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Give ’em a brrreak!
In some ways (my wife would say many), I haven’t grown up. As a child, I loved playing outside in the snow. If it was too powdery to make a snowman or build a fort, I was content just tromping through the drifts into the woods on my own arctic expeditions.
Four college winters in northern New Hampshire failed to dampen my enthusiasm for the cold. In fact, they probably influenced my decision to marry a girl from Maine and spend the last 45 winters in her home state. I enjoy cross-country skiing and snowshoeing, and the stack of books on my nightstand almost always contains one book about someone’s arctic adventure.
Two weeks ago on one of my crispy after-lunch refreshers, I walked past our neighborhood grade school. The playground was a mountainous landscape covered in pristine snow unsullied by the salt and sand the town has spread on the roads and sidewalks. Scores of 5- and 6-year-olds clad in a kaleidoscope of color swarmed over the giant mounds of snow, some of which were two and three times their height. Even my wool cap and fleece balaclava couldn’t muffle their shrieks of glee.
As I crunched along, I said to myself, those kids are experiencing an ecstasy that no child should be deprived of. Well, it turns out that in New York City, some thoughtless adults are doing just that (“A Casualty of a Frigid New York Winter: Outside School Recess,” by Ginia Bellafante, N.Y. Times, March 6, 2015). Although the official Department of Education policy cautions school administrators against using temperature alone as a criterion for canceling outside play, it does discourage sending children outside if wind chills will bring the effective temperature to less than zero degrees Fahrenheit, which sounds reasonable in a community unaccustomed to serious cold. However, it also discourages schools from allowing outside play if it is snowing or there is any ice on the playground.
Sadly, some cold-averse administrators have robbed hundreds of children of the chance to enjoy what has been an unusually snowy winter in the Northeast. In fact, no one can remember when the children in one unfortunate New York City grade school have been outside for recess. A conservative estimate is 40 consecutive days of incarceration.
This school is in the unenviable and unacceptable position of having no playground. Even in warmer weather, it relies on a nearby park that the parks department has chosen not to plow this winter. The tragic snow deprivation these children are suffering is just the tip of the iceberg. Despite ample evidence supporting the health and educational benefits of physical activity and recess, the New York City Department of Education does not mandate recess. Instead, it simply “encourages” schools to offer 20 minutes of outside activity.
I can understand why some school administrators are hesitant to send their young students out in the cold. It can take at least as long to bundle and unbundle a class of 5-year-olds as they will spend outside. But, at least teachers no longer have to contend with the thumb-lacerating metal buckles that made the old rubber galoshes such a painful challenge.
I am sure the list of willing volunteers to take playground duty on a frigid Friday afternoon is a short one. But, let’s remember that we are talking about young minds and bodies that need fresh air, even if it is cold fresh air, to keep them healthy and engaged in the learning process. For goodness sake, put on another layer, or three, and let them go out to enjoy the winter wonderland.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping With a Picky Eater.” E-mail him at pdnews@frontlinemedcom.com.
In some ways (my wife would say many), I haven’t grown up. As a child, I loved playing outside in the snow. If it was too powdery to make a snowman or build a fort, I was content just tromping through the drifts into the woods on my own arctic expeditions.
Four college winters in northern New Hampshire failed to dampen my enthusiasm for the cold. In fact, they probably influenced my decision to marry a girl from Maine and spend the last 45 winters in her home state. I enjoy cross-country skiing and snowshoeing, and the stack of books on my nightstand almost always contains one book about someone’s arctic adventure.
Two weeks ago on one of my crispy after-lunch refreshers, I walked past our neighborhood grade school. The playground was a mountainous landscape covered in pristine snow unsullied by the salt and sand the town has spread on the roads and sidewalks. Scores of 5- and 6-year-olds clad in a kaleidoscope of color swarmed over the giant mounds of snow, some of which were two and three times their height. Even my wool cap and fleece balaclava couldn’t muffle their shrieks of glee.
As I crunched along, I said to myself, those kids are experiencing an ecstasy that no child should be deprived of. Well, it turns out that in New York City, some thoughtless adults are doing just that (“A Casualty of a Frigid New York Winter: Outside School Recess,” by Ginia Bellafante, N.Y. Times, March 6, 2015). Although the official Department of Education policy cautions school administrators against using temperature alone as a criterion for canceling outside play, it does discourage sending children outside if wind chills will bring the effective temperature to less than zero degrees Fahrenheit, which sounds reasonable in a community unaccustomed to serious cold. However, it also discourages schools from allowing outside play if it is snowing or there is any ice on the playground.
Sadly, some cold-averse administrators have robbed hundreds of children of the chance to enjoy what has been an unusually snowy winter in the Northeast. In fact, no one can remember when the children in one unfortunate New York City grade school have been outside for recess. A conservative estimate is 40 consecutive days of incarceration.
This school is in the unenviable and unacceptable position of having no playground. Even in warmer weather, it relies on a nearby park that the parks department has chosen not to plow this winter. The tragic snow deprivation these children are suffering is just the tip of the iceberg. Despite ample evidence supporting the health and educational benefits of physical activity and recess, the New York City Department of Education does not mandate recess. Instead, it simply “encourages” schools to offer 20 minutes of outside activity.
I can understand why some school administrators are hesitant to send their young students out in the cold. It can take at least as long to bundle and unbundle a class of 5-year-olds as they will spend outside. But, at least teachers no longer have to contend with the thumb-lacerating metal buckles that made the old rubber galoshes such a painful challenge.
I am sure the list of willing volunteers to take playground duty on a frigid Friday afternoon is a short one. But, let’s remember that we are talking about young minds and bodies that need fresh air, even if it is cold fresh air, to keep them healthy and engaged in the learning process. For goodness sake, put on another layer, or three, and let them go out to enjoy the winter wonderland.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping With a Picky Eater.” E-mail him at pdnews@frontlinemedcom.com.
In some ways (my wife would say many), I haven’t grown up. As a child, I loved playing outside in the snow. If it was too powdery to make a snowman or build a fort, I was content just tromping through the drifts into the woods on my own arctic expeditions.
Four college winters in northern New Hampshire failed to dampen my enthusiasm for the cold. In fact, they probably influenced my decision to marry a girl from Maine and spend the last 45 winters in her home state. I enjoy cross-country skiing and snowshoeing, and the stack of books on my nightstand almost always contains one book about someone’s arctic adventure.
Two weeks ago on one of my crispy after-lunch refreshers, I walked past our neighborhood grade school. The playground was a mountainous landscape covered in pristine snow unsullied by the salt and sand the town has spread on the roads and sidewalks. Scores of 5- and 6-year-olds clad in a kaleidoscope of color swarmed over the giant mounds of snow, some of which were two and three times their height. Even my wool cap and fleece balaclava couldn’t muffle their shrieks of glee.
As I crunched along, I said to myself, those kids are experiencing an ecstasy that no child should be deprived of. Well, it turns out that in New York City, some thoughtless adults are doing just that (“A Casualty of a Frigid New York Winter: Outside School Recess,” by Ginia Bellafante, N.Y. Times, March 6, 2015). Although the official Department of Education policy cautions school administrators against using temperature alone as a criterion for canceling outside play, it does discourage sending children outside if wind chills will bring the effective temperature to less than zero degrees Fahrenheit, which sounds reasonable in a community unaccustomed to serious cold. However, it also discourages schools from allowing outside play if it is snowing or there is any ice on the playground.
Sadly, some cold-averse administrators have robbed hundreds of children of the chance to enjoy what has been an unusually snowy winter in the Northeast. In fact, no one can remember when the children in one unfortunate New York City grade school have been outside for recess. A conservative estimate is 40 consecutive days of incarceration.
This school is in the unenviable and unacceptable position of having no playground. Even in warmer weather, it relies on a nearby park that the parks department has chosen not to plow this winter. The tragic snow deprivation these children are suffering is just the tip of the iceberg. Despite ample evidence supporting the health and educational benefits of physical activity and recess, the New York City Department of Education does not mandate recess. Instead, it simply “encourages” schools to offer 20 minutes of outside activity.
I can understand why some school administrators are hesitant to send their young students out in the cold. It can take at least as long to bundle and unbundle a class of 5-year-olds as they will spend outside. But, at least teachers no longer have to contend with the thumb-lacerating metal buckles that made the old rubber galoshes such a painful challenge.
I am sure the list of willing volunteers to take playground duty on a frigid Friday afternoon is a short one. But, let’s remember that we are talking about young minds and bodies that need fresh air, even if it is cold fresh air, to keep them healthy and engaged in the learning process. For goodness sake, put on another layer, or three, and let them go out to enjoy the winter wonderland.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping With a Picky Eater.” E-mail him at pdnews@frontlinemedcom.com.
Dark circles under the eyes
How many times a week are we asked by our patients about “dark circles” under the eyes? The term “dark circles” is a catch-all term that refers to problems that have a vast range of genetic, environmental, and skin causes. However, it is a common frustrating problem with little structure in its definition and few foolproof treatments.
We propose a classification system for the definition of dark circles, and offer some clinical pearls in their treatment. Most patients, however, have dark circles with multifactorial causes that need to be addressed.
I. Infraorbital fat pad protrusion (“bags under my eyes”)
Blepharoplasty is the best solution and for now, the only solution for fat pad prominence. The fat may be removed in lower lid blepharoplasty or repositioned. Referral to a board certified plastic surgeon, oculoplastic surgeon, or dermatologic surgeon is recommended. If there is also significant tear trough deformity, fillers may be placed in the tear trough to help “camouflage” the appearance of the fat pad protrusion but it does not rid the patient of the fat pads.
II. Infraorbital edema (“puffiness”)
The infraorbital skin is very thin and highly sensitive to fluid compartmentalization. Seasonal allergies, sinus infections, crying, or water retention from high blood pressure or consumption of high sodium foods are some of the reasons the loose, thin epidermis becomes edematous. Recommendations for patients:
• Treat seasonal allergies with over-the-counter allergy medications, or see your doctor for prescription medications for resistant allergies or possible sinus infections.
• Switch your sleep position. Sleep position can be contributing to under-eye bags through gravity. Sleeping on your side or stomach can encourage fluids to collect under your eyes. If you’re a side sleeper, you may notice a heavier bag on the side you sleep on. Patients who wake up with puffy eyes can sleep on their backs and add an extra pillow under the head.
• Avoid rubbing eyes frequently, going to bed with makeup on, and harsh cleansers. Anything that irritates the eyes can cause fluids to pool. Sleeping in eye makeup can irritate eyes, causing undereye edema.
• Eye bags might be a sign of an underlying medical condition, if they appear suddenly and none of the above conditions apply. Thyroid, cardiovascular, or kidney problems can cause under-eye fluid retention and the patients need to see their primary care doctors for further evaluation.
• Place an ice pack, slices of cucumbers, chilled tea bags, or even a package of frozen peas on eyes. This can constrict leaky blood vessels and lessen the periorbital edema.
• A few topical eye creams have been developed, such as Neotensil, that temporarily reduce the appearance of lower eyelid puffiness. The product is a blend of polymers that provide compression, smoothing, and hydrating benefits to the skin. In addition, a makeup is often applied over it to reduce the appearance further.
III: Periorbital hyperpigmentation (“dark circles”)
Pigmentation of the periorbital skin is very common in skin of color because of the increased melanin content. Genetics, rubbing, and inflammatory skin diseases such as eczema may play a role in exacerbating the pigmentation of the thin under-eye skin. Recommendations for patients:
• Remind them to avoid rubbing the area – chronic rubbing and the development of lichen simplex chronicus can lead to dark, thickened under-eye skin.
• Retinoic acid creams can help slough the dark pigmented skin. However, it should be used in very small amounts with increasing use over several weeks to avoid severe irritation.
• Skin lightening creams with azaleic acid, kojic acid, and glycolic acid, can be found in varying strengths in dermatologist office preparations, over-the-counter creams, or prescriptions. Hydroquinone creams have demonstrated success in lightening under-eye hyperpigmentation. Strengths in over-the-counter preparations start at 1%-2% and in prescription strength can be compounded to higher than 4%.
• Chemical peels: Light chemical peels such as glycolic acid and Jessner’s peels will assist in lightening dark under-eye pigmentation. Dermatologists also can use peels with hydroquinone or retinoic acid for an added lightening benefit.
• Intense pulsed light (IPL) can help minimize under eye pigmentation, particularly UV-induced pigmentation.
IV: Infraorbital tear trough depression
Most often, dark circles aren’t about changes in the color of the skin at all. Instead, they’re created by a loss of volume in the area around the eye. This exposes the underlying blue veins and orbital bone, creating a hollow trough that shows up as a dark circle. These changes are often caused by genetics; however, significant weight loss and aging with resorption or displacement of the infraorbital fat pads can also expose under-eye tear trough depressions.
The best way to treat this problem is with a small amount of a hyaluronic acid filler placed by a dermatologist in the trough. Very small aliquots are needed in even the deepest trough but can give outstanding results. Caution however, must be taken as this is a highly specialized technique and injector dependent procedure. There are crucial vascular structures around the eye that need to be avoided, and overfilled troughs will give patients a puffy appearance that may pose a worse and more difficult problem to fix. Hyaluronic acid fillers are not approved by the Food and Drug Administration for treatment of under-eye depressions, so patients should be educated about the risks and benefits prior to undergoing these procedures.
V: Periorbital vascular prominence
With age, the skin around the eye becomes thinner, exposing the small capillaries and venules just below the thin epidermal layer. Vascular prominence can leave a bluish undertone to the infraorbital skin which can cast dark shadows and make the area appear dark or sallow.
• Eye creams that contain caffeine can constrict the underlying blood vessels and temporarily diminish small vessel prominence.
• For large blue veins, vascular lasers such as a long pulse Nd:Yag lasers can be recommended. But in darker skin types these lasers can cause hyperpigmented scars if not used with adequate skin cooling techniques. Proper eye protection should also be used.
VI: Periorbital static and dynamic rhytids
• Botulinum toxin placed in small aliquots around the orbital rim will reduce the dynamic rhytids in this area. Treatments spaced 3 months apart will ensure long-lasting benefits as botulinum toxin often wears off.
