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Treatment of the neck and lower face with botulinum toxin
.
The neck and the lower face are covered by thin layers of a vertical muscle, the anterior and posterior platysma muscle that is innervated by the cervical branch of the facial nerve. This muscle superficially blends with the muscles of the lower face, including the depressor anguli oris, depressor labii inferioris, mentalis, risorius, and orbicularis oris muscles. The inferior portion blends with the pectoralis and anterior deltoid muscles and lifts the skin of the neck.
Treatment of the platysma muscle and bands with botulinum toxin is an effective treatment for aging and sagging of the lower face and neck. Although treatment techniques differ and there are currently no standardized guidelines, the treatment starts by having the patient contract the neck muscles (I have them sit upright, with their head completely straight and say “E” with force). After evaluating the tension of the muscle, the muscle should be grasped and pulled away from the neck. Botulinum toxin is injected perpendicular to the muscle, with a dose of approximately 2 units, 2 cm apart along the vertical muscle. Approximately 20-40 units are used for the anterior and lateral bands.
To balance the opposing forces of the depressors of the lower face and improve jowling and downturning of the mouth, 10-20 units are also injected subdermally 1 cm above and 1 cm below the mandibular border.
Understanding the anatomy of the face and neck is crucial to proper injection. Side effects from improper injection include dysphagia, dysphonia, asymmetric smile, and weakness of the neck muscles. It is also important to set realistic expectations and address other components of neck aging, including actinic damage, as well as submental and jowl fat. The manufacturer of onabotulinumtoxinA (Botox Cosmetic) recently announced positive results of a second phase 3 clinical trial evaluating onabotulinumtoxinA for the treatment of moderate to severe platysma prominence. Results of the multicenter, randomized, double blind, placebo-controlled study evaluated the safety and efficacy of one treatment versus placebo in 426 adults with moderate to severe platysmal prominence. The results showed statistically significant improvement of platysma prominence from baseline, based on investigator and patient assessments, with no new safety signals, according to the company. The company expects to submit phase 3 data to the Food and Drug Administration by the end of this year and if approved, it will be the first neurotoxin approved for the treatment of platysmal bands.
Dr. Talakoub is in private practice in McLean, Va. Write to her at dermnews@mdedge.com. She had no relevant disclosures.
References
Brandt FS, Bellman B. Dermatol Surg. 1998 Nov;24(11):1232-4.
Matarasso A et al. Plast Reconstr Surg. 1999 Feb;103(2):645-52.
Rohrich RJ et al. Plast Reconstr Surg Glob Open. 2020 Jun 23;8(6):e2812.
.
The neck and the lower face are covered by thin layers of a vertical muscle, the anterior and posterior platysma muscle that is innervated by the cervical branch of the facial nerve. This muscle superficially blends with the muscles of the lower face, including the depressor anguli oris, depressor labii inferioris, mentalis, risorius, and orbicularis oris muscles. The inferior portion blends with the pectoralis and anterior deltoid muscles and lifts the skin of the neck.
Treatment of the platysma muscle and bands with botulinum toxin is an effective treatment for aging and sagging of the lower face and neck. Although treatment techniques differ and there are currently no standardized guidelines, the treatment starts by having the patient contract the neck muscles (I have them sit upright, with their head completely straight and say “E” with force). After evaluating the tension of the muscle, the muscle should be grasped and pulled away from the neck. Botulinum toxin is injected perpendicular to the muscle, with a dose of approximately 2 units, 2 cm apart along the vertical muscle. Approximately 20-40 units are used for the anterior and lateral bands.
To balance the opposing forces of the depressors of the lower face and improve jowling and downturning of the mouth, 10-20 units are also injected subdermally 1 cm above and 1 cm below the mandibular border.
Understanding the anatomy of the face and neck is crucial to proper injection. Side effects from improper injection include dysphagia, dysphonia, asymmetric smile, and weakness of the neck muscles. It is also important to set realistic expectations and address other components of neck aging, including actinic damage, as well as submental and jowl fat. The manufacturer of onabotulinumtoxinA (Botox Cosmetic) recently announced positive results of a second phase 3 clinical trial evaluating onabotulinumtoxinA for the treatment of moderate to severe platysma prominence. Results of the multicenter, randomized, double blind, placebo-controlled study evaluated the safety and efficacy of one treatment versus placebo in 426 adults with moderate to severe platysmal prominence. The results showed statistically significant improvement of platysma prominence from baseline, based on investigator and patient assessments, with no new safety signals, according to the company. The company expects to submit phase 3 data to the Food and Drug Administration by the end of this year and if approved, it will be the first neurotoxin approved for the treatment of platysmal bands.
Dr. Talakoub is in private practice in McLean, Va. Write to her at dermnews@mdedge.com. She had no relevant disclosures.
References
Brandt FS, Bellman B. Dermatol Surg. 1998 Nov;24(11):1232-4.
Matarasso A et al. Plast Reconstr Surg. 1999 Feb;103(2):645-52.
Rohrich RJ et al. Plast Reconstr Surg Glob Open. 2020 Jun 23;8(6):e2812.
.
The neck and the lower face are covered by thin layers of a vertical muscle, the anterior and posterior platysma muscle that is innervated by the cervical branch of the facial nerve. This muscle superficially blends with the muscles of the lower face, including the depressor anguli oris, depressor labii inferioris, mentalis, risorius, and orbicularis oris muscles. The inferior portion blends with the pectoralis and anterior deltoid muscles and lifts the skin of the neck.
Treatment of the platysma muscle and bands with botulinum toxin is an effective treatment for aging and sagging of the lower face and neck. Although treatment techniques differ and there are currently no standardized guidelines, the treatment starts by having the patient contract the neck muscles (I have them sit upright, with their head completely straight and say “E” with force). After evaluating the tension of the muscle, the muscle should be grasped and pulled away from the neck. Botulinum toxin is injected perpendicular to the muscle, with a dose of approximately 2 units, 2 cm apart along the vertical muscle. Approximately 20-40 units are used for the anterior and lateral bands.
To balance the opposing forces of the depressors of the lower face and improve jowling and downturning of the mouth, 10-20 units are also injected subdermally 1 cm above and 1 cm below the mandibular border.
Understanding the anatomy of the face and neck is crucial to proper injection. Side effects from improper injection include dysphagia, dysphonia, asymmetric smile, and weakness of the neck muscles. It is also important to set realistic expectations and address other components of neck aging, including actinic damage, as well as submental and jowl fat. The manufacturer of onabotulinumtoxinA (Botox Cosmetic) recently announced positive results of a second phase 3 clinical trial evaluating onabotulinumtoxinA for the treatment of moderate to severe platysma prominence. Results of the multicenter, randomized, double blind, placebo-controlled study evaluated the safety and efficacy of one treatment versus placebo in 426 adults with moderate to severe platysmal prominence. The results showed statistically significant improvement of platysma prominence from baseline, based on investigator and patient assessments, with no new safety signals, according to the company. The company expects to submit phase 3 data to the Food and Drug Administration by the end of this year and if approved, it will be the first neurotoxin approved for the treatment of platysmal bands.
Dr. Talakoub is in private practice in McLean, Va. Write to her at dermnews@mdedge.com. She had no relevant disclosures.
References
Brandt FS, Bellman B. Dermatol Surg. 1998 Nov;24(11):1232-4.
Matarasso A et al. Plast Reconstr Surg. 1999 Feb;103(2):645-52.
Rohrich RJ et al. Plast Reconstr Surg Glob Open. 2020 Jun 23;8(6):e2812.
Treating poikiloderma
and is one of the most frustrating dermatologic problems to treat.
Poikiloderma is an area of mottled pigmentation (hyper and hypo) with telangiectasias and atrophy often present on the V of the chest, lateral neck, and lateral face. It is always present in sun-exposed areas but shaded areas of the neck, such as the area under the chin, are spared. Cumulative UV radiation is the predominant underlying cause; however, postmenopausal hormonal changes and contact sensitization with perfumes and cosmetics can exacerbate the condition.
Breaking down the subtypes will help direct the treatment options. There are two main types of poikiloderma – telangiectatic and hyperpigmented – and of course, an overlap between the two. Choosing which subtype is dominant is based primarily on clinical presentation and dermoscopic findings. Atrophy is ubiquitous, thus collagen remodeling is a necessary treatment for both.
In my clinical practice, the pigmentation component of poikiloderma in all skin types is pretreated and posttreated with topical hydroquinone and/or oral tranexamic acid to avoid recurrence after any laser treatment. In the majority of my patients with poikiloderma, I first treat the pigmentation with hydroquinone and tranexamic acid (if the patient is a candidate) to minimize the pigment as much as possible and then treat the telangiectasias with lasers. I try to avoid laser treatment of the hyperpigmentation if at all possible.
Telangiectatic poikiloderma is characterized by a linear and reticular dilated network of vessels. Laser treatment options include IPL, V-beam, and KTP lasers. Multiple treatments are usually necessary and if the patient has concomitant flushing and burning symptoms associated with poikiloderma, topical rosacea treatments such as topical oxymetazoline, as well as avoidance of fragrance, and strict use of a broad spectrum mineral sunscreen, should be initiated prior to laser treatments.
Hyperpigmented poikiloderma is characterized by mottled hyperpigmentation caused by the increased melanin irregularly distributed in the basal layer of the epidermis and melanophages within the dermis. The best treatment for this is with 1,927-nm fractionated resurfacing modalities. Although IPL has been used in this area and is often recommended in the literature for the lentigines, in my experience, the results are transient and it is much harder to blend the color of the skin with the surrounding area of the neck, lateral chest, shoulders, and arms. The 1,927-nm fractionated laser allows for a smoother transition and blending of the skin and also helps with some collagen remodeling of the dermis.
Atrophy is visualized under dermoscopy as a white polka dot–like print with flattened, atrophic epidermis and an elastotic papillary dermis in between the hyperemic telangiectatic network. With every case of poikiloderma, there is some atrophy present; therefore, I combine platelet rich plasma (PRP), PRP with microneedling, or very light treatments with the Fraxel dual (1927/1550) laser to help improve architectural changes of the dermis.
As with any condition of the chest and neck, there is a very fine line between treatment efficacy and complications. All treatments, particularly lasers, should be used with considerable caution and test spots and with the expectation that the treatment will mitigate, not resolve the condition. Sun avoidance, use of daily mineral SPF, and avoidance of fragrance should be emphasized. If expectations are set properly, patients are often satisfied with small improvements as this condition can be very troubling and difficult to treat.
Dr. Talakoub is in private practice in McLean, Va. Write to her at dermnews@mdedge.com. She had no relevant disclosures.
References
Geronemus R. Arch Dermatol. 1990 Apr;126(4):547-8.
Goldman MP and Weiss RA. Plast Reconstr Surg. 2001 May;107(6):1376-81.
