Each year, the American Contact Dermatitis Society names an Allergen of the Year with the purpose of promoting greater awareness of a key allergen and its impact on patients. Often, the Allergen of the Year is an emerging allergen that may represent an underrecognized or novel cause of allergic contact dermatitis (ACD).In 2020, the American Contact Dermatitis Society chose isobornyl acrylate as the Allergen of the Year.¹ Not only has isobornyl acrylate been implicated in an epidemic of contact allergy to diabetic devices, but it also illustrates the challenges of investigating contact allergy to medical devices in general.

What Is Isobornyl Acrylate?

Isobornyl acrylate, also known as the isobornyl ester of acrylic acid, is a chemical used in glues, adhesives, coatings, sealants, inks, and paints. Similar to other acrylates, such as those involved in gel nail treatments, it is photopolymerizable; that is, when exposed to UV light, it can transform from a liquid monomer into a hard polymer, contributing to its utility as an adhesive. Prior to its recent implication in diabetic device contact allergy, isobornyl acrylate was not thought to be a common skin sensitizer. In a 2013 Dutch study of patients with acrylate allergy, only 1 of 14 patients with a contact allergy to other acrylates had a positive patch test reaction to isobornyl acrylate, which led the authors to conclude that adding it to their acrylate patch test series was not indicated.²

Isobornyl Acrylate in Diabetic Devices

Devices such as glucose monitoring systems and insulin pumps are used by millions of patients with diabetes worldwide. Not only are continuous glucose monitoring devices more convenient than self-monitoring of blood glucose, but they also are associated with a reduction in hemoglobin A_1c levels and lower risk for hypoglycemia.³ However, these devices have been increasingly recognized as a source of irritant contact dermatitis and ACD.

Early cases of contact allergy to isobornyl acrylate in diabetic devices were reported in 1995 when 2 Belgian patients using insulin pumps developed ACD.⁴ The patients had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum and other allergens including acrylates. In addition, patch testing with plastic scrapings from their insulin pumps also was positive, and it was determined that the glue affixing the needle to the plastic had diffused into the plastic. The patients were switched to insulin pumps produced by heat staking instead of glue, and their symptoms resolved. In retrospect, this case series may seem prescient, as it was written 2 decades before isobornyl acrylate became recognized as a widespread cause of ACD in users of diabetic devices. Admittedly, other acrylate components of the glue also were positive on patch testing in these patients, so it was not until much later that the focus turned more exclusively to isobornyl acrylate.⁴

Similar to the insulin pumps in the 1995 Belgian series, diffusion of glue to other parts of modern glucose sensors also appears to cause isobornyl acrylate contact allergy. This theory was supported by a 2017 study from Belgian and Swedish investigators in which gas chromatography–mass spectrometry was used to identify concentrations of isobornyl acrylate in various components of a popular continuous glucose monitoring sensor.⁵ The concentration of isobornyl acrylate was approximately 100-fold higher at the site where the top and bottom plastic components of the sensor were joined as compared to the adhesive patch in contact with the patient’s skin. Therefore, the adhesive patch itself was not the source of the isobornyl acrylate exposure; rather, the isobornyl acrylate diffused into the adhesive patch from the glue used to join the components of the sensor together.⁵ One ramification is that patients with diabetic device contact allergy can have a false-negative patch test result if the adhesive patch is tested by itself, whereas they may react to patch testing with the whole sensor or an acetonic extract thereof.

Frequency of Sensitization to Isobornyl Acrylate

It is difficult to estimate the frequency of sensitization to isobornyl acrylate among users of diabetic devices, in part because those with mild allergy may not seek medical treatment. Nevertheless, there are studies that demonstrate a high prevalence of sensitization among users with suspected allergy. In a 2019 Finnish study of 6567 patients using an isobornyl acrylate–containing glucose sensor, 63 were patch tested for suspected ACD.⁶ Of these 63 patients, 51 (81%) had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum. These findings were consistent with the original 2017 study from Belgium and Sweden, in which 10 of 11 (91%) patients who used an isobornyl acrylate–containing glucose sensor and had suspected contact allergy had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum compared to no positive reactions in the 14 control patients.⁵ Given that there are more than 1.5 million users of this isobornyl acrylate–containing glucose sensor across 46 countries,⁷ it requires no stretch of the imagination to understand why investigators refer to isobornyl acrylate allergy as an epidemic, even if only a small percentage of users are sensitized to the device.

The Journey to Discover Isobornyl Acrylate as a Culprit Allergen

Similar to the discoveries of radiography and penicillin, the discovery of isobornyl acrylate as a culprit allergen in a modern glucose sensor was purely accidental. In 2016, a 9-year-old boy with diabetes presented to a Belgian dermatology department with ACD to a glucose sensor.¹ A patch test nurse serendipitously applied isobornyl acrylate—0.01%, 0.05%, and 0.1% in petrolatum—which was not intended to be applied as part of the typical acrylate series. The only positive patch test reactions in this patient were to isobornyl acrylate at all 3 concentrations. This lucky error inspired isobornyl acrylate to be tested at multiple other dermatology departments in Europe in patients with ACD to their glucose sensors, leading to its discovery as a culprit allergen.¹

One challenge facing investigators was obtaining information and materials from the diabetic device industry. Medical device manufacturers are not required to disclose chemicals present in a device on its label.⁸ Therefore, for patients or investigators to determine whether a potential allergen is present in a given device, they must request that information from the manufacturer, which can be a time-consuming and frustrating effort. Luckily, investigators collaborated with one another, and Belgian investigators suggested that Swedish investigators performing chemical analyses on a glucose monitoring device should focus on isobornyl acrylate, which enabled its detection in an extract from the device.⁵

Testing for Isobornyl Acrylate Allergy in Your Clinic

Patients with suspected ACD to a diabetic device—insulin pump or glucose sensor—should be patch tested with isobornyl acrylate, in addition to other previously reported allergens. The vehicle typically is petrolatum, and the commonly tested concentration is 0.1%. Testing with lower concentrations such as 0.01% can result in false-negative reactions,⁹ and testing at higher concentrations such as 0.3% can result in irritant skin reactions.² Isobornyl acrylate 0.1% in petrolatum currently is available from one commercial allergen supplier (Chemotechnique Diagnostics). A positive patch test reaction to isobornyl acrylate 0.1% in petrolatum is shown in the Figure.

Management of Diabetic Device ACD

For patients with diabetic device ACD, there are several strategies that can reduce direct contact between the device and the patient’s skin. Methods that have been tried with varying success to allow patients to continue using their glucose sensors include barrier sprays (eg, Cavilon [3M], Silesse Skin Barrier [ConvaTec]); barrier pads (eg, Compeed [HRA Pharma], Surround skin protectors [Eakin], DuoDERM dressings [ConvaTec], Tegaderm dressings [3M]); and topical corticosteroids, calcineurin inhibitors, and phosphodiesterase 4 inhibitors. Nevertheless, a 2019 Finnish study showed that only 14 of 63 (22%) patients with ACD to their isobornyl acrylate–containing glucose sensor were able to continue using the device, with all 14 requiring use of a barrier agent. Despite using the barrier agent, 13 (93%) of these patients had residual dermatitis.⁶ There also is concern that use of barrier methods might hamper the proper functioning of glucose sensors and related devices.

Patients with known isobornyl acrylate contact allergy also may switch to a different diabetic device. A 2019 German study showed that in 5 patients with isobornyl acrylate ACD, none had reactions to the one particular system that has been shown by gas chromatography–mass spectrometry to not contain isobornyl acrylate.¹⁰ However, as a word of caution, the same device also has been associated with ACD^11,12 but has been resolved by using heat staking during the production process.¹³ As manufacturers update device components, identification of other isobornyl acrylate–free devices may require a degree of trial and error, as neither isobornyl acrylate nor any other potential allergen is listed on device labels.

Final Interpretation

Isobornyl acrylate is not a common sensitizer in general patch test populations but is a recently identified major culprit in ACD to diabetic devices. Patch testing with isobornyl acrylate 0.1% in petrolatum is not necessary in standard screening panels but should be considered in patients with suspected ACD to glucose sensors or insulin pumps. If a patient with ACD wants to continue to experience the convenience provided by a diabetic device, options include using topical steroids or barrier agents and/or changing the brand of the diabetic device, though none of these methods are foolproof. Hopefully, the identification of isobornyl acrylate as a culprit allergen will help to improve the lives of patients who use diabetic devices worldwide.

Each year, the American Contact Dermatitis Society names an Allergen of the Year with the purpose of promoting greater awareness of a key allergen and its impact on patients. Often, the Allergen of the Year is an emerging allergen that may represent an underrecognized or novel cause of allergic contact dermatitis (ACD).In 2020, the American Contact Dermatitis Society chose isobornyl acrylate as the Allergen of the Year.¹ Not only has isobornyl acrylate been implicated in an epidemic of contact allergy to diabetic devices, but it also illustrates the challenges of investigating contact allergy to medical devices in general.

What Is Isobornyl Acrylate?

Isobornyl acrylate, also known as the isobornyl ester of acrylic acid, is a chemical used in glues, adhesives, coatings, sealants, inks, and paints. Similar to other acrylates, such as those involved in gel nail treatments, it is photopolymerizable; that is, when exposed to UV light, it can transform from a liquid monomer into a hard polymer, contributing to its utility as an adhesive. Prior to its recent implication in diabetic device contact allergy, isobornyl acrylate was not thought to be a common skin sensitizer. In a 2013 Dutch study of patients with acrylate allergy, only 1 of 14 patients with a contact allergy to other acrylates had a positive patch test reaction to isobornyl acrylate, which led the authors to conclude that adding it to their acrylate patch test series was not indicated.²

Isobornyl Acrylate in Diabetic Devices

Devices such as glucose monitoring systems and insulin pumps are used by millions of patients with diabetes worldwide. Not only are continuous glucose monitoring devices more convenient than self-monitoring of blood glucose, but they also are associated with a reduction in hemoglobin A_1c levels and lower risk for hypoglycemia.³ However, these devices have been increasingly recognized as a source of irritant contact dermatitis and ACD.

Early cases of contact allergy to isobornyl acrylate in diabetic devices were reported in 1995 when 2 Belgian patients using insulin pumps developed ACD.⁴ The patients had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum and other allergens including acrylates. In addition, patch testing with plastic scrapings from their insulin pumps also was positive, and it was determined that the glue affixing the needle to the plastic had diffused into the plastic. The patients were switched to insulin pumps produced by heat staking instead of glue, and their symptoms resolved. In retrospect, this case series may seem prescient, as it was written 2 decades before isobornyl acrylate became recognized as a widespread cause of ACD in users of diabetic devices. Admittedly, other acrylate components of the glue also were positive on patch testing in these patients, so it was not until much later that the focus turned more exclusively to isobornyl acrylate.⁴

Similar to the insulin pumps in the 1995 Belgian series, diffusion of glue to other parts of modern glucose sensors also appears to cause isobornyl acrylate contact allergy. This theory was supported by a 2017 study from Belgian and Swedish investigators in which gas chromatography–mass spectrometry was used to identify concentrations of isobornyl acrylate in various components of a popular continuous glucose monitoring sensor.⁵ The concentration of isobornyl acrylate was approximately 100-fold higher at the site where the top and bottom plastic components of the sensor were joined as compared to the adhesive patch in contact with the patient’s skin. Therefore, the adhesive patch itself was not the source of the isobornyl acrylate exposure; rather, the isobornyl acrylate diffused into the adhesive patch from the glue used to join the components of the sensor together.⁵ One ramification is that patients with diabetic device contact allergy can have a false-negative patch test result if the adhesive patch is tested by itself, whereas they may react to patch testing with the whole sensor or an acetonic extract thereof.

Frequency of Sensitization to Isobornyl Acrylate

It is difficult to estimate the frequency of sensitization to isobornyl acrylate among users of diabetic devices, in part because those with mild allergy may not seek medical treatment. Nevertheless, there are studies that demonstrate a high prevalence of sensitization among users with suspected allergy. In a 2019 Finnish study of 6567 patients using an isobornyl acrylate–containing glucose sensor, 63 were patch tested for suspected ACD.⁶ Of these 63 patients, 51 (81%) had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum. These findings were consistent with the original 2017 study from Belgium and Sweden, in which 10 of 11 (91%) patients who used an isobornyl acrylate–containing glucose sensor and had suspected contact allergy had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum compared to no positive reactions in the 14 control patients.⁵ Given that there are more than 1.5 million users of this isobornyl acrylate–containing glucose sensor across 46 countries,⁷ it requires no stretch of the imagination to understand why investigators refer to isobornyl acrylate allergy as an epidemic, even if only a small percentage of users are sensitized to the device.

The Journey to Discover Isobornyl Acrylate as a Culprit Allergen

Similar to the discoveries of radiography and penicillin, the discovery of isobornyl acrylate as a culprit allergen in a modern glucose sensor was purely accidental. In 2016, a 9-year-old boy with diabetes presented to a Belgian dermatology department with ACD to a glucose sensor.¹ A patch test nurse serendipitously applied isobornyl acrylate—0.01%, 0.05%, and 0.1% in petrolatum—which was not intended to be applied as part of the typical acrylate series. The only positive patch test reactions in this patient were to isobornyl acrylate at all 3 concentrations. This lucky error inspired isobornyl acrylate to be tested at multiple other dermatology departments in Europe in patients with ACD to their glucose sensors, leading to its discovery as a culprit allergen.¹

One challenge facing investigators was obtaining information and materials from the diabetic device industry. Medical device manufacturers are not required to disclose chemicals present in a device on its label.⁸ Therefore, for patients or investigators to determine whether a potential allergen is present in a given device, they must request that information from the manufacturer, which can be a time-consuming and frustrating effort. Luckily, investigators collaborated with one another, and Belgian investigators suggested that Swedish investigators performing chemical analyses on a glucose monitoring device should focus on isobornyl acrylate, which enabled its detection in an extract from the device.⁵

Testing for Isobornyl Acrylate Allergy in Your Clinic

Patients with suspected ACD to a diabetic device—insulin pump or glucose sensor—should be patch tested with isobornyl acrylate, in addition to other previously reported allergens. The vehicle typically is petrolatum, and the commonly tested concentration is 0.1%. Testing with lower concentrations such as 0.01% can result in false-negative reactions,⁹ and testing at higher concentrations such as 0.3% can result in irritant skin reactions.² Isobornyl acrylate 0.1% in petrolatum currently is available from one commercial allergen supplier (Chemotechnique Diagnostics). A positive patch test reaction to isobornyl acrylate 0.1% in petrolatum is shown in the Figure.

Management of Diabetic Device ACD

For patients with diabetic device ACD, there are several strategies that can reduce direct contact between the device and the patient’s skin. Methods that have been tried with varying success to allow patients to continue using their glucose sensors include barrier sprays (eg, Cavilon [3M], Silesse Skin Barrier [ConvaTec]); barrier pads (eg, Compeed [HRA Pharma], Surround skin protectors [Eakin], DuoDERM dressings [ConvaTec], Tegaderm dressings [3M]); and topical corticosteroids, calcineurin inhibitors, and phosphodiesterase 4 inhibitors. Nevertheless, a 2019 Finnish study showed that only 14 of 63 (22%) patients with ACD to their isobornyl acrylate–containing glucose sensor were able to continue using the device, with all 14 requiring use of a barrier agent. Despite using the barrier agent, 13 (93%) of these patients had residual dermatitis.⁶ There also is concern that use of barrier methods might hamper the proper functioning of glucose sensors and related devices.

Patients with known isobornyl acrylate contact allergy also may switch to a different diabetic device. A 2019 German study showed that in 5 patients with isobornyl acrylate ACD, none had reactions to the one particular system that has been shown by gas chromatography–mass spectrometry to not contain isobornyl acrylate.¹⁰ However, as a word of caution, the same device also has been associated with ACD^11,12 but has been resolved by using heat staking during the production process.¹³ As manufacturers update device components, identification of other isobornyl acrylate–free devices may require a degree of trial and error, as neither isobornyl acrylate nor any other potential allergen is listed on device labels.

Final Interpretation

Isobornyl acrylate is not a common sensitizer in general patch test populations but is a recently identified major culprit in ACD to diabetic devices. Patch testing with isobornyl acrylate 0.1% in petrolatum is not necessary in standard screening panels but should be considered in patients with suspected ACD to glucose sensors or insulin pumps. If a patient with ACD wants to continue to experience the convenience provided by a diabetic device, options include using topical steroids or barrier agents and/or changing the brand of the diabetic device, though none of these methods are foolproof. Hopefully, the identification of isobornyl acrylate as a culprit allergen will help to improve the lives of patients who use diabetic devices worldwide.

Each year, the American Contact Dermatitis Society names an Allergen of the Year with the purpose of promoting greater awareness of a key allergen and its impact on patients. Often, the Allergen of the Year is an emerging allergen that may represent an underrecognized or novel cause of allergic contact dermatitis (ACD).In 2020, the American Contact Dermatitis Society chose isobornyl acrylate as the Allergen of the Year.¹ Not only has isobornyl acrylate been implicated in an epidemic of contact allergy to diabetic devices, but it also illustrates the challenges of investigating contact allergy to medical devices in general.

What Is Isobornyl Acrylate?

Isobornyl acrylate, also known as the isobornyl ester of acrylic acid, is a chemical used in glues, adhesives, coatings, sealants, inks, and paints. Similar to other acrylates, such as those involved in gel nail treatments, it is photopolymerizable; that is, when exposed to UV light, it can transform from a liquid monomer into a hard polymer, contributing to its utility as an adhesive. Prior to its recent implication in diabetic device contact allergy, isobornyl acrylate was not thought to be a common skin sensitizer. In a 2013 Dutch study of patients with acrylate allergy, only 1 of 14 patients with a contact allergy to other acrylates had a positive patch test reaction to isobornyl acrylate, which led the authors to conclude that adding it to their acrylate patch test series was not indicated.²

Isobornyl Acrylate in Diabetic Devices

Devices such as glucose monitoring systems and insulin pumps are used by millions of patients with diabetes worldwide. Not only are continuous glucose monitoring devices more convenient than self-monitoring of blood glucose, but they also are associated with a reduction in hemoglobin A_1c levels and lower risk for hypoglycemia.³ However, these devices have been increasingly recognized as a source of irritant contact dermatitis and ACD.