• Laser resurfacing with CO2, fractionated CO2, or erbium lasers may also be used to treat periorbital rhytides.
Additional tips for your patients:
• For most of the types of infraorbital issues, makeup can help conceal some skin imperfections. Patients should choose a concealer that matches or is slightly lighter than their skin tone. If the patient has mild discoloration, choose a liquid formula. For more prominent imperfections, a cream full-coverage concealer works best.
• Recommend that patients avoid smoking, which dehydrates the skin and causes premature aging and collagen degradation.
• Remind patients to apply a sunscreen around the eye area. Hyperpigmentation and tear troughs can accentuate with UV-induced skin pigmentation. Physical blocking sunscreens may be less irritating than chemical blockers for those with sensitive eyelid skin.
• Remind patients to apply a moisturizer to the eye area nightly to keep the skin from becoming dry, irritated, and dehydrated.
• Advise patients not to break the bank with over-the-counter creams that promise cures for under-eye circles. Most over-the-counter preparations provide temporary, mild benefits at most, and often do not provide any lasting benefit.
Dr. Talakoub and Dr. Wesley are co-contributors to a monthly Aesthetic Dermatology column in Dermatology News. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is an update by Dr. Wesley of a previous column by Dr. Talakoub.
How many times a week are we asked by our patients about “dark circles” under the eyes? The term “dark circles” is a catch-all term that refers to problems that have a vast range of genetic, environmental, and skin causes. However, it is a common frustrating problem with little structure in its definition and few foolproof treatments.
We propose a classification system for the definition of dark circles, and offer some clinical pearls in their treatment. Most patients, however, have dark circles with multifactorial causes that need to be addressed.
I. Infraorbital fat pad protrusion (“bags under my eyes”)
Blepharoplasty is the best solution and for now, the only solution for fat pad prominence. The fat may be removed in lower lid blepharoplasty or repositioned. Referral to a board certified plastic surgeon, oculoplastic surgeon, or dermatologic surgeon is recommended. If there is also significant tear trough deformity, fillers may be placed in the tear trough to help “camouflage” the appearance of the fat pad protrusion but it does not rid the patient of the fat pads.
II. Infraorbital edema (“puffiness”)
The infraorbital skin is very thin and highly sensitive to fluid compartmentalization. Seasonal allergies, sinus infections, crying, or water retention from high blood pressure or consumption of high sodium foods are some of the reasons the loose, thin epidermis becomes edematous. Recommendations for patients:
• Treat seasonal allergies with over-the-counter allergy medications, or see your doctor for prescription medications for resistant allergies or possible sinus infections.
• Switch your sleep position. Sleep position can be contributing to under-eye bags through gravity. Sleeping on your side or stomach can encourage fluids to collect under your eyes. If you’re a side sleeper, you may notice a heavier bag on the side you sleep on. Patients who wake up with puffy eyes can sleep on their backs and add an extra pillow under the head.
• Avoid rubbing eyes frequently, going to bed with makeup on, and harsh cleansers. Anything that irritates the eyes can cause fluids to pool. Sleeping in eye makeup can irritate eyes, causing undereye edema.
• Eye bags might be a sign of an underlying medical condition, if they appear suddenly and none of the above conditions apply. Thyroid, cardiovascular, or kidney problems can cause under-eye fluid retention and the patients need to see their primary care doctors for further evaluation.
• Place an ice pack, slices of cucumbers, chilled tea bags, or even a package of frozen peas on eyes. This can constrict leaky blood vessels and lessen the periorbital edema.
• A few topical eye creams have been developed, such as Neotensil, that temporarily reduce the appearance of lower eyelid puffiness. The product is a blend of polymers that provide compression, smoothing, and hydrating benefits to the skin. In addition, a makeup is often applied over it to reduce the appearance further.
III: Periorbital hyperpigmentation (“dark circles”)
Pigmentation of the periorbital skin is very common in skin of color because of the increased melanin content. Genetics, rubbing, and inflammatory skin diseases such as eczema may play a role in exacerbating the pigmentation of the thin under-eye skin. Recommendations for patients:
• Remind them to avoid rubbing the area – chronic rubbing and the development of lichen simplex chronicus can lead to dark, thickened under-eye skin.
• Retinoic acid creams can help slough the dark pigmented skin. However, it should be used in very small amounts with increasing use over several weeks to avoid severe irritation.
• Skin lightening creams with azaleic acid, kojic acid, and glycolic acid, can be found in varying strengths in dermatologist office preparations, over-the-counter creams, or prescriptions. Hydroquinone creams have demonstrated success in lightening under-eye hyperpigmentation. Strengths in over-the-counter preparations start at 1%-2% and in prescription strength can be compounded to higher than 4%.
• Chemical peels: Light chemical peels such as glycolic acid and Jessner’s peels will assist in lightening dark under-eye pigmentation. Dermatologists also can use peels with hydroquinone or retinoic acid for an added lightening benefit.
• Intense pulsed light (IPL) can help minimize under eye pigmentation, particularly UV-induced pigmentation.
IV: Infraorbital tear trough depression
Most often, dark circles aren’t about changes in the color of the skin at all. Instead, they’re created by a loss of volume in the area around the eye. This exposes the underlying blue veins and orbital bone, creating a hollow trough that shows up as a dark circle. These changes are often caused by genetics; however, significant weight loss and aging with resorption or displacement of the infraorbital fat pads can also expose under-eye tear trough depressions.
The best way to treat this problem is with a small amount of a hyaluronic acid filler placed by a dermatologist in the trough. Very small aliquots are needed in even the deepest trough but can give outstanding results. Caution however, must be taken as this is a highly specialized technique and injector dependent procedure. There are crucial vascular structures around the eye that need to be avoided, and overfilled troughs will give patients a puffy appearance that may pose a worse and more difficult problem to fix. Hyaluronic acid fillers are not approved by the Food and Drug Administration for treatment of under-eye depressions, so patients should be educated about the risks and benefits prior to undergoing these procedures.
V: Periorbital vascular prominence
With age, the skin around the eye becomes thinner, exposing the small capillaries and venules just below the thin epidermal layer. Vascular prominence can leave a bluish undertone to the infraorbital skin which can cast dark shadows and make the area appear dark or sallow.
• Eye creams that contain caffeine can constrict the underlying blood vessels and temporarily diminish small vessel prominence.
• For large blue veins, vascular lasers such as a long pulse Nd:Yag lasers can be recommended. But in darker skin types these lasers can cause hyperpigmented scars if not used with adequate skin cooling techniques. Proper eye protection should also be used.
VI: Periorbital static and dynamic rhytids
• Botulinum toxin placed in small aliquots around the orbital rim will reduce the dynamic rhytids in this area. Treatments spaced 3 months apart will ensure long-lasting benefits as botulinum toxin often wears off.
• Laser resurfacing with CO2, fractionated CO2, or erbium lasers may also be used to treat periorbital rhytides.
Additional tips for your patients:
• For most of the types of infraorbital issues, makeup can help conceal some skin imperfections. Patients should choose a concealer that matches or is slightly lighter than their skin tone. If the patient has mild discoloration, choose a liquid formula. For more prominent imperfections, a cream full-coverage concealer works best.
• Recommend that patients avoid smoking, which dehydrates the skin and causes premature aging and collagen degradation.
• Remind patients to apply a sunscreen around the eye area. Hyperpigmentation and tear troughs can accentuate with UV-induced skin pigmentation. Physical blocking sunscreens may be less irritating than chemical blockers for those with sensitive eyelid skin.
• Remind patients to apply a moisturizer to the eye area nightly to keep the skin from becoming dry, irritated, and dehydrated.
• Advise patients not to break the bank with over-the-counter creams that promise cures for under-eye circles. Most over-the-counter preparations provide temporary, mild benefits at most, and often do not provide any lasting benefit.
Dr. Talakoub and Dr. Wesley are co-contributors to a monthly Aesthetic Dermatology column in Dermatology News. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is an update by Dr. Wesley of a previous column by Dr. Talakoub.
How many times a week are we asked by our patients about “dark circles” under the eyes? The term “dark circles” is a catch-all term that refers to problems that have a vast range of genetic, environmental, and skin causes. However, it is a common frustrating problem with little structure in its definition and few foolproof treatments.
We propose a classification system for the definition of dark circles, and offer some clinical pearls in their treatment. Most patients, however, have dark circles with multifactorial causes that need to be addressed.
I. Infraorbital fat pad protrusion (“bags under my eyes”)
Blepharoplasty is the best solution and for now, the only solution for fat pad prominence. The fat may be removed in lower lid blepharoplasty or repositioned. Referral to a board certified plastic surgeon, oculoplastic surgeon, or dermatologic surgeon is recommended. If there is also significant tear trough deformity, fillers may be placed in the tear trough to help “camouflage” the appearance of the fat pad protrusion but it does not rid the patient of the fat pads.
II. Infraorbital edema (“puffiness”)
The infraorbital skin is very thin and highly sensitive to fluid compartmentalization. Seasonal allergies, sinus infections, crying, or water retention from high blood pressure or consumption of high sodium foods are some of the reasons the loose, thin epidermis becomes edematous. Recommendations for patients:
• Treat seasonal allergies with over-the-counter allergy medications, or see your doctor for prescription medications for resistant allergies or possible sinus infections.
• Switch your sleep position. Sleep position can be contributing to under-eye bags through gravity. Sleeping on your side or stomach can encourage fluids to collect under your eyes. If you’re a side sleeper, you may notice a heavier bag on the side you sleep on. Patients who wake up with puffy eyes can sleep on their backs and add an extra pillow under the head.
• Avoid rubbing eyes frequently, going to bed with makeup on, and harsh cleansers. Anything that irritates the eyes can cause fluids to pool. Sleeping in eye makeup can irritate eyes, causing undereye edema.
• Eye bags might be a sign of an underlying medical condition, if they appear suddenly and none of the above conditions apply. Thyroid, cardiovascular, or kidney problems can cause under-eye fluid retention and the patients need to see their primary care doctors for further evaluation.
• Place an ice pack, slices of cucumbers, chilled tea bags, or even a package of frozen peas on eyes. This can constrict leaky blood vessels and lessen the periorbital edema.
• A few topical eye creams have been developed, such as Neotensil, that temporarily reduce the appearance of lower eyelid puffiness. The product is a blend of polymers that provide compression, smoothing, and hydrating benefits to the skin. In addition, a makeup is often applied over it to reduce the appearance further.
III: Periorbital hyperpigmentation (“dark circles”)
Pigmentation of the periorbital skin is very common in skin of color because of the increased melanin content. Genetics, rubbing, and inflammatory skin diseases such as eczema may play a role in exacerbating the pigmentation of the thin under-eye skin. Recommendations for patients:
• Remind them to avoid rubbing the area – chronic rubbing and the development of lichen simplex chronicus can lead to dark, thickened under-eye skin.
• Retinoic acid creams can help slough the dark pigmented skin. However, it should be used in very small amounts with increasing use over several weeks to avoid severe irritation.
• Skin lightening creams with azaleic acid, kojic acid, and glycolic acid, can be found in varying strengths in dermatologist office preparations, over-the-counter creams, or prescriptions. Hydroquinone creams have demonstrated success in lightening under-eye hyperpigmentation. Strengths in over-the-counter preparations start at 1%-2% and in prescription strength can be compounded to higher than 4%.
• Chemical peels: Light chemical peels such as glycolic acid and Jessner’s peels will assist in lightening dark under-eye pigmentation. Dermatologists also can use peels with hydroquinone or retinoic acid for an added lightening benefit.
• Intense pulsed light (IPL) can help minimize under eye pigmentation, particularly UV-induced pigmentation.
IV: Infraorbital tear trough depression
Most often, dark circles aren’t about changes in the color of the skin at all. Instead, they’re created by a loss of volume in the area around the eye. This exposes the underlying blue veins and orbital bone, creating a hollow trough that shows up as a dark circle. These changes are often caused by genetics; however, significant weight loss and aging with resorption or displacement of the infraorbital fat pads can also expose under-eye tear trough depressions.
The best way to treat this problem is with a small amount of a hyaluronic acid filler placed by a dermatologist in the trough. Very small aliquots are needed in even the deepest trough but can give outstanding results. Caution however, must be taken as this is a highly specialized technique and injector dependent procedure. There are crucial vascular structures around the eye that need to be avoided, and overfilled troughs will give patients a puffy appearance that may pose a worse and more difficult problem to fix. Hyaluronic acid fillers are not approved by the Food and Drug Administration for treatment of under-eye depressions, so patients should be educated about the risks and benefits prior to undergoing these procedures.
V: Periorbital vascular prominence
With age, the skin around the eye becomes thinner, exposing the small capillaries and venules just below the thin epidermal layer. Vascular prominence can leave a bluish undertone to the infraorbital skin which can cast dark shadows and make the area appear dark or sallow.
• Eye creams that contain caffeine can constrict the underlying blood vessels and temporarily diminish small vessel prominence.
• For large blue veins, vascular lasers such as a long pulse Nd:Yag lasers can be recommended. But in darker skin types these lasers can cause hyperpigmented scars if not used with adequate skin cooling techniques. Proper eye protection should also be used.
VI: Periorbital static and dynamic rhytids
• Botulinum toxin placed in small aliquots around the orbital rim will reduce the dynamic rhytids in this area. Treatments spaced 3 months apart will ensure long-lasting benefits as botulinum toxin often wears off.
• Laser resurfacing with CO2, fractionated CO2, or erbium lasers may also be used to treat periorbital rhytides.
Additional tips for your patients:
• For most of the types of infraorbital issues, makeup can help conceal some skin imperfections. Patients should choose a concealer that matches or is slightly lighter than their skin tone. If the patient has mild discoloration, choose a liquid formula. For more prominent imperfections, a cream full-coverage concealer works best.
• Recommend that patients avoid smoking, which dehydrates the skin and causes premature aging and collagen degradation.
• Remind patients to apply a sunscreen around the eye area. Hyperpigmentation and tear troughs can accentuate with UV-induced skin pigmentation. Physical blocking sunscreens may be less irritating than chemical blockers for those with sensitive eyelid skin.