Katoulis AC and Stavrianeas NG. Poikiloderma of Civatte. In: Rigopoulos D, Katoulis AC, editors. Hyperpigmentation (Boca Raton, Fla.: CRC Press, 2017). Chapter 12.
and is one of the most frustrating dermatologic problems to treat.
Poikiloderma is an area of mottled pigmentation (hyper and hypo) with telangiectasias and atrophy often present on the V of the chest, lateral neck, and lateral face. It is always present in sun-exposed areas but shaded areas of the neck, such as the area under the chin, are spared. Cumulative UV radiation is the predominant underlying cause; however, postmenopausal hormonal changes and contact sensitization with perfumes and cosmetics can exacerbate the condition.
Breaking down the subtypes will help direct the treatment options. There are two main types of poikiloderma – telangiectatic and hyperpigmented – and of course, an overlap between the two. Choosing which subtype is dominant is based primarily on clinical presentation and dermoscopic findings. Atrophy is ubiquitous, thus collagen remodeling is a necessary treatment for both.
In my clinical practice, the pigmentation component of poikiloderma in all skin types is pretreated and posttreated with topical hydroquinone and/or oral tranexamic acid to avoid recurrence after any laser treatment. In the majority of my patients with poikiloderma, I first treat the pigmentation with hydroquinone and tranexamic acid (if the patient is a candidate) to minimize the pigment as much as possible and then treat the telangiectasias with lasers. I try to avoid laser treatment of the hyperpigmentation if at all possible.
Telangiectatic poikiloderma is characterized by a linear and reticular dilated network of vessels. Laser treatment options include IPL, V-beam, and KTP lasers. Multiple treatments are usually necessary and if the patient has concomitant flushing and burning symptoms associated with poikiloderma, topical rosacea treatments such as topical oxymetazoline, as well as avoidance of fragrance, and strict use of a broad spectrum mineral sunscreen, should be initiated prior to laser treatments.
Hyperpigmented poikiloderma is characterized by mottled hyperpigmentation caused by the increased melanin irregularly distributed in the basal layer of the epidermis and melanophages within the dermis. The best treatment for this is with 1,927-nm fractionated resurfacing modalities. Although IPL has been used in this area and is often recommended in the literature for the lentigines, in my experience, the results are transient and it is much harder to blend the color of the skin with the surrounding area of the neck, lateral chest, shoulders, and arms. The 1,927-nm fractionated laser allows for a smoother transition and blending of the skin and also helps with some collagen remodeling of the dermis.
Atrophy is visualized under dermoscopy as a white polka dot–like print with flattened, atrophic epidermis and an elastotic papillary dermis in between the hyperemic telangiectatic network. With every case of poikiloderma, there is some atrophy present; therefore, I combine platelet rich plasma (PRP), PRP with microneedling, or very light treatments with the Fraxel dual (1927/1550) laser to help improve architectural changes of the dermis.
As with any condition of the chest and neck, there is a very fine line between treatment efficacy and complications. All treatments, particularly lasers, should be used with considerable caution and test spots and with the expectation that the treatment will mitigate, not resolve the condition. Sun avoidance, use of daily mineral SPF, and avoidance of fragrance should be emphasized. If expectations are set properly, patients are often satisfied with small improvements as this condition can be very troubling and difficult to treat.
Dr. Talakoub is in private practice in McLean, Va. Write to her at dermnews@mdedge.com. She had no relevant disclosures.
References
Geronemus R. Arch Dermatol. 1990 Apr;126(4):547-8.
Goldman MP and Weiss RA. Plast Reconstr Surg. 2001 May;107(6):1376-81.
Katoulis AC and Stavrianeas NG. Poikiloderma of Civatte. In: Rigopoulos D, Katoulis AC, editors. Hyperpigmentation (Boca Raton, Fla.: CRC Press, 2017). Chapter 12.
and is one of the most frustrating dermatologic problems to treat.
Poikiloderma is an area of mottled pigmentation (hyper and hypo) with telangiectasias and atrophy often present on the V of the chest, lateral neck, and lateral face. It is always present in sun-exposed areas but shaded areas of the neck, such as the area under the chin, are spared. Cumulative UV radiation is the predominant underlying cause; however, postmenopausal hormonal changes and contact sensitization with perfumes and cosmetics can exacerbate the condition.
Breaking down the subtypes will help direct the treatment options. There are two main types of poikiloderma – telangiectatic and hyperpigmented – and of course, an overlap between the two. Choosing which subtype is dominant is based primarily on clinical presentation and dermoscopic findings. Atrophy is ubiquitous, thus collagen remodeling is a necessary treatment for both.
In my clinical practice, the pigmentation component of poikiloderma in all skin types is pretreated and posttreated with topical hydroquinone and/or oral tranexamic acid to avoid recurrence after any laser treatment. In the majority of my patients with poikiloderma, I first treat the pigmentation with hydroquinone and tranexamic acid (if the patient is a candidate) to minimize the pigment as much as possible and then treat the telangiectasias with lasers. I try to avoid laser treatment of the hyperpigmentation if at all possible.
Telangiectatic poikiloderma is characterized by a linear and reticular dilated network of vessels. Laser treatment options include IPL, V-beam, and KTP lasers. Multiple treatments are usually necessary and if the patient has concomitant flushing and burning symptoms associated with poikiloderma, topical rosacea treatments such as topical oxymetazoline, as well as avoidance of fragrance, and strict use of a broad spectrum mineral sunscreen, should be initiated prior to laser treatments.
Hyperpigmented poikiloderma is characterized by mottled hyperpigmentation caused by the increased melanin irregularly distributed in the basal layer of the epidermis and melanophages within the dermis. The best treatment for this is with 1,927-nm fractionated resurfacing modalities. Although IPL has been used in this area and is often recommended in the literature for the lentigines, in my experience, the results are transient and it is much harder to blend the color of the skin with the surrounding area of the neck, lateral chest, shoulders, and arms. The 1,927-nm fractionated laser allows for a smoother transition and blending of the skin and also helps with some collagen remodeling of the dermis.
Atrophy is visualized under dermoscopy as a white polka dot–like print with flattened, atrophic epidermis and an elastotic papillary dermis in between the hyperemic telangiectatic network. With every case of poikiloderma, there is some atrophy present; therefore, I combine platelet rich plasma (PRP), PRP with microneedling, or very light treatments with the Fraxel dual (1927/1550) laser to help improve architectural changes of the dermis.
As with any condition of the chest and neck, there is a very fine line between treatment efficacy and complications. All treatments, particularly lasers, should be used with considerable caution and test spots and with the expectation that the treatment will mitigate, not resolve the condition. Sun avoidance, use of daily mineral SPF, and avoidance of fragrance should be emphasized. If expectations are set properly, patients are often satisfied with small improvements as this condition can be very troubling and difficult to treat.
Dr. Talakoub is in private practice in McLean, Va. Write to her at dermnews@mdedge.com. She had no relevant disclosures.
References
Geronemus R. Arch Dermatol. 1990 Apr;126(4):547-8.
Goldman MP and Weiss RA. Plast Reconstr Surg. 2001 May;107(6):1376-81.
Katoulis AC and Stavrianeas NG. Poikiloderma of Civatte. In: Rigopoulos D, Katoulis AC, editors. Hyperpigmentation (Boca Raton, Fla.: CRC Press, 2017). Chapter 12.
Treatment of craniofacial hyperhidrosis
Hyperhidrosis has a significant impact on a person’s physical, psychological, and social aspects of life. The lack of treatment options and associated stigma limits access to care and treatment options.
Primary hyperhidrosis does not have an underlying cause; is symmetrical; can worsen with anxiety, fear, or stress; and may have a familial component. Palmar and axillary hyperhidrosis are the most common types of hyperhidrosis. The incidence of craniofacial hyperhidrosis has not been clearly defined but it is most commonly reported on the forehead, where the concentration of eccrine sweat glands is highest.
Treatment options for craniofacial hyperhidrosis include topical aluminum chloride, which blocks the eccrine sweat duct or causes eccrine cell atrophy. Although this option is a common treatment for palmar and axillary hyperhidrosis, use on the face has not been thoroughly studied, and may also cause skin irritation.
Topical and oral glycopyrrolate can be effective for all types of hyperhidrosis, but must be used daily and can have systemic side effects, with variable efficacy and longevity. Oral oxybutynin, beta-blockers, clonidine, and benzodiazepines have also been used with some limited studies available in patients with generalized hyperhidrosis.
Surgical treatments such as videothoracoscopy sympathectomy can be used in severe or recalcitrant cases of hyperhidrosis with good efficacy. However, surgical complications and inherent surgical risks limit these treatment options unless other modalities are exhausted.
OnabotulinumtoxinA is Food and Drug Administration approved for treating severe primary axillary hyperhidrosis, but is used off label for palmar, plantar, and craniofacial hyperhidrosis with great results and few side effects. Clinical pearls and guidelines for the use of botulinum toxin A in craniofacial hyperhidrosis were outlined by Wolosker and colleagues in a review article. As with any injection of neurotoxin, knowledge of the facial anatomy is critical to avoiding muscle paralysis.
double diluted. Treatment effects usually last 3 months, similar to cosmetic uses. Wolosker uses a dilution of 100 U botulinum toxin in 1.0 mL saline, which I find slightly more difficult to control and more likely to have loss of toxin.
In my experience, I have found the following dosing to be most effective with the least side effects for the following (dosages vary and can be titrated up to response):
- Upper lip: 6-10 U.
- Chin: 6-10 U.
- Forehead: 15-30 U. (Avoid 1 cm above the brow unless risks of brow drop are reviewed and acceptable to the patient. In my experience patients would rather have a lower brow than obstructive sweating in their brow that can irritate the eyes, blur vision, and smudge skincare and makeup.)
- Nose: 10 U
- Cheeks: 10 U per side (staying very superficial with injections).
- Scalp: 30-50 U (using serial injections 1-2 cm apart in the area affected by hyperhidrosis).
Side effects include temporary erythema, bruising, and edema, as well as muscle paralysis and asymmetry if proper injection technique is not used, the dose is not diluted properly, or the injection is too deep.
There are scattered case studies of symbiotic techniques to help the penetration of botulinum toxin when treating craniofacial hyperhidrosis, including microneedling, radiofrequency, long-pulsed diode laser, and ultrasound. But the safety and efficacy of these procedures have not been properly evaluated.
In all of my patients with craniofacial hyperhidrosis treated with botulinum toxin, quality of life is significantly improved with almost no complications. Botulinum toxin is a safe, relatively quick in-office procedure to treat craniofacial hyperhidrosis that can be used to help patients – particularly those who experience anxiety or have social and occupational impairment related to their disease.
This procedure is cosmetic in nature, and therefore, not covered by insurance.
Dr. Talakoub is in private practice in McLean, Va. Write to her at dermnews@mdedge.com. She had no relevant disclosures.
References
Parashar K et al. Am J Clin Dermatol. 2023 Mar;24(2):187-98.
Doolittle J et al. Arch Dermatol Res. 2016 Dec;308(10):743-9.