Early cases of contact allergy to isobornyl acrylate in diabetic devices were reported in 1995 when 2 Belgian patients using insulin pumps developed ACD.⁴ The patients had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum and other allergens including acrylates. In addition, patch testing with plastic scrapings from their insulin pumps also was positive, and it was determined that the glue affixing the needle to the plastic had diffused into the plastic. The patients were switched to insulin pumps produced by heat staking instead of glue, and their symptoms resolved. In retrospect, this case series may seem prescient, as it was written 2 decades before isobornyl acrylate became recognized as a widespread cause of ACD in users of diabetic devices. Admittedly, other acrylate components of the glue also were positive on patch testing in these patients, so it was not until much later that the focus turned more exclusively to isobornyl acrylate.⁴

Similar to the insulin pumps in the 1995 Belgian series, diffusion of glue to other parts of modern glucose sensors also appears to cause isobornyl acrylate contact allergy. This theory was supported by a 2017 study from Belgian and Swedish investigators in which gas chromatography–mass spectrometry was used to identify concentrations of isobornyl acrylate in various components of a popular continuous glucose monitoring sensor.⁵ The concentration of isobornyl acrylate was approximately 100-fold higher at the site where the top and bottom plastic components of the sensor were joined as compared to the adhesive patch in contact with the patient’s skin. Therefore, the adhesive patch itself was not the source of the isobornyl acrylate exposure; rather, the isobornyl acrylate diffused into the adhesive patch from the glue used to join the components of the sensor together.⁵ One ramification is that patients with diabetic device contact allergy can have a false-negative patch test result if the adhesive patch is tested by itself, whereas they may react to patch testing with the whole sensor or an acetonic extract thereof.

Frequency of Sensitization to Isobornyl Acrylate

It is difficult to estimate the frequency of sensitization to isobornyl acrylate among users of diabetic devices, in part because those with mild allergy may not seek medical treatment. Nevertheless, there are studies that demonstrate a high prevalence of sensitization among users with suspected allergy. In a 2019 Finnish study of 6567 patients using an isobornyl acrylate–containing glucose sensor, 63 were patch tested for suspected ACD.⁶ Of these 63 patients, 51 (81%) had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum. These findings were consistent with the original 2017 study from Belgium and Sweden, in which 10 of 11 (91%) patients who used an isobornyl acrylate–containing glucose sensor and had suspected contact allergy had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum compared to no positive reactions in the 14 control patients.⁵ Given that there are more than 1.5 million users of this isobornyl acrylate–containing glucose sensor across 46 countries,⁷ it requires no stretch of the imagination to understand why investigators refer to isobornyl acrylate allergy as an epidemic, even if only a small percentage of users are sensitized to the device.

The Journey to Discover Isobornyl Acrylate as a Culprit Allergen

Similar to the discoveries of radiography and penicillin, the discovery of isobornyl acrylate as a culprit allergen in a modern glucose sensor was purely accidental. In 2016, a 9-year-old boy with diabetes presented to a Belgian dermatology department with ACD to a glucose sensor.¹ A patch test nurse serendipitously applied isobornyl acrylate—0.01%, 0.05%, and 0.1% in petrolatum—which was not intended to be applied as part of the typical acrylate series. The only positive patch test reactions in this patient were to isobornyl acrylate at all 3 concentrations. This lucky error inspired isobornyl acrylate to be tested at multiple other dermatology departments in Europe in patients with ACD to their glucose sensors, leading to its discovery as a culprit allergen.¹

One challenge facing investigators was obtaining information and materials from the diabetic device industry. Medical device manufacturers are not required to disclose chemicals present in a device on its label.⁸ Therefore, for patients or investigators to determine whether a potential allergen is present in a given device, they must request that information from the manufacturer, which can be a time-consuming and frustrating effort. Luckily, investigators collaborated with one another, and Belgian investigators suggested that Swedish investigators performing chemical analyses on a glucose monitoring device should focus on isobornyl acrylate, which enabled its detection in an extract from the device.⁵

Testing for Isobornyl Acrylate Allergy in Your Clinic

Patients with suspected ACD to a diabetic device—insulin pump or glucose sensor—should be patch tested with isobornyl acrylate, in addition to other previously reported allergens. The vehicle typically is petrolatum, and the commonly tested concentration is 0.1%. Testing with lower concentrations such as 0.01% can result in false-negative reactions,⁹ and testing at higher concentrations such as 0.3% can result in irritant skin reactions.² Isobornyl acrylate 0.1% in petrolatum currently is available from one commercial allergen supplier (Chemotechnique Diagnostics). A positive patch test reaction to isobornyl acrylate 0.1% in petrolatum is shown in the Figure.

Management of Diabetic Device ACD

For patients with diabetic device ACD, there are several strategies that can reduce direct contact between the device and the patient’s skin. Methods that have been tried with varying success to allow patients to continue using their glucose sensors include barrier sprays (eg, Cavilon [3M], Silesse Skin Barrier [ConvaTec]); barrier pads (eg, Compeed [HRA Pharma], Surround skin protectors [Eakin], DuoDERM dressings [ConvaTec], Tegaderm dressings [3M]); and topical corticosteroids, calcineurin inhibitors, and phosphodiesterase 4 inhibitors. Nevertheless, a 2019 Finnish study showed that only 14 of 63 (22%) patients with ACD to their isobornyl acrylate–containing glucose sensor were able to continue using the device, with all 14 requiring use of a barrier agent. Despite using the barrier agent, 13 (93%) of these patients had residual dermatitis.⁶ There also is concern that use of barrier methods might hamper the proper functioning of glucose sensors and related devices.

Patients with known isobornyl acrylate contact allergy also may switch to a different diabetic device. A 2019 German study showed that in 5 patients with isobornyl acrylate ACD, none had reactions to the one particular system that has been shown by gas chromatography–mass spectrometry to not contain isobornyl acrylate.¹⁰ However, as a word of caution, the same device also has been associated with ACD^11,12 but has been resolved by using heat staking during the production process.¹³ As manufacturers update device components, identification of other isobornyl acrylate–free devices may require a degree of trial and error, as neither isobornyl acrylate nor any other potential allergen is listed on device labels.

Final Interpretation

Isobornyl acrylate is not a common sensitizer in general patch test populations but is a recently identified major culprit in ACD to diabetic devices. Patch testing with isobornyl acrylate 0.1% in petrolatum is not necessary in standard screening panels but should be considered in patients with suspected ACD to glucose sensors or insulin pumps. If a patient with ACD wants to continue to experience the convenience provided by a diabetic device, options include using topical steroids or barrier agents and/or changing the brand of the diabetic device, though none of these methods are foolproof. Hopefully, the identification of isobornyl acrylate as a culprit allergen will help to improve the lives of patients who use diabetic devices worldwide.

Practice Gap

Anxiety is common in patients undergoing surgery with general anesthesia and may be exacerbated in patients undergoing dermatologic surgery with local anesthesia. Apprehension might be worse for nail surgery patients because the nail unit is highly innervated and vascular. Many patients fear the anesthetic injections, and there often is pain postoperatively. Perioperative anxiety correlates with increased postoperative pain,¹ analgesic use,² and delayed recovery.³ Several alternatives have been proposed to decrease perioperative anxiety, including nonpharmacologic interventions such as using educational videos, personalized music, hand holding, art activities, and virtual reality, as well as pharmacologic interventions such as benzodiazepines. However, these techniques have not been well studied for nail surgery.

The Technique

Patients generally are anxious about nail surgery secondary to the pain associated with the local anesthetic infiltration; hence, it is crucial to decrease anxiety during this initial step. In our practice, we provide patients with a palm-sized stress ball made of closed-cell polyurethane foam rubber before surgery. Patients are then instructed to hold the stress ball with the free hand and squeeze it whenever they feel anxious or when they feel any discomfort related to the procedure (Figure). A variety of balls can be bought for less than $1 each, thus making it a cost-effective option.

Practice Implications

Holding a stress ball has been found to reduce both pain and anxiety in patients undergoing conscious surgery.⁴ Furthermore, squeezing a stress ball perioperatively may increase feelings of empowerment, given that patients have direct control over the object, which in turn may have a positive effect on anxiety and patient satisfaction without interfering with the surgical procedure.⁵ Holding a stress ball is a safe, widely accessible, and inexpensive technique that may aid in decreasing patients’ anxiety related to nail surgery. Nonetheless, controlled clinical trials assessing the efficacy of this method in reducing anxiety related to nail surgery are needed to determine its benefit compared to other methods.

Practice Gap

Anxiety is common in patients undergoing surgery with general anesthesia and may be exacerbated in patients undergoing dermatologic surgery with local anesthesia. Apprehension might be worse for nail surgery patients because the nail unit is highly innervated and vascular. Many patients fear the anesthetic injections, and there often is pain postoperatively. Perioperative anxiety correlates with increased postoperative pain,¹ analgesic use,² and delayed recovery.³ Several alternatives have been proposed to decrease perioperative anxiety, including nonpharmacologic interventions such as using educational videos, personalized music, hand holding, art activities, and virtual reality, as well as pharmacologic interventions such as benzodiazepines. However, these techniques have not been well studied for nail surgery.

The Technique

Patients generally are anxious about nail surgery secondary to the pain associated with the local anesthetic infiltration; hence, it is crucial to decrease anxiety during this initial step. In our practice, we provide patients with a palm-sized stress ball made of closed-cell polyurethane foam rubber before surgery. Patients are then instructed to hold the stress ball with the free hand and squeeze it whenever they feel anxious or when they feel any discomfort related to the procedure (Figure). A variety of balls can be bought for less than $1 each, thus making it a cost-effective option.

Practice Implications

Holding a stress ball has been found to reduce both pain and anxiety in patients undergoing conscious surgery.⁴ Furthermore, squeezing a stress ball perioperatively may increase feelings of empowerment, given that patients have direct control over the object, which in turn may have a positive effect on anxiety and patient satisfaction without interfering with the surgical procedure.⁵ Holding a stress ball is a safe, widely accessible, and inexpensive technique that may aid in decreasing patients’ anxiety related to nail surgery. Nonetheless, controlled clinical trials assessing the efficacy of this method in reducing anxiety related to nail surgery are needed to determine its benefit compared to other methods.

Practice Gap

Anxiety is common in patients undergoing surgery with general anesthesia and may be exacerbated in patients undergoing dermatologic surgery with local anesthesia. Apprehension might be worse for nail surgery patients because the nail unit is highly innervated and vascular. Many patients fear the anesthetic injections, and there often is pain postoperatively. Perioperative anxiety correlates with increased postoperative pain,¹ analgesic use,² and delayed recovery.³ Several alternatives have been proposed to decrease perioperative anxiety, including nonpharmacologic interventions such as using educational videos, personalized music, hand holding, art activities, and virtual reality, as well as pharmacologic interventions such as benzodiazepines. However, these techniques have not been well studied for nail surgery.

The Technique

Patients generally are anxious about nail surgery secondary to the pain associated with the local anesthetic infiltration; hence, it is crucial to decrease anxiety during this initial step. In our practice, we provide patients with a palm-sized stress ball made of closed-cell polyurethane foam rubber before surgery. Patients are then instructed to hold the stress ball with the free hand and squeeze it whenever they feel anxious or when they feel any discomfort related to the procedure (Figure). A variety of balls can be bought for less than $1 each, thus making it a cost-effective option.

Practice Implications

Holding a stress ball has been found to reduce both pain and anxiety in patients undergoing conscious surgery.⁴ Furthermore, squeezing a stress ball perioperatively may increase feelings of empowerment, given that patients have direct control over the object, which in turn may have a positive effect on anxiety and patient satisfaction without interfering with the surgical procedure.⁵ Holding a stress ball is a safe, widely accessible, and inexpensive technique that may aid in decreasing patients’ anxiety related to nail surgery. Nonetheless, controlled clinical trials assessing the efficacy of this method in reducing anxiety related to nail surgery are needed to determine its benefit compared to other methods.

Dermatologic treatment of patients with skin of color offers specific challenges. Studies have reported structural, morphologic, and physiologic distinctions among different ethnic groups,¹ which may account for distinct clinical presentations of skin disease seen in patients with skin of color. Patients with skin of color are at increased risk for specific dermatologic conditions, such as postinflammatory hyperpigmentation, keloid development, and central centrifugal cicatricial alopecia.^2,3 Furthermore, although skin cancer is less prevalent in patients with skin of color, it often presents at a more advanced stage and with a worse prognosis compared to white patients.⁴

Individuals with skin of color make up the majority of the world’s population and a rapidly expanding portion of the US population. By the year 2044, more than half of all Americans are projected to belong to an ethnic group that is currently a minority. By 2060, the population of citizens identifying with 2 or more races will increase by 226%, the Asian population is projected to grow by 128%, the Hispanic population will increase by 115%, and the black population will increase by 42%.⁵ The racial and ethnic composition of the United States is evolving, and dermatologic care must evolve accordingly to address patients’ unique concerns. It is essential for future dermatologists to be knowledgeable about dermatologic conditions presenting in patients of various ethnic backgrounds.

Prior studies have demonstrated the need for increased exposure, education, and training in diseases pertaining to skin of color in US dermatology residency programs.^6-8 The aim of this study was to assess if dermatologists in-training feel that their residency curriculum sufficiently educates them on the needs of patients with skin of color.

Methods

A 10-question anonymous survey was emailed to 109 dermatology residency programs to evaluate the attitudes of dermatology residents about their exposure to patients with skin of color and their skin-of-color curriculum. The study included individuals 18 years or older who were current residents in a dermatology program accredited by the Accreditation Council for Graduate Medical Education. Responses were measured on a 1 to 3 Likert scale, ranging from agree, neutral, and disagree. Data were analyzed using the Fisher exact test, and the statistical significance was set at P<.05.

Results

Forty-three dermatology residents completed the survey. Respondents self-selected their regions, with 8 (19%) from the Northeast (NE), 7 (16%) from the Southeast (SE), 12 (28%) from the Midwest (MW), 8 (19%) from the Southwest (SW), and 8 (18%) from the Northwest (NW)(Table 1). Overall, 31 (72%) respondents agreed that their practice treats a diverse patient population. Respondents who agreed most often were from the NE, SE, and SW. Less than two-thirds of respondents from the MW agreed, and only half of respondents from the NW agreed (Table 2). Although 37% of all respondents agreed that a dedicated multiethnic skin clinic is important for residents, 5 (63%) NE residents disagreed with this statement compared to 5 (42%) MW residents and 5 (63%) NW residents who agreed (P<.005). Overall, 39 (91%) respondents agreed that dedicated lectures on skin conditions in skin of color patients are important to gain competence in treating patients. Only 4 respondents were neutral to this question, 2 (17%) MW residents and 2 (25%) SW residents. When asked if reading textbook chapters on multiethnic skin is important to gain competence, 36 (83%) respondents agreed. Two respondents disagreed, 1 (13%) from the NE and 1 (8%) from the MW. Overall, 23% of respondents agreed that a rotation dedicated to skin of color is important to build competency. There was a significant difference in responses between the NE and MW (P=.032) and between the NE and NW (P=.019). Furthermore, 19 (44%) respondents agreed that having a faculty member or departmental expert is important for residents to gain competence in treating conditions affecting skin of color. Again, there was a significant difference in responses between the NE and MW (P=.003) and between the SE and MW (P=.009).

When asked the number of hours of lecture per month necessary to gain competence in conditions affecting patients with skin of color, 67% agreed that 1 to 5 hours was sufficient (Table 3). There were significant differences in the responses between the NE and SE (P=.024) and the SE and MW (P=.007). Of all respondents, 53% reported 1 to 5 months of clinical training are needed to gain competence in treating conditions affecting patients with skin of color, with significant differences in responses between the NE and MW (P<.001), the NE and SW (P=.019), and the SE and MW (P=.015)(Table 4).

Comment

Responses varied by practicing region. Less ethnically diverse regions, such as the MW and NW, were more likely to agree that dedicated clinics and rotations are important to gain competence compared to more ethnically diverse regions such as the NE, SE, and SW. Overall, more residents reported that dedicated lectures and textbook chapters were important to gain competency compared to dedicated clinics or rotations.

Although interactive lectures and textbook readings are important for obtaining a foundational understanding of dermatologic disease, they cannot substitute for clinical interactions and hands-on experience treating patients with skin of color.⁹ Not only do clinical interactions encourage independent reading and the study of encountered diagnoses, but intercommunication with patients may have a more profound and lasting impact on residents’ education.

Different regions of the United States have varying distributions of patients with skin of color, and dermatology residency program training reflects these disparities.⁶ In areas of less diversity, dermatology residents examine, diagnose, and treat substantially fewer patients with skin of color. The desire for more diverse training supports the prior findings of Nijhawan et al⁶ and is reflected in the responses we received in our study, whereby residents from the less ethnically diversified regions of the MW and NW were more likely to agree that clinics and rotations were necessary for training in preparation to sufficiently address the needs of patients with skin of color.

One way to compensate for the lack of ethnic diversity encountered in areas such as the MW and NW would be to develop educational programs featuring experts on skin of color.⁶ These specialists would not only train dermatology residents in areas of the country currently lacking ethnic diversity but also expand the expertise for treating patients with skin of color. Additionally, dedicated multiethnic skin clinics and externships devoted solely to treating patients with skin of color could be encouraged for residency training.⁶ Finally, community outreach through volunteer clinics may provide residents exposure to patients with skin of color seeking dermatologic care.¹⁰

This study was limited by the small number of respondents, but we were able to extract important trends and data from the collected responses. It is possible that respondents felt strongly about topics involving patients with skin of color, and the results were skewed to reflect individual bias. Additional limitations included not asking respondents for program names and population density (eg, urban, suburban, rural). Future studies should be directed toward analyzing how the diversity of the local population influences training in patients with skin of color, comparing program directors’ perceptions with residents’ perceptions on training in skin of color, and assessing patient perception of residents’ training in skin of color.

Conclusion

In the last decade it has become increasingly apparent that the US population is diversifying and that patients with skin of color will comprise a substantial proportion of the future population,^8,11 which emphasizes the need for dermatology residency programs to ensure that residents receive adequate training and exposure to patients with skin of color as well as the distinct skin diseases seen more commonly in these populations.¹²

Dermatologic treatment of patients with skin of color offers specific challenges. Studies have reported structural, morphologic, and physiologic distinctions among different ethnic groups,¹ which may account for distinct clinical presentations of skin disease seen in patients with skin of color. Patients with skin of color are at increased risk for specific dermatologic conditions, such as postinflammatory hyperpigmentation, keloid development, and central centrifugal cicatricial alopecia.^2,3 Furthermore, although skin cancer is less prevalent in patients with skin of color, it often presents at a more advanced stage and with a worse prognosis compared to white patients.⁴

Individuals with skin of color make up the majority of the world’s population and a rapidly expanding portion of the US population. By the year 2044, more than half of all Americans are projected to belong to an ethnic group that is currently a minority. By 2060, the population of citizens identifying with 2 or more races will increase by 226%, the Asian population is projected to grow by 128%, the Hispanic population will increase by 115%, and the black population will increase by 42%.⁵ The racial and ethnic composition of the United States is evolving, and dermatologic care must evolve accordingly to address patients’ unique concerns. It is essential for future dermatologists to be knowledgeable about dermatologic conditions presenting in patients of various ethnic backgrounds.

Prior studies have demonstrated the need for increased exposure, education, and training in diseases pertaining to skin of color in US dermatology residency programs.^6-8 The aim of this study was to assess if dermatologists in-training feel that their residency curriculum sufficiently educates them on the needs of patients with skin of color.