• Remind patients to apply a moisturizer to the eye area nightly to keep the skin from becoming dry, irritated, and dehydrated.
• Advise patients not to break the bank with over-the-counter creams that promise cures for under-eye circles. Most over-the-counter preparations provide temporary, mild benefits at most, and often do not provide any lasting benefit.
Dr. Talakoub and Dr. Wesley are co-contributors to a monthly Aesthetic Dermatology column in Dermatology News. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is an update by Dr. Wesley of a previous column by Dr. Talakoub.
Patented knowledge
The other day I had a chat with a chiropractor I’ll call Stan. Stan was excited about a new technique he has used to build his practice, whose clients now number several celebrities (some of whom I’d even heard of). “I specialize in muscular work and performance enhancement,” he said. “Performers with strenuous routines and a lot of stress need to sustain peak performance.”
A colleague out West whom Stan described as “very brilliant” had developed this technique. “It’s patented,” he said.
Stan went on to describe how this method has given him a whole new sense of the body. “I can actually feel the small transverse muscles of the vertebrae respond under my fingers,” he said. “The results are amazing.”
“How did you learn this technique?” I asked him.
“I took courses with the inventor,” he said. “His courses are patented, and can only be taught by accredited instructors. That ensures that the method is being done right. There are nine levels of certification.”
“Nine?”
“Yes, you have to keep taking more courses, learning new things. It’s very exciting.”
“By the way,” I asked, “how do you know that this method works better than the older ones you learned when you went to school?”
“Oh, you can feel and see the difference,” he said. “If you’re asking if there are studies or things like that, I guess there aren’t. But there’s no question that it’s better.”
“Do they teach this technique in chiropractic school?”
“No. As I said, it’s patented.”
“In that case,” I said, “it seems your professional schools are teaching inferior treatment methods.”
That gave Stan some pause. While he was thinking, I continued.
“It’s interesting,” I said. “In my profession, if someone came up with a treatment that was better than what everyone else was doing, he would need to do studies that proved he was right. He would also feel ethically bound to let everyone else know about the method, so all patients could be treated that way.”
Stan’s blank look suggested that this line of analysis had not occurred to him.
“But you must have some special techniques you use in your practice,” he said.
“No,” I said, “actually I don’t. I just practice conventional dermatology. Nothing special or unique about what I do.”
“What about the teaching hospitals in Boston,” he went on. “Don’t they do things no one else does?”
“Possibly,” I said. “But if they come up with a new technique, they have to convince others in the profession – and insurance companies – that their innovation is better in some measurable way.”
I’d gone as far as I wanted to. “It’s exciting that your patients do so well,” I said. “By the way,” I said, “what are celebrities really like up close and personal?”
“Most of them are very nice people,” he said. “They work hard to be good at what they do.”
“Do they ever complain that your treatment didn’t work, didn’t give their performance the boost they were expecting?”
“No,” he said. “Not one. They’re all happy.”
“That is really amazing,” I said. Stan nodded in agreement, though I don’t think he knew what I found so remarkable about it.
Stan is no cynic. He truly believes that what he does is valid, and that it helps his patients more than other treatments do. His patients believe it too.
Nor is our own profession as selfless and sharing as I made it sound. Hospitals love to trumpet their cyberknife technology or state-of-the-art orthopedic techniques or comprehensive cancer care, implying that they do whatever they do better than anyone else can.
Patients love to read this. They want to believe they’re seeing the “top” doctor, the one with the best results. Boston magazine (and the equivalent in every other city) publishes a list of “Top Doctors” this time of year.
Patients sometimes say, “I came to you because you did such a great job clearing up my sister’s acne,” or “You cleared my older son’s wart when nobody else could – one freeze, and it was gone. You’re a miracle worker!”
Oh sure I am. Nobody sprays liquid nitrogen the way I do.
I didn’t patent it, though. Teddy Roosevelt banned patent medicines in this country in 1906. But I guess in some quarters, patented never has gone away.
Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.
The other day I had a chat with a chiropractor I’ll call Stan. Stan was excited about a new technique he has used to build his practice, whose clients now number several celebrities (some of whom I’d even heard of). “I specialize in muscular work and performance enhancement,” he said. “Performers with strenuous routines and a lot of stress need to sustain peak performance.”
A colleague out West whom Stan described as “very brilliant” had developed this technique. “It’s patented,” he said.
Stan went on to describe how this method has given him a whole new sense of the body. “I can actually feel the small transverse muscles of the vertebrae respond under my fingers,” he said. “The results are amazing.”
“How did you learn this technique?” I asked him.
“I took courses with the inventor,” he said. “His courses are patented, and can only be taught by accredited instructors. That ensures that the method is being done right. There are nine levels of certification.”
“Nine?”
“Yes, you have to keep taking more courses, learning new things. It’s very exciting.”
“By the way,” I asked, “how do you know that this method works better than the older ones you learned when you went to school?”
“Oh, you can feel and see the difference,” he said. “If you’re asking if there are studies or things like that, I guess there aren’t. But there’s no question that it’s better.”
“Do they teach this technique in chiropractic school?”
“No. As I said, it’s patented.”
“In that case,” I said, “it seems your professional schools are teaching inferior treatment methods.”
That gave Stan some pause. While he was thinking, I continued.
“It’s interesting,” I said. “In my profession, if someone came up with a treatment that was better than what everyone else was doing, he would need to do studies that proved he was right. He would also feel ethically bound to let everyone else know about the method, so all patients could be treated that way.”
Stan’s blank look suggested that this line of analysis had not occurred to him.
“But you must have some special techniques you use in your practice,” he said.
“No,” I said, “actually I don’t. I just practice conventional dermatology. Nothing special or unique about what I do.”
“What about the teaching hospitals in Boston,” he went on. “Don’t they do things no one else does?”
“Possibly,” I said. “But if they come up with a new technique, they have to convince others in the profession – and insurance companies – that their innovation is better in some measurable way.”
I’d gone as far as I wanted to. “It’s exciting that your patients do so well,” I said. “By the way,” I said, “what are celebrities really like up close and personal?”
“Most of them are very nice people,” he said. “They work hard to be good at what they do.”
“Do they ever complain that your treatment didn’t work, didn’t give their performance the boost they were expecting?”
“No,” he said. “Not one. They’re all happy.”
“That is really amazing,” I said. Stan nodded in agreement, though I don’t think he knew what I found so remarkable about it.
Stan is no cynic. He truly believes that what he does is valid, and that it helps his patients more than other treatments do. His patients believe it too.
Nor is our own profession as selfless and sharing as I made it sound. Hospitals love to trumpet their cyberknife technology or state-of-the-art orthopedic techniques or comprehensive cancer care, implying that they do whatever they do better than anyone else can.
Patients love to read this. They want to believe they’re seeing the “top” doctor, the one with the best results. Boston magazine (and the equivalent in every other city) publishes a list of “Top Doctors” this time of year.
Patients sometimes say, “I came to you because you did such a great job clearing up my sister’s acne,” or “You cleared my older son’s wart when nobody else could – one freeze, and it was gone. You’re a miracle worker!”
Oh sure I am. Nobody sprays liquid nitrogen the way I do.
I didn’t patent it, though. Teddy Roosevelt banned patent medicines in this country in 1906. But I guess in some quarters, patented never has gone away.
Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.
The other day I had a chat with a chiropractor I’ll call Stan. Stan was excited about a new technique he has used to build his practice, whose clients now number several celebrities (some of whom I’d even heard of). “I specialize in muscular work and performance enhancement,” he said. “Performers with strenuous routines and a lot of stress need to sustain peak performance.”
A colleague out West whom Stan described as “very brilliant” had developed this technique. “It’s patented,” he said.
Stan went on to describe how this method has given him a whole new sense of the body. “I can actually feel the small transverse muscles of the vertebrae respond under my fingers,” he said. “The results are amazing.”
“How did you learn this technique?” I asked him.
“I took courses with the inventor,” he said. “His courses are patented, and can only be taught by accredited instructors. That ensures that the method is being done right. There are nine levels of certification.”
“Nine?”
“Yes, you have to keep taking more courses, learning new things. It’s very exciting.”
“By the way,” I asked, “how do you know that this method works better than the older ones you learned when you went to school?”
“Oh, you can feel and see the difference,” he said. “If you’re asking if there are studies or things like that, I guess there aren’t. But there’s no question that it’s better.”
“Do they teach this technique in chiropractic school?”
“No. As I said, it’s patented.”
“In that case,” I said, “it seems your professional schools are teaching inferior treatment methods.”
That gave Stan some pause. While he was thinking, I continued.
“It’s interesting,” I said. “In my profession, if someone came up with a treatment that was better than what everyone else was doing, he would need to do studies that proved he was right. He would also feel ethically bound to let everyone else know about the method, so all patients could be treated that way.”
Stan’s blank look suggested that this line of analysis had not occurred to him.
“But you must have some special techniques you use in your practice,” he said.
“No,” I said, “actually I don’t. I just practice conventional dermatology. Nothing special or unique about what I do.”
“What about the teaching hospitals in Boston,” he went on. “Don’t they do things no one else does?”
“Possibly,” I said. “But if they come up with a new technique, they have to convince others in the profession – and insurance companies – that their innovation is better in some measurable way.”
I’d gone as far as I wanted to. “It’s exciting that your patients do so well,” I said. “By the way,” I said, “what are celebrities really like up close and personal?”
“Most of them are very nice people,” he said. “They work hard to be good at what they do.”
“Do they ever complain that your treatment didn’t work, didn’t give their performance the boost they were expecting?”
“No,” he said. “Not one. They’re all happy.”
“That is really amazing,” I said. Stan nodded in agreement, though I don’t think he knew what I found so remarkable about it.
Stan is no cynic. He truly believes that what he does is valid, and that it helps his patients more than other treatments do. His patients believe it too.
Nor is our own profession as selfless and sharing as I made it sound. Hospitals love to trumpet their cyberknife technology or state-of-the-art orthopedic techniques or comprehensive cancer care, implying that they do whatever they do better than anyone else can.
Patients love to read this. They want to believe they’re seeing the “top” doctor, the one with the best results. Boston magazine (and the equivalent in every other city) publishes a list of “Top Doctors” this time of year.
Patients sometimes say, “I came to you because you did such a great job clearing up my sister’s acne,” or “You cleared my older son’s wart when nobody else could – one freeze, and it was gone. You’re a miracle worker!”
Oh sure I am. Nobody sprays liquid nitrogen the way I do.
I didn’t patent it, though. Teddy Roosevelt banned patent medicines in this country in 1906. But I guess in some quarters, patented never has gone away.
Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.
Questions on stroke ambulance feasibility
The TPA ambulance, armed with its own CT scanner, has arrived in the United States after several successful years in Germany.
Now what?
Like all new advances, it’s a difficult balance between costs and benefits. The money, in the end, is what it really comes down to. Will the cost of a CT ambulance, the equipment needed to send images to a radiologist, the extra training for EMTs, the price of stocking TPA on board, and maybe even having a neurologist on the ride (or telemedicine for one to see the patient) be offset by money saved on rehabilitation costs, better recoveries, fewer complications, even returning a patient to work?
I have no idea. I’m not sure anyone else does, either.
Certainly, I support the idea of improved stroke care. Although far from ideal, TPA is the only thing we have right now, and the sooner it’s given, the better. Most neurologists will agree. But who’s going to pay for this?
The insurance companies, obviously. But money is finite. What if we upgrade all these ambulances, only to find that there’s no significant cost savings on rehab and recovery when TPA is used in the field? Then the money comes out of doctors’ and nurses’ salaries, higher premiums for everyone, and a cutback in treatment for some other disorder. I’m pretty sure it won’t be taken out of an insurance executive’s year-end bonus.
And just try explaining that to the family of a stroke victim.
It’s not practical to put a CT scanner in every ambulance, so where do we put those so equipped? Again, there’s no easy answer. In areas with large retirement communities? Seems like a safe bet, but young people have strokes, too. Only in cities? More people live in cities, but those in rural areas may be too far from a hospital to receive TPA early. Shouldn’t they have one, too?
Who’s going to make the decision to send the TPA ambulance vs. the regular ambulance? That’s another tough question. The layman who calls in usually isn’t sure what’s going on, only that an ambulance is needed. The dispatcher often can’t tell over the phone if the patient has had a stroke, seizure, or psychogenic event. Should a neurologist or emergency medicine physician make the decision? Maybe, but how much extra time will it take to get one on the line? And, even then, they’ll be making a critical decision with sparse, secondhand information. What if the special ambulance is mistakenly sent to deal with a conversion disorder, only to have a legitimate stroke occur elsewhere when it’s no longer immediately available? That, inevitably, will lead to a lawsuit because the wrong ambulance was sent.
I’m not against the stroke ambulance – far from it – but there are still a lot questions to be answered. Putting a CT scanner and TPA in an ambulance is, comparatively, the easiest part.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
The TPA ambulance, armed with its own CT scanner, has arrived in the United States after several successful years in Germany.
Now what?
Like all new advances, it’s a difficult balance between costs and benefits. The money, in the end, is what it really comes down to. Will the cost of a CT ambulance, the equipment needed to send images to a radiologist, the extra training for EMTs, the price of stocking TPA on board, and maybe even having a neurologist on the ride (or telemedicine for one to see the patient) be offset by money saved on rehabilitation costs, better recoveries, fewer complications, even returning a patient to work?
I have no idea. I’m not sure anyone else does, either.
Certainly, I support the idea of improved stroke care. Although far from ideal, TPA is the only thing we have right now, and the sooner it’s given, the better. Most neurologists will agree. But who’s going to pay for this?
The insurance companies, obviously. But money is finite. What if we upgrade all these ambulances, only to find that there’s no significant cost savings on rehab and recovery when TPA is used in the field? Then the money comes out of doctors’ and nurses’ salaries, higher premiums for everyone, and a cutback in treatment for some other disorder. I’m pretty sure it won’t be taken out of an insurance executive’s year-end bonus.
And just try explaining that to the family of a stroke victim.
It’s not practical to put a CT scanner in every ambulance, so where do we put those so equipped? Again, there’s no easy answer. In areas with large retirement communities? Seems like a safe bet, but young people have strokes, too. Only in cities? More people live in cities, but those in rural areas may be too far from a hospital to receive TPA early. Shouldn’t they have one, too?