Wolosker N et al. J Vasc Bras. 2020 Nov 16;19:e20190152.
Garcia-Souto F et al. Dermatol Ther. 2021 Jan;34(1):e14658.
Ebrahim H et al. J Clin Aesthet Dermatol. 2022 Sep;15(9):40-4.
Campanati A et al. Toxins (Basel). 2022 May 27;14(6):3727.
Hyperhidrosis has a significant impact on a person’s physical, psychological, and social aspects of life. The lack of treatment options and associated stigma limits access to care and treatment options.
Primary hyperhidrosis does not have an underlying cause; is symmetrical; can worsen with anxiety, fear, or stress; and may have a familial component. Palmar and axillary hyperhidrosis are the most common types of hyperhidrosis. The incidence of craniofacial hyperhidrosis has not been clearly defined but it is most commonly reported on the forehead, where the concentration of eccrine sweat glands is highest.
Treatment options for craniofacial hyperhidrosis include topical aluminum chloride, which blocks the eccrine sweat duct or causes eccrine cell atrophy. Although this option is a common treatment for palmar and axillary hyperhidrosis, use on the face has not been thoroughly studied, and may also cause skin irritation.
Topical and oral glycopyrrolate can be effective for all types of hyperhidrosis, but must be used daily and can have systemic side effects, with variable efficacy and longevity. Oral oxybutynin, beta-blockers, clonidine, and benzodiazepines have also been used with some limited studies available in patients with generalized hyperhidrosis.
Surgical treatments such as videothoracoscopy sympathectomy can be used in severe or recalcitrant cases of hyperhidrosis with good efficacy. However, surgical complications and inherent surgical risks limit these treatment options unless other modalities are exhausted.
OnabotulinumtoxinA is Food and Drug Administration approved for treating severe primary axillary hyperhidrosis, but is used off label for palmar, plantar, and craniofacial hyperhidrosis with great results and few side effects. Clinical pearls and guidelines for the use of botulinum toxin A in craniofacial hyperhidrosis were outlined by Wolosker and colleagues in a review article. As with any injection of neurotoxin, knowledge of the facial anatomy is critical to avoiding muscle paralysis.
double diluted. Treatment effects usually last 3 months, similar to cosmetic uses. Wolosker uses a dilution of 100 U botulinum toxin in 1.0 mL saline, which I find slightly more difficult to control and more likely to have loss of toxin.
In my experience, I have found the following dosing to be most effective with the least side effects for the following (dosages vary and can be titrated up to response):
- Upper lip: 6-10 U.
- Chin: 6-10 U.
- Forehead: 15-30 U. (Avoid 1 cm above the brow unless risks of brow drop are reviewed and acceptable to the patient. In my experience patients would rather have a lower brow than obstructive sweating in their brow that can irritate the eyes, blur vision, and smudge skincare and makeup.)
- Nose: 10 U
- Cheeks: 10 U per side (staying very superficial with injections).
- Scalp: 30-50 U (using serial injections 1-2 cm apart in the area affected by hyperhidrosis).
Side effects include temporary erythema, bruising, and edema, as well as muscle paralysis and asymmetry if proper injection technique is not used, the dose is not diluted properly, or the injection is too deep.
There are scattered case studies of symbiotic techniques to help the penetration of botulinum toxin when treating craniofacial hyperhidrosis, including microneedling, radiofrequency, long-pulsed diode laser, and ultrasound. But the safety and efficacy of these procedures have not been properly evaluated.
In all of my patients with craniofacial hyperhidrosis treated with botulinum toxin, quality of life is significantly improved with almost no complications. Botulinum toxin is a safe, relatively quick in-office procedure to treat craniofacial hyperhidrosis that can be used to help patients – particularly those who experience anxiety or have social and occupational impairment related to their disease.
This procedure is cosmetic in nature, and therefore, not covered by insurance.
Dr. Talakoub is in private practice in McLean, Va. Write to her at dermnews@mdedge.com. She had no relevant disclosures.
References
Parashar K et al. Am J Clin Dermatol. 2023 Mar;24(2):187-98.
Doolittle J et al. Arch Dermatol Res. 2016 Dec;308(10):743-9.
Wolosker N et al. J Vasc Bras. 2020 Nov 16;19:e20190152.
Garcia-Souto F et al. Dermatol Ther. 2021 Jan;34(1):e14658.
Ebrahim H et al. J Clin Aesthet Dermatol. 2022 Sep;15(9):40-4.
Campanati A et al. Toxins (Basel). 2022 May 27;14(6):3727.
Hyperhidrosis has a significant impact on a person’s physical, psychological, and social aspects of life. The lack of treatment options and associated stigma limits access to care and treatment options.
Primary hyperhidrosis does not have an underlying cause; is symmetrical; can worsen with anxiety, fear, or stress; and may have a familial component. Palmar and axillary hyperhidrosis are the most common types of hyperhidrosis. The incidence of craniofacial hyperhidrosis has not been clearly defined but it is most commonly reported on the forehead, where the concentration of eccrine sweat glands is highest.
Treatment options for craniofacial hyperhidrosis include topical aluminum chloride, which blocks the eccrine sweat duct or causes eccrine cell atrophy. Although this option is a common treatment for palmar and axillary hyperhidrosis, use on the face has not been thoroughly studied, and may also cause skin irritation.
Topical and oral glycopyrrolate can be effective for all types of hyperhidrosis, but must be used daily and can have systemic side effects, with variable efficacy and longevity. Oral oxybutynin, beta-blockers, clonidine, and benzodiazepines have also been used with some limited studies available in patients with generalized hyperhidrosis.
Surgical treatments such as videothoracoscopy sympathectomy can be used in severe or recalcitrant cases of hyperhidrosis with good efficacy. However, surgical complications and inherent surgical risks limit these treatment options unless other modalities are exhausted.
OnabotulinumtoxinA is Food and Drug Administration approved for treating severe primary axillary hyperhidrosis, but is used off label for palmar, plantar, and craniofacial hyperhidrosis with great results and few side effects. Clinical pearls and guidelines for the use of botulinum toxin A in craniofacial hyperhidrosis were outlined by Wolosker and colleagues in a review article. As with any injection of neurotoxin, knowledge of the facial anatomy is critical to avoiding muscle paralysis.
double diluted. Treatment effects usually last 3 months, similar to cosmetic uses. Wolosker uses a dilution of 100 U botulinum toxin in 1.0 mL saline, which I find slightly more difficult to control and more likely to have loss of toxin.
In my experience, I have found the following dosing to be most effective with the least side effects for the following (dosages vary and can be titrated up to response):
- Upper lip: 6-10 U.
- Chin: 6-10 U.
- Forehead: 15-30 U. (Avoid 1 cm above the brow unless risks of brow drop are reviewed and acceptable to the patient. In my experience patients would rather have a lower brow than obstructive sweating in their brow that can irritate the eyes, blur vision, and smudge skincare and makeup.)
- Nose: 10 U
- Cheeks: 10 U per side (staying very superficial with injections).
- Scalp: 30-50 U (using serial injections 1-2 cm apart in the area affected by hyperhidrosis).
Side effects include temporary erythema, bruising, and edema, as well as muscle paralysis and asymmetry if proper injection technique is not used, the dose is not diluted properly, or the injection is too deep.
There are scattered case studies of symbiotic techniques to help the penetration of botulinum toxin when treating craniofacial hyperhidrosis, including microneedling, radiofrequency, long-pulsed diode laser, and ultrasound. But the safety and efficacy of these procedures have not been properly evaluated.
In all of my patients with craniofacial hyperhidrosis treated with botulinum toxin, quality of life is significantly improved with almost no complications. Botulinum toxin is a safe, relatively quick in-office procedure to treat craniofacial hyperhidrosis that can be used to help patients – particularly those who experience anxiety or have social and occupational impairment related to their disease.
This procedure is cosmetic in nature, and therefore, not covered by insurance.
Dr. Talakoub is in private practice in McLean, Va. Write to her at dermnews@mdedge.com. She had no relevant disclosures.
References
Parashar K et al. Am J Clin Dermatol. 2023 Mar;24(2):187-98.
Doolittle J et al. Arch Dermatol Res. 2016 Dec;308(10):743-9.
Wolosker N et al. J Vasc Bras. 2020 Nov 16;19:e20190152.
Garcia-Souto F et al. Dermatol Ther. 2021 Jan;34(1):e14658.
Ebrahim H et al. J Clin Aesthet Dermatol. 2022 Sep;15(9):40-4.
Campanati A et al. Toxins (Basel). 2022 May 27;14(6):3727.
Microtox and Mesotox
The terms when they mention one of these terms.
Let’s settle the nomenclature confusion. In this column, I define and outline suggested terminology based on studies and my 15 years of experience using neuromodulators. If any readers or colleagues disagree, please write to me and we can discuss the alternatives in a subsequent article; if you agree, please also write to me so we can collaboratively correct the discrepancies in the literature accordingly.
The term mesotherapy, originating from the Greek “mesos” referring to the early embryonic mesoderm, was identified in the 1950’s by Dr. Michel Pistor, a French physician who administered drugs intradermally. The term was defined as a minimally invasive technique by which drugs or bioactive substances are given in small quantities through dermal micropunctures. Drugs administered intradermally diffuse very slowly and therefore, stay in the tissue longer than those administered intramuscularly.
Thus, Mesotox is defined not by the concentration of the neuromodulator or location, but by the depth of injection in the superficial dermis. It can be delivered through individual injections or through a microneedling pen.
Microtox refers to the dilution of the neuromodulator at concentrations below the proposed dilution guidelines of the manufacturer: Less than 2.5 U per 0.1 mL for onabotulinumtoxinA (OBA), incobotulinumtoxinA (IBA), and prabotulinumtoxinA (PBA); and less than 10 U per 0.1 mL for abobotulinumtoxinA (ABO), This method allows for the injection of superficial cutaneous muscles softening the dynamic rhytids without complete paralysis.
Mesotox is widely used off label for facial lifting, reduction in skin laxity or crepiness, flushing of rosacea, acne, hyperhidrosis of the face, keloids, seborrhea, neck rejuvenation, contouring of the mandibular border, and scalp oiliness. Based on a review of articles using this technique, dilution methods were less than 2.5 U per 1 mL (OBA, IBA) and less than 10 U per 0.1 mL (ABO) depth of injection was the superficial to mid-dermis with injection points 0.5 cm to 1 cm apart.
In a study by Atwa and colleagues, 25 patients with mild facial skin laxity received intradermal Botox-A on one side and saline on the other. This split face study showed a highly significant difference with facial lifting on the treated side. Mesotox injection points vary based on the clinical indication and area being treated.
The treatment of dynamic muscles using standard neuromodulator dosing protocols include the treatment of the glabella, crow’s feet, forehead lines, masseter hypertrophy, bunny lines, gummy smile, perioral lines, mentalis hypertonia, platysmal bands, and marionette lines.