Methods

A 10-question anonymous survey was emailed to 109 dermatology residency programs to evaluate the attitudes of dermatology residents about their exposure to patients with skin of color and their skin-of-color curriculum. The study included individuals 18 years or older who were current residents in a dermatology program accredited by the Accreditation Council for Graduate Medical Education. Responses were measured on a 1 to 3 Likert scale, ranging from agree, neutral, and disagree. Data were analyzed using the Fisher exact test, and the statistical significance was set at P<.05.

Results

Forty-three dermatology residents completed the survey. Respondents self-selected their regions, with 8 (19%) from the Northeast (NE), 7 (16%) from the Southeast (SE), 12 (28%) from the Midwest (MW), 8 (19%) from the Southwest (SW), and 8 (18%) from the Northwest (NW)(Table 1). Overall, 31 (72%) respondents agreed that their practice treats a diverse patient population. Respondents who agreed most often were from the NE, SE, and SW. Less than two-thirds of respondents from the MW agreed, and only half of respondents from the NW agreed (Table 2). Although 37% of all respondents agreed that a dedicated multiethnic skin clinic is important for residents, 5 (63%) NE residents disagreed with this statement compared to 5 (42%) MW residents and 5 (63%) NW residents who agreed (P<.005). Overall, 39 (91%) respondents agreed that dedicated lectures on skin conditions in skin of color patients are important to gain competence in treating patients. Only 4 respondents were neutral to this question, 2 (17%) MW residents and 2 (25%) SW residents. When asked if reading textbook chapters on multiethnic skin is important to gain competence, 36 (83%) respondents agreed. Two respondents disagreed, 1 (13%) from the NE and 1 (8%) from the MW. Overall, 23% of respondents agreed that a rotation dedicated to skin of color is important to build competency. There was a significant difference in responses between the NE and MW (P=.032) and between the NE and NW (P=.019). Furthermore, 19 (44%) respondents agreed that having a faculty member or departmental expert is important for residents to gain competence in treating conditions affecting skin of color. Again, there was a significant difference in responses between the NE and MW (P=.003) and between the SE and MW (P=.009).

When asked the number of hours of lecture per month necessary to gain competence in conditions affecting patients with skin of color, 67% agreed that 1 to 5 hours was sufficient (Table 3). There were significant differences in the responses between the NE and SE (P=.024) and the SE and MW (P=.007). Of all respondents, 53% reported 1 to 5 months of clinical training are needed to gain competence in treating conditions affecting patients with skin of color, with significant differences in responses between the NE and MW (P<.001), the NE and SW (P=.019), and the SE and MW (P=.015)(Table 4).

Comment

Responses varied by practicing region. Less ethnically diverse regions, such as the MW and NW, were more likely to agree that dedicated clinics and rotations are important to gain competence compared to more ethnically diverse regions such as the NE, SE, and SW. Overall, more residents reported that dedicated lectures and textbook chapters were important to gain competency compared to dedicated clinics or rotations.

Although interactive lectures and textbook readings are important for obtaining a foundational understanding of dermatologic disease, they cannot substitute for clinical interactions and hands-on experience treating patients with skin of color.⁹ Not only do clinical interactions encourage independent reading and the study of encountered diagnoses, but intercommunication with patients may have a more profound and lasting impact on residents’ education.

Different regions of the United States have varying distributions of patients with skin of color, and dermatology residency program training reflects these disparities.⁶ In areas of less diversity, dermatology residents examine, diagnose, and treat substantially fewer patients with skin of color. The desire for more diverse training supports the prior findings of Nijhawan et al⁶ and is reflected in the responses we received in our study, whereby residents from the less ethnically diversified regions of the MW and NW were more likely to agree that clinics and rotations were necessary for training in preparation to sufficiently address the needs of patients with skin of color.

One way to compensate for the lack of ethnic diversity encountered in areas such as the MW and NW would be to develop educational programs featuring experts on skin of color.⁶ These specialists would not only train dermatology residents in areas of the country currently lacking ethnic diversity but also expand the expertise for treating patients with skin of color. Additionally, dedicated multiethnic skin clinics and externships devoted solely to treating patients with skin of color could be encouraged for residency training.⁶ Finally, community outreach through volunteer clinics may provide residents exposure to patients with skin of color seeking dermatologic care.¹⁰

This study was limited by the small number of respondents, but we were able to extract important trends and data from the collected responses. It is possible that respondents felt strongly about topics involving patients with skin of color, and the results were skewed to reflect individual bias. Additional limitations included not asking respondents for program names and population density (eg, urban, suburban, rural). Future studies should be directed toward analyzing how the diversity of the local population influences training in patients with skin of color, comparing program directors’ perceptions with residents’ perceptions on training in skin of color, and assessing patient perception of residents’ training in skin of color.

Conclusion

In the last decade it has become increasingly apparent that the US population is diversifying and that patients with skin of color will comprise a substantial proportion of the future population,^8,11 which emphasizes the need for dermatology residency programs to ensure that residents receive adequate training and exposure to patients with skin of color as well as the distinct skin diseases seen more commonly in these populations.¹²

Dermatologic treatment of patients with skin of color offers specific challenges. Studies have reported structural, morphologic, and physiologic distinctions among different ethnic groups,¹ which may account for distinct clinical presentations of skin disease seen in patients with skin of color. Patients with skin of color are at increased risk for specific dermatologic conditions, such as postinflammatory hyperpigmentation, keloid development, and central centrifugal cicatricial alopecia.^2,3 Furthermore, although skin cancer is less prevalent in patients with skin of color, it often presents at a more advanced stage and with a worse prognosis compared to white patients.⁴

Individuals with skin of color make up the majority of the world’s population and a rapidly expanding portion of the US population. By the year 2044, more than half of all Americans are projected to belong to an ethnic group that is currently a minority. By 2060, the population of citizens identifying with 2 or more races will increase by 226%, the Asian population is projected to grow by 128%, the Hispanic population will increase by 115%, and the black population will increase by 42%.⁵ The racial and ethnic composition of the United States is evolving, and dermatologic care must evolve accordingly to address patients’ unique concerns. It is essential for future dermatologists to be knowledgeable about dermatologic conditions presenting in patients of various ethnic backgrounds.

Prior studies have demonstrated the need for increased exposure, education, and training in diseases pertaining to skin of color in US dermatology residency programs.^6-8 The aim of this study was to assess if dermatologists in-training feel that their residency curriculum sufficiently educates them on the needs of patients with skin of color.

Methods

A 10-question anonymous survey was emailed to 109 dermatology residency programs to evaluate the attitudes of dermatology residents about their exposure to patients with skin of color and their skin-of-color curriculum. The study included individuals 18 years or older who were current residents in a dermatology program accredited by the Accreditation Council for Graduate Medical Education. Responses were measured on a 1 to 3 Likert scale, ranging from agree, neutral, and disagree. Data were analyzed using the Fisher exact test, and the statistical significance was set at P<.05.

Results

Forty-three dermatology residents completed the survey. Respondents self-selected their regions, with 8 (19%) from the Northeast (NE), 7 (16%) from the Southeast (SE), 12 (28%) from the Midwest (MW), 8 (19%) from the Southwest (SW), and 8 (18%) from the Northwest (NW)(Table 1). Overall, 31 (72%) respondents agreed that their practice treats a diverse patient population. Respondents who agreed most often were from the NE, SE, and SW. Less than two-thirds of respondents from the MW agreed, and only half of respondents from the NW agreed (Table 2). Although 37% of all respondents agreed that a dedicated multiethnic skin clinic is important for residents, 5 (63%) NE residents disagreed with this statement compared to 5 (42%) MW residents and 5 (63%) NW residents who agreed (P<.005). Overall, 39 (91%) respondents agreed that dedicated lectures on skin conditions in skin of color patients are important to gain competence in treating patients. Only 4 respondents were neutral to this question, 2 (17%) MW residents and 2 (25%) SW residents. When asked if reading textbook chapters on multiethnic skin is important to gain competence, 36 (83%) respondents agreed. Two respondents disagreed, 1 (13%) from the NE and 1 (8%) from the MW. Overall, 23% of respondents agreed that a rotation dedicated to skin of color is important to build competency. There was a significant difference in responses between the NE and MW (P=.032) and between the NE and NW (P=.019). Furthermore, 19 (44%) respondents agreed that having a faculty member or departmental expert is important for residents to gain competence in treating conditions affecting skin of color. Again, there was a significant difference in responses between the NE and MW (P=.003) and between the SE and MW (P=.009).

When asked the number of hours of lecture per month necessary to gain competence in conditions affecting patients with skin of color, 67% agreed that 1 to 5 hours was sufficient (Table 3). There were significant differences in the responses between the NE and SE (P=.024) and the SE and MW (P=.007). Of all respondents, 53% reported 1 to 5 months of clinical training are needed to gain competence in treating conditions affecting patients with skin of color, with significant differences in responses between the NE and MW (P<.001), the NE and SW (P=.019), and the SE and MW (P=.015)(Table 4).

Comment

Responses varied by practicing region. Less ethnically diverse regions, such as the MW and NW, were more likely to agree that dedicated clinics and rotations are important to gain competence compared to more ethnically diverse regions such as the NE, SE, and SW. Overall, more residents reported that dedicated lectures and textbook chapters were important to gain competency compared to dedicated clinics or rotations.

Although interactive lectures and textbook readings are important for obtaining a foundational understanding of dermatologic disease, they cannot substitute for clinical interactions and hands-on experience treating patients with skin of color.⁹ Not only do clinical interactions encourage independent reading and the study of encountered diagnoses, but intercommunication with patients may have a more profound and lasting impact on residents’ education.

Different regions of the United States have varying distributions of patients with skin of color, and dermatology residency program training reflects these disparities.⁶ In areas of less diversity, dermatology residents examine, diagnose, and treat substantially fewer patients with skin of color. The desire for more diverse training supports the prior findings of Nijhawan et al⁶ and is reflected in the responses we received in our study, whereby residents from the less ethnically diversified regions of the MW and NW were more likely to agree that clinics and rotations were necessary for training in preparation to sufficiently address the needs of patients with skin of color.

One way to compensate for the lack of ethnic diversity encountered in areas such as the MW and NW would be to develop educational programs featuring experts on skin of color.⁶ These specialists would not only train dermatology residents in areas of the country currently lacking ethnic diversity but also expand the expertise for treating patients with skin of color. Additionally, dedicated multiethnic skin clinics and externships devoted solely to treating patients with skin of color could be encouraged for residency training.⁶ Finally, community outreach through volunteer clinics may provide residents exposure to patients with skin of color seeking dermatologic care.¹⁰

This study was limited by the small number of respondents, but we were able to extract important trends and data from the collected responses. It is possible that respondents felt strongly about topics involving patients with skin of color, and the results were skewed to reflect individual bias. Additional limitations included not asking respondents for program names and population density (eg, urban, suburban, rural). Future studies should be directed toward analyzing how the diversity of the local population influences training in patients with skin of color, comparing program directors’ perceptions with residents’ perceptions on training in skin of color, and assessing patient perception of residents’ training in skin of color.

Conclusion

In the last decade it has become increasingly apparent that the US population is diversifying and that patients with skin of color will comprise a substantial proportion of the future population,^8,11 which emphasizes the need for dermatology residency programs to ensure that residents receive adequate training and exposure to patients with skin of color as well as the distinct skin diseases seen more commonly in these populations.¹²

Case Report

A 37-year-old woman presented to the dermatology clinic with an itchy rash involving the right hand. The rash had been present for 10 days but had become increasingly pruritic and vesicular over the last 5 days. She denied new exposures or other household members with similar symptoms. The patient reported that she had purchased a 4-toed, white-bellied African pygmy hedgehog (Atelerix albiventris) approximately 4 months prior. Upon questioning, she stated that she handled the hedgehog a couple of times a week and always washed her hands with soap and water immediately after. The patient’s medical and personal history were otherwise unremarkable.

Review of systems, including fevers, chills, and night sweats, was negative. Clinical examination revealed erythema with overlying vesicles and pustules on the right radial palm, radial dorsal hand, and interdigital web space of the first and second digit (Figure 1). The eruption was actively discharging serous exudate. No other lesions were present.

Comment

Tinea manuum is a dermatophytic epidermal infection of the hand. The most common causative organisms are Trichophyton rubrum, T mentagrophytes, and Epidermophyton floccosum. Infection can be acquired from contact with an infected person or animal, fomites, soil, or autoinoculation. Tinea manuum often is associated with tinea pedis. The hand that is used to excoriate the pruritic feet becomes infected, resulting in the classic two feet–one hand syndrome, which this patient did not have.¹

Dermatophytes colonize keratin-containing tissues—skin, hair, and nails—utilizing the keratin for nutrients, and they do not invade living tissue in immunocompetent hosts. Dermatophytes cause clinical disease from an allergic host response to fungal antigens or their metabolic products.¹ Tinea incognito results from the use of corticosteroids to treat a cutaneous fungal infection. The immunomodulatory effects of corticosteroids alter the appearance of the lesion. Hallmark signs and symptoms of a tinea infection, including scale, prominent border, erythema, and pruritus, can be reduced with corticosteroid use, giving the false impression that the lesion is resolving.^2,3 

The diagnosis of tinea manuum can be made clinically and often is supported with the findings of a KOH preparation. Scraping from an active scaling border generally provides the best results for obtaining fungal elements. For vesiculobullous lesions, the roof of a vesicle can provide an adequate specimen. Fungal culture and specific dermatophyte testing mediums can be used as confirmatory tests or allow for speciation, which help establish the diagnosis.¹

Trichophyton mentagrophytes is a species complex—a group of closely related organisms that share morphologic appearance to the point that boundaries between them often are unclear. It can be identified by gross and microscopic morphology; however, variants of T mentagrophytes (eg, Trichophyton interdigitale, Trichophyton erinacei) require a confirmatory test or molecular analysis to be correctly identified.^4-6 The laboratory used at our facility does not routinely attempt to identify the variant due to of lack of clinical significance.^7,8

Anthropophilic fungi such as T rubrum, E floccosum, and T interdigitale generally do not cause a robust immunologic reaction. Infection usually is chronic in nature, though cases of pustular and vesicular tinea have been described.^9,10Trichophyton erinacei and T mentagrophytes are zoophilic dermatophytes that cause an acute host response and are more likely to present with vesiculobullous lesions. Trichophyton erinacei is the most common fungal pathogen associated with A albiventris and has been isolated from its epidermal mites and quills,^11,12 which likely facilitates interspecies transmission and compromises the cutaneous barrier of human hosts when the hedgehog is handled.

Atelerix albiventris is the most common domesticated hedgehog in the United States. These mild-mannered, nocturnal insectivores are unique, low-maintenance pets that have recently gained popularity. They are notable for their propensity to curl into a ball when frightened (Figure 5). The spines are not barbed and do not detach, as those of a porcupine do, but are still capable of piercing the skin. Atelerix albiventris is known to cause zoonotic dermatosis in humans and should be handled with gloves.¹³ Performing a KOH preparation early in the diagnostic workup can help initiate antifungal therapy, as results of fungal culture can take several weeks.

Conclusion

This case illustrates the importance of close follow-up of skin lesions that only partially respond to initial treatment and maintaining a high index of suspicion as exotic pets become popular.

Case Report

A 37-year-old woman presented to the dermatology clinic with an itchy rash involving the right hand. The rash had been present for 10 days but had become increasingly pruritic and vesicular over the last 5 days. She denied new exposures or other household members with similar symptoms. The patient reported that she had purchased a 4-toed, white-bellied African pygmy hedgehog (Atelerix albiventris) approximately 4 months prior. Upon questioning, she stated that she handled the hedgehog a couple of times a week and always washed her hands with soap and water immediately after. The patient’s medical and personal history were otherwise unremarkable.

Review of systems, including fevers, chills, and night sweats, was negative. Clinical examination revealed erythema with overlying vesicles and pustules on the right radial palm, radial dorsal hand, and interdigital web space of the first and second digit (Figure 1). The eruption was actively discharging serous exudate. No other lesions were present.

Comment

Tinea manuum is a dermatophytic epidermal infection of the hand. The most common causative organisms are Trichophyton rubrum, T mentagrophytes, and Epidermophyton floccosum. Infection can be acquired from contact with an infected person or animal, fomites, soil, or autoinoculation. Tinea manuum often is associated with tinea pedis. The hand that is used to excoriate the pruritic feet becomes infected, resulting in the classic two feet–one hand syndrome, which this patient did not have.¹

Dermatophytes colonize keratin-containing tissues—skin, hair, and nails—utilizing the keratin for nutrients, and they do not invade living tissue in immunocompetent hosts. Dermatophytes cause clinical disease from an allergic host response to fungal antigens or their metabolic products.¹ Tinea incognito results from the use of corticosteroids to treat a cutaneous fungal infection. The immunomodulatory effects of corticosteroids alter the appearance of the lesion. Hallmark signs and symptoms of a tinea infection, including scale, prominent border, erythema, and pruritus, can be reduced with corticosteroid use, giving the false impression that the lesion is resolving.^2,3 

The diagnosis of tinea manuum can be made clinically and often is supported with the findings of a KOH preparation. Scraping from an active scaling border generally provides the best results for obtaining fungal elements. For vesiculobullous lesions, the roof of a vesicle can provide an adequate specimen. Fungal culture and specific dermatophyte testing mediums can be used as confirmatory tests or allow for speciation, which help establish the diagnosis.¹

Trichophyton mentagrophytes is a species complex—a group of closely related organisms that share morphologic appearance to the point that boundaries between them often are unclear. It can be identified by gross and microscopic morphology; however, variants of T mentagrophytes (eg, Trichophyton interdigitale, Trichophyton erinacei) require a confirmatory test or molecular analysis to be correctly identified.^4-6 The laboratory used at our facility does not routinely attempt to identify the variant due to of lack of clinical significance.^7,8

Anthropophilic fungi such as T rubrum, E floccosum, and T interdigitale generally do not cause a robust immunologic reaction. Infection usually is chronic in nature, though cases of pustular and vesicular tinea have been described.^9,10Trichophyton erinacei and T mentagrophytes are zoophilic dermatophytes that cause an acute host response and are more likely to present with vesiculobullous lesions. Trichophyton erinacei is the most common fungal pathogen associated with A albiventris and has been isolated from its epidermal mites and quills,^11,12 which likely facilitates interspecies transmission and compromises the cutaneous barrier of human hosts when the hedgehog is handled.

Atelerix albiventris is the most common domesticated hedgehog in the United States. These mild-mannered, nocturnal insectivores are unique, low-maintenance pets that have recently gained popularity. They are notable for their propensity to curl into a ball when frightened (Figure 5). The spines are not barbed and do not detach, as those of a porcupine do, but are still capable of piercing the skin. Atelerix albiventris is known to cause zoonotic dermatosis in humans and should be handled with gloves.¹³ Performing a KOH preparation early in the diagnostic workup can help initiate antifungal therapy, as results of fungal culture can take several weeks.

Conclusion

This case illustrates the importance of close follow-up of skin lesions that only partially respond to initial treatment and maintaining a high index of suspicion as exotic pets become popular.