Who’s going to make the decision to send the TPA ambulance vs. the regular ambulance? That’s another tough question. The layman who calls in usually isn’t sure what’s going on, only that an ambulance is needed. The dispatcher often can’t tell over the phone if the patient has had a stroke, seizure, or psychogenic event. Should a neurologist or emergency medicine physician make the decision? Maybe, but how much extra time will it take to get one on the line? And, even then, they’ll be making a critical decision with sparse, secondhand information. What if the special ambulance is mistakenly sent to deal with a conversion disorder, only to have a legitimate stroke occur elsewhere when it’s no longer immediately available? That, inevitably, will lead to a lawsuit because the wrong ambulance was sent.
I’m not against the stroke ambulance – far from it – but there are still a lot questions to be answered. Putting a CT scanner and TPA in an ambulance is, comparatively, the easiest part.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
The TPA ambulance, armed with its own CT scanner, has arrived in the United States after several successful years in Germany.
Now what?
Like all new advances, it’s a difficult balance between costs and benefits. The money, in the end, is what it really comes down to. Will the cost of a CT ambulance, the equipment needed to send images to a radiologist, the extra training for EMTs, the price of stocking TPA on board, and maybe even having a neurologist on the ride (or telemedicine for one to see the patient) be offset by money saved on rehabilitation costs, better recoveries, fewer complications, even returning a patient to work?
I have no idea. I’m not sure anyone else does, either.
Certainly, I support the idea of improved stroke care. Although far from ideal, TPA is the only thing we have right now, and the sooner it’s given, the better. Most neurologists will agree. But who’s going to pay for this?
The insurance companies, obviously. But money is finite. What if we upgrade all these ambulances, only to find that there’s no significant cost savings on rehab and recovery when TPA is used in the field? Then the money comes out of doctors’ and nurses’ salaries, higher premiums for everyone, and a cutback in treatment for some other disorder. I’m pretty sure it won’t be taken out of an insurance executive’s year-end bonus.
And just try explaining that to the family of a stroke victim.
It’s not practical to put a CT scanner in every ambulance, so where do we put those so equipped? Again, there’s no easy answer. In areas with large retirement communities? Seems like a safe bet, but young people have strokes, too. Only in cities? More people live in cities, but those in rural areas may be too far from a hospital to receive TPA early. Shouldn’t they have one, too?
Who’s going to make the decision to send the TPA ambulance vs. the regular ambulance? That’s another tough question. The layman who calls in usually isn’t sure what’s going on, only that an ambulance is needed. The dispatcher often can’t tell over the phone if the patient has had a stroke, seizure, or psychogenic event. Should a neurologist or emergency medicine physician make the decision? Maybe, but how much extra time will it take to get one on the line? And, even then, they’ll be making a critical decision with sparse, secondhand information. What if the special ambulance is mistakenly sent to deal with a conversion disorder, only to have a legitimate stroke occur elsewhere when it’s no longer immediately available? That, inevitably, will lead to a lawsuit because the wrong ambulance was sent.
I’m not against the stroke ambulance – far from it – but there are still a lot questions to be answered. Putting a CT scanner and TPA in an ambulance is, comparatively, the easiest part.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
Kinetin and the skin
Kinetin (N6-furfuryladenine or 6-furfurylaminopurine) is a plant cytokinin or phytohormone that promotes cell division, delays senescence in plants, and is reputed to aid in the restoration of skin barrier function and, possibly, in reducing the signs and symptoms of rosacea (Clin. Exp. Dermatol. 2007;32:693-5; Plant Sci. 1999;148:37-45).
Kinetin is believed to develop in cellular DNA as a product of the oxidative, secondary modification of DNA (Plant Sci. 1999;148:37-45). In 1955, it became the first cytokinin isolated from DNA (from herring sperm) as an artifactual rearrangement product of the autoclaving process (J. Cosmet. Dermatol. 2007;6:243-9; Int. J. Biol. Macromol. 2007;40:182-92).
It has since been found to be present in human urine as well as DNA freshly extracted from human cells (Int. J. Biol. Macromol. 2007;40:182-92). The preponderance of amassed experimental evidence suggests that endogenous kinetin acts in vitro and in vivo as a potent antioxidant (Plant Sci. 1999;148:37-45). Currently, it is used as an anti-aging agent in various cosmetic products (J. Cosmet. Dermatol. 2007;6:243-9; J. Cosmet. Dermatol. 2010;9:218-25). Synthetic kinetin is thought to have the capacity to neutralize free radicals as well as limit the damage to DNA and fibroblasts (Photochem. Photobiol. 2012;88:748-52).
In vitro results
Olsen et al. demonstrated in vitro in 1999 that kinetin dose-dependently protected DNA against oxidative damage mediated by the Fenton reaction, and noted that kinetin had previously been linked to anti-aging activity in plants, fruit flies, and human cells in culture (Biochem. Biophys. Res. Commun. 1999;265:499-502). The following year, Verbeke et al. showed in vitro that kinetin potently inhibited damage caused by oxidation and glycoxidation (Biochem. Biophys. Res. Commun. 2000;276:1265-70).
In 2006, Vicanova et al. analyzed the effects of active ingredients from topical and systemic skin care formulations in vitro, finding that kinetin affected the upper dermis by enhancing deposits of fibrillin-1 and elastin fibers as well as their organization perpendicular to the dermal-epidermal junction. In the epidermis, kinetin stimulated keratinocyte production. Further, the investigators noted that the combination of topically applied kinetin with Imedeen Time Perfection ingredients (i.e., BioMarine Complex, grape seed extract, tomato extract, and vitamin C) supplemented systemically into culture medium yielded complementary benefits to dermal and epidermal development (Ann. N.Y. Acad. Sci. 2006;1067:337-42).
It is worth noting that in a study by Tournas et al. published the same month, investigators found that the topical application of a combination of vitamins C and E and ferulic acid yielded photoprotection to pig skin at 5 times the minimal erythema dose (MED) while individual antioxidants to which it was compared (i.e., coenzyme Q10, idebenone, and kinetin) delivered no photoprotective effects (J. Invest. Dermatol. 2006;126:1185-7). Nevertheless, Barciszewski et al. have observed that kinetin is the first stable secondary DNA damage product characterized by well defined cytokinin and anti-aging activity, with data showing that it has delayed human cellular aging in culture (Int. J. Biol. Macromol. 2007;40:182-92).
Rosacea
In 2007, Wu et al. performed a 12-week open-label study in 15 women and 3 men (aged 30-67 years) to ascertain the tolerability and efficacy of kinetin 0.1% lotion in the treatment of mild to moderate facial rosacea. Patients (17 of whom completed the study) applied the lotion twice daily, also daily applying an SPF 30 sunscreen. By week 4, significant improvements were observed in the reduction of skin roughness and mottled hyperpigmentation. Subject assessments at each 4-week interval after baseline and after 12 weeks revealed that kinetin 0.1% was well tolerated and effective for mild to moderate inflammatory rosacea (Clin. Exp. Dermatol. 2007;32:693-5).
Anti-aging
A 2002 study by J.L. McCullough and G.D. Weinstein represented the first evidence of the efficacy of topical kinetin in human beings, with twice-daily application for 24 weeks found to ameliorate skin texture, color, and blotchiness while diminishing rhytides and transepidermal water loss (J. Cosmet. Dermatol. 2002;15:29-32).
Two years later, T. Kimura and K. Doi showed that topical administration of kinetin improved the texture, wrinkling, and pigmentation of aged skin of hairless descendants of Mexican hairless dogs, resulting in notable depigmentation and rejuvenation after 100 days of treatment (Rejuvenation Res. 2004;7:32-9).In 2007, Chiu et al. conducted a randomized, double-blind, placebo-controlled, split-face comparative study in 52 Taiwanese subjects aged 30-60 years (90% of whom were female, all of whom had Fitzpatrick skin types II, III, or IV) to evaluate the clinical anti-aging effects and efficacy differences between kinetin plus niacinamide (kinetin 0.03%, niacinamide 4%) and niacinamide 4% alone versus vehicle placebo.
In the combination group, significant and sustained decreases were observed in counts of spots, pores, wrinkles, and evenness as well as persistent reductions in erythema index at weeks 8 and 12. At week 12, stratum corneum hydration status also was significantly enhanced in this group. In the niacinamide-only group, pore and evenness counts were significantly decreased at week 8, with declines in wrinkle counts emerging at week 12. The investigators concluded that kinetin and niacinamide display synergistic and dynamic anti-aging effects, showing substantial potential as topical anti-aging cosmeceutical agents (J. Cosmet. Dermatol. 2007;6:243-9).
However, Levin et al. noted in 2010 that while the effects of kinetin have been established in plants and its antioxidant properties have been displayed in vitro, the anti-aging effects and clinical efficacy ascribed to kinetin have been based on limited evidence, with no studies extant on the percutaneous absorption of kinetin. They added that research elucidating the mechanisms through which kinetin appears to improve skin barrier function, texture, and pigmentation also are lacking (J. Clin. Aesthet. Dermatol. 2010;3:22-41).
In 2012, Campos et al. assessed the effects on hydration, viscoelastic characteristics, and photoprotection of cosmetic preparations containing a dispersion of liposome with magnesium ascorbyl phosphate, alpha-lipoic acid, and kinetin. They observed that the formulation protected hairless mouse skin barrier function against UV harm. After 4 weeks of application on human skin, the combination product was found to have improved moisturization of the stratum corneum, also delivering hydration effects to deeper skin layers. The researchers concluded that the cosmetic formulation containing kinetin shows promise as a cutaneous anti-aging product (Photochem. Photobiol. 2012;88:748-52).
Conclusion
While some experimental and clinical results appear to suggest an anti-aging effect exerted by topically applied kinetin, much more research – particularly randomized controlled and comparison studies – are needed to provide a clearer picture as to the mechanisms and appropriate role of kinetin in the dermatologic armamentarium.
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy,Topix Pharmaceuticals, and Unilever.
Kinetin (N6-furfuryladenine or 6-furfurylaminopurine) is a plant cytokinin or phytohormone that promotes cell division, delays senescence in plants, and is reputed to aid in the restoration of skin barrier function and, possibly, in reducing the signs and symptoms of rosacea (Clin. Exp. Dermatol. 2007;32:693-5; Plant Sci. 1999;148:37-45).
Kinetin is believed to develop in cellular DNA as a product of the oxidative, secondary modification of DNA (Plant Sci. 1999;148:37-45). In 1955, it became the first cytokinin isolated from DNA (from herring sperm) as an artifactual rearrangement product of the autoclaving process (J. Cosmet. Dermatol. 2007;6:243-9; Int. J. Biol. Macromol. 2007;40:182-92).
It has since been found to be present in human urine as well as DNA freshly extracted from human cells (Int. J. Biol. Macromol. 2007;40:182-92). The preponderance of amassed experimental evidence suggests that endogenous kinetin acts in vitro and in vivo as a potent antioxidant (Plant Sci. 1999;148:37-45). Currently, it is used as an anti-aging agent in various cosmetic products (J. Cosmet. Dermatol. 2007;6:243-9; J. Cosmet. Dermatol. 2010;9:218-25). Synthetic kinetin is thought to have the capacity to neutralize free radicals as well as limit the damage to DNA and fibroblasts (Photochem. Photobiol. 2012;88:748-52).
In vitro results
Olsen et al. demonstrated in vitro in 1999 that kinetin dose-dependently protected DNA against oxidative damage mediated by the Fenton reaction, and noted that kinetin had previously been linked to anti-aging activity in plants, fruit flies, and human cells in culture (Biochem. Biophys. Res. Commun. 1999;265:499-502). The following year, Verbeke et al. showed in vitro that kinetin potently inhibited damage caused by oxidation and glycoxidation (Biochem. Biophys. Res. Commun. 2000;276:1265-70).
In 2006, Vicanova et al. analyzed the effects of active ingredients from topical and systemic skin care formulations in vitro, finding that kinetin affected the upper dermis by enhancing deposits of fibrillin-1 and elastin fibers as well as their organization perpendicular to the dermal-epidermal junction. In the epidermis, kinetin stimulated keratinocyte production. Further, the investigators noted that the combination of topically applied kinetin with Imedeen Time Perfection ingredients (i.e., BioMarine Complex, grape seed extract, tomato extract, and vitamin C) supplemented systemically into culture medium yielded complementary benefits to dermal and epidermal development (Ann. N.Y. Acad. Sci. 2006;1067:337-42).
It is worth noting that in a study by Tournas et al. published the same month, investigators found that the topical application of a combination of vitamins C and E and ferulic acid yielded photoprotection to pig skin at 5 times the minimal erythema dose (MED) while individual antioxidants to which it was compared (i.e., coenzyme Q10, idebenone, and kinetin) delivered no photoprotective effects (J. Invest. Dermatol. 2006;126:1185-7). Nevertheless, Barciszewski et al. have observed that kinetin is the first stable secondary DNA damage product characterized by well defined cytokinin and anti-aging activity, with data showing that it has delayed human cellular aging in culture (Int. J. Biol. Macromol. 2007;40:182-92).
Rosacea
In 2007, Wu et al. performed a 12-week open-label study in 15 women and 3 men (aged 30-67 years) to ascertain the tolerability and efficacy of kinetin 0.1% lotion in the treatment of mild to moderate facial rosacea. Patients (17 of whom completed the study) applied the lotion twice daily, also daily applying an SPF 30 sunscreen. By week 4, significant improvements were observed in the reduction of skin roughness and mottled hyperpigmentation. Subject assessments at each 4-week interval after baseline and after 12 weeks revealed that kinetin 0.1% was well tolerated and effective for mild to moderate inflammatory rosacea (Clin. Exp. Dermatol. 2007;32:693-5).
Anti-aging
A 2002 study by J.L. McCullough and G.D. Weinstein represented the first evidence of the efficacy of topical kinetin in human beings, with twice-daily application for 24 weeks found to ameliorate skin texture, color, and blotchiness while diminishing rhytides and transepidermal water loss (J. Cosmet. Dermatol. 2002;15:29-32).