However, hyperdilute neuromodulators or Microtox can effectively be used alone or in combination with standard dosing for the following off-label uses. Used in combination with standard dosing of the forehead lines, I use Microtox in the lateral brow to soften the frontalis muscle without dropping the brow in patients with a low-set brow or lid laxity. I also use it for the jelly roll of the eyes and to open the aperture of the eyes. Along the nose, Microtox can also be used to treat a sagging nasal tip, decrease the width of the ala, and treat overactive facial muscles adjacent to the nose resulting in an overactive nasolabial fold.
Similarly, Microtox can be used to treat lateral smile lines and downward extensions of the crow’s feet. In all of the aforementioned treatment areas, I recommend approximately 0.5-1 U of toxin in each area divided at 1-cm intervals.Mesotox and Microtox are both highly effective strategies to treat the aging face. However, the nomenclature is not interchangeable. I propose that the term Mesotox be used only to articulate or define the superficial injection of a neuromodulator for the improvement of the skin that does not involve the injection into or paralysis of a cutaneous muscle (“tox” being used generically for all neuromodulators). I also propose that the term Microtox should be used to define the dilution of a neuromodulator beyond the manufacturer-recommended dilution protocols – used for the paralysis of a cutaneous muscle. In addition, I recommend that the terms MicroBotox and MesoBotox no longer be used. These procedures all have risks, and adverse events associated with Microtox and Mesotox are similar to those of any neuromodulator injection at FDA-recommended maximum doses, and dilution and storage protocols and proper injection techniques need to be followed. Expertise and training is crucial and treatment by a board-certified dermatologist or plastic surgeon is imperative.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to her at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Awaida CJ et al. Plast Reconstr Surg. 2018 Sep;142(3):640-9.
Calvani F et al. Plast Surg (Oakv). 2019 May;27(2):156-61.
Iranmanesh B et al. J Cosmet Dermatol. 2022 Oct;21(10):4160-70.
Kandhari R et al. J Cutan Aesthet Surg. 2022 Apr-Jun;15(2):101-7.
Lewandowski M et al. Molecules. 2022 May 13;27(10):3143.
Mammucari M et al. Eur Rev Med Pharmacol Sci. 2011 Jun;15(6):682-94.
Park KY et al. Ann Dermatol. 2018 Dec;30(6):688-93.
Pistor M. Chir Dent Fr. 1976;46:59-60.
Rho NK, Gil YC. Toxins (Basel). 2021 Nov 19;13(11):817.
Wu WTL. Plast Reconstr Surg. 2015 Nov;136(5 Suppl):92S-100S.
Zhang H et al. Clin Cosmet Investig Dermatol. 2021 Apr 30;14:407-17.
The terms when they mention one of these terms.
Let’s settle the nomenclature confusion. In this column, I define and outline suggested terminology based on studies and my 15 years of experience using neuromodulators. If any readers or colleagues disagree, please write to me and we can discuss the alternatives in a subsequent article; if you agree, please also write to me so we can collaboratively correct the discrepancies in the literature accordingly.
The term mesotherapy, originating from the Greek “mesos” referring to the early embryonic mesoderm, was identified in the 1950’s by Dr. Michel Pistor, a French physician who administered drugs intradermally. The term was defined as a minimally invasive technique by which drugs or bioactive substances are given in small quantities through dermal micropunctures. Drugs administered intradermally diffuse very slowly and therefore, stay in the tissue longer than those administered intramuscularly.
Thus, Mesotox is defined not by the concentration of the neuromodulator or location, but by the depth of injection in the superficial dermis. It can be delivered through individual injections or through a microneedling pen.
Microtox refers to the dilution of the neuromodulator at concentrations below the proposed dilution guidelines of the manufacturer: Less than 2.5 U per 0.1 mL for onabotulinumtoxinA (OBA), incobotulinumtoxinA (IBA), and prabotulinumtoxinA (PBA); and less than 10 U per 0.1 mL for abobotulinumtoxinA (ABO), This method allows for the injection of superficial cutaneous muscles softening the dynamic rhytids without complete paralysis.
Mesotox is widely used off label for facial lifting, reduction in skin laxity or crepiness, flushing of rosacea, acne, hyperhidrosis of the face, keloids, seborrhea, neck rejuvenation, contouring of the mandibular border, and scalp oiliness. Based on a review of articles using this technique, dilution methods were less than 2.5 U per 1 mL (OBA, IBA) and less than 10 U per 0.1 mL (ABO) depth of injection was the superficial to mid-dermis with injection points 0.5 cm to 1 cm apart.
In a study by Atwa and colleagues, 25 patients with mild facial skin laxity received intradermal Botox-A on one side and saline on the other. This split face study showed a highly significant difference with facial lifting on the treated side. Mesotox injection points vary based on the clinical indication and area being treated.
The treatment of dynamic muscles using standard neuromodulator dosing protocols include the treatment of the glabella, crow’s feet, forehead lines, masseter hypertrophy, bunny lines, gummy smile, perioral lines, mentalis hypertonia, platysmal bands, and marionette lines.
However, hyperdilute neuromodulators or Microtox can effectively be used alone or in combination with standard dosing for the following off-label uses. Used in combination with standard dosing of the forehead lines, I use Microtox in the lateral brow to soften the frontalis muscle without dropping the brow in patients with a low-set brow or lid laxity. I also use it for the jelly roll of the eyes and to open the aperture of the eyes. Along the nose, Microtox can also be used to treat a sagging nasal tip, decrease the width of the ala, and treat overactive facial muscles adjacent to the nose resulting in an overactive nasolabial fold.
Similarly, Microtox can be used to treat lateral smile lines and downward extensions of the crow’s feet. In all of the aforementioned treatment areas, I recommend approximately 0.5-1 U of toxin in each area divided at 1-cm intervals.Mesotox and Microtox are both highly effective strategies to treat the aging face. However, the nomenclature is not interchangeable. I propose that the term Mesotox be used only to articulate or define the superficial injection of a neuromodulator for the improvement of the skin that does not involve the injection into or paralysis of a cutaneous muscle (“tox” being used generically for all neuromodulators). I also propose that the term Microtox should be used to define the dilution of a neuromodulator beyond the manufacturer-recommended dilution protocols – used for the paralysis of a cutaneous muscle. In addition, I recommend that the terms MicroBotox and MesoBotox no longer be used. These procedures all have risks, and adverse events associated with Microtox and Mesotox are similar to those of any neuromodulator injection at FDA-recommended maximum doses, and dilution and storage protocols and proper injection techniques need to be followed. Expertise and training is crucial and treatment by a board-certified dermatologist or plastic surgeon is imperative.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to her at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Awaida CJ et al. Plast Reconstr Surg. 2018 Sep;142(3):640-9.
Calvani F et al. Plast Surg (Oakv). 2019 May;27(2):156-61.
Iranmanesh B et al. J Cosmet Dermatol. 2022 Oct;21(10):4160-70.
Kandhari R et al. J Cutan Aesthet Surg. 2022 Apr-Jun;15(2):101-7.
Lewandowski M et al. Molecules. 2022 May 13;27(10):3143.
Mammucari M et al. Eur Rev Med Pharmacol Sci. 2011 Jun;15(6):682-94.
Park KY et al. Ann Dermatol. 2018 Dec;30(6):688-93.
Pistor M. Chir Dent Fr. 1976;46:59-60.
Rho NK, Gil YC. Toxins (Basel). 2021 Nov 19;13(11):817.
Wu WTL. Plast Reconstr Surg. 2015 Nov;136(5 Suppl):92S-100S.
Zhang H et al. Clin Cosmet Investig Dermatol. 2021 Apr 30;14:407-17.
The terms when they mention one of these terms.
Let’s settle the nomenclature confusion. In this column, I define and outline suggested terminology based on studies and my 15 years of experience using neuromodulators. If any readers or colleagues disagree, please write to me and we can discuss the alternatives in a subsequent article; if you agree, please also write to me so we can collaboratively correct the discrepancies in the literature accordingly.
The term mesotherapy, originating from the Greek “mesos” referring to the early embryonic mesoderm, was identified in the 1950’s by Dr. Michel Pistor, a French physician who administered drugs intradermally. The term was defined as a minimally invasive technique by which drugs or bioactive substances are given in small quantities through dermal micropunctures. Drugs administered intradermally diffuse very slowly and therefore, stay in the tissue longer than those administered intramuscularly.
Thus, Mesotox is defined not by the concentration of the neuromodulator or location, but by the depth of injection in the superficial dermis. It can be delivered through individual injections or through a microneedling pen.
Microtox refers to the dilution of the neuromodulator at concentrations below the proposed dilution guidelines of the manufacturer: Less than 2.5 U per 0.1 mL for onabotulinumtoxinA (OBA), incobotulinumtoxinA (IBA), and prabotulinumtoxinA (PBA); and less than 10 U per 0.1 mL for abobotulinumtoxinA (ABO), This method allows for the injection of superficial cutaneous muscles softening the dynamic rhytids without complete paralysis.
Mesotox is widely used off label for facial lifting, reduction in skin laxity or crepiness, flushing of rosacea, acne, hyperhidrosis of the face, keloids, seborrhea, neck rejuvenation, contouring of the mandibular border, and scalp oiliness. Based on a review of articles using this technique, dilution methods were less than 2.5 U per 1 mL (OBA, IBA) and less than 10 U per 0.1 mL (ABO) depth of injection was the superficial to mid-dermis with injection points 0.5 cm to 1 cm apart.
In a study by Atwa and colleagues, 25 patients with mild facial skin laxity received intradermal Botox-A on one side and saline on the other. This split face study showed a highly significant difference with facial lifting on the treated side. Mesotox injection points vary based on the clinical indication and area being treated.
The treatment of dynamic muscles using standard neuromodulator dosing protocols include the treatment of the glabella, crow’s feet, forehead lines, masseter hypertrophy, bunny lines, gummy smile, perioral lines, mentalis hypertonia, platysmal bands, and marionette lines.
However, hyperdilute neuromodulators or Microtox can effectively be used alone or in combination with standard dosing for the following off-label uses. Used in combination with standard dosing of the forehead lines, I use Microtox in the lateral brow to soften the frontalis muscle without dropping the brow in patients with a low-set brow or lid laxity. I also use it for the jelly roll of the eyes and to open the aperture of the eyes. Along the nose, Microtox can also be used to treat a sagging nasal tip, decrease the width of the ala, and treat overactive facial muscles adjacent to the nose resulting in an overactive nasolabial fold.