Case Report

A 37-year-old woman presented to the dermatology clinic with an itchy rash involving the right hand. The rash had been present for 10 days but had become increasingly pruritic and vesicular over the last 5 days. She denied new exposures or other household members with similar symptoms. The patient reported that she had purchased a 4-toed, white-bellied African pygmy hedgehog (Atelerix albiventris) approximately 4 months prior. Upon questioning, she stated that she handled the hedgehog a couple of times a week and always washed her hands with soap and water immediately after. The patient’s medical and personal history were otherwise unremarkable.

Review of systems, including fevers, chills, and night sweats, was negative. Clinical examination revealed erythema with overlying vesicles and pustules on the right radial palm, radial dorsal hand, and interdigital web space of the first and second digit (Figure 1). The eruption was actively discharging serous exudate. No other lesions were present.

Comment

Tinea manuum is a dermatophytic epidermal infection of the hand. The most common causative organisms are Trichophyton rubrum, T mentagrophytes, and Epidermophyton floccosum. Infection can be acquired from contact with an infected person or animal, fomites, soil, or autoinoculation. Tinea manuum often is associated with tinea pedis. The hand that is used to excoriate the pruritic feet becomes infected, resulting in the classic two feet–one hand syndrome, which this patient did not have.¹

Dermatophytes colonize keratin-containing tissues—skin, hair, and nails—utilizing the keratin for nutrients, and they do not invade living tissue in immunocompetent hosts. Dermatophytes cause clinical disease from an allergic host response to fungal antigens or their metabolic products.¹ Tinea incognito results from the use of corticosteroids to treat a cutaneous fungal infection. The immunomodulatory effects of corticosteroids alter the appearance of the lesion. Hallmark signs and symptoms of a tinea infection, including scale, prominent border, erythema, and pruritus, can be reduced with corticosteroid use, giving the false impression that the lesion is resolving.^2,3 

The diagnosis of tinea manuum can be made clinically and often is supported with the findings of a KOH preparation. Scraping from an active scaling border generally provides the best results for obtaining fungal elements. For vesiculobullous lesions, the roof of a vesicle can provide an adequate specimen. Fungal culture and specific dermatophyte testing mediums can be used as confirmatory tests or allow for speciation, which help establish the diagnosis.¹

Trichophyton mentagrophytes is a species complex—a group of closely related organisms that share morphologic appearance to the point that boundaries between them often are unclear. It can be identified by gross and microscopic morphology; however, variants of T mentagrophytes (eg, Trichophyton interdigitale, Trichophyton erinacei) require a confirmatory test or molecular analysis to be correctly identified.^4-6 The laboratory used at our facility does not routinely attempt to identify the variant due to of lack of clinical significance.^7,8

Anthropophilic fungi such as T rubrum, E floccosum, and T interdigitale generally do not cause a robust immunologic reaction. Infection usually is chronic in nature, though cases of pustular and vesicular tinea have been described.^9,10Trichophyton erinacei and T mentagrophytes are zoophilic dermatophytes that cause an acute host response and are more likely to present with vesiculobullous lesions. Trichophyton erinacei is the most common fungal pathogen associated with A albiventris and has been isolated from its epidermal mites and quills,^11,12 which likely facilitates interspecies transmission and compromises the cutaneous barrier of human hosts when the hedgehog is handled.

Atelerix albiventris is the most common domesticated hedgehog in the United States. These mild-mannered, nocturnal insectivores are unique, low-maintenance pets that have recently gained popularity. They are notable for their propensity to curl into a ball when frightened (Figure 5). The spines are not barbed and do not detach, as those of a porcupine do, but are still capable of piercing the skin. Atelerix albiventris is known to cause zoonotic dermatosis in humans and should be handled with gloves.¹³ Performing a KOH preparation early in the diagnostic workup can help initiate antifungal therapy, as results of fungal culture can take several weeks.

Conclusion

This case illustrates the importance of close follow-up of skin lesions that only partially respond to initial treatment and maintaining a high index of suspicion as exotic pets become popular.

To the Editor:

It is with great interest that I read the article by Ware et al,¹ “Racial Limitations of Fitzpatrick Skin Type.” Within my own department, the issue of the appropriateness of using Fitzpatrick skin type (FST) as a surrogate to describe skin color has been raised with mixed responses.

As in many dermatology residency programs across the country, first-year dermatology residents are asked to describe the morphology of a lesion/eruption seen on a patient during Grand Rounds. Preceding the morphologic description, many providers describe the appearance of the patient including their skin color, as constitutive skin color can impact understanding of the morphologic descriptions, favor different diagnoses based on disease epidemiology, and guide subsequent treatment recommendations.^2,3 During one of my first Grand Rounds as an early dermatology resident, a patient was described as a “well-appearing brown boy,” which led to a lively discussion regarding the terms that should be used to describe skin color, with some in the audience preferring FST, others including myself preferring degree of pigmentation (eg, light, moderate, dark), and lastly others preferring an inferred ethnicity based on the patient’s appearance. One audience member commented, “I am brown, therefore I think it is fine to say ‘brown boy,’” which adds to findings from Ware et al¹ that there may be differences in what providers prefer to utilize to describe a patient’s skin color based on their own constitutive skin color.

I inquired with 2 other first-year dermatology residents with skin of color at other programs. When asked what terminology they use to describe a patient for Grand Rounds or in clinic, one resident replied, “It’s stylistic but if it’s your one liner [for assessment and plan] use their ethnicity [whereas] if it’s [for] a physical exam use their Fitzpatrick skin type.” The other resident replied, “I use Fitzpatrick skin type even though it’s technically subjective and therefore not appropriate for use within objective data, such as the physical exam, however it’s a language that most colleagues understand as a substitute for skin color.” I also raised the same question to an attending dermatologist at a primarily skin-of-color community hospital. She replied, “I think when unsure about ethnicity, Fitzpatrick type is an appropriate way to describe someone. It’s not really correct to say [a patient’s ethnicity] when you don’t know for sure.”

Unfortunately, as Ware and colleagues¹ indicated, there is no consensus by which to objectively classify nonwhite skin color. Within the dermatology literature, it has been proposed that race should not be used to express skin color, and this article proposes that FST is an inappropriate surrogate for race/ethnicity.⁴ Although I agree that appropriate use of FST should be emphasized in training, is there a vocabulary that Ware et al¹ recommend we use instead? Does the Skin of Color Society have suggestions on preferred language among its members? Finally, what efforts are being made to develop “culturally appropriate and clinically relevant methods for describing skin of color,” as the authors stated, within our own Skin of Color Society, or to whom does this responsibility ultimately fall?

References

1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.

2. Sachdeva S. Fitzpatrick skin typing: applications in dermatology. Indian J Dermatol Venereol Leprol. 2009;75:93-96.

3. Kelly AP, Taylor SC, Lim HW, et al. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. New York, NY: McGraw-Hill Education; 2016.

4. Bigby M, Thaler D. Describing patients’ “race” in clinical presentations should be abandoned. J Am Acad Dermatol. 2006;54:1074-1076.

Author’s Response

My colleagues and I thank Dr. Pimentel for his insights regarding the article, “Racial Limitations of Fitzpatrick Skin Type.”¹ The conundrum on how to appropriately categorize skin color for descriptive and epidemiologic purposes continues to remain unsolved today. However, attempts have been made in the past. For example, in September 2006, Dr. Susan C. Taylor (Philadelphia, Pennsylvania), formed and chaired a workshop session titled “A New Classification System for All Skin Types.” Dermatology leaders with skin of color expertise were invited from around the world for a weekend in New York, New York, to brainstorm a new skin color classification system. This endeavor did not produce any successful alternatives, but it has remained a pertinent topic of discussion in academic dermatology, including the Skin of Color Society, since then.

When unsure about ethnicity, my colleagues and I continue to advocate that the Fitzpatrick scale is not an appropriate substitute to describe skin color. This usage of Fitzpatrick skin type (FST) perpetuates the idea that the Fitzpatrick scale is a suitable proxy to describe ethnicity or race, which it is not. It is important to remember that race is a social classification construct, not a biological one.² The topic of race in contemporary culture undoubtedly invokes strong emotional connotations. The language around race is constantly evolving. I would argue that fear and discomfort of using incorrect racial language promotes the inappropriate use of FST, as the FST may be perceived as a more scientific and pseudoapplicable form of classification. To gain knowledge about a patient’s ethnicity/race to assess epidemiologic ethnic trends, we recommend asking the patient in an intake form or during consultation to self-identify his/her ethnicity or race,³ which takes the guesswork out for providers. However, caution must be exercised to avoid using race and ethnicity to later describe skin color.

Until a more culturally and medically relevant method of skin color classification is created, my colleagues and I recommend using basic color adjectives such as brown, black, pink, tan, or white supplemented with light, medium, or dark predescriptors. For example, “A 35-year-old self-identified African American woman with a dark brown skin hue presents with a 2-week flare of itchy, dark purple plaques with white scale on the scalp and extensor surfaces of the knees and elbows.” These basic descriptions for constitutive skin color conjure ample visual information for the listener/reader to understand morphologic descriptions, presentation of erythema, changes in pigmentation, and more. For a more specific skin color classification, we recommend developing a user-friendly Pantone-like color system to classify constitutive skin color.⁴

Jessica E. Dawson, MD

From the University of Washington School of Medicine, Seattle.

The author reports no conflict of interest.

Correspondence: Jessica E. Dawson, MD, University of Washington School of Medicine, 1959 NE Pacific St, Seattle, WA 98195 (jessdawsonmed@gmail.com).

References

1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.

2. Ifekwunigwe JO, Wagner JK, Yu JH, et al. A qualitative analysis of how anthropologists interpret the race construct. Am Anthropol. 2017;119:422-434.

3. Hasnain-Wynia R, Baker DW. Obtaining data on patient race, ethnicity, and primary language in health care organizations: current challenges and proposed solutions. Health Serv Res. 2006;41:1501-1518.

4. What is the Pantone color system? Pantone website. https://www.pantone.com/color-systems/pantone-color-systems-explained. Accesed May 13, 2020.

To the Editor:

It is with great interest that I read the article by Ware et al,¹ “Racial Limitations of Fitzpatrick Skin Type.” Within my own department, the issue of the appropriateness of using Fitzpatrick skin type (FST) as a surrogate to describe skin color has been raised with mixed responses.

As in many dermatology residency programs across the country, first-year dermatology residents are asked to describe the morphology of a lesion/eruption seen on a patient during Grand Rounds. Preceding the morphologic description, many providers describe the appearance of the patient including their skin color, as constitutive skin color can impact understanding of the morphologic descriptions, favor different diagnoses based on disease epidemiology, and guide subsequent treatment recommendations.^2,3 During one of my first Grand Rounds as an early dermatology resident, a patient was described as a “well-appearing brown boy,” which led to a lively discussion regarding the terms that should be used to describe skin color, with some in the audience preferring FST, others including myself preferring degree of pigmentation (eg, light, moderate, dark), and lastly others preferring an inferred ethnicity based on the patient’s appearance. One audience member commented, “I am brown, therefore I think it is fine to say ‘brown boy,’” which adds to findings from Ware et al¹ that there may be differences in what providers prefer to utilize to describe a patient’s skin color based on their own constitutive skin color.

I inquired with 2 other first-year dermatology residents with skin of color at other programs. When asked what terminology they use to describe a patient for Grand Rounds or in clinic, one resident replied, “It’s stylistic but if it’s your one liner [for assessment and plan] use their ethnicity [whereas] if it’s [for] a physical exam use their Fitzpatrick skin type.” The other resident replied, “I use Fitzpatrick skin type even though it’s technically subjective and therefore not appropriate for use within objective data, such as the physical exam, however it’s a language that most colleagues understand as a substitute for skin color.” I also raised the same question to an attending dermatologist at a primarily skin-of-color community hospital. She replied, “I think when unsure about ethnicity, Fitzpatrick type is an appropriate way to describe someone. It’s not really correct to say [a patient’s ethnicity] when you don’t know for sure.”

Unfortunately, as Ware and colleagues¹ indicated, there is no consensus by which to objectively classify nonwhite skin color. Within the dermatology literature, it has been proposed that race should not be used to express skin color, and this article proposes that FST is an inappropriate surrogate for race/ethnicity.⁴ Although I agree that appropriate use of FST should be emphasized in training, is there a vocabulary that Ware et al¹ recommend we use instead? Does the Skin of Color Society have suggestions on preferred language among its members? Finally, what efforts are being made to develop “culturally appropriate and clinically relevant methods for describing skin of color,” as the authors stated, within our own Skin of Color Society, or to whom does this responsibility ultimately fall?

References

1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.

2. Sachdeva S. Fitzpatrick skin typing: applications in dermatology. Indian J Dermatol Venereol Leprol. 2009;75:93-96.

3. Kelly AP, Taylor SC, Lim HW, et al. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. New York, NY: McGraw-Hill Education; 2016.

4. Bigby M, Thaler D. Describing patients’ “race” in clinical presentations should be abandoned. J Am Acad Dermatol. 2006;54:1074-1076.

Author’s Response

My colleagues and I thank Dr. Pimentel for his insights regarding the article, “Racial Limitations of Fitzpatrick Skin Type.”¹ The conundrum on how to appropriately categorize skin color for descriptive and epidemiologic purposes continues to remain unsolved today. However, attempts have been made in the past. For example, in September 2006, Dr. Susan C. Taylor (Philadelphia, Pennsylvania), formed and chaired a workshop session titled “A New Classification System for All Skin Types.” Dermatology leaders with skin of color expertise were invited from around the world for a weekend in New York, New York, to brainstorm a new skin color classification system. This endeavor did not produce any successful alternatives, but it has remained a pertinent topic of discussion in academic dermatology, including the Skin of Color Society, since then.

When unsure about ethnicity, my colleagues and I continue to advocate that the Fitzpatrick scale is not an appropriate substitute to describe skin color. This usage of Fitzpatrick skin type (FST) perpetuates the idea that the Fitzpatrick scale is a suitable proxy to describe ethnicity or race, which it is not. It is important to remember that race is a social classification construct, not a biological one.² The topic of race in contemporary culture undoubtedly invokes strong emotional connotations. The language around race is constantly evolving. I would argue that fear and discomfort of using incorrect racial language promotes the inappropriate use of FST, as the FST may be perceived as a more scientific and pseudoapplicable form of classification. To gain knowledge about a patient’s ethnicity/race to assess epidemiologic ethnic trends, we recommend asking the patient in an intake form or during consultation to self-identify his/her ethnicity or race,³ which takes the guesswork out for providers. However, caution must be exercised to avoid using race and ethnicity to later describe skin color.

Until a more culturally and medically relevant method of skin color classification is created, my colleagues and I recommend using basic color adjectives such as brown, black, pink, tan, or white supplemented with light, medium, or dark predescriptors. For example, “A 35-year-old self-identified African American woman with a dark brown skin hue presents with a 2-week flare of itchy, dark purple plaques with white scale on the scalp and extensor surfaces of the knees and elbows.” These basic descriptions for constitutive skin color conjure ample visual information for the listener/reader to understand morphologic descriptions, presentation of erythema, changes in pigmentation, and more. For a more specific skin color classification, we recommend developing a user-friendly Pantone-like color system to classify constitutive skin color.⁴

Jessica E. Dawson, MD

From the University of Washington School of Medicine, Seattle.

The author reports no conflict of interest.

Correspondence: Jessica E. Dawson, MD, University of Washington School of Medicine, 1959 NE Pacific St, Seattle, WA 98195 (jessdawsonmed@gmail.com).

References

1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.

2. Ifekwunigwe JO, Wagner JK, Yu JH, et al. A qualitative analysis of how anthropologists interpret the race construct. Am Anthropol. 2017;119:422-434.

3. Hasnain-Wynia R, Baker DW. Obtaining data on patient race, ethnicity, and primary language in health care organizations: current challenges and proposed solutions. Health Serv Res. 2006;41:1501-1518.

4. What is the Pantone color system? Pantone website. https://www.pantone.com/color-systems/pantone-color-systems-explained. Accesed May 13, 2020.

To the Editor:

It is with great interest that I read the article by Ware et al,¹ “Racial Limitations of Fitzpatrick Skin Type.” Within my own department, the issue of the appropriateness of using Fitzpatrick skin type (FST) as a surrogate to describe skin color has been raised with mixed responses.

As in many dermatology residency programs across the country, first-year dermatology residents are asked to describe the morphology of a lesion/eruption seen on a patient during Grand Rounds. Preceding the morphologic description, many providers describe the appearance of the patient including their skin color, as constitutive skin color can impact understanding of the morphologic descriptions, favor different diagnoses based on disease epidemiology, and guide subsequent treatment recommendations.^2,3 During one of my first Grand Rounds as an early dermatology resident, a patient was described as a “well-appearing brown boy,” which led to a lively discussion regarding the terms that should be used to describe skin color, with some in the audience preferring FST, others including myself preferring degree of pigmentation (eg, light, moderate, dark), and lastly others preferring an inferred ethnicity based on the patient’s appearance. One audience member commented, “I am brown, therefore I think it is fine to say ‘brown boy,’” which adds to findings from Ware et al¹ that there may be differences in what providers prefer to utilize to describe a patient’s skin color based on their own constitutive skin color.

I inquired with 2 other first-year dermatology residents with skin of color at other programs. When asked what terminology they use to describe a patient for Grand Rounds or in clinic, one resident replied, “It’s stylistic but if it’s your one liner [for assessment and plan] use their ethnicity [whereas] if it’s [for] a physical exam use their Fitzpatrick skin type.” The other resident replied, “I use Fitzpatrick skin type even though it’s technically subjective and therefore not appropriate for use within objective data, such as the physical exam, however it’s a language that most colleagues understand as a substitute for skin color.” I also raised the same question to an attending dermatologist at a primarily skin-of-color community hospital. She replied, “I think when unsure about ethnicity, Fitzpatrick type is an appropriate way to describe someone. It’s not really correct to say [a patient’s ethnicity] when you don’t know for sure.”

Unfortunately, as Ware and colleagues¹ indicated, there is no consensus by which to objectively classify nonwhite skin color. Within the dermatology literature, it has been proposed that race should not be used to express skin color, and this article proposes that FST is an inappropriate surrogate for race/ethnicity.⁴ Although I agree that appropriate use of FST should be emphasized in training, is there a vocabulary that Ware et al¹ recommend we use instead? Does the Skin of Color Society have suggestions on preferred language among its members? Finally, what efforts are being made to develop “culturally appropriate and clinically relevant methods for describing skin of color,” as the authors stated, within our own Skin of Color Society, or to whom does this responsibility ultimately fall?

References

1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.

2. Sachdeva S. Fitzpatrick skin typing: applications in dermatology. Indian J Dermatol Venereol Leprol. 2009;75:93-96.

3. Kelly AP, Taylor SC, Lim HW, et al. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. New York, NY: McGraw-Hill Education; 2016.

4. Bigby M, Thaler D. Describing patients’ “race” in clinical presentations should be abandoned. J Am Acad Dermatol. 2006;54:1074-1076.