Two years later, T. Kimura and K. Doi showed that topical administration of kinetin improved the texture, wrinkling, and pigmentation of aged skin of hairless descendants of Mexican hairless dogs, resulting in notable depigmentation and rejuvenation after 100 days of treatment (Rejuvenation Res. 2004;7:32-9).In 2007, Chiu et al. conducted a randomized, double-blind, placebo-controlled, split-face comparative study in 52 Taiwanese subjects aged 30-60 years (90% of whom were female, all of whom had Fitzpatrick skin types II, III, or IV) to evaluate the clinical anti-aging effects and efficacy differences between kinetin plus niacinamide (kinetin 0.03%, niacinamide 4%) and niacinamide 4% alone versus vehicle placebo.
In the combination group, significant and sustained decreases were observed in counts of spots, pores, wrinkles, and evenness as well as persistent reductions in erythema index at weeks 8 and 12. At week 12, stratum corneum hydration status also was significantly enhanced in this group. In the niacinamide-only group, pore and evenness counts were significantly decreased at week 8, with declines in wrinkle counts emerging at week 12. The investigators concluded that kinetin and niacinamide display synergistic and dynamic anti-aging effects, showing substantial potential as topical anti-aging cosmeceutical agents (J. Cosmet. Dermatol. 2007;6:243-9).
However, Levin et al. noted in 2010 that while the effects of kinetin have been established in plants and its antioxidant properties have been displayed in vitro, the anti-aging effects and clinical efficacy ascribed to kinetin have been based on limited evidence, with no studies extant on the percutaneous absorption of kinetin. They added that research elucidating the mechanisms through which kinetin appears to improve skin barrier function, texture, and pigmentation also are lacking (J. Clin. Aesthet. Dermatol. 2010;3:22-41).
In 2012, Campos et al. assessed the effects on hydration, viscoelastic characteristics, and photoprotection of cosmetic preparations containing a dispersion of liposome with magnesium ascorbyl phosphate, alpha-lipoic acid, and kinetin. They observed that the formulation protected hairless mouse skin barrier function against UV harm. After 4 weeks of application on human skin, the combination product was found to have improved moisturization of the stratum corneum, also delivering hydration effects to deeper skin layers. The researchers concluded that the cosmetic formulation containing kinetin shows promise as a cutaneous anti-aging product (Photochem. Photobiol. 2012;88:748-52).
Conclusion
While some experimental and clinical results appear to suggest an anti-aging effect exerted by topically applied kinetin, much more research – particularly randomized controlled and comparison studies – are needed to provide a clearer picture as to the mechanisms and appropriate role of kinetin in the dermatologic armamentarium.
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy,Topix Pharmaceuticals, and Unilever.
Kinetin (N6-furfuryladenine or 6-furfurylaminopurine) is a plant cytokinin or phytohormone that promotes cell division, delays senescence in plants, and is reputed to aid in the restoration of skin barrier function and, possibly, in reducing the signs and symptoms of rosacea (Clin. Exp. Dermatol. 2007;32:693-5; Plant Sci. 1999;148:37-45).
Kinetin is believed to develop in cellular DNA as a product of the oxidative, secondary modification of DNA (Plant Sci. 1999;148:37-45). In 1955, it became the first cytokinin isolated from DNA (from herring sperm) as an artifactual rearrangement product of the autoclaving process (J. Cosmet. Dermatol. 2007;6:243-9; Int. J. Biol. Macromol. 2007;40:182-92).
It has since been found to be present in human urine as well as DNA freshly extracted from human cells (Int. J. Biol. Macromol. 2007;40:182-92). The preponderance of amassed experimental evidence suggests that endogenous kinetin acts in vitro and in vivo as a potent antioxidant (Plant Sci. 1999;148:37-45). Currently, it is used as an anti-aging agent in various cosmetic products (J. Cosmet. Dermatol. 2007;6:243-9; J. Cosmet. Dermatol. 2010;9:218-25). Synthetic kinetin is thought to have the capacity to neutralize free radicals as well as limit the damage to DNA and fibroblasts (Photochem. Photobiol. 2012;88:748-52).
In vitro results
Olsen et al. demonstrated in vitro in 1999 that kinetin dose-dependently protected DNA against oxidative damage mediated by the Fenton reaction, and noted that kinetin had previously been linked to anti-aging activity in plants, fruit flies, and human cells in culture (Biochem. Biophys. Res. Commun. 1999;265:499-502). The following year, Verbeke et al. showed in vitro that kinetin potently inhibited damage caused by oxidation and glycoxidation (Biochem. Biophys. Res. Commun. 2000;276:1265-70).
In 2006, Vicanova et al. analyzed the effects of active ingredients from topical and systemic skin care formulations in vitro, finding that kinetin affected the upper dermis by enhancing deposits of fibrillin-1 and elastin fibers as well as their organization perpendicular to the dermal-epidermal junction. In the epidermis, kinetin stimulated keratinocyte production. Further, the investigators noted that the combination of topically applied kinetin with Imedeen Time Perfection ingredients (i.e., BioMarine Complex, grape seed extract, tomato extract, and vitamin C) supplemented systemically into culture medium yielded complementary benefits to dermal and epidermal development (Ann. N.Y. Acad. Sci. 2006;1067:337-42).
It is worth noting that in a study by Tournas et al. published the same month, investigators found that the topical application of a combination of vitamins C and E and ferulic acid yielded photoprotection to pig skin at 5 times the minimal erythema dose (MED) while individual antioxidants to which it was compared (i.e., coenzyme Q10, idebenone, and kinetin) delivered no photoprotective effects (J. Invest. Dermatol. 2006;126:1185-7). Nevertheless, Barciszewski et al. have observed that kinetin is the first stable secondary DNA damage product characterized by well defined cytokinin and anti-aging activity, with data showing that it has delayed human cellular aging in culture (Int. J. Biol. Macromol. 2007;40:182-92).
Rosacea
In 2007, Wu et al. performed a 12-week open-label study in 15 women and 3 men (aged 30-67 years) to ascertain the tolerability and efficacy of kinetin 0.1% lotion in the treatment of mild to moderate facial rosacea. Patients (17 of whom completed the study) applied the lotion twice daily, also daily applying an SPF 30 sunscreen. By week 4, significant improvements were observed in the reduction of skin roughness and mottled hyperpigmentation. Subject assessments at each 4-week interval after baseline and after 12 weeks revealed that kinetin 0.1% was well tolerated and effective for mild to moderate inflammatory rosacea (Clin. Exp. Dermatol. 2007;32:693-5).
Anti-aging
A 2002 study by J.L. McCullough and G.D. Weinstein represented the first evidence of the efficacy of topical kinetin in human beings, with twice-daily application for 24 weeks found to ameliorate skin texture, color, and blotchiness while diminishing rhytides and transepidermal water loss (J. Cosmet. Dermatol. 2002;15:29-32).
Two years later, T. Kimura and K. Doi showed that topical administration of kinetin improved the texture, wrinkling, and pigmentation of aged skin of hairless descendants of Mexican hairless dogs, resulting in notable depigmentation and rejuvenation after 100 days of treatment (Rejuvenation Res. 2004;7:32-9).In 2007, Chiu et al. conducted a randomized, double-blind, placebo-controlled, split-face comparative study in 52 Taiwanese subjects aged 30-60 years (90% of whom were female, all of whom had Fitzpatrick skin types II, III, or IV) to evaluate the clinical anti-aging effects and efficacy differences between kinetin plus niacinamide (kinetin 0.03%, niacinamide 4%) and niacinamide 4% alone versus vehicle placebo.
In the combination group, significant and sustained decreases were observed in counts of spots, pores, wrinkles, and evenness as well as persistent reductions in erythema index at weeks 8 and 12. At week 12, stratum corneum hydration status also was significantly enhanced in this group. In the niacinamide-only group, pore and evenness counts were significantly decreased at week 8, with declines in wrinkle counts emerging at week 12. The investigators concluded that kinetin and niacinamide display synergistic and dynamic anti-aging effects, showing substantial potential as topical anti-aging cosmeceutical agents (J. Cosmet. Dermatol. 2007;6:243-9).
However, Levin et al. noted in 2010 that while the effects of kinetin have been established in plants and its antioxidant properties have been displayed in vitro, the anti-aging effects and clinical efficacy ascribed to kinetin have been based on limited evidence, with no studies extant on the percutaneous absorption of kinetin. They added that research elucidating the mechanisms through which kinetin appears to improve skin barrier function, texture, and pigmentation also are lacking (J. Clin. Aesthet. Dermatol. 2010;3:22-41).
In 2012, Campos et al. assessed the effects on hydration, viscoelastic characteristics, and photoprotection of cosmetic preparations containing a dispersion of liposome with magnesium ascorbyl phosphate, alpha-lipoic acid, and kinetin. They observed that the formulation protected hairless mouse skin barrier function against UV harm. After 4 weeks of application on human skin, the combination product was found to have improved moisturization of the stratum corneum, also delivering hydration effects to deeper skin layers. The researchers concluded that the cosmetic formulation containing kinetin shows promise as a cutaneous anti-aging product (Photochem. Photobiol. 2012;88:748-52).
Conclusion
While some experimental and clinical results appear to suggest an anti-aging effect exerted by topically applied kinetin, much more research – particularly randomized controlled and comparison studies – are needed to provide a clearer picture as to the mechanisms and appropriate role of kinetin in the dermatologic armamentarium.
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy,Topix Pharmaceuticals, and Unilever.
First Refusal
Treatment success in psoriasis, as in any dermatologic condition, is dependent on many factors. The willingness of patients to follow our suggested therapeutic plans certainly is one of the most important components of this process.
Halioua et al1 analyzed the issue of treatment refusal, which they defined as “a patient actively refusing to take treatment despite physician recommendations,” among psoriasis patients. Treatment refusal is a more complex phenomenon than nonadherence, as it requires an affirmative act that goes beyond more passive acts of not filling prescriptions, taking a medication sporadically, or forgetting to take a medication. Their objective was to investigate refusal of topical treatments by patients living with psoriasis in France as well as the factors that influence such refusal.1
The authors evaluated responses to an Internet study.1 Responses from participants who refused topical therapy (n=50) were compared to individuals who successfully applied topical treatment (n=205). Individuals receiving phototherapy, biologic therapy, and oral treatment were not included in the analysis. Spearman rank correlations completed by Fisher exact tests and Student t tests were performed.1
The researchers found that objective aspects of psoriasis, including comorbidities, localization of lesions, and symptoms associated with psoriasis, were not significant predictors of treatment refusal. The factors that did appear to influence refusal related more to patient perception of disease and its treatment.1
First, treatment refusal was defined by patient attitude toward treatment. In the treatment refusal group, significantly fewer participants reported believing that psoriasis can be managed (20.0% vs 38.5%; P<.01), and significantly more participants in the treatment refusal group reported believing that topical psoriasis treatments never work (58.0% vs 27.5%; odds ratio, 2.09; P<.0001). Additionally, significantly fewer participants in the treatment refusal group were willing to stay on prescription medications long-term (30.0% vs 77.6%; P<.001), and significantly more patients in the treatment refusal group believed that all creams (prescription or over-the-counter) work the same (54.0% vs 31.7%; odds ratio, 1.07; P=.003).1
The physician-patient relationship also influenced refusal. In the treatment refusal group, 60% of participants reported no longer consulting physicians for psoriasis treatment. The main reasons for cessation of medical care were lack of improvement of psoriasis (40%) and feeling that the physician did not take psoriasis seriously (20%). In the treatment acceptance group, only 10% of participants no longer consulted physicians.1 Among participants who continued to consult their physician (40% for the treatment refusal group and 90.2% for the treatment acceptance group), significantly fewer participants in the treatment refusal group reported that they were substantially helped by their physician (50.0% vs 73.0%; P=.03) and that they always followed physician recommendations (65.0% vs 85.4%; P=.02). Additionally, significantly fewer participants in the treatment refusal group considered that their physician took the time to listen to what he/she had to say (65.0% vs 85.9%; P=.02) and that their physician had provided clear instructions on how to utilize the treatment (65.0% vs 83.2%; P=.046).1
Therefore, treatment refusal is an important factor to be considered in the management of psoriasis. The findings of this study indicate possible strategies to reduce patient refusal. For example, enhanced education about the therapeutic options for psoriasis and their benefits could counter negative perceptions about these therapies. It also appears that increased focus on the physician-patient relationship may have a positive impact in this area.
Reference
1. Halioua B, Maury Le Breton A, de Fontaubert A, et al. Treatment refusal among patients with psoriasis [published online ahead of print]. J Dermatolog Treat. 2015;2:1-5.
Treatment success in psoriasis, as in any dermatologic condition, is dependent on many factors. The willingness of patients to follow our suggested therapeutic plans certainly is one of the most important components of this process.