Similarly, Microtox can be used to treat lateral smile lines and downward extensions of the crow’s feet. In all of the aforementioned treatment areas, I recommend approximately 0.5-1 U of toxin in each area divided at 1-cm intervals.Mesotox and Microtox are both highly effective strategies to treat the aging face. However, the nomenclature is not interchangeable. I propose that the term Mesotox be used only to articulate or define the superficial injection of a neuromodulator for the improvement of the skin that does not involve the injection into or paralysis of a cutaneous muscle (“tox” being used generically for all neuromodulators). I also propose that the term Microtox should be used to define the dilution of a neuromodulator beyond the manufacturer-recommended dilution protocols – used for the paralysis of a cutaneous muscle. In addition, I recommend that the terms MicroBotox and MesoBotox no longer be used. These procedures all have risks, and adverse events associated with Microtox and Mesotox are similar to those of any neuromodulator injection at FDA-recommended maximum doses, and dilution and storage protocols and proper injection techniques need to be followed. Expertise and training is crucial and treatment by a board-certified dermatologist or plastic surgeon is imperative.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to her at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Awaida CJ et al. Plast Reconstr Surg. 2018 Sep;142(3):640-9.
Calvani F et al. Plast Surg (Oakv). 2019 May;27(2):156-61.
Iranmanesh B et al. J Cosmet Dermatol. 2022 Oct;21(10):4160-70.
Kandhari R et al. J Cutan Aesthet Surg. 2022 Apr-Jun;15(2):101-7.
Lewandowski M et al. Molecules. 2022 May 13;27(10):3143.
Mammucari M et al. Eur Rev Med Pharmacol Sci. 2011 Jun;15(6):682-94.
Park KY et al. Ann Dermatol. 2018 Dec;30(6):688-93.
Pistor M. Chir Dent Fr. 1976;46:59-60.
Rho NK, Gil YC. Toxins (Basel). 2021 Nov 19;13(11):817.
Wu WTL. Plast Reconstr Surg. 2015 Nov;136(5 Suppl):92S-100S.
Zhang H et al. Clin Cosmet Investig Dermatol. 2021 Apr 30;14:407-17.
Low-dose oral minoxidil for the treatment of alopecia
Other than oral finasteride, vitamins, and topicals, there has been little advancement in the treatment of AGA leaving many (including me) desperate for anything remotely new.
Oral minoxidil is a peripheral vasodilator approved by the Food and Drug Administration for use in patients with hypertensive disease taken at doses ranging between 10 mg to 40 mg daily. Animal studies have shown that minoxidil affects the hair growth cycle by shortening the telogen phase and prolonging the anagen phase.
Recent case studies have also shown growing evidence for the off-label use of low-dose oral minoxidil (LDOM) for treating different types of alopecia. Topical minoxidil is metabolized into its active metabolite minoxidil sulfate, by sulfotransferase enzymes located in the outer root sheath of hair follicles. The expression of sulfotransferase varies greatly in the scalp of different individuals, and this difference is directly correlated to the wide range of responses to minoxidil treatment. LDOM is, however, more widely effective because it requires decreased follicular enzymatic activity to form its active metabolite as compared with its topical form.
In a retrospective series by Beach and colleagues evaluating the efficacy and tolerability of LDOM for treating AGA, there was increased scalp hair growth in 33 of 51 patients (65%) and decreased hair shedding in 14 of the 51 patients (27%) with LDOM. Patients with nonscarring alopecia were most likely to show improvement. Side effects were dose dependent and infrequent. The most frequent adverse effects were hypertrichosis, lightheadedness, edema, and tachycardia. No life-threatening adverse effects were observed. Although there has been a recently reported case report of severe pericardial effusion, edema, and anasarca in a woman with frontal fibrosing alopecia treated with LDOM, life threatening side effects are rare.3
To compare the efficacy of topical versus oral minoxidil, Ramos and colleagues performed a 24-week prospective study of low-dose (1 mg/day) oral minoxidil, compared with topical 5% minoxidil, in the treatment of 52 women with female pattern hair loss. Blinded analysis of trichoscopic images were evaluated to compare the change in total hair density in a target area from baseline to week 24 by three dermatologists.
Results after 24 weeks of treatment showed an increase in total hair density (12%) among the women taking oral minoxidil, compared with 7.2% in women who applied topical minoxidil (P =.09).
In the armamentarium of hair-loss treatments, dermatologists have limited choices. LDOM can be used in patients with both scarring and nonscarring alopecia if monitored regularly. Treatment doses I recommend are 1.25-5 mg daily titrated up slowly in properly selected patients without contraindications and those who are not taking other vasodilators. Self-reported dizziness, edema, and headache are common and treatments for facial hypertrichosis in women are always discussed. Clinical efficacy can be evaluated after 10-12 months of therapy and concomitant spironolactone can be given to mitigate the side effect of hypertrichosis.Patient selection is crucial as patients with severe scarring alopecia and those with active inflammatory diseases of the scalp may not see similar results. Similar to other hair loss treatments, treatment courses of 10-12 months are often needed to see visible signs of hair growth.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Beach RA et al. J Am Acad Dermatol. 2021 Mar;84(3):761-3.
Dlova et al. JAAD Case Reports. 2022 Oct;28:94-6.
Jimenez-Cauhe J et al. J Am Acad Dermatol. 2021 Jan;84(1):222-3.
Ramos PM et al. J Eur Acad Dermatol Venereol. 2020 Jan;34(1):e40-1.
Ramos PM et al. J Am Acad Dermatol. 2020 Jan;82(1):252-3.
Randolph M and Tosti A. J Am Acad Dermatol. 2021 Mar;84(3):737-46.
Vañó-Galván S et al. J Am Acad Dermatol. 2021 Jun;84(6):1644-51.
Other than oral finasteride, vitamins, and topicals, there has been little advancement in the treatment of AGA leaving many (including me) desperate for anything remotely new.
Oral minoxidil is a peripheral vasodilator approved by the Food and Drug Administration for use in patients with hypertensive disease taken at doses ranging between 10 mg to 40 mg daily. Animal studies have shown that minoxidil affects the hair growth cycle by shortening the telogen phase and prolonging the anagen phase.
Recent case studies have also shown growing evidence for the off-label use of low-dose oral minoxidil (LDOM) for treating different types of alopecia. Topical minoxidil is metabolized into its active metabolite minoxidil sulfate, by sulfotransferase enzymes located in the outer root sheath of hair follicles. The expression of sulfotransferase varies greatly in the scalp of different individuals, and this difference is directly correlated to the wide range of responses to minoxidil treatment. LDOM is, however, more widely effective because it requires decreased follicular enzymatic activity to form its active metabolite as compared with its topical form.
In a retrospective series by Beach and colleagues evaluating the efficacy and tolerability of LDOM for treating AGA, there was increased scalp hair growth in 33 of 51 patients (65%) and decreased hair shedding in 14 of the 51 patients (27%) with LDOM. Patients with nonscarring alopecia were most likely to show improvement. Side effects were dose dependent and infrequent. The most frequent adverse effects were hypertrichosis, lightheadedness, edema, and tachycardia. No life-threatening adverse effects were observed. Although there has been a recently reported case report of severe pericardial effusion, edema, and anasarca in a woman with frontal fibrosing alopecia treated with LDOM, life threatening side effects are rare.3
To compare the efficacy of topical versus oral minoxidil, Ramos and colleagues performed a 24-week prospective study of low-dose (1 mg/day) oral minoxidil, compared with topical 5% minoxidil, in the treatment of 52 women with female pattern hair loss. Blinded analysis of trichoscopic images were evaluated to compare the change in total hair density in a target area from baseline to week 24 by three dermatologists.
Results after 24 weeks of treatment showed an increase in total hair density (12%) among the women taking oral minoxidil, compared with 7.2% in women who applied topical minoxidil (P =.09).
In the armamentarium of hair-loss treatments, dermatologists have limited choices. LDOM can be used in patients with both scarring and nonscarring alopecia if monitored regularly. Treatment doses I recommend are 1.25-5 mg daily titrated up slowly in properly selected patients without contraindications and those who are not taking other vasodilators. Self-reported dizziness, edema, and headache are common and treatments for facial hypertrichosis in women are always discussed. Clinical efficacy can be evaluated after 10-12 months of therapy and concomitant spironolactone can be given to mitigate the side effect of hypertrichosis.Patient selection is crucial as patients with severe scarring alopecia and those with active inflammatory diseases of the scalp may not see similar results. Similar to other hair loss treatments, treatment courses of 10-12 months are often needed to see visible signs of hair growth.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Beach RA et al. J Am Acad Dermatol. 2021 Mar;84(3):761-3.
Dlova et al. JAAD Case Reports. 2022 Oct;28:94-6.
Jimenez-Cauhe J et al. J Am Acad Dermatol. 2021 Jan;84(1):222-3.
Ramos PM et al. J Eur Acad Dermatol Venereol. 2020 Jan;34(1):e40-1.
Ramos PM et al. J Am Acad Dermatol. 2020 Jan;82(1):252-3.
Randolph M and Tosti A. J Am Acad Dermatol. 2021 Mar;84(3):737-46.
Vañó-Galván S et al. J Am Acad Dermatol. 2021 Jun;84(6):1644-51.
Other than oral finasteride, vitamins, and topicals, there has been little advancement in the treatment of AGA leaving many (including me) desperate for anything remotely new.
Oral minoxidil is a peripheral vasodilator approved by the Food and Drug Administration for use in patients with hypertensive disease taken at doses ranging between 10 mg to 40 mg daily. Animal studies have shown that minoxidil affects the hair growth cycle by shortening the telogen phase and prolonging the anagen phase.
Recent case studies have also shown growing evidence for the off-label use of low-dose oral minoxidil (LDOM) for treating different types of alopecia. Topical minoxidil is metabolized into its active metabolite minoxidil sulfate, by sulfotransferase enzymes located in the outer root sheath of hair follicles. The expression of sulfotransferase varies greatly in the scalp of different individuals, and this difference is directly correlated to the wide range of responses to minoxidil treatment. LDOM is, however, more widely effective because it requires decreased follicular enzymatic activity to form its active metabolite as compared with its topical form.
In a retrospective series by Beach and colleagues evaluating the efficacy and tolerability of LDOM for treating AGA, there was increased scalp hair growth in 33 of 51 patients (65%) and decreased hair shedding in 14 of the 51 patients (27%) with LDOM. Patients with nonscarring alopecia were most likely to show improvement. Side effects were dose dependent and infrequent. The most frequent adverse effects were hypertrichosis, lightheadedness, edema, and tachycardia. No life-threatening adverse effects were observed. Although there has been a recently reported case report of severe pericardial effusion, edema, and anasarca in a woman with frontal fibrosing alopecia treated with LDOM, life threatening side effects are rare.3
To compare the efficacy of topical versus oral minoxidil, Ramos and colleagues performed a 24-week prospective study of low-dose (1 mg/day) oral minoxidil, compared with topical 5% minoxidil, in the treatment of 52 women with female pattern hair loss. Blinded analysis of trichoscopic images were evaluated to compare the change in total hair density in a target area from baseline to week 24 by three dermatologists.
Results after 24 weeks of treatment showed an increase in total hair density (12%) among the women taking oral minoxidil, compared with 7.2% in women who applied topical minoxidil (P =.09).