Author’s Response

My colleagues and I thank Dr. Pimentel for his insights regarding the article, “Racial Limitations of Fitzpatrick Skin Type.”¹ The conundrum on how to appropriately categorize skin color for descriptive and epidemiologic purposes continues to remain unsolved today. However, attempts have been made in the past. For example, in September 2006, Dr. Susan C. Taylor (Philadelphia, Pennsylvania), formed and chaired a workshop session titled “A New Classification System for All Skin Types.” Dermatology leaders with skin of color expertise were invited from around the world for a weekend in New York, New York, to brainstorm a new skin color classification system. This endeavor did not produce any successful alternatives, but it has remained a pertinent topic of discussion in academic dermatology, including the Skin of Color Society, since then.

When unsure about ethnicity, my colleagues and I continue to advocate that the Fitzpatrick scale is not an appropriate substitute to describe skin color. This usage of Fitzpatrick skin type (FST) perpetuates the idea that the Fitzpatrick scale is a suitable proxy to describe ethnicity or race, which it is not. It is important to remember that race is a social classification construct, not a biological one.² The topic of race in contemporary culture undoubtedly invokes strong emotional connotations. The language around race is constantly evolving. I would argue that fear and discomfort of using incorrect racial language promotes the inappropriate use of FST, as the FST may be perceived as a more scientific and pseudoapplicable form of classification. To gain knowledge about a patient’s ethnicity/race to assess epidemiologic ethnic trends, we recommend asking the patient in an intake form or during consultation to self-identify his/her ethnicity or race,³ which takes the guesswork out for providers. However, caution must be exercised to avoid using race and ethnicity to later describe skin color.

Until a more culturally and medically relevant method of skin color classification is created, my colleagues and I recommend using basic color adjectives such as brown, black, pink, tan, or white supplemented with light, medium, or dark predescriptors. For example, “A 35-year-old self-identified African American woman with a dark brown skin hue presents with a 2-week flare of itchy, dark purple plaques with white scale on the scalp and extensor surfaces of the knees and elbows.” These basic descriptions for constitutive skin color conjure ample visual information for the listener/reader to understand morphologic descriptions, presentation of erythema, changes in pigmentation, and more. For a more specific skin color classification, we recommend developing a user-friendly Pantone-like color system to classify constitutive skin color.⁴

Jessica E. Dawson, MD

From the University of Washington School of Medicine, Seattle.

The author reports no conflict of interest.

Correspondence: Jessica E. Dawson, MD, University of Washington School of Medicine, 1959 NE Pacific St, Seattle, WA 98195 (jessdawsonmed@gmail.com).

References

1. Ware OR, Dawson JE, Shinohara MM, et al. Racial limitations of Fitzpatrick skin type. Cutis. 2020;105:77-80.

2. Ifekwunigwe JO, Wagner JK, Yu JH, et al. A qualitative analysis of how anthropologists interpret the race construct. Am Anthropol. 2017;119:422-434.

3. Hasnain-Wynia R, Baker DW. Obtaining data on patient race, ethnicity, and primary language in health care organizations: current challenges and proposed solutions. Health Serv Res. 2006;41:1501-1518.

4. What is the Pantone color system? Pantone website. https://www.pantone.com/color-systems/pantone-color-systems-explained. Accesed May 13, 2020.

Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease that can have devastating effects on many organs. Despite the considerable morbidity and mortality associated with SLE, treatment options have been largely unchanged since the 1950s.¹ It was not until the last decade that a new biologic medication was approved, and several other promising treatments currently are being evaluated in clinical trials. Dermatologists are most likely to encounter cutaneous lupus erythematosus (CLE) with or without SLE, which can present with a variety of skin manifestations. Cutaneous lupus erythematosus can have devastating effects on quality of life and can be a visible sign of the internal activity and damage of SLE.^2,3 Although many trials have been completed evaluating SLE treatments, few medications have been evaluated specifically for CLE despite the availability of validated measures of CLE skin activity.⁴ There is a recent shortage of antimalarial medications, the current first-line therapy for CLE, due to both an import alert in the United States on quinacrine placed in 2019 as well as the use of hydroxychloroquine and chloroquine in treating coronavirus disease 2019.^5,6 Due to this shortage, the need for new and effective treatments is more critical than ever, as alternatives to first-line therapy frequently require immunosuppression. We review recent drug approvals for SLE and their efficacy in CLE. We also provide an update on new agents currently being studied to treat this disease.

Belimumab

Belimumab is a B-lymphocyte stimulator–specific inhibitor that was first approved for treatment of SLE in 2011. It was the first monoclonal antibody approved to treat SLE.⁷ B-lymphocyte stimulator plays a critical role in B-cell survival; thus, its inhibition increases apoptosis of autoreactive B cells involved in the pathogenesis of SLE. More recently, belimumab was approved for pediatric SLE in April 2019 based on the PLUTO study, a phase 2 randomized, double-blind study of 93 patients.⁸ Although patients with cutaneous manifestations of lupus were included in trials for belimumab, they lacked CLE-specific outcome measurements to truly evaluate the efficacy in treating skin disease.⁹ This medication currently is not approved by the US Food and Drug Administration (FDA) for CLE; however, it is used off label in some cases for recalcitrant disease.¹⁰

Baricitinib

Baricitinib is a selective and reversible inhibitor of JAK1 and JAK2 that was granted fast-track status by the FDA in December 2018. In a phase 2 trial, baricitinib was superior to placebo plus standard of care, primarily for arthritis and lupus nephritis.¹¹ Although improvement of cutaneous disease was measured as an end point, it did not show significant improvement in disease. The presence of skin disease was high, but the activity of disease was low, which can make it difficult to show meaningful improvement, as there is not much room for patients to objectively improve.¹² Showing meaningful improvement in skin disease often is difficult in phase 2 trials, especially when the trial design is focused on SLE rather than CLE activity. Further studies of baricitinib that include more severe patients with CLE disease are needed to truly understand its effects on the skin.

Lenalidomide

There have been several CLE studies in the last several years surrounding lenalidomide, an analog of thalidomide.^13-15 This molecule has a number of immunomodulatory effects including antiangiogenic effects, increased natural killer cell–dependent cytotoxicity, and cytokine and interleukin inhibition. Lenalidomide is of particular interest in treating CLE, as it was shown to be more potent than thalidomide at low doses and with a better side-effect profile. Multiple small, open-label trials have shown lenalidomide to be both safe and efficacious in the treatment of CLE.^13,14 In addition, iberdomide, a derivative of lenalidomide, recently completed a phase 2 dose-escalation study showing improvement in both SLE and CLE end points.¹⁶ A phase 2b proof-of-concept study currently is underway (ClinicalTrials.gov Identifier NCT03161483).

Monoclonal Antibodies

Many developing therapies target specific components of the type I interferon pathway, which is a primary driver of CLE lesions. Innate immune system pathways involving type I interferon were shown to be active in the pathogenesis of CLE, and levels of interferon correlate with skin disease activity.¹⁷ One molecule in development that targets this pathway is BIIB059, a humanized IgG1 monoclonal antibody that binds to blood dendritic cell antigen 2. This cell surface protein is uniquely expressed on plasmacytoid dendritic cells, which are the main source of type I interferon overproduction in SLE. The binding of this antibody to the blood dendritic cell antigen 2 receptor both blocks type I interferon production and decreases the overall number of active plasmacytoid dendritic cells present.¹⁸ In the completed phase 1b study, a response in cutaneous disease was shown through a reduction in the CLE disease area and severity index score following single-dose administration.¹⁹ More recently, a phase 2 study met primary end points in both SLE and CLE compared to placebo.²⁰

Anifrolumab is a human IgG1k monoclonal antibody that binds to type I interferon receptor, blocking all type I interferon signaling. Following a successful phase 2 trial, it failed to meet its primary end point in its first phase 3 trial.²¹ Several secondary end points suggested a clinical benefit. A second phase 3 trial of 362 patients randomized to treatment with anifrolumab or placebo over 48 weeks showed anifrolumab to be superior to placebo for multiple end points, including the overall disease primary end point as well as a notable reduction in skin activity.²²

Final Thoughts

Outside of the approval of belimumab, there have been no new FDA-approved treatments for SLE since the approval of antimalarial agents nearly 50 years ago. For CLE specifically, there is an even greater scarcity of evidence-based treatments. Recently studied medications, such as belimumab and lenalidomide, are available off label for CLE patients when other options have failed. Recent studies have evaluated the efficacy of these agents in the treatment of CLE using the CLE disease area and severity index.^10,13,14 Enrollment in CLE trials is difficult due to the rarity of the disease, and careful attention must be paid to evaluating skin end points. As experts in CLE and the nuances of these assessments, it is critical that dermatologists be involved in clinical trials. Future SLE trials must consider CLE as an important end point for CLE patients to get access to much-needed novel therapies.

Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease that can have devastating effects on many organs. Despite the considerable morbidity and mortality associated with SLE, treatment options have been largely unchanged since the 1950s.¹ It was not until the last decade that a new biologic medication was approved, and several other promising treatments currently are being evaluated in clinical trials. Dermatologists are most likely to encounter cutaneous lupus erythematosus (CLE) with or without SLE, which can present with a variety of skin manifestations. Cutaneous lupus erythematosus can have devastating effects on quality of life and can be a visible sign of the internal activity and damage of SLE.^2,3 Although many trials have been completed evaluating SLE treatments, few medications have been evaluated specifically for CLE despite the availability of validated measures of CLE skin activity.⁴ There is a recent shortage of antimalarial medications, the current first-line therapy for CLE, due to both an import alert in the United States on quinacrine placed in 2019 as well as the use of hydroxychloroquine and chloroquine in treating coronavirus disease 2019.^5,6 Due to this shortage, the need for new and effective treatments is more critical than ever, as alternatives to first-line therapy frequently require immunosuppression. We review recent drug approvals for SLE and their efficacy in CLE. We also provide an update on new agents currently being studied to treat this disease.

Belimumab

Belimumab is a B-lymphocyte stimulator–specific inhibitor that was first approved for treatment of SLE in 2011. It was the first monoclonal antibody approved to treat SLE.⁷ B-lymphocyte stimulator plays a critical role in B-cell survival; thus, its inhibition increases apoptosis of autoreactive B cells involved in the pathogenesis of SLE. More recently, belimumab was approved for pediatric SLE in April 2019 based on the PLUTO study, a phase 2 randomized, double-blind study of 93 patients.⁸ Although patients with cutaneous manifestations of lupus were included in trials for belimumab, they lacked CLE-specific outcome measurements to truly evaluate the efficacy in treating skin disease.⁹ This medication currently is not approved by the US Food and Drug Administration (FDA) for CLE; however, it is used off label in some cases for recalcitrant disease.¹⁰

Baricitinib

Baricitinib is a selective and reversible inhibitor of JAK1 and JAK2 that was granted fast-track status by the FDA in December 2018. In a phase 2 trial, baricitinib was superior to placebo plus standard of care, primarily for arthritis and lupus nephritis.¹¹ Although improvement of cutaneous disease was measured as an end point, it did not show significant improvement in disease. The presence of skin disease was high, but the activity of disease was low, which can make it difficult to show meaningful improvement, as there is not much room for patients to objectively improve.¹² Showing meaningful improvement in skin disease often is difficult in phase 2 trials, especially when the trial design is focused on SLE rather than CLE activity. Further studies of baricitinib that include more severe patients with CLE disease are needed to truly understand its effects on the skin.

Lenalidomide

There have been several CLE studies in the last several years surrounding lenalidomide, an analog of thalidomide.^13-15 This molecule has a number of immunomodulatory effects including antiangiogenic effects, increased natural killer cell–dependent cytotoxicity, and cytokine and interleukin inhibition. Lenalidomide is of particular interest in treating CLE, as it was shown to be more potent than thalidomide at low doses and with a better side-effect profile. Multiple small, open-label trials have shown lenalidomide to be both safe and efficacious in the treatment of CLE.^13,14 In addition, iberdomide, a derivative of lenalidomide, recently completed a phase 2 dose-escalation study showing improvement in both SLE and CLE end points.¹⁶ A phase 2b proof-of-concept study currently is underway (ClinicalTrials.gov Identifier NCT03161483).

Monoclonal Antibodies

Many developing therapies target specific components of the type I interferon pathway, which is a primary driver of CLE lesions. Innate immune system pathways involving type I interferon were shown to be active in the pathogenesis of CLE, and levels of interferon correlate with skin disease activity.¹⁷ One molecule in development that targets this pathway is BIIB059, a humanized IgG1 monoclonal antibody that binds to blood dendritic cell antigen 2. This cell surface protein is uniquely expressed on plasmacytoid dendritic cells, which are the main source of type I interferon overproduction in SLE. The binding of this antibody to the blood dendritic cell antigen 2 receptor both blocks type I interferon production and decreases the overall number of active plasmacytoid dendritic cells present.¹⁸ In the completed phase 1b study, a response in cutaneous disease was shown through a reduction in the CLE disease area and severity index score following single-dose administration.¹⁹ More recently, a phase 2 study met primary end points in both SLE and CLE compared to placebo.²⁰

Anifrolumab is a human IgG1k monoclonal antibody that binds to type I interferon receptor, blocking all type I interferon signaling. Following a successful phase 2 trial, it failed to meet its primary end point in its first phase 3 trial.²¹ Several secondary end points suggested a clinical benefit. A second phase 3 trial of 362 patients randomized to treatment with anifrolumab or placebo over 48 weeks showed anifrolumab to be superior to placebo for multiple end points, including the overall disease primary end point as well as a notable reduction in skin activity.²²

Final Thoughts

Outside of the approval of belimumab, there have been no new FDA-approved treatments for SLE since the approval of antimalarial agents nearly 50 years ago. For CLE specifically, there is an even greater scarcity of evidence-based treatments. Recently studied medications, such as belimumab and lenalidomide, are available off label for CLE patients when other options have failed. Recent studies have evaluated the efficacy of these agents in the treatment of CLE using the CLE disease area and severity index.^10,13,14 Enrollment in CLE trials is difficult due to the rarity of the disease, and careful attention must be paid to evaluating skin end points. As experts in CLE and the nuances of these assessments, it is critical that dermatologists be involved in clinical trials. Future SLE trials must consider CLE as an important end point for CLE patients to get access to much-needed novel therapies.

Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease that can have devastating effects on many organs. Despite the considerable morbidity and mortality associated with SLE, treatment options have been largely unchanged since the 1950s.¹ It was not until the last decade that a new biologic medication was approved, and several other promising treatments currently are being evaluated in clinical trials. Dermatologists are most likely to encounter cutaneous lupus erythematosus (CLE) with or without SLE, which can present with a variety of skin manifestations. Cutaneous lupus erythematosus can have devastating effects on quality of life and can be a visible sign of the internal activity and damage of SLE.^2,3 Although many trials have been completed evaluating SLE treatments, few medications have been evaluated specifically for CLE despite the availability of validated measures of CLE skin activity.⁴ There is a recent shortage of antimalarial medications, the current first-line therapy for CLE, due to both an import alert in the United States on quinacrine placed in 2019 as well as the use of hydroxychloroquine and chloroquine in treating coronavirus disease 2019.^5,6 Due to this shortage, the need for new and effective treatments is more critical than ever, as alternatives to first-line therapy frequently require immunosuppression. We review recent drug approvals for SLE and their efficacy in CLE. We also provide an update on new agents currently being studied to treat this disease.

Belimumab

Belimumab is a B-lymphocyte stimulator–specific inhibitor that was first approved for treatment of SLE in 2011. It was the first monoclonal antibody approved to treat SLE.⁷ B-lymphocyte stimulator plays a critical role in B-cell survival; thus, its inhibition increases apoptosis of autoreactive B cells involved in the pathogenesis of SLE. More recently, belimumab was approved for pediatric SLE in April 2019 based on the PLUTO study, a phase 2 randomized, double-blind study of 93 patients.⁸ Although patients with cutaneous manifestations of lupus were included in trials for belimumab, they lacked CLE-specific outcome measurements to truly evaluate the efficacy in treating skin disease.⁹ This medication currently is not approved by the US Food and Drug Administration (FDA) for CLE; however, it is used off label in some cases for recalcitrant disease.¹⁰

Baricitinib

Baricitinib is a selective and reversible inhibitor of JAK1 and JAK2 that was granted fast-track status by the FDA in December 2018. In a phase 2 trial, baricitinib was superior to placebo plus standard of care, primarily for arthritis and lupus nephritis.¹¹ Although improvement of cutaneous disease was measured as an end point, it did not show significant improvement in disease. The presence of skin disease was high, but the activity of disease was low, which can make it difficult to show meaningful improvement, as there is not much room for patients to objectively improve.¹² Showing meaningful improvement in skin disease often is difficult in phase 2 trials, especially when the trial design is focused on SLE rather than CLE activity. Further studies of baricitinib that include more severe patients with CLE disease are needed to truly understand its effects on the skin.

Lenalidomide

There have been several CLE studies in the last several years surrounding lenalidomide, an analog of thalidomide.^13-15 This molecule has a number of immunomodulatory effects including antiangiogenic effects, increased natural killer cell–dependent cytotoxicity, and cytokine and interleukin inhibition. Lenalidomide is of particular interest in treating CLE, as it was shown to be more potent than thalidomide at low doses and with a better side-effect profile. Multiple small, open-label trials have shown lenalidomide to be both safe and efficacious in the treatment of CLE.^13,14 In addition, iberdomide, a derivative of lenalidomide, recently completed a phase 2 dose-escalation study showing improvement in both SLE and CLE end points.¹⁶ A phase 2b proof-of-concept study currently is underway (ClinicalTrials.gov Identifier NCT03161483).

Monoclonal Antibodies

Many developing therapies target specific components of the type I interferon pathway, which is a primary driver of CLE lesions. Innate immune system pathways involving type I interferon were shown to be active in the pathogenesis of CLE, and levels of interferon correlate with skin disease activity.¹⁷ One molecule in development that targets this pathway is BIIB059, a humanized IgG1 monoclonal antibody that binds to blood dendritic cell antigen 2. This cell surface protein is uniquely expressed on plasmacytoid dendritic cells, which are the main source of type I interferon overproduction in SLE. The binding of this antibody to the blood dendritic cell antigen 2 receptor both blocks type I interferon production and decreases the overall number of active plasmacytoid dendritic cells present.¹⁸ In the completed phase 1b study, a response in cutaneous disease was shown through a reduction in the CLE disease area and severity index score following single-dose administration.¹⁹ More recently, a phase 2 study met primary end points in both SLE and CLE compared to placebo.²⁰

Anifrolumab is a human IgG1k monoclonal antibody that binds to type I interferon receptor, blocking all type I interferon signaling. Following a successful phase 2 trial, it failed to meet its primary end point in its first phase 3 trial.²¹ Several secondary end points suggested a clinical benefit. A second phase 3 trial of 362 patients randomized to treatment with anifrolumab or placebo over 48 weeks showed anifrolumab to be superior to placebo for multiple end points, including the overall disease primary end point as well as a notable reduction in skin activity.²²

Final Thoughts

Outside of the approval of belimumab, there have been no new FDA-approved treatments for SLE since the approval of antimalarial agents nearly 50 years ago. For CLE specifically, there is an even greater scarcity of evidence-based treatments. Recently studied medications, such as belimumab and lenalidomide, are available off label for CLE patients when other options have failed. Recent studies have evaluated the efficacy of these agents in the treatment of CLE using the CLE disease area and severity index.^10,13,14 Enrollment in CLE trials is difficult due to the rarity of the disease, and careful attention must be paid to evaluating skin end points. As experts in CLE and the nuances of these assessments, it is critical that dermatologists be involved in clinical trials. Future SLE trials must consider CLE as an important end point for CLE patients to get access to much-needed novel therapies.