Halioua et al1 analyzed the issue of treatment refusal, which they defined as “a patient actively refusing to take treatment despite physician recommendations,” among psoriasis patients. Treatment refusal is a more complex phenomenon than nonadherence, as it requires an affirmative act that goes beyond more passive acts of not filling prescriptions, taking a medication sporadically, or forgetting to take a medication. Their objective was to investigate refusal of topical treatments by patients living with psoriasis in France as well as the factors that influence such refusal.1
The authors evaluated responses to an Internet study.1 Responses from participants who refused topical therapy (n=50) were compared to individuals who successfully applied topical treatment (n=205). Individuals receiving phototherapy, biologic therapy, and oral treatment were not included in the analysis. Spearman rank correlations completed by Fisher exact tests and Student t tests were performed.1
The researchers found that objective aspects of psoriasis, including comorbidities, localization of lesions, and symptoms associated with psoriasis, were not significant predictors of treatment refusal. The factors that did appear to influence refusal related more to patient perception of disease and its treatment.1
First, treatment refusal was defined by patient attitude toward treatment. In the treatment refusal group, significantly fewer participants reported believing that psoriasis can be managed (20.0% vs 38.5%; P<.01), and significantly more participants in the treatment refusal group reported believing that topical psoriasis treatments never work (58.0% vs 27.5%; odds ratio, 2.09; P<.0001). Additionally, significantly fewer participants in the treatment refusal group were willing to stay on prescription medications long-term (30.0% vs 77.6%; P<.001), and significantly more patients in the treatment refusal group believed that all creams (prescription or over-the-counter) work the same (54.0% vs 31.7%; odds ratio, 1.07; P=.003).1
The physician-patient relationship also influenced refusal. In the treatment refusal group, 60% of participants reported no longer consulting physicians for psoriasis treatment. The main reasons for cessation of medical care were lack of improvement of psoriasis (40%) and feeling that the physician did not take psoriasis seriously (20%). In the treatment acceptance group, only 10% of participants no longer consulted physicians.1 Among participants who continued to consult their physician (40% for the treatment refusal group and 90.2% for the treatment acceptance group), significantly fewer participants in the treatment refusal group reported that they were substantially helped by their physician (50.0% vs 73.0%; P=.03) and that they always followed physician recommendations (65.0% vs 85.4%; P=.02). Additionally, significantly fewer participants in the treatment refusal group considered that their physician took the time to listen to what he/she had to say (65.0% vs 85.9%; P=.02) and that their physician had provided clear instructions on how to utilize the treatment (65.0% vs 83.2%; P=.046).1
Therefore, treatment refusal is an important factor to be considered in the management of psoriasis. The findings of this study indicate possible strategies to reduce patient refusal. For example, enhanced education about the therapeutic options for psoriasis and their benefits could counter negative perceptions about these therapies. It also appears that increased focus on the physician-patient relationship may have a positive impact in this area.
Treatment success in psoriasis, as in any dermatologic condition, is dependent on many factors. The willingness of patients to follow our suggested therapeutic plans certainly is one of the most important components of this process.
Halioua et al1 analyzed the issue of treatment refusal, which they defined as “a patient actively refusing to take treatment despite physician recommendations,” among psoriasis patients. Treatment refusal is a more complex phenomenon than nonadherence, as it requires an affirmative act that goes beyond more passive acts of not filling prescriptions, taking a medication sporadically, or forgetting to take a medication. Their objective was to investigate refusal of topical treatments by patients living with psoriasis in France as well as the factors that influence such refusal.1
The authors evaluated responses to an Internet study.1 Responses from participants who refused topical therapy (n=50) were compared to individuals who successfully applied topical treatment (n=205). Individuals receiving phototherapy, biologic therapy, and oral treatment were not included in the analysis. Spearman rank correlations completed by Fisher exact tests and Student t tests were performed.1
The researchers found that objective aspects of psoriasis, including comorbidities, localization of lesions, and symptoms associated with psoriasis, were not significant predictors of treatment refusal. The factors that did appear to influence refusal related more to patient perception of disease and its treatment.1
First, treatment refusal was defined by patient attitude toward treatment. In the treatment refusal group, significantly fewer participants reported believing that psoriasis can be managed (20.0% vs 38.5%; P<.01), and significantly more participants in the treatment refusal group reported believing that topical psoriasis treatments never work (58.0% vs 27.5%; odds ratio, 2.09; P<.0001). Additionally, significantly fewer participants in the treatment refusal group were willing to stay on prescription medications long-term (30.0% vs 77.6%; P<.001), and significantly more patients in the treatment refusal group believed that all creams (prescription or over-the-counter) work the same (54.0% vs 31.7%; odds ratio, 1.07; P=.003).1
The physician-patient relationship also influenced refusal. In the treatment refusal group, 60% of participants reported no longer consulting physicians for psoriasis treatment. The main reasons for cessation of medical care were lack of improvement of psoriasis (40%) and feeling that the physician did not take psoriasis seriously (20%). In the treatment acceptance group, only 10% of participants no longer consulted physicians.1 Among participants who continued to consult their physician (40% for the treatment refusal group and 90.2% for the treatment acceptance group), significantly fewer participants in the treatment refusal group reported that they were substantially helped by their physician (50.0% vs 73.0%; P=.03) and that they always followed physician recommendations (65.0% vs 85.4%; P=.02). Additionally, significantly fewer participants in the treatment refusal group considered that their physician took the time to listen to what he/she had to say (65.0% vs 85.9%; P=.02) and that their physician had provided clear instructions on how to utilize the treatment (65.0% vs 83.2%; P=.046).1
Therefore, treatment refusal is an important factor to be considered in the management of psoriasis. The findings of this study indicate possible strategies to reduce patient refusal. For example, enhanced education about the therapeutic options for psoriasis and their benefits could counter negative perceptions about these therapies. It also appears that increased focus on the physician-patient relationship may have a positive impact in this area.
Reference
1. Halioua B, Maury Le Breton A, de Fontaubert A, et al. Treatment refusal among patients with psoriasis [published online ahead of print]. J Dermatolog Treat. 2015;2:1-5.
Reference
1. Halioua B, Maury Le Breton A, de Fontaubert A, et al. Treatment refusal among patients with psoriasis [published online ahead of print]. J Dermatolog Treat. 2015;2:1-5.
Moms can (almost) have it all
They say you can’t have it all, and they’re right. But you can have most of it. By that I mean you can achieve a work-life balance that will enable you to thrive in your career while you raise your dream family. While this goal may never be easy, and you may always feel like you want to do more, give more, and reach more, that’s just the nature of the beast. We are all overachievers. That’s how we’re programmed; it’s in our DNA. Why else would we have taken on so much debt and sacrificed so many years for a career? And while many of us specifically chose hospital medicine so we could offset our stressful, hectic work life with plenty of time off for self and family, our reality is still replete with everyday challenges and, frequently, burnout.
We eagerly seek out best practices to optimize patient care, but how often do we seek advice from trusted colleagues on their “best practices” for balancing work and home? While talking with some of my female colleagues recently, I expressed my dismay that my dishwasher had broken and I frequently found myself washing dinner dishes as I juggled homework for my two 6-year-olds and responded to a seemingly incessant pager. One laughed as she recalled the pains she went through to have not one, but two dishwashers installed in her kitchen during her remodel. Washing dishes by hand simply wasn’t realistic for her. Her two little boys demanded whatever physical and emotional energy she had left after a stressful day at the hospital.
It is okay to admit that you don’t have all the answers, and it is cathartic to accept that you may never be the homemaker your mother was and forget about matching your grandmothers’ skillsets. At some Alcoholics Anonymous meetings, new members stand up and introduce themselves by saying, “Hello, my name is ___, and I am an alcoholic.” I personally felt like a huge weight had been lifted from my shoulders when one day, I finally acknowledged I didn’t have all the answers and I could never follow all of the parenting experts’ advice. After all, experts come and go, and with it, their expert recommendations. I don’t even want to abide by the “no more than 30 minutes of screen time per day” mantra. My parents raised five children on rerun after rerun of “The Andy Griffith Show,” “The Brady Bunch,” and other sitcoms, not to mention movies and musicals, and every one of us has a terminal degree, and still remember how much fun we had as children. My parents set high expectations, and they taught us how to reach them, plain and simple. We worked hard and we got to play hard, too.
The bottom line is that different techniques work for different people. Find out which ones work for you and your family and pursue them, regardless of what others may think. And above all, don’t let guilt get the best of you, because it will eat away at you and potentially destroy all you want to accomplish. You know, the guilt of missing a soccer game or a school play, or even the guilt of stopping for fast food when you are just too tired to cook a nutritious meal. Give yourself a break. The realistic goal is to optimize your work-life balance; the elusive one is to perfect it.
Dr. Hester is a hospitalist at Baltimore-Washington Medical Center in Glen Burnie, Md. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at healthsavvy@aol.com.
They say you can’t have it all, and they’re right. But you can have most of it. By that I mean you can achieve a work-life balance that will enable you to thrive in your career while you raise your dream family. While this goal may never be easy, and you may always feel like you want to do more, give more, and reach more, that’s just the nature of the beast. We are all overachievers. That’s how we’re programmed; it’s in our DNA. Why else would we have taken on so much debt and sacrificed so many years for a career? And while many of us specifically chose hospital medicine so we could offset our stressful, hectic work life with plenty of time off for self and family, our reality is still replete with everyday challenges and, frequently, burnout.
We eagerly seek out best practices to optimize patient care, but how often do we seek advice from trusted colleagues on their “best practices” for balancing work and home? While talking with some of my female colleagues recently, I expressed my dismay that my dishwasher had broken and I frequently found myself washing dinner dishes as I juggled homework for my two 6-year-olds and responded to a seemingly incessant pager. One laughed as she recalled the pains she went through to have not one, but two dishwashers installed in her kitchen during her remodel. Washing dishes by hand simply wasn’t realistic for her. Her two little boys demanded whatever physical and emotional energy she had left after a stressful day at the hospital.
It is okay to admit that you don’t have all the answers, and it is cathartic to accept that you may never be the homemaker your mother was and forget about matching your grandmothers’ skillsets. At some Alcoholics Anonymous meetings, new members stand up and introduce themselves by saying, “Hello, my name is ___, and I am an alcoholic.” I personally felt like a huge weight had been lifted from my shoulders when one day, I finally acknowledged I didn’t have all the answers and I could never follow all of the parenting experts’ advice. After all, experts come and go, and with it, their expert recommendations. I don’t even want to abide by the “no more than 30 minutes of screen time per day” mantra. My parents raised five children on rerun after rerun of “The Andy Griffith Show,” “The Brady Bunch,” and other sitcoms, not to mention movies and musicals, and every one of us has a terminal degree, and still remember how much fun we had as children. My parents set high expectations, and they taught us how to reach them, plain and simple. We worked hard and we got to play hard, too.
The bottom line is that different techniques work for different people. Find out which ones work for you and your family and pursue them, regardless of what others may think. And above all, don’t let guilt get the best of you, because it will eat away at you and potentially destroy all you want to accomplish. You know, the guilt of missing a soccer game or a school play, or even the guilt of stopping for fast food when you are just too tired to cook a nutritious meal. Give yourself a break. The realistic goal is to optimize your work-life balance; the elusive one is to perfect it.
Dr. Hester is a hospitalist at Baltimore-Washington Medical Center in Glen Burnie, Md. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at healthsavvy@aol.com.
They say you can’t have it all, and they’re right. But you can have most of it. By that I mean you can achieve a work-life balance that will enable you to thrive in your career while you raise your dream family. While this goal may never be easy, and you may always feel like you want to do more, give more, and reach more, that’s just the nature of the beast. We are all overachievers. That’s how we’re programmed; it’s in our DNA. Why else would we have taken on so much debt and sacrificed so many years for a career? And while many of us specifically chose hospital medicine so we could offset our stressful, hectic work life with plenty of time off for self and family, our reality is still replete with everyday challenges and, frequently, burnout.
We eagerly seek out best practices to optimize patient care, but how often do we seek advice from trusted colleagues on their “best practices” for balancing work and home? While talking with some of my female colleagues recently, I expressed my dismay that my dishwasher had broken and I frequently found myself washing dinner dishes as I juggled homework for my two 6-year-olds and responded to a seemingly incessant pager. One laughed as she recalled the pains she went through to have not one, but two dishwashers installed in her kitchen during her remodel. Washing dishes by hand simply wasn’t realistic for her. Her two little boys demanded whatever physical and emotional energy she had left after a stressful day at the hospital.
It is okay to admit that you don’t have all the answers, and it is cathartic to accept that you may never be the homemaker your mother was and forget about matching your grandmothers’ skillsets. At some Alcoholics Anonymous meetings, new members stand up and introduce themselves by saying, “Hello, my name is ___, and I am an alcoholic.” I personally felt like a huge weight had been lifted from my shoulders when one day, I finally acknowledged I didn’t have all the answers and I could never follow all of the parenting experts’ advice. After all, experts come and go, and with it, their expert recommendations. I don’t even want to abide by the “no more than 30 minutes of screen time per day” mantra. My parents raised five children on rerun after rerun of “The Andy Griffith Show,” “The Brady Bunch,” and other sitcoms, not to mention movies and musicals, and every one of us has a terminal degree, and still remember how much fun we had as children. My parents set high expectations, and they taught us how to reach them, plain and simple. We worked hard and we got to play hard, too.
The bottom line is that different techniques work for different people. Find out which ones work for you and your family and pursue them, regardless of what others may think. And above all, don’t let guilt get the best of you, because it will eat away at you and potentially destroy all you want to accomplish. You know, the guilt of missing a soccer game or a school play, or even the guilt of stopping for fast food when you are just too tired to cook a nutritious meal. Give yourself a break. The realistic goal is to optimize your work-life balance; the elusive one is to perfect it.
Dr. Hester is a hospitalist at Baltimore-Washington Medical Center in Glen Burnie, Md. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at healthsavvy@aol.com.
Patience, my dear
When I am trying to help parents deal with their picky eaters, the most frustrating challenge is getting the parents to sit back and silently watch their child not eating. Despite their claims that they want their child to eat a healthy and varied diet, many parents can’t muster up either the patience or the fortitude to watch their child ignore a plate of healthy but unpreferred food. Going to bed “hungry” just doesn’t seem to happen. Before the pajamas are even out of the bottom drawer, the child is offered an alternative serving of something on the child’s short list of nutritionally sketchy “will eats.”
Parents will dredge up any excuse they can find, including the eco-conscious claim that throwing the uneaten food will swamp the town landfill. Neither the reality that the amount thrown out is minuscule nor the concept of composting seems to convince them not to worry. The more prevalent excuse is that if their child doesn’t eat something he will become malnourished or lose weight – a strange claim in a country plagued by obesity. Or heaven forbid, the child will be sentenced to suffer the pangs of “hunger” until morning.
As part of an epidemic loss of common sense, North American parents seem to also have lost their ability to be patient. It takes time to break old habits and develop new ones. They fail to appreciate that the process of change will grind to a halt if they continue to offer alternatives that enable an old habit to persist.
The challenge facing the parent of a 3-year-old picky eater is no different than the one facing our nation’s school lunch program. It is just a matter of scale. In an attempt to stop our epidemic of child obesity, the Congress passed the Healthy, Hunger-Free Kids Act in 2010. The nutritional standards it mandated were finalized by the Department of Agriculture in 2012 and put into effect in the 2012-2013 school year.