In the armamentarium of hair-loss treatments, dermatologists have limited choices. LDOM can be used in patients with both scarring and nonscarring alopecia if monitored regularly. Treatment doses I recommend are 1.25-5 mg daily titrated up slowly in properly selected patients without contraindications and those who are not taking other vasodilators. Self-reported dizziness, edema, and headache are common and treatments for facial hypertrichosis in women are always discussed. Clinical efficacy can be evaluated after 10-12 months of therapy and concomitant spironolactone can be given to mitigate the side effect of hypertrichosis.Patient selection is crucial as patients with severe scarring alopecia and those with active inflammatory diseases of the scalp may not see similar results. Similar to other hair loss treatments, treatment courses of 10-12 months are often needed to see visible signs of hair growth.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Beach RA et al. J Am Acad Dermatol. 2021 Mar;84(3):761-3.
Dlova et al. JAAD Case Reports. 2022 Oct;28:94-6.
Jimenez-Cauhe J et al. J Am Acad Dermatol. 2021 Jan;84(1):222-3.
Ramos PM et al. J Eur Acad Dermatol Venereol. 2020 Jan;34(1):e40-1.
Ramos PM et al. J Am Acad Dermatol. 2020 Jan;82(1):252-3.
Randolph M and Tosti A. J Am Acad Dermatol. 2021 Mar;84(3):737-46.
Vañó-Galván S et al. J Am Acad Dermatol. 2021 Jun;84(6):1644-51.
Understanding filler reversal with hyaluronidase
Hyaluronic acid is the most common filler used in the United States for cosmetic procedures. . However, there has been little research and there are no formal clinical guidelines on its use. Hyaluronidase is approved by the Food and Drug Administration for several indications, but its use in cosmetic procedures is off-label.
Hyaluronic acid filler complications can be local and transient or delayed and/or dangerous. Local reactions generally improve over time or respond to symptomatic care. But granulomatous reactions, misplaced injection, adverse aesthetic outcomes, and vascular occlusion are some of the detrimental outcomes that require immediate treatment, often using hyaluronidase, a naturally occurring enzyme that degrades hyaluronic acid.
Hyaluronic acid products vary in concentration, cross-linking, type of cross-linker used, and particle size, and therefore display different degradation patterns with hyaluronidase. The three hyaluronidase products available also vary in concentration, source, and enzyme activity. Hyaluronidase has a half-life of 2 minutes but has a duration of action of 24-48 hours depending on the product used.
In an interesting study by Casabona G et al., the dose and activity of five hyaluronidase products available worldwide were used to degrade five different fillers (Juvederm Volbella, Voluma, and Ultraplus; Belotero, and Belotero Balance) with various concentrations and cross-linking in human skin. The results showed that the Vycross products (Juvederm Voluma) are the least sensitive to hyaluronidase and require the greatest concentration of hyaluronidase and a longer time for dissolution requiring up to three times more hyaluronidase to degrade the same volume of other hyaluronic acid products.
In addition, the ovine hyaluronidase product marketed in the United States as Vitrase had the greatest activity against the range of hyaluronic acids used in the trial. Higher concentrations of hyaluronidase also could produce type-I hypersensitivity reactions and angioedema in susceptible patients as evidenced by eosinophilic tissue reactions at concentrations greater than 300 IU.
Hyaluronidase is stored at cool temperatures (35-46° F). It can be reconstituted with saline, water, or bacteriostatic saline for reducing injection site pain; however, it should not be mixed with local anesthetic. The volume of diluent used depends on the surface area treated and ranges from 1 mL to 10 mL. Smaller volumes are used for more concentrated local injection and larger volumes for more precise dosing.
For impending necrosis, hyaluronidase should be used within minutes to hours of blanching of the skin and the area should be flooded every 30 minutes until the tissue has reperfused. Depending on the type of filler used, the volume of injection varies and the area should continually be injected and tissue response observed. A high-dosed large-volume protocol allows the tissue perfusion to gradually infiltrate the vessel walls. Recommendations are 2 mL of bacteriostatic saline diluted with a vial of hyaluronidase. Retrobulbar injection of hyaluronidase within minutes of retinal artery occlusion in doses of 150-200 units in 2-4 mL of diluent into the inferolateral orbit by an experienced ophthalmologist or oculoplastic surgeon is recommended.
Although there is no consensus, there are various clinical studies using hyaluronidase dilutions varying between 5 and 30 units to break down 0.1mg/mL of hyaluronic acid for the reversal of facial hyaluronic acid fillers. In my clinical experience, the recommendation is that, apart from necrosis, the concentration used is titrated to clinical efficacy, which can also be done over multiple appointments every 48 hours until the desired outcome is achieved.
Complications from hyaluronidase injection include local tissue erythema, edema, pain, allergic reactions, and anaphylaxis. An intradermal patch test of 10-20 units of hyaluronidase in the forearm can be done in patients with a history of allergy to hyaluronidase, which, in people with sensitivity, results in a wheal within 30 minutes of injection. If a patient has a positive patch test, hyaluronidase cannot be used. In addition, a history of allergic reactions to bees may pose a heightened reaction to hyaluronidase and is a contraindication to use.
It is recommended that any practitioner using hyaluronic acid fillers keep 2-3 vials of hyaluronidase available at all times in the event of a vascular emergency. Stability, storage, and expiration dates should also be monitored closely.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub has no relevant disclosures.
References
Casabona G et al. Dermatol Surg. 2018 Nov;44 Suppl 1:S42-S50.
DeLorenzi C. Aesthet Surg J. 2017 Jul 1;37(7):814-25.
Juhász MLW et al. Dermatol Surg. 2017 Jun;43(6):841-7.
King M. J Clin Aesthet Dermatol. 2016 Nov; 9(11):E6–8.
Kim M et al. J Clin Aesthet Dermatol. 2018 Jun;11(6):E61-8.
Hyaluronic acid is the most common filler used in the United States for cosmetic procedures. . However, there has been little research and there are no formal clinical guidelines on its use. Hyaluronidase is approved by the Food and Drug Administration for several indications, but its use in cosmetic procedures is off-label.
Hyaluronic acid filler complications can be local and transient or delayed and/or dangerous. Local reactions generally improve over time or respond to symptomatic care. But granulomatous reactions, misplaced injection, adverse aesthetic outcomes, and vascular occlusion are some of the detrimental outcomes that require immediate treatment, often using hyaluronidase, a naturally occurring enzyme that degrades hyaluronic acid.
Hyaluronic acid products vary in concentration, cross-linking, type of cross-linker used, and particle size, and therefore display different degradation patterns with hyaluronidase. The three hyaluronidase products available also vary in concentration, source, and enzyme activity. Hyaluronidase has a half-life of 2 minutes but has a duration of action of 24-48 hours depending on the product used.
In an interesting study by Casabona G et al., the dose and activity of five hyaluronidase products available worldwide were used to degrade five different fillers (Juvederm Volbella, Voluma, and Ultraplus; Belotero, and Belotero Balance) with various concentrations and cross-linking in human skin. The results showed that the Vycross products (Juvederm Voluma) are the least sensitive to hyaluronidase and require the greatest concentration of hyaluronidase and a longer time for dissolution requiring up to three times more hyaluronidase to degrade the same volume of other hyaluronic acid products.
In addition, the ovine hyaluronidase product marketed in the United States as Vitrase had the greatest activity against the range of hyaluronic acids used in the trial. Higher concentrations of hyaluronidase also could produce type-I hypersensitivity reactions and angioedema in susceptible patients as evidenced by eosinophilic tissue reactions at concentrations greater than 300 IU.
Hyaluronidase is stored at cool temperatures (35-46° F). It can be reconstituted with saline, water, or bacteriostatic saline for reducing injection site pain; however, it should not be mixed with local anesthetic. The volume of diluent used depends on the surface area treated and ranges from 1 mL to 10 mL. Smaller volumes are used for more concentrated local injection and larger volumes for more precise dosing.
For impending necrosis, hyaluronidase should be used within minutes to hours of blanching of the skin and the area should be flooded every 30 minutes until the tissue has reperfused. Depending on the type of filler used, the volume of injection varies and the area should continually be injected and tissue response observed. A high-dosed large-volume protocol allows the tissue perfusion to gradually infiltrate the vessel walls. Recommendations are 2 mL of bacteriostatic saline diluted with a vial of hyaluronidase. Retrobulbar injection of hyaluronidase within minutes of retinal artery occlusion in doses of 150-200 units in 2-4 mL of diluent into the inferolateral orbit by an experienced ophthalmologist or oculoplastic surgeon is recommended.
Although there is no consensus, there are various clinical studies using hyaluronidase dilutions varying between 5 and 30 units to break down 0.1mg/mL of hyaluronic acid for the reversal of facial hyaluronic acid fillers. In my clinical experience, the recommendation is that, apart from necrosis, the concentration used is titrated to clinical efficacy, which can also be done over multiple appointments every 48 hours until the desired outcome is achieved.
Complications from hyaluronidase injection include local tissue erythema, edema, pain, allergic reactions, and anaphylaxis. An intradermal patch test of 10-20 units of hyaluronidase in the forearm can be done in patients with a history of allergy to hyaluronidase, which, in people with sensitivity, results in a wheal within 30 minutes of injection. If a patient has a positive patch test, hyaluronidase cannot be used. In addition, a history of allergic reactions to bees may pose a heightened reaction to hyaluronidase and is a contraindication to use.
It is recommended that any practitioner using hyaluronic acid fillers keep 2-3 vials of hyaluronidase available at all times in the event of a vascular emergency. Stability, storage, and expiration dates should also be monitored closely.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub has no relevant disclosures.
References
Casabona G et al. Dermatol Surg. 2018 Nov;44 Suppl 1:S42-S50.
DeLorenzi C. Aesthet Surg J. 2017 Jul 1;37(7):814-25.
Juhász MLW et al. Dermatol Surg. 2017 Jun;43(6):841-7.
King M. J Clin Aesthet Dermatol. 2016 Nov; 9(11):E6–8.
Kim M et al. J Clin Aesthet Dermatol. 2018 Jun;11(6):E61-8.
Hyaluronic acid is the most common filler used in the United States for cosmetic procedures. . However, there has been little research and there are no formal clinical guidelines on its use. Hyaluronidase is approved by the Food and Drug Administration for several indications, but its use in cosmetic procedures is off-label.
Hyaluronic acid filler complications can be local and transient or delayed and/or dangerous. Local reactions generally improve over time or respond to symptomatic care. But granulomatous reactions, misplaced injection, adverse aesthetic outcomes, and vascular occlusion are some of the detrimental outcomes that require immediate treatment, often using hyaluronidase, a naturally occurring enzyme that degrades hyaluronic acid.
Hyaluronic acid products vary in concentration, cross-linking, type of cross-linker used, and particle size, and therefore display different degradation patterns with hyaluronidase. The three hyaluronidase products available also vary in concentration, source, and enzyme activity. Hyaluronidase has a half-life of 2 minutes but has a duration of action of 24-48 hours depending on the product used.