Experts may be moving toward accepting cannabis as a useful tool to treat neuropathic pain, a recent debate on the topic suggests. During the debate, one expert argued for, and another against, there being sufficient evidence for the use of cannabis to treat neuropathic pain, but in the end, they agreed that some patients do benefit.

Anatoliy Sizov/Getty Images

The discussion took place at the Congress of the European Academy of Neurology (EAN) 2020, which transitioned to a virtual online meeting because of the COVID-19 pandemic.

The cannabis plant has 460 constituents. The two main components are tetrahydrocannabinol (THC) and cannabidiol (CBD). It can be consumed by swallowing oil extracts, by the sublingual route, or by smoking or eating the plant. Cannabis medications already in use include oral THC (nabilone, dronabinol) and an oral mucosal spray, nabiximols (Sativex).

Arguing that therapeutic cannabis is helpful for neuropathic pain, Elon Eisenberg, MD, professor of neurology and pain medicine, Israel Institute of Technology, Haifa, cited a number of encouraging randomized, controlled trials and meta-analyses of studies on the subject.
 

Opioid substitute

Dr. Eisenberg discussed three relevant articles. One was a 2016 viewpoint article published in JAMA that concluded that “cannabis seems to be a substitute, a rather good one, for opioids,” said Dr. Eisenberg.

A “comprehensive” 440-page review, published by the National Academies Press in 2017, evaluated the evidence to that point and “came to the conclusion there is substantial evidence that cannabis is an effective treatment for chronic pain in adults,” said Dr. Eisenberg.

And a 2018 position paper from the European Pain Federation determined that “the quantity and quality of evidence is such that cannabis-based medicines may be reasonably considered for chronic neuropathic pain,” he said.

He noted that the most recent results from an Israeli prospective cohort registry study that is following more than 851 patients who are taking cannabis over 1 year are positive. Analyses show a steady reduction in pain intensity and improvements in catastrophizing and disability. Importantly, he said, participants are using fewer opioids. However, about 40% of patients in that registry study experienced some adverse event, although most were not serious, said Dr. Eisenberg.
 

Not convinced

Arguing on the other side – that therapeutic cannabis is not helpful for neuropathic pain – was Nadine Attal, MD, PhD, professor of therapeutics and pain at the University Versailles Saint Quentin, France. She questioned the quality of some of the research to date and stressed that studies should consider neuropathic pain as a primary outcome – not spasticity or pain in general. They should also be double-blind, randomized, and placebo controlled, she said.

In addition, she said these studies should enroll at least 10 patients per group and should continue for 3 weeks or longer.

Dr. Attal wondered which of the many plant derivatives (phytocannabinoids) are used in cannabis studies.

She discussed four meta-analyses or reviews on the topic, some of which she said are “heterogeneous” and don’t provide convincing evidence for cannabis use in neuropathic pain.

For example, one review examined only marijuana, and all studies in it were short term. One of the studies in this review was of spasticity. Another review included two studies of cancer pain, and the most positive study in NP used short-term inhaled THC.

“There is no evidence to date that cannabinoids, including nabiximols or oral THC, administered for at least 3 weeks are more effective than placebo in neuropathic pain,” she concluded.
 

Some responders

However, Dr. Attal acknowledged that cannabis might be effective for some patients. In her experience, which has been borne out by some observational studies, patients with paroxysmal pain, or sudden stabbing pain, seem to get more relief from cannabis. “It’s absolutely possible that there’s a subgroup of symptoms or a subgroup of patients with specific symptoms who are much better responders to cannabis than others,” she said.

Asked if patients experience increased pain after withdrawing from cannabis, Dr. Eisenberg said he has observed that many patients stop taking cannabis when they start feeling better, but he hasn’t seen severe withdrawal symptoms.

However, there are other concerns related to cannabis use, said Dr. Eisenberg. A major concern regards driving a vehicle. In Israel, getting behind the wheel is prohibited within 6 hours of using cannabis.

But Dr. Eisenberg pointed out that published data on the safety of cannabis and driving were based on recreational users. “We need to keep in mind that recreational users typically use other substances, so we’re not sure the data is accurate,” he said.

There are increasing reports of stroke, transient ischemic attack, and MI among cannabis users. This is especially concerning because many of these cases involve young male adults who have no risk factors, said Dr. Eisenberg.

One conference delegate asked whether legal issues make it difficult to properly investigate cannabis in large studies. Dr. Eisenberg noted that legal concerns may help explain why there have not been any new randomized, controlled trials for about 2 years. “In the U.S., you can’t do clinical trials; cannabis is still regarded as schedule I substance,” he said.

Some physicians “are reluctant to deal with cannabis unless they get better data,” he said. “Doing research on cannabis seems to be somehow out of the mainstream.” Moreover, the research is difficult to carry out, owing to the complexity of the cannabis plant, which has many constituents. Perhaps it’s a matter of identifying and adding particular components to better demonstrate reduced pain, said Dr. Eisenberg.

Another complicating factor is that bioavailability differs considerably from one patient to another, “sometimes even by 10-fold,” he said.

Dr. Attal’s group will be starting a study next January that will enroll a large sample of patients with neuropathic pain or spasticity. In that study, cannabis will be dispensed through pharmacies and primary care. The aim of the study is “to see how it works in a real-life setting,” she said

Those participating in the virtual session were asked to vote on which side they agreed with. About 57% voted in favor of cannabis use, 14% voted against, and 28% had no opinion.

Dr. Eisenberg has received research grants from Rafa Laboratories, Saga Medical Ltd., Israel Pain Association, and Teva Israel. Dr. Attal has received support from Merck Sharp & Dohme, Sanofi, Ipsen, Novartis, Aptinyx, Air Liquide, Lilly, and Grunenthal.

A version of this article originally appeared on Medscape.com.

Experts may be moving toward accepting cannabis as a useful tool to treat neuropathic pain, a recent debate on the topic suggests. During the debate, one expert argued for, and another against, there being sufficient evidence for the use of cannabis to treat neuropathic pain, but in the end, they agreed that some patients do benefit.

Anatoliy Sizov/Getty Images

The discussion took place at the Congress of the European Academy of Neurology (EAN) 2020, which transitioned to a virtual online meeting because of the COVID-19 pandemic.

The cannabis plant has 460 constituents. The two main components are tetrahydrocannabinol (THC) and cannabidiol (CBD). It can be consumed by swallowing oil extracts, by the sublingual route, or by smoking or eating the plant. Cannabis medications already in use include oral THC (nabilone, dronabinol) and an oral mucosal spray, nabiximols (Sativex).

Arguing that therapeutic cannabis is helpful for neuropathic pain, Elon Eisenberg, MD, professor of neurology and pain medicine, Israel Institute of Technology, Haifa, cited a number of encouraging randomized, controlled trials and meta-analyses of studies on the subject.
 

Opioid substitute

Dr. Eisenberg discussed three relevant articles. One was a 2016 viewpoint article published in JAMA that concluded that “cannabis seems to be a substitute, a rather good one, for opioids,” said Dr. Eisenberg.

A “comprehensive” 440-page review, published by the National Academies Press in 2017, evaluated the evidence to that point and “came to the conclusion there is substantial evidence that cannabis is an effective treatment for chronic pain in adults,” said Dr. Eisenberg.

And a 2018 position paper from the European Pain Federation determined that “the quantity and quality of evidence is such that cannabis-based medicines may be reasonably considered for chronic neuropathic pain,” he said.

He noted that the most recent results from an Israeli prospective cohort registry study that is following more than 851 patients who are taking cannabis over 1 year are positive. Analyses show a steady reduction in pain intensity and improvements in catastrophizing and disability. Importantly, he said, participants are using fewer opioids. However, about 40% of patients in that registry study experienced some adverse event, although most were not serious, said Dr. Eisenberg.
 

Not convinced

Arguing on the other side – that therapeutic cannabis is not helpful for neuropathic pain – was Nadine Attal, MD, PhD, professor of therapeutics and pain at the University Versailles Saint Quentin, France. She questioned the quality of some of the research to date and stressed that studies should consider neuropathic pain as a primary outcome – not spasticity or pain in general. They should also be double-blind, randomized, and placebo controlled, she said.

In addition, she said these studies should enroll at least 10 patients per group and should continue for 3 weeks or longer.

Dr. Attal wondered which of the many plant derivatives (phytocannabinoids) are used in cannabis studies.

She discussed four meta-analyses or reviews on the topic, some of which she said are “heterogeneous” and don’t provide convincing evidence for cannabis use in neuropathic pain.

For example, one review examined only marijuana, and all studies in it were short term. One of the studies in this review was of spasticity. Another review included two studies of cancer pain, and the most positive study in NP used short-term inhaled THC.

“There is no evidence to date that cannabinoids, including nabiximols or oral THC, administered for at least 3 weeks are more effective than placebo in neuropathic pain,” she concluded.
 

Some responders

However, Dr. Attal acknowledged that cannabis might be effective for some patients. In her experience, which has been borne out by some observational studies, patients with paroxysmal pain, or sudden stabbing pain, seem to get more relief from cannabis. “It’s absolutely possible that there’s a subgroup of symptoms or a subgroup of patients with specific symptoms who are much better responders to cannabis than others,” she said.

Asked if patients experience increased pain after withdrawing from cannabis, Dr. Eisenberg said he has observed that many patients stop taking cannabis when they start feeling better, but he hasn’t seen severe withdrawal symptoms.

However, there are other concerns related to cannabis use, said Dr. Eisenberg. A major concern regards driving a vehicle. In Israel, getting behind the wheel is prohibited within 6 hours of using cannabis.

But Dr. Eisenberg pointed out that published data on the safety of cannabis and driving were based on recreational users. “We need to keep in mind that recreational users typically use other substances, so we’re not sure the data is accurate,” he said.

There are increasing reports of stroke, transient ischemic attack, and MI among cannabis users. This is especially concerning because many of these cases involve young male adults who have no risk factors, said Dr. Eisenberg.

One conference delegate asked whether legal issues make it difficult to properly investigate cannabis in large studies. Dr. Eisenberg noted that legal concerns may help explain why there have not been any new randomized, controlled trials for about 2 years. “In the U.S., you can’t do clinical trials; cannabis is still regarded as schedule I substance,” he said.

Some physicians “are reluctant to deal with cannabis unless they get better data,” he said. “Doing research on cannabis seems to be somehow out of the mainstream.” Moreover, the research is difficult to carry out, owing to the complexity of the cannabis plant, which has many constituents. Perhaps it’s a matter of identifying and adding particular components to better demonstrate reduced pain, said Dr. Eisenberg.

Another complicating factor is that bioavailability differs considerably from one patient to another, “sometimes even by 10-fold,” he said.

Dr. Attal’s group will be starting a study next January that will enroll a large sample of patients with neuropathic pain or spasticity. In that study, cannabis will be dispensed through pharmacies and primary care. The aim of the study is “to see how it works in a real-life setting,” she said

Those participating in the virtual session were asked to vote on which side they agreed with. About 57% voted in favor of cannabis use, 14% voted against, and 28% had no opinion.

Dr. Eisenberg has received research grants from Rafa Laboratories, Saga Medical Ltd., Israel Pain Association, and Teva Israel. Dr. Attal has received support from Merck Sharp & Dohme, Sanofi, Ipsen, Novartis, Aptinyx, Air Liquide, Lilly, and Grunenthal.

A version of this article originally appeared on Medscape.com.

Experts may be moving toward accepting cannabis as a useful tool to treat neuropathic pain, a recent debate on the topic suggests. During the debate, one expert argued for, and another against, there being sufficient evidence for the use of cannabis to treat neuropathic pain, but in the end, they agreed that some patients do benefit.

Anatoliy Sizov/Getty Images

The discussion took place at the Congress of the European Academy of Neurology (EAN) 2020, which transitioned to a virtual online meeting because of the COVID-19 pandemic.

The cannabis plant has 460 constituents. The two main components are tetrahydrocannabinol (THC) and cannabidiol (CBD). It can be consumed by swallowing oil extracts, by the sublingual route, or by smoking or eating the plant. Cannabis medications already in use include oral THC (nabilone, dronabinol) and an oral mucosal spray, nabiximols (Sativex).

Arguing that therapeutic cannabis is helpful for neuropathic pain, Elon Eisenberg, MD, professor of neurology and pain medicine, Israel Institute of Technology, Haifa, cited a number of encouraging randomized, controlled trials and meta-analyses of studies on the subject.
 

Opioid substitute

Dr. Eisenberg discussed three relevant articles. One was a 2016 viewpoint article published in JAMA that concluded that “cannabis seems to be a substitute, a rather good one, for opioids,” said Dr. Eisenberg.

A “comprehensive” 440-page review, published by the National Academies Press in 2017, evaluated the evidence to that point and “came to the conclusion there is substantial evidence that cannabis is an effective treatment for chronic pain in adults,” said Dr. Eisenberg.

And a 2018 position paper from the European Pain Federation determined that “the quantity and quality of evidence is such that cannabis-based medicines may be reasonably considered for chronic neuropathic pain,” he said.

He noted that the most recent results from an Israeli prospective cohort registry study that is following more than 851 patients who are taking cannabis over 1 year are positive. Analyses show a steady reduction in pain intensity and improvements in catastrophizing and disability. Importantly, he said, participants are using fewer opioids. However, about 40% of patients in that registry study experienced some adverse event, although most were not serious, said Dr. Eisenberg.
 

Not convinced

Arguing on the other side – that therapeutic cannabis is not helpful for neuropathic pain – was Nadine Attal, MD, PhD, professor of therapeutics and pain at the University Versailles Saint Quentin, France. She questioned the quality of some of the research to date and stressed that studies should consider neuropathic pain as a primary outcome – not spasticity or pain in general. They should also be double-blind, randomized, and placebo controlled, she said.

In addition, she said these studies should enroll at least 10 patients per group and should continue for 3 weeks or longer.

Dr. Attal wondered which of the many plant derivatives (phytocannabinoids) are used in cannabis studies.

She discussed four meta-analyses or reviews on the topic, some of which she said are “heterogeneous” and don’t provide convincing evidence for cannabis use in neuropathic pain.

For example, one review examined only marijuana, and all studies in it were short term. One of the studies in this review was of spasticity. Another review included two studies of cancer pain, and the most positive study in NP used short-term inhaled THC.

“There is no evidence to date that cannabinoids, including nabiximols or oral THC, administered for at least 3 weeks are more effective than placebo in neuropathic pain,” she concluded.
 

Some responders

However, Dr. Attal acknowledged that cannabis might be effective for some patients. In her experience, which has been borne out by some observational studies, patients with paroxysmal pain, or sudden stabbing pain, seem to get more relief from cannabis. “It’s absolutely possible that there’s a subgroup of symptoms or a subgroup of patients with specific symptoms who are much better responders to cannabis than others,” she said.

Asked if patients experience increased pain after withdrawing from cannabis, Dr. Eisenberg said he has observed that many patients stop taking cannabis when they start feeling better, but he hasn’t seen severe withdrawal symptoms.

However, there are other concerns related to cannabis use, said Dr. Eisenberg. A major concern regards driving a vehicle. In Israel, getting behind the wheel is prohibited within 6 hours of using cannabis.

But Dr. Eisenberg pointed out that published data on the safety of cannabis and driving were based on recreational users. “We need to keep in mind that recreational users typically use other substances, so we’re not sure the data is accurate,” he said.

There are increasing reports of stroke, transient ischemic attack, and MI among cannabis users. This is especially concerning because many of these cases involve young male adults who have no risk factors, said Dr. Eisenberg.

One conference delegate asked whether legal issues make it difficult to properly investigate cannabis in large studies. Dr. Eisenberg noted that legal concerns may help explain why there have not been any new randomized, controlled trials for about 2 years. “In the U.S., you can’t do clinical trials; cannabis is still regarded as schedule I substance,” he said.

Some physicians “are reluctant to deal with cannabis unless they get better data,” he said. “Doing research on cannabis seems to be somehow out of the mainstream.” Moreover, the research is difficult to carry out, owing to the complexity of the cannabis plant, which has many constituents. Perhaps it’s a matter of identifying and adding particular components to better demonstrate reduced pain, said Dr. Eisenberg.

Another complicating factor is that bioavailability differs considerably from one patient to another, “sometimes even by 10-fold,” he said.

Dr. Attal’s group will be starting a study next January that will enroll a large sample of patients with neuropathic pain or spasticity. In that study, cannabis will be dispensed through pharmacies and primary care. The aim of the study is “to see how it works in a real-life setting,” she said

Those participating in the virtual session were asked to vote on which side they agreed with. About 57% voted in favor of cannabis use, 14% voted against, and 28% had no opinion.

Dr. Eisenberg has received research grants from Rafa Laboratories, Saga Medical Ltd., Israel Pain Association, and Teva Israel. Dr. Attal has received support from Merck Sharp & Dohme, Sanofi, Ipsen, Novartis, Aptinyx, Air Liquide, Lilly, and Grunenthal.

A version of this article originally appeared on Medscape.com.

Having a diagnosis of atopic dermatitis (AD) was associated with a greater risk of developing anxiety, depression, bipolar disorder, and other major neuropsychiatric disorders in children, adolescents, and adults, according to a study presented at the annual meeting of the Society for Investigative Dermatology, held virtually.

“The risk increase ranges from as low as 5% up to 59%, depending on the outcome, with generally greater effects observed among the adults,” Joy Wan, MD, a postdoctoral dermatology fellow at the University of Pennsylvania, Philadelphia, said in her presentation. The risk was independent of other atopic disease, gender, age, and socioeconomic status.

Dr. Wan and colleagues conducted a cohort study of patients with AD in the United Kingdom using data from the Health Improvement Network (THIN) electronic records database, matching AD patients in THIN with up to five patients without AD, similar in age and also registered to general practices. The researchers validated AD disease status using an algorithm that identified patients with a diagnostic code and two therapy codes related to AD. Outcomes of interest included anxiety, depression, bipolar disorder, obsessive-compulsive disorder, ADHD, schizophrenia, and autism. Patients entered into the cohort when they were diagnosed with AD, registered by a practice, or when data from a practice was reported to THIN. The researchers stopped following patients when they developed a neuropsychiatric outcome of interest, left a practice, died, or when the study ended.