Before the first tray of healthier alternatives could slide down the polished stainless steel of a cafeteria line, there were complaints from the “lunch ladies,” aka the School Nutrition Association, a group with support from some food industry giants. Like the parent of a picky eater, the “lunch ladies” predicted that kids wouldn’t eat that healthy stuff and food would be wasted. Healthy less processed food would be more expensive (and of course less profitable for industries that process). And surprise, surprise, they were correct. Some grade school kids even organized their own protests.
However, common sense suggests that with time behavior would change if the standards were maintained. A recently released study by the Rudd Center for Food Policy and Obesity at the University of Connecticut, Hartford, “New School Meal Regulations Increase Fruit Consumption and Do Not Increase Total Plate Waste” (Child Obesity 2015 [doi:10.1089/chi.2015.0019]), has found that in the three urban school districts sampled that the percentage of students choosing fruit for lunch rose from 54% in 2012 to 66% 2014. There also was less wasted because 84% of the students ate their entrées, including fruit, in 2014. This was up from 71% at the beginning of the 3-year survey. There was a significant increase in vegetable consumption, from 45.6% in 2012 to 63.6% in 2014.
The study was far from robust in that it compared data from only 1 day in each school year over the study period. The authors noted that each year fewer children in the cohort were eating school lunches, a phenomenon they suspect may be due to the tendency of older children to take less advantage of school lunches.
Regardless of its deficiencies, the study seems to support the basic principle that giving children better choices and waiting patiently will result in more nutritionally sound eating patterns. There is no question that in the short term that providing healthier school meals is more costly. However, this gap should narrow as the lunch ladies learn more cost-effective strategies for food procurement and preparation. The Department of Agriculture is already providing funds for the school departments who are struggling financially to comply with the new standards.
Unfortunately, some impatient members of Congress are like many parents of picky eaters and are trying to roll back the nutritional standards rather than wait for the inevitable change. None of us likes the thought of wasting food or money. But when managing unhealthy eating behaviors, sometimes waste has to happen.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping With a Picky Eater.” E-mail him at pdnews@frontlinemedcom.com.
When I am trying to help parents deal with their picky eaters, the most frustrating challenge is getting the parents to sit back and silently watch their child not eating. Despite their claims that they want their child to eat a healthy and varied diet, many parents can’t muster up either the patience or the fortitude to watch their child ignore a plate of healthy but unpreferred food. Going to bed “hungry” just doesn’t seem to happen. Before the pajamas are even out of the bottom drawer, the child is offered an alternative serving of something on the child’s short list of nutritionally sketchy “will eats.”
Parents will dredge up any excuse they can find, including the eco-conscious claim that throwing the uneaten food will swamp the town landfill. Neither the reality that the amount thrown out is minuscule nor the concept of composting seems to convince them not to worry. The more prevalent excuse is that if their child doesn’t eat something he will become malnourished or lose weight – a strange claim in a country plagued by obesity. Or heaven forbid, the child will be sentenced to suffer the pangs of “hunger” until morning.
As part of an epidemic loss of common sense, North American parents seem to also have lost their ability to be patient. It takes time to break old habits and develop new ones. They fail to appreciate that the process of change will grind to a halt if they continue to offer alternatives that enable an old habit to persist.
The challenge facing the parent of a 3-year-old picky eater is no different than the one facing our nation’s school lunch program. It is just a matter of scale. In an attempt to stop our epidemic of child obesity, the Congress passed the Healthy, Hunger-Free Kids Act in 2010. The nutritional standards it mandated were finalized by the Department of Agriculture in 2012 and put into effect in the 2012-2013 school year.
Before the first tray of healthier alternatives could slide down the polished stainless steel of a cafeteria line, there were complaints from the “lunch ladies,” aka the School Nutrition Association, a group with support from some food industry giants. Like the parent of a picky eater, the “lunch ladies” predicted that kids wouldn’t eat that healthy stuff and food would be wasted. Healthy less processed food would be more expensive (and of course less profitable for industries that process). And surprise, surprise, they were correct. Some grade school kids even organized their own protests.
However, common sense suggests that with time behavior would change if the standards were maintained. A recently released study by the Rudd Center for Food Policy and Obesity at the University of Connecticut, Hartford, “New School Meal Regulations Increase Fruit Consumption and Do Not Increase Total Plate Waste” (Child Obesity 2015 [doi:10.1089/chi.2015.0019]), has found that in the three urban school districts sampled that the percentage of students choosing fruit for lunch rose from 54% in 2012 to 66% 2014. There also was less wasted because 84% of the students ate their entrées, including fruit, in 2014. This was up from 71% at the beginning of the 3-year survey. There was a significant increase in vegetable consumption, from 45.6% in 2012 to 63.6% in 2014.
The study was far from robust in that it compared data from only 1 day in each school year over the study period. The authors noted that each year fewer children in the cohort were eating school lunches, a phenomenon they suspect may be due to the tendency of older children to take less advantage of school lunches.
Regardless of its deficiencies, the study seems to support the basic principle that giving children better choices and waiting patiently will result in more nutritionally sound eating patterns. There is no question that in the short term that providing healthier school meals is more costly. However, this gap should narrow as the lunch ladies learn more cost-effective strategies for food procurement and preparation. The Department of Agriculture is already providing funds for the school departments who are struggling financially to comply with the new standards.
Unfortunately, some impatient members of Congress are like many parents of picky eaters and are trying to roll back the nutritional standards rather than wait for the inevitable change. None of us likes the thought of wasting food or money. But when managing unhealthy eating behaviors, sometimes waste has to happen.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping With a Picky Eater.” E-mail him at pdnews@frontlinemedcom.com.
When I am trying to help parents deal with their picky eaters, the most frustrating challenge is getting the parents to sit back and silently watch their child not eating. Despite their claims that they want their child to eat a healthy and varied diet, many parents can’t muster up either the patience or the fortitude to watch their child ignore a plate of healthy but unpreferred food. Going to bed “hungry” just doesn’t seem to happen. Before the pajamas are even out of the bottom drawer, the child is offered an alternative serving of something on the child’s short list of nutritionally sketchy “will eats.”
Parents will dredge up any excuse they can find, including the eco-conscious claim that throwing the uneaten food will swamp the town landfill. Neither the reality that the amount thrown out is minuscule nor the concept of composting seems to convince them not to worry. The more prevalent excuse is that if their child doesn’t eat something he will become malnourished or lose weight – a strange claim in a country plagued by obesity. Or heaven forbid, the child will be sentenced to suffer the pangs of “hunger” until morning.
As part of an epidemic loss of common sense, North American parents seem to also have lost their ability to be patient. It takes time to break old habits and develop new ones. They fail to appreciate that the process of change will grind to a halt if they continue to offer alternatives that enable an old habit to persist.
The challenge facing the parent of a 3-year-old picky eater is no different than the one facing our nation’s school lunch program. It is just a matter of scale. In an attempt to stop our epidemic of child obesity, the Congress passed the Healthy, Hunger-Free Kids Act in 2010. The nutritional standards it mandated were finalized by the Department of Agriculture in 2012 and put into effect in the 2012-2013 school year.
Before the first tray of healthier alternatives could slide down the polished stainless steel of a cafeteria line, there were complaints from the “lunch ladies,” aka the School Nutrition Association, a group with support from some food industry giants. Like the parent of a picky eater, the “lunch ladies” predicted that kids wouldn’t eat that healthy stuff and food would be wasted. Healthy less processed food would be more expensive (and of course less profitable for industries that process). And surprise, surprise, they were correct. Some grade school kids even organized their own protests.
However, common sense suggests that with time behavior would change if the standards were maintained. A recently released study by the Rudd Center for Food Policy and Obesity at the University of Connecticut, Hartford, “New School Meal Regulations Increase Fruit Consumption and Do Not Increase Total Plate Waste” (Child Obesity 2015 [doi:10.1089/chi.2015.0019]), has found that in the three urban school districts sampled that the percentage of students choosing fruit for lunch rose from 54% in 2012 to 66% 2014. There also was less wasted because 84% of the students ate their entrées, including fruit, in 2014. This was up from 71% at the beginning of the 3-year survey. There was a significant increase in vegetable consumption, from 45.6% in 2012 to 63.6% in 2014.
The study was far from robust in that it compared data from only 1 day in each school year over the study period. The authors noted that each year fewer children in the cohort were eating school lunches, a phenomenon they suspect may be due to the tendency of older children to take less advantage of school lunches.
Regardless of its deficiencies, the study seems to support the basic principle that giving children better choices and waiting patiently will result in more nutritionally sound eating patterns. There is no question that in the short term that providing healthier school meals is more costly. However, this gap should narrow as the lunch ladies learn more cost-effective strategies for food procurement and preparation. The Department of Agriculture is already providing funds for the school departments who are struggling financially to comply with the new standards.
Unfortunately, some impatient members of Congress are like many parents of picky eaters and are trying to roll back the nutritional standards rather than wait for the inevitable change. None of us likes the thought of wasting food or money. But when managing unhealthy eating behaviors, sometimes waste has to happen.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping With a Picky Eater.” E-mail him at pdnews@frontlinemedcom.com.
Microbiome and innate immunity in the respiratory tract – a primer
The pathogenesis of respiratory infections such as acute otitis media (AOM), sinusitis, and pneumonia involves complex interactions among bacteria, respiratory viruses, and host immune responses.
My clinical and laboratory group and others have described respiratory infections as resulting from the growth of a single otopathogen, such as Streptococcus pneumoniae (Spn), nontypeable Haemophilus influenzae (NTHi), or Moraxella catarrhalis (Mcat) in the nasopharynx (NP) followed by ascension to the middle ear, sinuses, or descent to the lungs. Recent research from my group and others has resulted in a shift from a single pathogen focus toward consideration of respiratory infections as a polymicrobial disease. Bacterial and viral interactions are critical in respiratory infection pathogenesis. Commensal bacteria can alter virulence of bacterial pathogens and interfere with antibiotic treatment.
The traditional view of the immune system is that it is an assembly of human tissues, cells, and molecules that work to eliminate pathogens. Recent discoveries indicate that commensals play a central role in regulating human immune responses. Thus, the key questions in the field are:
1) How do members of the NP microbiome and innate immune responses maintain health in young children over time?
2) Do specific deleterious members of the NP microbiome alter host innate immune responses in a manner that predisposes to respiratory infections?
3) How does the microbiome and innate response in the NP differ when recovery, relapse of infection, or persistent infection occurs?
Virtually all young children are colonized by Spn, NTHi, or Mcat during the first 3 years of life. My group and others have shown that competitive interactions among bacteria influence whether these potential pathogens successfully colonize and cause respiratory infections. Recent studies have demonstrated that hundreds of different bacterial species colonize the upper respiratory tract. Diverse communities have been shown to be more stable and resistant to invasion by foreign species. Data from cross-sectional studies demonstrate that specific commensals, including Dolosigranulum, Corynebacterium, and Lactococcus, are associated with decreased risk of respiratory infections. Prior studies have been limited by the use of culture-based methods or have been cross sectional in design. Therefore, the optimal levels of diversity and NP commensals critical for maintaining health in the upper respiratory tract of children are currently unknown and under study by my group and others. Studies that utilize high-throughput culture-independent molecular detection methods are now used to identify optimal levels of diversity and commensal members of the microbiome critical for maintaining health homeostasis.
The innate immune system constitutes the first line of defense against respiratory pathogen colonization and respiratory virus infection. It relies on pattern recognition receptors on innate immune cells to detect evolutionarily conserved pathogen-associated molecular patterns expressed on pathogen surfaces. Toll-like receptors (TLRs) are crucial in the innate immune response; TLR 3, 7, and 8 recognize respiratory infection-associated viral pathogens. TLR2, 4, and 5 recognize respiratory infection-associated bacterial pathogens, and TLR9 and TLR13 recognize both viral and bacterial pathogens. The activation of TLRs triggers signaling cascades and regulates the expression of a wide range of cytokines leading to antimicrobial and inflammatory responses. Cytokines (there are dozens) associated with the pathogenesis, development, severity, and clinical outcomes of respiratory infections identify hypotheses that our group is exploring to expand our understanding of how innate responses might be manipulated to favor the child host. Importantly, it has already been shown that cytokine profiles differ in the NP depending on the number and type of bacteria and viruses involved.
My group recently has shown that serum IL-10 levels are significantly higher in AOM from Spn than are the levels associated with NTHi and Mcat, suggesting use of detection of this cytokine as a serum biomarker. Others have shown that the levels of IL-1-beta, TNF-alpha, IL-6, IL-8, IL-10, and IL-17a in middle ear fluids from children with recurrent AOM correlate significantly with higher bacterial load (and worse disease). Previous studies on cytokine responses associated with AOM have focused on limited numbers of cytokines and have not examined any relationship with commensals of the NP microbiome. Moreover, the subset of children who experience excessively frequent respiratory infections likely have disturbances in their microbiome (made worse with antibiotics) and innate immune response. Because of our growing knowledge about the microbiome and innate immune response, I see a compelling need to assess interactions of the NP microbiome and innate immune responses in children that are associated with sustained health and control of respiratory infections.
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. Dr. Pichichero said the work was supported by a National Institutes of Health grant, and he had no relevant conflicts of interest. E-mail him at pdnews@frontlinemedcom.com.
The pathogenesis of respiratory infections such as acute otitis media (AOM), sinusitis, and pneumonia involves complex interactions among bacteria, respiratory viruses, and host immune responses.
My clinical and laboratory group and others have described respiratory infections as resulting from the growth of a single otopathogen, such as Streptococcus pneumoniae (Spn), nontypeable Haemophilus influenzae (NTHi), or Moraxella catarrhalis (Mcat) in the nasopharynx (NP) followed by ascension to the middle ear, sinuses, or descent to the lungs. Recent research from my group and others has resulted in a shift from a single pathogen focus toward consideration of respiratory infections as a polymicrobial disease. Bacterial and viral interactions are critical in respiratory infection pathogenesis. Commensal bacteria can alter virulence of bacterial pathogens and interfere with antibiotic treatment.