In an interesting study by Casabona G et al., the dose and activity of five hyaluronidase products available worldwide were used to degrade five different fillers (Juvederm Volbella, Voluma, and Ultraplus; Belotero, and Belotero Balance) with various concentrations and cross-linking in human skin. The results showed that the Vycross products (Juvederm Voluma) are the least sensitive to hyaluronidase and require the greatest concentration of hyaluronidase and a longer time for dissolution requiring up to three times more hyaluronidase to degrade the same volume of other hyaluronic acid products.
In addition, the ovine hyaluronidase product marketed in the United States as Vitrase had the greatest activity against the range of hyaluronic acids used in the trial. Higher concentrations of hyaluronidase also could produce type-I hypersensitivity reactions and angioedema in susceptible patients as evidenced by eosinophilic tissue reactions at concentrations greater than 300 IU.
Hyaluronidase is stored at cool temperatures (35-46° F). It can be reconstituted with saline, water, or bacteriostatic saline for reducing injection site pain; however, it should not be mixed with local anesthetic. The volume of diluent used depends on the surface area treated and ranges from 1 mL to 10 mL. Smaller volumes are used for more concentrated local injection and larger volumes for more precise dosing.
For impending necrosis, hyaluronidase should be used within minutes to hours of blanching of the skin and the area should be flooded every 30 minutes until the tissue has reperfused. Depending on the type of filler used, the volume of injection varies and the area should continually be injected and tissue response observed. A high-dosed large-volume protocol allows the tissue perfusion to gradually infiltrate the vessel walls. Recommendations are 2 mL of bacteriostatic saline diluted with a vial of hyaluronidase. Retrobulbar injection of hyaluronidase within minutes of retinal artery occlusion in doses of 150-200 units in 2-4 mL of diluent into the inferolateral orbit by an experienced ophthalmologist or oculoplastic surgeon is recommended.
Although there is no consensus, there are various clinical studies using hyaluronidase dilutions varying between 5 and 30 units to break down 0.1mg/mL of hyaluronic acid for the reversal of facial hyaluronic acid fillers. In my clinical experience, the recommendation is that, apart from necrosis, the concentration used is titrated to clinical efficacy, which can also be done over multiple appointments every 48 hours until the desired outcome is achieved.
Complications from hyaluronidase injection include local tissue erythema, edema, pain, allergic reactions, and anaphylaxis. An intradermal patch test of 10-20 units of hyaluronidase in the forearm can be done in patients with a history of allergy to hyaluronidase, which, in people with sensitivity, results in a wheal within 30 minutes of injection. If a patient has a positive patch test, hyaluronidase cannot be used. In addition, a history of allergic reactions to bees may pose a heightened reaction to hyaluronidase and is a contraindication to use.
It is recommended that any practitioner using hyaluronic acid fillers keep 2-3 vials of hyaluronidase available at all times in the event of a vascular emergency. Stability, storage, and expiration dates should also be monitored closely.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub has no relevant disclosures.
References
Casabona G et al. Dermatol Surg. 2018 Nov;44 Suppl 1:S42-S50.
DeLorenzi C. Aesthet Surg J. 2017 Jul 1;37(7):814-25.
Juhász MLW et al. Dermatol Surg. 2017 Jun;43(6):841-7.
King M. J Clin Aesthet Dermatol. 2016 Nov; 9(11):E6–8.
Kim M et al. J Clin Aesthet Dermatol. 2018 Jun;11(6):E61-8.
Acid series: Trichloroacetic acid
– yet can be one of the most dangerous treatments in the hands of an untrained user.
TCA, in a clear colorless solution, is available in concentrations up to 100%, and has not been associated with allergic reactions or systemic toxicity. The available concentrations include those used for superficial depth peels (10%-30%), medium depth peels (35%-50%), and deep peels (greater than 50%).
TCA causes coagulation of the cellular membrane of epidermal proteins in the epidermis and, depending on the concentration, the dermis, which results in frosting of the skin. Repair of the epidermal cells induces resurfacing of the skin and neocollagenesis. TCA can be combined with other acids, including glycolic acid (Coleman peel), Jessner solution (Monheit peel), and solid CO2 (Brody peel). It has also been combined with lactic acid, mandelic acid, and salicylic acid in combination peels of various concentrations.
Although there are many studies, case reports, and textbooks related to this topic and the applications, combinations and treatment options for TCA peels, it is important to highlight here how many of these solutions – at high concentrations – are available directly to consumers, med spas, and the general public through online websites, including Amazon and overseas sites. Over the last 15 years, I have seen complications of this acid alone in people who have bought TCA online, related to applications not just on the face but on the body, neck, eyes, vaginal, and anal areas. Pigmentation, erosions, ulcers, and strictures are just some of the possible complications that occur not just with a more concentrated solution, but more often from application errors, aggressive layering of the acid, allowing the acid to sit on the skin too long, and improper tissue prepping and posttreatment skin care.
TCA can be an untamable acid, with little control over the depth of penetration even in the most controlled situations. The inability to be neutralize TCA creates an environment in which the depth of penetration and tissue coagulation is not a precise science. Once applied, the tissue reaction cannot be “stopped” or rapidly reversed making it highly variable in its mechanism. Patients of all skin types have the potential to develop complications as the epidermal and dermal thickness, moisture content, sebum production, and pigmentation are highly varied between individuals.
In my opinion, it is a dangerous product to have on the market – not just for the untrained medical providers using it but for estheticians and the general public who now can buy TCA anywhere.
But with effective training, reliable sourcing and appropriate preparation of the patient’s skin, however, a TCA peel can be a highly effective tool for difficult-to-treat dermatological problems, such as scarring and xanthelasma.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. She has no relevant disclosures. Write to them at dermnews@mdedge.com.
– yet can be one of the most dangerous treatments in the hands of an untrained user.
TCA, in a clear colorless solution, is available in concentrations up to 100%, and has not been associated with allergic reactions or systemic toxicity. The available concentrations include those used for superficial depth peels (10%-30%), medium depth peels (35%-50%), and deep peels (greater than 50%).
TCA causes coagulation of the cellular membrane of epidermal proteins in the epidermis and, depending on the concentration, the dermis, which results in frosting of the skin. Repair of the epidermal cells induces resurfacing of the skin and neocollagenesis. TCA can be combined with other acids, including glycolic acid (Coleman peel), Jessner solution (Monheit peel), and solid CO2 (Brody peel). It has also been combined with lactic acid, mandelic acid, and salicylic acid in combination peels of various concentrations.
Although there are many studies, case reports, and textbooks related to this topic and the applications, combinations and treatment options for TCA peels, it is important to highlight here how many of these solutions – at high concentrations – are available directly to consumers, med spas, and the general public through online websites, including Amazon and overseas sites. Over the last 15 years, I have seen complications of this acid alone in people who have bought TCA online, related to applications not just on the face but on the body, neck, eyes, vaginal, and anal areas. Pigmentation, erosions, ulcers, and strictures are just some of the possible complications that occur not just with a more concentrated solution, but more often from application errors, aggressive layering of the acid, allowing the acid to sit on the skin too long, and improper tissue prepping and posttreatment skin care.
TCA can be an untamable acid, with little control over the depth of penetration even in the most controlled situations. The inability to be neutralize TCA creates an environment in which the depth of penetration and tissue coagulation is not a precise science. Once applied, the tissue reaction cannot be “stopped” or rapidly reversed making it highly variable in its mechanism. Patients of all skin types have the potential to develop complications as the epidermal and dermal thickness, moisture content, sebum production, and pigmentation are highly varied between individuals.
In my opinion, it is a dangerous product to have on the market – not just for the untrained medical providers using it but for estheticians and the general public who now can buy TCA anywhere.
But with effective training, reliable sourcing and appropriate preparation of the patient’s skin, however, a TCA peel can be a highly effective tool for difficult-to-treat dermatological problems, such as scarring and xanthelasma.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. She has no relevant disclosures. Write to them at dermnews@mdedge.com.
– yet can be one of the most dangerous treatments in the hands of an untrained user.
TCA, in a clear colorless solution, is available in concentrations up to 100%, and has not been associated with allergic reactions or systemic toxicity. The available concentrations include those used for superficial depth peels (10%-30%), medium depth peels (35%-50%), and deep peels (greater than 50%).
TCA causes coagulation of the cellular membrane of epidermal proteins in the epidermis and, depending on the concentration, the dermis, which results in frosting of the skin. Repair of the epidermal cells induces resurfacing of the skin and neocollagenesis. TCA can be combined with other acids, including glycolic acid (Coleman peel), Jessner solution (Monheit peel), and solid CO2 (Brody peel). It has also been combined with lactic acid, mandelic acid, and salicylic acid in combination peels of various concentrations.
Although there are many studies, case reports, and textbooks related to this topic and the applications, combinations and treatment options for TCA peels, it is important to highlight here how many of these solutions – at high concentrations – are available directly to consumers, med spas, and the general public through online websites, including Amazon and overseas sites. Over the last 15 years, I have seen complications of this acid alone in people who have bought TCA online, related to applications not just on the face but on the body, neck, eyes, vaginal, and anal areas. Pigmentation, erosions, ulcers, and strictures are just some of the possible complications that occur not just with a more concentrated solution, but more often from application errors, aggressive layering of the acid, allowing the acid to sit on the skin too long, and improper tissue prepping and posttreatment skin care.
TCA can be an untamable acid, with little control over the depth of penetration even in the most controlled situations. The inability to be neutralize TCA creates an environment in which the depth of penetration and tissue coagulation is not a precise science. Once applied, the tissue reaction cannot be “stopped” or rapidly reversed making it highly variable in its mechanism. Patients of all skin types have the potential to develop complications as the epidermal and dermal thickness, moisture content, sebum production, and pigmentation are highly varied between individuals.
In my opinion, it is a dangerous product to have on the market – not just for the untrained medical providers using it but for estheticians and the general public who now can buy TCA anywhere.
But with effective training, reliable sourcing and appropriate preparation of the patient’s skin, however, a TCA peel can be a highly effective tool for difficult-to-treat dermatological problems, such as scarring and xanthelasma.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. She has no relevant disclosures. Write to them at dermnews@mdedge.com.
Mandelic acid
Acids peels are used to elicit a chemical exfoliation of the skin by hydrolyzing amide bonds between keratinocytes, reducing corneocyte adhesion, as well as inducing an inflammatory reaction stimulating tissue remodeling. Release of cytokines such as interleukin (IL)-1 and IL-6 by keratinocytes activates fibroblasts to increase the production of matrix metalloproteinases. These are involved in the production of hyaluronic acid and new collagen formation.