“Previous studies have found associations between atopic dermatitis and anxiety, depression, and attention-deficit/hyperactivity disorder. However, many previous studies had been cross-sectional and they were unable to evaluate the directionality of association between atopic dermatitis and neuropsychiatric outcomes, while other previous studies have relied on the self-report of atopic dermatitis and outcomes as well,” Dr. Wan said. “Thus, longitudinal studies, using validated measures of atopic dermatitis, and those that include the entire age span, are really needed.”

Overall, 434,859 children and adolescents under aged 18 with AD in the THIN database were matched to 1,983,589 controls, and 644,802 adults with AD were matched to almost 2,900,000 adults without AD. In the pediatric group, demographics were mostly balanced between children with and without AD: the average age ranged between about 5 and almost 6 years. In pediatric patients with AD, there was a higher rate of allergic rhinitis (6.2% vs. 4%) and asthma (13.5% vs. 9.3%) than in the control group.

For adults, the average age was about 48 years in both groups. Compared with patients who did not have AD, adults with AD also had higher rates of allergic rhinitis (15.2% vs. 9.6%) and asthma (19.9% vs. 12.6%).

After adjusting for age, gender, socioeconomic status, asthma, and allergic rhinitis, Dr. Wan and colleagues found greater rates of bipolar disorder (hazard ratio, 1.34; 95% confidence interval, 1.09-1.65), obsessive-compulsive disorder (HR, 1.30; 95% CI, 1.21-1.41), anxiety (HR, 1.09; 95% CI, 1.07-1.11), and depression (HR, 1.06; 95% CI, 1.04-1.08) among children and adolescents with AD, compared with controls.

In the adult cohort, a diagnosis of AD was associated with an increased risk of autism (HR, 1.53; 95% CI, 1.30-1.80), obsessive-compulsive disorder (HR, 1.49; 95% CI, 1.40-1.59), ADHD (HR, 1.31; 95% CI, 1.13-1.53), anxiety (HR, 1.17; 95% CI, 1.15-1.18), depression (HR, 1.15; 95% CI, 1.14-1.16), and bipolar disorder (HR, 1.12; 95% CI, 1.04-1.21), after adjusting for age, gender, socioeconomic status, asthma, and allergic rhinitis.

One reason for the increased associations among the adults, even for ADHD and autism, which are more characteristically diagnosed in childhood, Dr. Wan said, is that, since they looked at incident outcomes, “many children may already have had these prevalent comorbidities at the time of the entry in the cohort.”

She noted that the study may have observation bias or unknown confounders, but she hopes these results raise awareness of the association between AD and neuropsychiatric disorders, although more research is needed to determine how AD severity affects neuropsychiatric outcomes. “Additional work is needed to really understand the mechanisms that drive these associations, whether it’s mediated through symptoms of atopic dermatitis such as itch and poor sleep, or potentially the stigma of having a chronic skin disease, or perhaps shared pathophysiology between atopic dermatitis and these neuropsychiatric diseases,” she said.

The study was funded by a grant from Pfizer. Dr. Wan reports receiving research funding from Pfizer paid to the University of Pennsylvania.

Having a diagnosis of atopic dermatitis (AD) was associated with a greater risk of developing anxiety, depression, bipolar disorder, and other major neuropsychiatric disorders in children, adolescents, and adults, according to a study presented at the annual meeting of the Society for Investigative Dermatology, held virtually.

“The risk increase ranges from as low as 5% up to 59%, depending on the outcome, with generally greater effects observed among the adults,” Joy Wan, MD, a postdoctoral dermatology fellow at the University of Pennsylvania, Philadelphia, said in her presentation. The risk was independent of other atopic disease, gender, age, and socioeconomic status.

Dr. Wan and colleagues conducted a cohort study of patients with AD in the United Kingdom using data from the Health Improvement Network (THIN) electronic records database, matching AD patients in THIN with up to five patients without AD, similar in age and also registered to general practices. The researchers validated AD disease status using an algorithm that identified patients with a diagnostic code and two therapy codes related to AD. Outcomes of interest included anxiety, depression, bipolar disorder, obsessive-compulsive disorder, ADHD, schizophrenia, and autism. Patients entered into the cohort when they were diagnosed with AD, registered by a practice, or when data from a practice was reported to THIN. The researchers stopped following patients when they developed a neuropsychiatric outcome of interest, left a practice, died, or when the study ended.

“Previous studies have found associations between atopic dermatitis and anxiety, depression, and attention-deficit/hyperactivity disorder. However, many previous studies had been cross-sectional and they were unable to evaluate the directionality of association between atopic dermatitis and neuropsychiatric outcomes, while other previous studies have relied on the self-report of atopic dermatitis and outcomes as well,” Dr. Wan said. “Thus, longitudinal studies, using validated measures of atopic dermatitis, and those that include the entire age span, are really needed.”

Overall, 434,859 children and adolescents under aged 18 with AD in the THIN database were matched to 1,983,589 controls, and 644,802 adults with AD were matched to almost 2,900,000 adults without AD. In the pediatric group, demographics were mostly balanced between children with and without AD: the average age ranged between about 5 and almost 6 years. In pediatric patients with AD, there was a higher rate of allergic rhinitis (6.2% vs. 4%) and asthma (13.5% vs. 9.3%) than in the control group.

For adults, the average age was about 48 years in both groups. Compared with patients who did not have AD, adults with AD also had higher rates of allergic rhinitis (15.2% vs. 9.6%) and asthma (19.9% vs. 12.6%).

After adjusting for age, gender, socioeconomic status, asthma, and allergic rhinitis, Dr. Wan and colleagues found greater rates of bipolar disorder (hazard ratio, 1.34; 95% confidence interval, 1.09-1.65), obsessive-compulsive disorder (HR, 1.30; 95% CI, 1.21-1.41), anxiety (HR, 1.09; 95% CI, 1.07-1.11), and depression (HR, 1.06; 95% CI, 1.04-1.08) among children and adolescents with AD, compared with controls.

In the adult cohort, a diagnosis of AD was associated with an increased risk of autism (HR, 1.53; 95% CI, 1.30-1.80), obsessive-compulsive disorder (HR, 1.49; 95% CI, 1.40-1.59), ADHD (HR, 1.31; 95% CI, 1.13-1.53), anxiety (HR, 1.17; 95% CI, 1.15-1.18), depression (HR, 1.15; 95% CI, 1.14-1.16), and bipolar disorder (HR, 1.12; 95% CI, 1.04-1.21), after adjusting for age, gender, socioeconomic status, asthma, and allergic rhinitis.

One reason for the increased associations among the adults, even for ADHD and autism, which are more characteristically diagnosed in childhood, Dr. Wan said, is that, since they looked at incident outcomes, “many children may already have had these prevalent comorbidities at the time of the entry in the cohort.”

She noted that the study may have observation bias or unknown confounders, but she hopes these results raise awareness of the association between AD and neuropsychiatric disorders, although more research is needed to determine how AD severity affects neuropsychiatric outcomes. “Additional work is needed to really understand the mechanisms that drive these associations, whether it’s mediated through symptoms of atopic dermatitis such as itch and poor sleep, or potentially the stigma of having a chronic skin disease, or perhaps shared pathophysiology between atopic dermatitis and these neuropsychiatric diseases,” she said.

The study was funded by a grant from Pfizer. Dr. Wan reports receiving research funding from Pfizer paid to the University of Pennsylvania.

Having a diagnosis of atopic dermatitis (AD) was associated with a greater risk of developing anxiety, depression, bipolar disorder, and other major neuropsychiatric disorders in children, adolescents, and adults, according to a study presented at the annual meeting of the Society for Investigative Dermatology, held virtually.

“The risk increase ranges from as low as 5% up to 59%, depending on the outcome, with generally greater effects observed among the adults,” Joy Wan, MD, a postdoctoral dermatology fellow at the University of Pennsylvania, Philadelphia, said in her presentation. The risk was independent of other atopic disease, gender, age, and socioeconomic status.

Dr. Wan and colleagues conducted a cohort study of patients with AD in the United Kingdom using data from the Health Improvement Network (THIN) electronic records database, matching AD patients in THIN with up to five patients without AD, similar in age and also registered to general practices. The researchers validated AD disease status using an algorithm that identified patients with a diagnostic code and two therapy codes related to AD. Outcomes of interest included anxiety, depression, bipolar disorder, obsessive-compulsive disorder, ADHD, schizophrenia, and autism. Patients entered into the cohort when they were diagnosed with AD, registered by a practice, or when data from a practice was reported to THIN. The researchers stopped following patients when they developed a neuropsychiatric outcome of interest, left a practice, died, or when the study ended.

“Previous studies have found associations between atopic dermatitis and anxiety, depression, and attention-deficit/hyperactivity disorder. However, many previous studies had been cross-sectional and they were unable to evaluate the directionality of association between atopic dermatitis and neuropsychiatric outcomes, while other previous studies have relied on the self-report of atopic dermatitis and outcomes as well,” Dr. Wan said. “Thus, longitudinal studies, using validated measures of atopic dermatitis, and those that include the entire age span, are really needed.”

Overall, 434,859 children and adolescents under aged 18 with AD in the THIN database were matched to 1,983,589 controls, and 644,802 adults with AD were matched to almost 2,900,000 adults without AD. In the pediatric group, demographics were mostly balanced between children with and without AD: the average age ranged between about 5 and almost 6 years. In pediatric patients with AD, there was a higher rate of allergic rhinitis (6.2% vs. 4%) and asthma (13.5% vs. 9.3%) than in the control group.

For adults, the average age was about 48 years in both groups. Compared with patients who did not have AD, adults with AD also had higher rates of allergic rhinitis (15.2% vs. 9.6%) and asthma (19.9% vs. 12.6%).

After adjusting for age, gender, socioeconomic status, asthma, and allergic rhinitis, Dr. Wan and colleagues found greater rates of bipolar disorder (hazard ratio, 1.34; 95% confidence interval, 1.09-1.65), obsessive-compulsive disorder (HR, 1.30; 95% CI, 1.21-1.41), anxiety (HR, 1.09; 95% CI, 1.07-1.11), and depression (HR, 1.06; 95% CI, 1.04-1.08) among children and adolescents with AD, compared with controls.

In the adult cohort, a diagnosis of AD was associated with an increased risk of autism (HR, 1.53; 95% CI, 1.30-1.80), obsessive-compulsive disorder (HR, 1.49; 95% CI, 1.40-1.59), ADHD (HR, 1.31; 95% CI, 1.13-1.53), anxiety (HR, 1.17; 95% CI, 1.15-1.18), depression (HR, 1.15; 95% CI, 1.14-1.16), and bipolar disorder (HR, 1.12; 95% CI, 1.04-1.21), after adjusting for age, gender, socioeconomic status, asthma, and allergic rhinitis.

One reason for the increased associations among the adults, even for ADHD and autism, which are more characteristically diagnosed in childhood, Dr. Wan said, is that, since they looked at incident outcomes, “many children may already have had these prevalent comorbidities at the time of the entry in the cohort.”

She noted that the study may have observation bias or unknown confounders, but she hopes these results raise awareness of the association between AD and neuropsychiatric disorders, although more research is needed to determine how AD severity affects neuropsychiatric outcomes. “Additional work is needed to really understand the mechanisms that drive these associations, whether it’s mediated through symptoms of atopic dermatitis such as itch and poor sleep, or potentially the stigma of having a chronic skin disease, or perhaps shared pathophysiology between atopic dermatitis and these neuropsychiatric diseases,” she said.

The study was funded by a grant from Pfizer. Dr. Wan reports receiving research funding from Pfizer paid to the University of Pennsylvania.

Neuroimaging of patients with progressive multiple sclerosis (MS) shows that physical behavioral change therapy, specifically, constraint-induced movement therapy (CIMT), leads to improvement in neuroplasticity, compared with alternative interventions with medicines. “The findings suggest for the first time that physical behavioral change therapy can significantly stimulate cortical neuroplasticity in a degenerative central nervous system disorder,” said the authors of research presented at the virtual meeting of the Consortium of Multiple Sclerosis Centers (CMSC).

CIMT, an intervention involving 3.5 hours/day of therapist-supervised treatment over 10 consecutive weekdays, has been shown to significantly improve paretic limb use for patients with progressive MS, and the effects are long lasting.

For patients with asymmetric upper limb nonuse, the treatment “is highly successful for promoting increased use by the more-affected arm for everyday activities,” said lead author Victor W. Mark, MD, an associate professor and medical director of the Constraint-Induced Movement Therapy Research Programs at the University of Alabama at Birmingham. “The improvements after CIMT can be found to remain as much as 1 year after the completion of the treatment, and even later. That by itself is novel for MS,” he said.

The team’s previous research in Neurorehabilitation and Neural Repair showed that the CIMT intervention is associated with statistically significant changes in white matter integrity in the brain. In this new study, Dr. Mark and colleagues sought to determine whether the effects would also translate to improvements in cortical gray matter.
 

Promoting neuroplasticity, improving motor function

For their study, they enrolled 20 adults with chronic MS who were matched with respect to unilateral arm disability. The participants were randomly assigned to receive 35 hours of either CIMT or a holistic complementary alternative medicine program, which included yoga, aquatic therapy, massage, and/or relaxation techniques, over the course of 2 weeks.

Both groups expressed the same degree of expectancy of benefits from the intervention. Those who received CIMT showed a significantly larger effect size on the Motor Activity Log, a measure that has been validated against real-world upper-limb accelerometry, compared with the control group (d = 3.2, vs. d = 0.7).

Imaging with tensor-based morphometry showed an increase in the thickness of the primary motor cortex in patients who underwent CIMT but not those who received the alternative medicine treatment. Furthermore, a change in the primary motor cortex was observed in the CIMT group on voxel-based morphometry, suggesting an increase in cortical density or volume, or both. Similar changes were not seen in the alternative medicine group.

“We evaluated the density of the brain cortical gray area before and after treatment, and we found increased gray matter in the area of the brain that is concentrated with voluntary limb movement (the motor cortex),” Dr. Mark said. “As in (previous) studies, we did not find such changes, or any changes, after the other form of treatment,” he said.

The results are important, Dr. Mark noted, “because CIMT seems to specifically promote neuroplasticity changes that appear to be healthy, for what is otherwise a chronically progressive degenerative neurological disorder.”

In addition to the improvements in MS, CIMT has led to improvement in motor function for patients who have experienced other central nervous system injuries, including stroke, traumatic brain injury, cerebral palsy, and, in musicians, focal hand dystonia.

The new findings offer intriguing insights into the effects in progressive MS, commented rehabilitation specialist Patricia Bobryk, MHS, a physical therapist with the UCHealth Yampa Valley Medical Center, in Colorado Springs.

“There is more evidence for CIMT in the area of stroke, which is more acute onset and with more potential recovery, especially early on, so this is exciting initial work in terms of MS,” she said.

“If we’re trying to find new avenues in the brain for better pathways, rather than using something that’s damaged in MS, it makes perfect sense that CIMT really forces and drives those connections, because you’re doing a repetitive, high-intensity patterning throughout the day, so you set up that environment for things to progress, especially in motor functioning,” she said.
 

Repetition, ‘prevention of compensation’

CIMT was developed at the University of Alabama, Birmingham, 30 years ago and involves four components. The first, described as “massed practice,” involves intensive, repetitive arm movements of the affected arm. The second component involves “shaping,” in which the patient is encouraged to perform his or her best attempts at the movements.

For the third component, described as “prevention of compensation,” the patient’s more-functional arm is inhibited from being used in everyday activities by wearing a padded mitt.

“This permits the patient to brace him- or herself whenever needed, but the better hand nonetheless lacks the dexterity to take over the activities that should be performed by the worse arm,” Dr. Mark explained.

“The patient wears the padded mitt after hours, too, except when using water or when sleeping,” he said.

The fourth component is a set of behavioral enforcement techniques involving goal-setting; daily interviews and discussion of progress and challenges; nightly homework; diary keeping; and telephone follow-up.

Dr. Mark noted that the intervention could have benefits that are secondary to motor and movement function. “We consider that the improvement of limb activity in a motor-challenged person with MS could afford a way to offset the deleterious effects of inactivity that can occur, such as weight gain, diabetes, osteoporosis, cardiac disease, and other conditions associated with prolonged inactivity,” he said.

Although it was developed at the University of Alabama, CIMT is currently more widely practiced in Europe than the United States, likely because of differences in care support, which in Europe is provided through socialized medicine, Dr. Mark pointed out.

Although the detailed methods for conducting CIMT are published in peer-reviewed journals, Dr. Mark recommends hands-on and interactive teaching. Such training is offered to clinicians and affiliated physical therapists and occupational therapists through Mark’s program at the University of Alabama in a semiannual, week-long training course, which includes hands-on treatment practice with actual patients.
 

Proof of principle

In further commenting on the study, Kathy M. Zackowski, PhD, of the National MS Society, said the findings provide an intriguing proof of concept that should be tested in a larger cohort. “The question of how much a behavioral (therapy) can impact true brain structural change or change in the pathologic mechanism is intriguing and of high importance,” she said.

“It is important to take this information as ‘proof of principle’ of the importance of CIMT for improving upper limb activity,” according to Dr. Zackowski, senior director, patient management, care and rehabilitation research at the society.

“Importantly, this team needs to move forward testing their hypothesis in a larger randomized, clinical trial with a full control group in order to show causal evidence that one intervention caused the structural brain changes seen,” she said in an interview.

Dr. Zackowski added that a caveat of CIMT is that the approach assumes one limb is more impaired than the other, which is always the case in stroke but is true only in some cases of MS. “Therefore, this method may not be effective for everyone with MS, but offers another option for tailoring an intervention to a person’s abilities and interests,” she said.

“Another important detail is that CIMT is also being explored for lower extremity use,” she added. “This is exciting, as lower extremity dysfunction is a very common problem in MS, and may be useful in treating walking disability.”

The authors, Ms. Bobryk, and Dr. Zackowski have disclosed no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

Neuroimaging of patients with progressive multiple sclerosis (MS) shows that physical behavioral change therapy, specifically, constraint-induced movement therapy (CIMT), leads to improvement in neuroplasticity, compared with alternative interventions with medicines. “The findings suggest for the first time that physical behavioral change therapy can significantly stimulate cortical neuroplasticity in a degenerative central nervous system disorder,” said the authors of research presented at the virtual meeting of the Consortium of Multiple Sclerosis Centers (CMSC).

CIMT, an intervention involving 3.5 hours/day of therapist-supervised treatment over 10 consecutive weekdays, has been shown to significantly improve paretic limb use for patients with progressive MS, and the effects are long lasting.

For patients with asymmetric upper limb nonuse, the treatment “is highly successful for promoting increased use by the more-affected arm for everyday activities,” said lead author Victor W. Mark, MD, an associate professor and medical director of the Constraint-Induced Movement Therapy Research Programs at the University of Alabama at Birmingham. “The improvements after CIMT can be found to remain as much as 1 year after the completion of the treatment, and even later. That by itself is novel for MS,” he said.

The team’s previous research in Neurorehabilitation and Neural Repair showed that the CIMT intervention is associated with statistically significant changes in white matter integrity in the brain. In this new study, Dr. Mark and colleagues sought to determine whether the effects would also translate to improvements in cortical gray matter.
 