The traditional view of the immune system is that it is an assembly of human tissues, cells, and molecules that work to eliminate pathogens. Recent discoveries indicate that commensals play a central role in regulating human immune responses. Thus, the key questions in the field are:
1) How do members of the NP microbiome and innate immune responses maintain health in young children over time?
2) Do specific deleterious members of the NP microbiome alter host innate immune responses in a manner that predisposes to respiratory infections?
3) How does the microbiome and innate response in the NP differ when recovery, relapse of infection, or persistent infection occurs?
Virtually all young children are colonized by Spn, NTHi, or Mcat during the first 3 years of life. My group and others have shown that competitive interactions among bacteria influence whether these potential pathogens successfully colonize and cause respiratory infections. Recent studies have demonstrated that hundreds of different bacterial species colonize the upper respiratory tract. Diverse communities have been shown to be more stable and resistant to invasion by foreign species. Data from cross-sectional studies demonstrate that specific commensals, including Dolosigranulum, Corynebacterium, and Lactococcus, are associated with decreased risk of respiratory infections. Prior studies have been limited by the use of culture-based methods or have been cross sectional in design. Therefore, the optimal levels of diversity and NP commensals critical for maintaining health in the upper respiratory tract of children are currently unknown and under study by my group and others. Studies that utilize high-throughput culture-independent molecular detection methods are now used to identify optimal levels of diversity and commensal members of the microbiome critical for maintaining health homeostasis.
The innate immune system constitutes the first line of defense against respiratory pathogen colonization and respiratory virus infection. It relies on pattern recognition receptors on innate immune cells to detect evolutionarily conserved pathogen-associated molecular patterns expressed on pathogen surfaces. Toll-like receptors (TLRs) are crucial in the innate immune response; TLR 3, 7, and 8 recognize respiratory infection-associated viral pathogens. TLR2, 4, and 5 recognize respiratory infection-associated bacterial pathogens, and TLR9 and TLR13 recognize both viral and bacterial pathogens. The activation of TLRs triggers signaling cascades and regulates the expression of a wide range of cytokines leading to antimicrobial and inflammatory responses. Cytokines (there are dozens) associated with the pathogenesis, development, severity, and clinical outcomes of respiratory infections identify hypotheses that our group is exploring to expand our understanding of how innate responses might be manipulated to favor the child host. Importantly, it has already been shown that cytokine profiles differ in the NP depending on the number and type of bacteria and viruses involved.
My group recently has shown that serum IL-10 levels are significantly higher in AOM from Spn than are the levels associated with NTHi and Mcat, suggesting use of detection of this cytokine as a serum biomarker. Others have shown that the levels of IL-1-beta, TNF-alpha, IL-6, IL-8, IL-10, and IL-17a in middle ear fluids from children with recurrent AOM correlate significantly with higher bacterial load (and worse disease). Previous studies on cytokine responses associated with AOM have focused on limited numbers of cytokines and have not examined any relationship with commensals of the NP microbiome. Moreover, the subset of children who experience excessively frequent respiratory infections likely have disturbances in their microbiome (made worse with antibiotics) and innate immune response. Because of our growing knowledge about the microbiome and innate immune response, I see a compelling need to assess interactions of the NP microbiome and innate immune responses in children that are associated with sustained health and control of respiratory infections.
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. Dr. Pichichero said the work was supported by a National Institutes of Health grant, and he had no relevant conflicts of interest. E-mail him at pdnews@frontlinemedcom.com.
The pathogenesis of respiratory infections such as acute otitis media (AOM), sinusitis, and pneumonia involves complex interactions among bacteria, respiratory viruses, and host immune responses.
My clinical and laboratory group and others have described respiratory infections as resulting from the growth of a single otopathogen, such as Streptococcus pneumoniae (Spn), nontypeable Haemophilus influenzae (NTHi), or Moraxella catarrhalis (Mcat) in the nasopharynx (NP) followed by ascension to the middle ear, sinuses, or descent to the lungs. Recent research from my group and others has resulted in a shift from a single pathogen focus toward consideration of respiratory infections as a polymicrobial disease. Bacterial and viral interactions are critical in respiratory infection pathogenesis. Commensal bacteria can alter virulence of bacterial pathogens and interfere with antibiotic treatment.
The traditional view of the immune system is that it is an assembly of human tissues, cells, and molecules that work to eliminate pathogens. Recent discoveries indicate that commensals play a central role in regulating human immune responses. Thus, the key questions in the field are:
1) How do members of the NP microbiome and innate immune responses maintain health in young children over time?
2) Do specific deleterious members of the NP microbiome alter host innate immune responses in a manner that predisposes to respiratory infections?
3) How does the microbiome and innate response in the NP differ when recovery, relapse of infection, or persistent infection occurs?
Virtually all young children are colonized by Spn, NTHi, or Mcat during the first 3 years of life. My group and others have shown that competitive interactions among bacteria influence whether these potential pathogens successfully colonize and cause respiratory infections. Recent studies have demonstrated that hundreds of different bacterial species colonize the upper respiratory tract. Diverse communities have been shown to be more stable and resistant to invasion by foreign species. Data from cross-sectional studies demonstrate that specific commensals, including Dolosigranulum, Corynebacterium, and Lactococcus, are associated with decreased risk of respiratory infections. Prior studies have been limited by the use of culture-based methods or have been cross sectional in design. Therefore, the optimal levels of diversity and NP commensals critical for maintaining health in the upper respiratory tract of children are currently unknown and under study by my group and others. Studies that utilize high-throughput culture-independent molecular detection methods are now used to identify optimal levels of diversity and commensal members of the microbiome critical for maintaining health homeostasis.
The innate immune system constitutes the first line of defense against respiratory pathogen colonization and respiratory virus infection. It relies on pattern recognition receptors on innate immune cells to detect evolutionarily conserved pathogen-associated molecular patterns expressed on pathogen surfaces. Toll-like receptors (TLRs) are crucial in the innate immune response; TLR 3, 7, and 8 recognize respiratory infection-associated viral pathogens. TLR2, 4, and 5 recognize respiratory infection-associated bacterial pathogens, and TLR9 and TLR13 recognize both viral and bacterial pathogens. The activation of TLRs triggers signaling cascades and regulates the expression of a wide range of cytokines leading to antimicrobial and inflammatory responses. Cytokines (there are dozens) associated with the pathogenesis, development, severity, and clinical outcomes of respiratory infections identify hypotheses that our group is exploring to expand our understanding of how innate responses might be manipulated to favor the child host. Importantly, it has already been shown that cytokine profiles differ in the NP depending on the number and type of bacteria and viruses involved.
My group recently has shown that serum IL-10 levels are significantly higher in AOM from Spn than are the levels associated with NTHi and Mcat, suggesting use of detection of this cytokine as a serum biomarker. Others have shown that the levels of IL-1-beta, TNF-alpha, IL-6, IL-8, IL-10, and IL-17a in middle ear fluids from children with recurrent AOM correlate significantly with higher bacterial load (and worse disease). Previous studies on cytokine responses associated with AOM have focused on limited numbers of cytokines and have not examined any relationship with commensals of the NP microbiome. Moreover, the subset of children who experience excessively frequent respiratory infections likely have disturbances in their microbiome (made worse with antibiotics) and innate immune response. Because of our growing knowledge about the microbiome and innate immune response, I see a compelling need to assess interactions of the NP microbiome and innate immune responses in children that are associated with sustained health and control of respiratory infections.
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. Dr. Pichichero said the work was supported by a National Institutes of Health grant, and he had no relevant conflicts of interest. E-mail him at pdnews@frontlinemedcom.com.
My test-ordering evolution as a rheumatologist
Perhaps one of the biggest ways in which I’ve evolved as a doctor over the 4.5 years I’ve been in private practice is that I am not so shy about ordering tests anymore.
My point is illustrated by the case of a lovely lady I met when I was starting out in practice who complained of being in pain all the time. She was referred to me for a very low titer antinuclear antibody and a barely positive rheumatoid factor. She’d had a very long history of severe depression and anxiety. She clearly connected her symptoms to having stopped her antidepressants. She attributed her dry mouth to her benzodiazepine. I told her that I thought she had fibromyalgia and that, as she herself pointed out, it was probably related to her emotional health. We talked about the lack of any real pharmacologic treatment for the illness. We addressed self-care: that she needed to sleep better, exercise more, and treat her depression.
Three years later she came back to me with hand swelling, hypergammaglobulinemia, renal tubular acidosis, this time with significantly higher ANA and RF titers, and hypocomplementemia. You guessed it; she has Sjögren’s syndrome.
Seeing patients 40 hours a week has been incredibly challenging but also incredibly rewarding. While the large number of cases that I’ve seen has sharpened my clinical eye, it has also broadened my differential diagnoses and improved my knowledge of when it will be helpful to order more tests.
It used to be that I was extremely conservative about ordering tests. This comes from having gone to med school in the Philippines, where each test was paid for by the patient out of pocket and GDP per capita is $2,765 (compared with $53,041 for the United States) and minimum wage is less than 2 dollars a day. Every CBC has to count. If a professor asked you why you were ordering a test, “to establish a baseline” was an unacceptable reason. When I started residency here, I was incredulous that the admitted patients got a CBC and chem-7 daily. This seemed like a huge and unjustifiable waste to me.
Today, I am not so uptight. Of course, I am still extremely thoughtful about ordering tests. I do not order tests without knowing what I am looking for, or how the result will affect management. But I also recognize that there is a non-zero probability that what I suspect is fibromyalgia is something else, something with a different prognosis, better or worse, something that needs to be managed and monitored differently.
After all, “clinical judgment” does not mean relying on the history and physical exam alone. Good clinical judgment requires medical knowledge, informed by experience, supplemented by test results, and complemented by an open, inquisitive mind.
Dr. Chan practices rheumatology in Pawtucket, R.I.
Perhaps one of the biggest ways in which I’ve evolved as a doctor over the 4.5 years I’ve been in private practice is that I am not so shy about ordering tests anymore.
My point is illustrated by the case of a lovely lady I met when I was starting out in practice who complained of being in pain all the time. She was referred to me for a very low titer antinuclear antibody and a barely positive rheumatoid factor. She’d had a very long history of severe depression and anxiety. She clearly connected her symptoms to having stopped her antidepressants. She attributed her dry mouth to her benzodiazepine. I told her that I thought she had fibromyalgia and that, as she herself pointed out, it was probably related to her emotional health. We talked about the lack of any real pharmacologic treatment for the illness. We addressed self-care: that she needed to sleep better, exercise more, and treat her depression.
Three years later she came back to me with hand swelling, hypergammaglobulinemia, renal tubular acidosis, this time with significantly higher ANA and RF titers, and hypocomplementemia. You guessed it; she has Sjögren’s syndrome.
Seeing patients 40 hours a week has been incredibly challenging but also incredibly rewarding. While the large number of cases that I’ve seen has sharpened my clinical eye, it has also broadened my differential diagnoses and improved my knowledge of when it will be helpful to order more tests.
It used to be that I was extremely conservative about ordering tests. This comes from having gone to med school in the Philippines, where each test was paid for by the patient out of pocket and GDP per capita is $2,765 (compared with $53,041 for the United States) and minimum wage is less than 2 dollars a day. Every CBC has to count. If a professor asked you why you were ordering a test, “to establish a baseline” was an unacceptable reason. When I started residency here, I was incredulous that the admitted patients got a CBC and chem-7 daily. This seemed like a huge and unjustifiable waste to me.
Today, I am not so uptight. Of course, I am still extremely thoughtful about ordering tests. I do not order tests without knowing what I am looking for, or how the result will affect management. But I also recognize that there is a non-zero probability that what I suspect is fibromyalgia is something else, something with a different prognosis, better or worse, something that needs to be managed and monitored differently.
After all, “clinical judgment” does not mean relying on the history and physical exam alone. Good clinical judgment requires medical knowledge, informed by experience, supplemented by test results, and complemented by an open, inquisitive mind.
Dr. Chan practices rheumatology in Pawtucket, R.I.
Perhaps one of the biggest ways in which I’ve evolved as a doctor over the 4.5 years I’ve been in private practice is that I am not so shy about ordering tests anymore.
My point is illustrated by the case of a lovely lady I met when I was starting out in practice who complained of being in pain all the time. She was referred to me for a very low titer antinuclear antibody and a barely positive rheumatoid factor. She’d had a very long history of severe depression and anxiety. She clearly connected her symptoms to having stopped her antidepressants. She attributed her dry mouth to her benzodiazepine. I told her that I thought she had fibromyalgia and that, as she herself pointed out, it was probably related to her emotional health. We talked about the lack of any real pharmacologic treatment for the illness. We addressed self-care: that she needed to sleep better, exercise more, and treat her depression.
Three years later she came back to me with hand swelling, hypergammaglobulinemia, renal tubular acidosis, this time with significantly higher ANA and RF titers, and hypocomplementemia. You guessed it; she has Sjögren’s syndrome.
Seeing patients 40 hours a week has been incredibly challenging but also incredibly rewarding. While the large number of cases that I’ve seen has sharpened my clinical eye, it has also broadened my differential diagnoses and improved my knowledge of when it will be helpful to order more tests.
It used to be that I was extremely conservative about ordering tests. This comes from having gone to med school in the Philippines, where each test was paid for by the patient out of pocket and GDP per capita is $2,765 (compared with $53,041 for the United States) and minimum wage is less than 2 dollars a day. Every CBC has to count. If a professor asked you why you were ordering a test, “to establish a baseline” was an unacceptable reason. When I started residency here, I was incredulous that the admitted patients got a CBC and chem-7 daily. This seemed like a huge and unjustifiable waste to me.
Today, I am not so uptight. Of course, I am still extremely thoughtful about ordering tests. I do not order tests without knowing what I am looking for, or how the result will affect management. But I also recognize that there is a non-zero probability that what I suspect is fibromyalgia is something else, something with a different prognosis, better or worse, something that needs to be managed and monitored differently.
After all, “clinical judgment” does not mean relying on the history and physical exam alone. Good clinical judgment requires medical knowledge, informed by experience, supplemented by test results, and complemented by an open, inquisitive mind.
Dr. Chan practices rheumatology in Pawtucket, R.I.