Promoting neuroplasticity, improving motor function

For their study, they enrolled 20 adults with chronic MS who were matched with respect to unilateral arm disability. The participants were randomly assigned to receive 35 hours of either CIMT or a holistic complementary alternative medicine program, which included yoga, aquatic therapy, massage, and/or relaxation techniques, over the course of 2 weeks.

Both groups expressed the same degree of expectancy of benefits from the intervention. Those who received CIMT showed a significantly larger effect size on the Motor Activity Log, a measure that has been validated against real-world upper-limb accelerometry, compared with the control group (d = 3.2, vs. d = 0.7).

Imaging with tensor-based morphometry showed an increase in the thickness of the primary motor cortex in patients who underwent CIMT but not those who received the alternative medicine treatment. Furthermore, a change in the primary motor cortex was observed in the CIMT group on voxel-based morphometry, suggesting an increase in cortical density or volume, or both. Similar changes were not seen in the alternative medicine group.

“We evaluated the density of the brain cortical gray area before and after treatment, and we found increased gray matter in the area of the brain that is concentrated with voluntary limb movement (the motor cortex),” Dr. Mark said. “As in (previous) studies, we did not find such changes, or any changes, after the other form of treatment,” he said.

The results are important, Dr. Mark noted, “because CIMT seems to specifically promote neuroplasticity changes that appear to be healthy, for what is otherwise a chronically progressive degenerative neurological disorder.”

In addition to the improvements in MS, CIMT has led to improvement in motor function for patients who have experienced other central nervous system injuries, including stroke, traumatic brain injury, cerebral palsy, and, in musicians, focal hand dystonia.

The new findings offer intriguing insights into the effects in progressive MS, commented rehabilitation specialist Patricia Bobryk, MHS, a physical therapist with the UCHealth Yampa Valley Medical Center, in Colorado Springs.

“There is more evidence for CIMT in the area of stroke, which is more acute onset and with more potential recovery, especially early on, so this is exciting initial work in terms of MS,” she said.

“If we’re trying to find new avenues in the brain for better pathways, rather than using something that’s damaged in MS, it makes perfect sense that CIMT really forces and drives those connections, because you’re doing a repetitive, high-intensity patterning throughout the day, so you set up that environment for things to progress, especially in motor functioning,” she said.
 

Repetition, ‘prevention of compensation’

CIMT was developed at the University of Alabama, Birmingham, 30 years ago and involves four components. The first, described as “massed practice,” involves intensive, repetitive arm movements of the affected arm. The second component involves “shaping,” in which the patient is encouraged to perform his or her best attempts at the movements.

For the third component, described as “prevention of compensation,” the patient’s more-functional arm is inhibited from being used in everyday activities by wearing a padded mitt.

“This permits the patient to brace him- or herself whenever needed, but the better hand nonetheless lacks the dexterity to take over the activities that should be performed by the worse arm,” Dr. Mark explained.

“The patient wears the padded mitt after hours, too, except when using water or when sleeping,” he said.

The fourth component is a set of behavioral enforcement techniques involving goal-setting; daily interviews and discussion of progress and challenges; nightly homework; diary keeping; and telephone follow-up.

Dr. Mark noted that the intervention could have benefits that are secondary to motor and movement function. “We consider that the improvement of limb activity in a motor-challenged person with MS could afford a way to offset the deleterious effects of inactivity that can occur, such as weight gain, diabetes, osteoporosis, cardiac disease, and other conditions associated with prolonged inactivity,” he said.

Although it was developed at the University of Alabama, CIMT is currently more widely practiced in Europe than the United States, likely because of differences in care support, which in Europe is provided through socialized medicine, Dr. Mark pointed out.

Although the detailed methods for conducting CIMT are published in peer-reviewed journals, Dr. Mark recommends hands-on and interactive teaching. Such training is offered to clinicians and affiliated physical therapists and occupational therapists through Mark’s program at the University of Alabama in a semiannual, week-long training course, which includes hands-on treatment practice with actual patients.
 

Proof of principle

In further commenting on the study, Kathy M. Zackowski, PhD, of the National MS Society, said the findings provide an intriguing proof of concept that should be tested in a larger cohort. “The question of how much a behavioral (therapy) can impact true brain structural change or change in the pathologic mechanism is intriguing and of high importance,” she said.

“It is important to take this information as ‘proof of principle’ of the importance of CIMT for improving upper limb activity,” according to Dr. Zackowski, senior director, patient management, care and rehabilitation research at the society.

“Importantly, this team needs to move forward testing their hypothesis in a larger randomized, clinical trial with a full control group in order to show causal evidence that one intervention caused the structural brain changes seen,” she said in an interview.

Dr. Zackowski added that a caveat of CIMT is that the approach assumes one limb is more impaired than the other, which is always the case in stroke but is true only in some cases of MS. “Therefore, this method may not be effective for everyone with MS, but offers another option for tailoring an intervention to a person’s abilities and interests,” she said.

“Another important detail is that CIMT is also being explored for lower extremity use,” she added. “This is exciting, as lower extremity dysfunction is a very common problem in MS, and may be useful in treating walking disability.”

The authors, Ms. Bobryk, and Dr. Zackowski have disclosed no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

Neuroimaging of patients with progressive multiple sclerosis (MS) shows that physical behavioral change therapy, specifically, constraint-induced movement therapy (CIMT), leads to improvement in neuroplasticity, compared with alternative interventions with medicines. “The findings suggest for the first time that physical behavioral change therapy can significantly stimulate cortical neuroplasticity in a degenerative central nervous system disorder,” said the authors of research presented at the virtual meeting of the Consortium of Multiple Sclerosis Centers (CMSC).

CIMT, an intervention involving 3.5 hours/day of therapist-supervised treatment over 10 consecutive weekdays, has been shown to significantly improve paretic limb use for patients with progressive MS, and the effects are long lasting.

For patients with asymmetric upper limb nonuse, the treatment “is highly successful for promoting increased use by the more-affected arm for everyday activities,” said lead author Victor W. Mark, MD, an associate professor and medical director of the Constraint-Induced Movement Therapy Research Programs at the University of Alabama at Birmingham. “The improvements after CIMT can be found to remain as much as 1 year after the completion of the treatment, and even later. That by itself is novel for MS,” he said.

The team’s previous research in Neurorehabilitation and Neural Repair showed that the CIMT intervention is associated with statistically significant changes in white matter integrity in the brain. In this new study, Dr. Mark and colleagues sought to determine whether the effects would also translate to improvements in cortical gray matter.
 

Promoting neuroplasticity, improving motor function

For their study, they enrolled 20 adults with chronic MS who were matched with respect to unilateral arm disability. The participants were randomly assigned to receive 35 hours of either CIMT or a holistic complementary alternative medicine program, which included yoga, aquatic therapy, massage, and/or relaxation techniques, over the course of 2 weeks.

Both groups expressed the same degree of expectancy of benefits from the intervention. Those who received CIMT showed a significantly larger effect size on the Motor Activity Log, a measure that has been validated against real-world upper-limb accelerometry, compared with the control group (d = 3.2, vs. d = 0.7).

Imaging with tensor-based morphometry showed an increase in the thickness of the primary motor cortex in patients who underwent CIMT but not those who received the alternative medicine treatment. Furthermore, a change in the primary motor cortex was observed in the CIMT group on voxel-based morphometry, suggesting an increase in cortical density or volume, or both. Similar changes were not seen in the alternative medicine group.

“We evaluated the density of the brain cortical gray area before and after treatment, and we found increased gray matter in the area of the brain that is concentrated with voluntary limb movement (the motor cortex),” Dr. Mark said. “As in (previous) studies, we did not find such changes, or any changes, after the other form of treatment,” he said.

The results are important, Dr. Mark noted, “because CIMT seems to specifically promote neuroplasticity changes that appear to be healthy, for what is otherwise a chronically progressive degenerative neurological disorder.”

In addition to the improvements in MS, CIMT has led to improvement in motor function for patients who have experienced other central nervous system injuries, including stroke, traumatic brain injury, cerebral palsy, and, in musicians, focal hand dystonia.

The new findings offer intriguing insights into the effects in progressive MS, commented rehabilitation specialist Patricia Bobryk, MHS, a physical therapist with the UCHealth Yampa Valley Medical Center, in Colorado Springs.

“There is more evidence for CIMT in the area of stroke, which is more acute onset and with more potential recovery, especially early on, so this is exciting initial work in terms of MS,” she said.

“If we’re trying to find new avenues in the brain for better pathways, rather than using something that’s damaged in MS, it makes perfect sense that CIMT really forces and drives those connections, because you’re doing a repetitive, high-intensity patterning throughout the day, so you set up that environment for things to progress, especially in motor functioning,” she said.
 

Repetition, ‘prevention of compensation’

CIMT was developed at the University of Alabama, Birmingham, 30 years ago and involves four components. The first, described as “massed practice,” involves intensive, repetitive arm movements of the affected arm. The second component involves “shaping,” in which the patient is encouraged to perform his or her best attempts at the movements.

For the third component, described as “prevention of compensation,” the patient’s more-functional arm is inhibited from being used in everyday activities by wearing a padded mitt.

“This permits the patient to brace him- or herself whenever needed, but the better hand nonetheless lacks the dexterity to take over the activities that should be performed by the worse arm,” Dr. Mark explained.

“The patient wears the padded mitt after hours, too, except when using water or when sleeping,” he said.

The fourth component is a set of behavioral enforcement techniques involving goal-setting; daily interviews and discussion of progress and challenges; nightly homework; diary keeping; and telephone follow-up.

Dr. Mark noted that the intervention could have benefits that are secondary to motor and movement function. “We consider that the improvement of limb activity in a motor-challenged person with MS could afford a way to offset the deleterious effects of inactivity that can occur, such as weight gain, diabetes, osteoporosis, cardiac disease, and other conditions associated with prolonged inactivity,” he said.

Although it was developed at the University of Alabama, CIMT is currently more widely practiced in Europe than the United States, likely because of differences in care support, which in Europe is provided through socialized medicine, Dr. Mark pointed out.

Although the detailed methods for conducting CIMT are published in peer-reviewed journals, Dr. Mark recommends hands-on and interactive teaching. Such training is offered to clinicians and affiliated physical therapists and occupational therapists through Mark’s program at the University of Alabama in a semiannual, week-long training course, which includes hands-on treatment practice with actual patients.
 

Proof of principle

In further commenting on the study, Kathy M. Zackowski, PhD, of the National MS Society, said the findings provide an intriguing proof of concept that should be tested in a larger cohort. “The question of how much a behavioral (therapy) can impact true brain structural change or change in the pathologic mechanism is intriguing and of high importance,” she said.

“It is important to take this information as ‘proof of principle’ of the importance of CIMT for improving upper limb activity,” according to Dr. Zackowski, senior director, patient management, care and rehabilitation research at the society.

“Importantly, this team needs to move forward testing their hypothesis in a larger randomized, clinical trial with a full control group in order to show causal evidence that one intervention caused the structural brain changes seen,” she said in an interview.

Dr. Zackowski added that a caveat of CIMT is that the approach assumes one limb is more impaired than the other, which is always the case in stroke but is true only in some cases of MS. “Therefore, this method may not be effective for everyone with MS, but offers another option for tailoring an intervention to a person’s abilities and interests,” she said.

“Another important detail is that CIMT is also being explored for lower extremity use,” she added. “This is exciting, as lower extremity dysfunction is a very common problem in MS, and may be useful in treating walking disability.”

The authors, Ms. Bobryk, and Dr. Zackowski have disclosed no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

I grew up in a family that was pretty much devoid of physical demonstrations of affection. I certainly felt that my folks loved me, but there was no hugging. I don’t recall ever seeing my parents kiss or touch each other. My dad would occasionally physically tease my mother. For example, I can remember one incident at the dinner table when he was playfully and gently laying a hand on my mother’s arm just as she was raising her fork to her mouth. After about three of these gentle holds, she lifted her water glass and tossed its contents in his face. This was the full extent of physicality in our family.

kate_sept2004/thinkstock

It wasn’t just my parents. I can’t remember aunts or uncles or cousins ever hugging us when we met. Grandmothers of course would request a hug. I never knew either of my grandfathers, but I suspect they would not have been the hugging kind.

I never felt I was missing out on anything, because in the generally WASPish atmosphere of the community in which I grew up I saw very few public displays of affection. But somewhere over time, hugging crept into the American repertoire of expression. This incursion may have been a ripple effect from the flower power, free love hippiedom of the ‘60s and ‘70s. Or it may have been a symptom of globalization as Americans became more familiar with other cultures in which physical expression was more common.

Whatever the reason for the more widespread adoption of hugging in our social vocabulary with my somewhat physically impoverished upbringing, it took me longer than most folks to comfortably include it in my greeting options. Although I may have come to the dance late, I have fully adopted hugging as a way to greet people with whom I have more than a passing acquaintance.

In fact, the ability to comfortably hug former coworkers, old friends I haven’t seen in years, and parents with whom I had shared a particularly troublesome child is what I miss most about the restrictions that have come with the COVID-19 pandemic. Now when I meet folks in the grocery store with whom I share a special affection that magnetic spark still leaps between our eyes, just visible over our face masks, but mentally and physically we take a step back and say to ourselves that this hug shouldn’t happen and it isn’t going to happen. And that makes me sad.

One of the great perks of practicing pediatrics in a small town and then remaining there in retirement is that nearly every week I encounter one or two people with whom I have a long and sometimes emotionally charged relationship. Nurses with whom I sweated over difficult delivery room resuscitations. Parents for whom their anxiety was getting in the way of their ability to parent. Parents and caregivers of complex multiply disabled children who are now adults. Peers who have lost a spouse or a child. I’m sure you have your own list of people who send off that we-need-to-hug spark.

I can envision a day sometime in the relatively near future that I will be able to hug my two grandchildren whom I haven’t hugged even though they live a short 10-minute walk away. But I have trouble imagining when I will again be able to enjoy and be enriched by those special grocery store hugs that I have grown to savor.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.

I grew up in a family that was pretty much devoid of physical demonstrations of affection. I certainly felt that my folks loved me, but there was no hugging. I don’t recall ever seeing my parents kiss or touch each other. My dad would occasionally physically tease my mother. For example, I can remember one incident at the dinner table when he was playfully and gently laying a hand on my mother’s arm just as she was raising her fork to her mouth. After about three of these gentle holds, she lifted her water glass and tossed its contents in his face. This was the full extent of physicality in our family.

kate_sept2004/thinkstock

It wasn’t just my parents. I can’t remember aunts or uncles or cousins ever hugging us when we met. Grandmothers of course would request a hug. I never knew either of my grandfathers, but I suspect they would not have been the hugging kind.

I never felt I was missing out on anything, because in the generally WASPish atmosphere of the community in which I grew up I saw very few public displays of affection. But somewhere over time, hugging crept into the American repertoire of expression. This incursion may have been a ripple effect from the flower power, free love hippiedom of the ‘60s and ‘70s. Or it may have been a symptom of globalization as Americans became more familiar with other cultures in which physical expression was more common.

Whatever the reason for the more widespread adoption of hugging in our social vocabulary with my somewhat physically impoverished upbringing, it took me longer than most folks to comfortably include it in my greeting options. Although I may have come to the dance late, I have fully adopted hugging as a way to greet people with whom I have more than a passing acquaintance.

In fact, the ability to comfortably hug former coworkers, old friends I haven’t seen in years, and parents with whom I had shared a particularly troublesome child is what I miss most about the restrictions that have come with the COVID-19 pandemic. Now when I meet folks in the grocery store with whom I share a special affection that magnetic spark still leaps between our eyes, just visible over our face masks, but mentally and physically we take a step back and say to ourselves that this hug shouldn’t happen and it isn’t going to happen. And that makes me sad.

One of the great perks of practicing pediatrics in a small town and then remaining there in retirement is that nearly every week I encounter one or two people with whom I have a long and sometimes emotionally charged relationship. Nurses with whom I sweated over difficult delivery room resuscitations. Parents for whom their anxiety was getting in the way of their ability to parent. Parents and caregivers of complex multiply disabled children who are now adults. Peers who have lost a spouse or a child. I’m sure you have your own list of people who send off that we-need-to-hug spark.

I can envision a day sometime in the relatively near future that I will be able to hug my two grandchildren whom I haven’t hugged even though they live a short 10-minute walk away. But I have trouble imagining when I will again be able to enjoy and be enriched by those special grocery store hugs that I have grown to savor.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.

I grew up in a family that was pretty much devoid of physical demonstrations of affection. I certainly felt that my folks loved me, but there was no hugging. I don’t recall ever seeing my parents kiss or touch each other. My dad would occasionally physically tease my mother. For example, I can remember one incident at the dinner table when he was playfully and gently laying a hand on my mother’s arm just as she was raising her fork to her mouth. After about three of these gentle holds, she lifted her water glass and tossed its contents in his face. This was the full extent of physicality in our family.

kate_sept2004/thinkstock

It wasn’t just my parents. I can’t remember aunts or uncles or cousins ever hugging us when we met. Grandmothers of course would request a hug. I never knew either of my grandfathers, but I suspect they would not have been the hugging kind.

I never felt I was missing out on anything, because in the generally WASPish atmosphere of the community in which I grew up I saw very few public displays of affection. But somewhere over time, hugging crept into the American repertoire of expression. This incursion may have been a ripple effect from the flower power, free love hippiedom of the ‘60s and ‘70s. Or it may have been a symptom of globalization as Americans became more familiar with other cultures in which physical expression was more common.

Whatever the reason for the more widespread adoption of hugging in our social vocabulary with my somewhat physically impoverished upbringing, it took me longer than most folks to comfortably include it in my greeting options. Although I may have come to the dance late, I have fully adopted hugging as a way to greet people with whom I have more than a passing acquaintance.

In fact, the ability to comfortably hug former coworkers, old friends I haven’t seen in years, and parents with whom I had shared a particularly troublesome child is what I miss most about the restrictions that have come with the COVID-19 pandemic. Now when I meet folks in the grocery store with whom I share a special affection that magnetic spark still leaps between our eyes, just visible over our face masks, but mentally and physically we take a step back and say to ourselves that this hug shouldn’t happen and it isn’t going to happen. And that makes me sad.

One of the great perks of practicing pediatrics in a small town and then remaining there in retirement is that nearly every week I encounter one or two people with whom I have a long and sometimes emotionally charged relationship. Nurses with whom I sweated over difficult delivery room resuscitations. Parents for whom their anxiety was getting in the way of their ability to parent. Parents and caregivers of complex multiply disabled children who are now adults. Peers who have lost a spouse or a child. I’m sure you have your own list of people who send off that we-need-to-hug spark.

I can envision a day sometime in the relatively near future that I will be able to hug my two grandchildren whom I haven’t hugged even though they live a short 10-minute walk away. But I have trouble imagining when I will again be able to enjoy and be enriched by those special grocery store hugs that I have grown to savor.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.