Mandelic acid was derived from bitter almonds (mandel is the German word for almond). It is a white powder originally used as an antibiotic for the treatment of urinary tract infections. Its antibacterial properties make it an excellent product for the topical treatment of acne, as well as for use in topical preparations to treat hyperpigmentation and photoaging. In cosmetic use, mandelic acid is a slow acting chemical peel that can be used in all skin types, including sensitive and rosacea-prone skin, as well as skin of color. Its large molecular size allows for the slow penetration of the acid on the skin and thus it can be carefully titrated.
Studies have shown its efficacy in reducing sebum content, acne, acne scarring, and hyperpigmentation. In clinical practice however, the most effective use of this acid is on sensitive skin. It is a great tool for clinicians to use as an effective exfoliant in less acid tolerant skin types. In commercially available concentrations of 5%-45%, mandelic acid can be used alone or in combination with other beta hydroxy peels, depending on the indication.
Most dermatologists and patients prefer in-office peels that induce noticeable peeling and resurfacing of the skin. Mandelic acid is one of the largest alpha hydroxy acids, a lipophilic acid that penetrates the skin slowly and uniformly, making it an ideal peel in sensitive or aging and thin skin types. Although many mandelic acid peels are available, however, there is a paucity of studies comparing their benefits and efficacies.
Dr. Lily Talakoub and Dr. Naissan O. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
1. Wójcik A et al. Dermatol Alergol. 2013 Jun;30(3):140-5.
2. Soleymani T et al. J Clin Aesthet Dermatol. 2018;11(8):21-8.
Acids peels are used to elicit a chemical exfoliation of the skin by hydrolyzing amide bonds between keratinocytes, reducing corneocyte adhesion, as well as inducing an inflammatory reaction stimulating tissue remodeling. Release of cytokines such as interleukin (IL)-1 and IL-6 by keratinocytes activates fibroblasts to increase the production of matrix metalloproteinases. These are involved in the production of hyaluronic acid and new collagen formation.
Mandelic acid was derived from bitter almonds (mandel is the German word for almond). It is a white powder originally used as an antibiotic for the treatment of urinary tract infections. Its antibacterial properties make it an excellent product for the topical treatment of acne, as well as for use in topical preparations to treat hyperpigmentation and photoaging. In cosmetic use, mandelic acid is a slow acting chemical peel that can be used in all skin types, including sensitive and rosacea-prone skin, as well as skin of color. Its large molecular size allows for the slow penetration of the acid on the skin and thus it can be carefully titrated.
Studies have shown its efficacy in reducing sebum content, acne, acne scarring, and hyperpigmentation. In clinical practice however, the most effective use of this acid is on sensitive skin. It is a great tool for clinicians to use as an effective exfoliant in less acid tolerant skin types. In commercially available concentrations of 5%-45%, mandelic acid can be used alone or in combination with other beta hydroxy peels, depending on the indication.
Most dermatologists and patients prefer in-office peels that induce noticeable peeling and resurfacing of the skin. Mandelic acid is one of the largest alpha hydroxy acids, a lipophilic acid that penetrates the skin slowly and uniformly, making it an ideal peel in sensitive or aging and thin skin types. Although many mandelic acid peels are available, however, there is a paucity of studies comparing their benefits and efficacies.
Dr. Lily Talakoub and Dr. Naissan O. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
1. Wójcik A et al. Dermatol Alergol. 2013 Jun;30(3):140-5.
2. Soleymani T et al. J Clin Aesthet Dermatol. 2018;11(8):21-8.
Acids peels are used to elicit a chemical exfoliation of the skin by hydrolyzing amide bonds between keratinocytes, reducing corneocyte adhesion, as well as inducing an inflammatory reaction stimulating tissue remodeling. Release of cytokines such as interleukin (IL)-1 and IL-6 by keratinocytes activates fibroblasts to increase the production of matrix metalloproteinases. These are involved in the production of hyaluronic acid and new collagen formation.
Mandelic acid was derived from bitter almonds (mandel is the German word for almond). It is a white powder originally used as an antibiotic for the treatment of urinary tract infections. Its antibacterial properties make it an excellent product for the topical treatment of acne, as well as for use in topical preparations to treat hyperpigmentation and photoaging. In cosmetic use, mandelic acid is a slow acting chemical peel that can be used in all skin types, including sensitive and rosacea-prone skin, as well as skin of color. Its large molecular size allows for the slow penetration of the acid on the skin and thus it can be carefully titrated.
Studies have shown its efficacy in reducing sebum content, acne, acne scarring, and hyperpigmentation. In clinical practice however, the most effective use of this acid is on sensitive skin. It is a great tool for clinicians to use as an effective exfoliant in less acid tolerant skin types. In commercially available concentrations of 5%-45%, mandelic acid can be used alone or in combination with other beta hydroxy peels, depending on the indication.
Most dermatologists and patients prefer in-office peels that induce noticeable peeling and resurfacing of the skin. Mandelic acid is one of the largest alpha hydroxy acids, a lipophilic acid that penetrates the skin slowly and uniformly, making it an ideal peel in sensitive or aging and thin skin types. Although many mandelic acid peels are available, however, there is a paucity of studies comparing their benefits and efficacies.
Dr. Lily Talakoub and Dr. Naissan O. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
1. Wójcik A et al. Dermatol Alergol. 2013 Jun;30(3):140-5.
2. Soleymani T et al. J Clin Aesthet Dermatol. 2018;11(8):21-8.
Acid series: Azelaic acid
However, it has many positive qualities, including being gentle enough to use daily and is safe to use in pregnancy. It is antibacterial, comedolytic, keratolytic, and has antioxidant activity. Unfortunately, in the last decade the formulations of azelaic acid have not been changed considerably. The 20% cream, 15% gel, and 15% foam vehicles are often too irritating and drying to be used in the population it is intended for: those with rosacea, or with inflamed or sensitive skin.
Azelaic acid is a dicarboxylic acid produced by Pityrosporum ovale. It inhibits the synthesis of cellular proteins and is bactericidal against Propionibacterium acnes and Staphylococcus epidermidis. Azelaic acid is both keratolytic and comedolytic by decreasing keratohyalin granules and reducing filaggrin in the epidermis. It not only scavenges free oxygen radicals, thereby reducing inflammation, but is also a tyrosinase inhibitor – making it a safe, non–hydroquinone-based alternative to skin lightening.
Azelaic acid has little toxicity, it is ingested regularly as it is found in wheat, barley, and rye. Topical side effects are usually mild and can subside with increased use. The most common side effects include erythema, local stinging, pruritus, scaling, and a burning sensation. It is considered safe in pregnancy and a great alternative to medications for acne in pregnant or nursing patients.
The largest constraint with azelaic acid preparations on the market – and most likely the reason it has not been more widely used for acne, rosacea, antiaging, and hyperpigmentation – is the formulation. The foam and gel preparations are irritating and difficult to use on dry or sensitive skin. The 20% cream preparations are slightly better tolerated; however, in vitro skin-penetration studies have shown that cutaneous penetration of azelaic acid is greater after application of a 15% gel (aqueous-based vehicle) and 15% foam (hydrophilic oil-in-water emulsion) as compared with the 20% cream formulations.
In my clinical experience, azelaic acid can only be used in rosacea patients with oily or nonsensitive skin. The majority of my rosacea patients cannot tolerate the burning sensation, albeit transient and mild. Acne patients who do not have dry skin and pregnant patients with mild acne are a great population for integrating azelaic acid into an acne regimen. I also use azelaic acid as an alternative for mild melasma and lentigines in patients who are tapering off hydroquinone or cannot use hydroquinone. In the future, we need better, creamier, nonirritating formulations to be developed and more studies of higher concentrations of this acid for both prescription/patient at-home use, as well as more elegant in-office localized peel systems using azelaic acid.
Dr. Talakoub and Dr. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
Fitton A and Goa KL. Drugs. 1991 May;41(5):780-98.
Del Rosso JQ. J Clin Aesthet Dermatol. 2017 Mar;10(3):37-40.
Breathnach AC et al. Clin Dermatol. Apr-Jun 1989;7(2):106-19.
However, it has many positive qualities, including being gentle enough to use daily and is safe to use in pregnancy. It is antibacterial, comedolytic, keratolytic, and has antioxidant activity. Unfortunately, in the last decade the formulations of azelaic acid have not been changed considerably. The 20% cream, 15% gel, and 15% foam vehicles are often too irritating and drying to be used in the population it is intended for: those with rosacea, or with inflamed or sensitive skin.
Azelaic acid is a dicarboxylic acid produced by Pityrosporum ovale. It inhibits the synthesis of cellular proteins and is bactericidal against Propionibacterium acnes and Staphylococcus epidermidis. Azelaic acid is both keratolytic and comedolytic by decreasing keratohyalin granules and reducing filaggrin in the epidermis. It not only scavenges free oxygen radicals, thereby reducing inflammation, but is also a tyrosinase inhibitor – making it a safe, non–hydroquinone-based alternative to skin lightening.
Azelaic acid has little toxicity, it is ingested regularly as it is found in wheat, barley, and rye. Topical side effects are usually mild and can subside with increased use. The most common side effects include erythema, local stinging, pruritus, scaling, and a burning sensation. It is considered safe in pregnancy and a great alternative to medications for acne in pregnant or nursing patients.
The largest constraint with azelaic acid preparations on the market – and most likely the reason it has not been more widely used for acne, rosacea, antiaging, and hyperpigmentation – is the formulation. The foam and gel preparations are irritating and difficult to use on dry or sensitive skin. The 20% cream preparations are slightly better tolerated; however, in vitro skin-penetration studies have shown that cutaneous penetration of azelaic acid is greater after application of a 15% gel (aqueous-based vehicle) and 15% foam (hydrophilic oil-in-water emulsion) as compared with the 20% cream formulations.
In my clinical experience, azelaic acid can only be used in rosacea patients with oily or nonsensitive skin. The majority of my rosacea patients cannot tolerate the burning sensation, albeit transient and mild. Acne patients who do not have dry skin and pregnant patients with mild acne are a great population for integrating azelaic acid into an acne regimen. I also use azelaic acid as an alternative for mild melasma and lentigines in patients who are tapering off hydroquinone or cannot use hydroquinone. In the future, we need better, creamier, nonirritating formulations to be developed and more studies of higher concentrations of this acid for both prescription/patient at-home use, as well as more elegant in-office localized peel systems using azelaic acid.
Dr. Talakoub and Dr. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
Fitton A and Goa KL. Drugs. 1991 May;41(5):780-98.
Del Rosso JQ. J Clin Aesthet Dermatol. 2017 Mar;10(3):37-40.
Breathnach AC et al. Clin Dermatol. Apr-Jun 1989;7(2):106-19.
However, it has many positive qualities, including being gentle enough to use daily and is safe to use in pregnancy. It is antibacterial, comedolytic, keratolytic, and has antioxidant activity. Unfortunately, in the last decade the formulations of azelaic acid have not been changed considerably. The 20% cream, 15% gel, and 15% foam vehicles are often too irritating and drying to be used in the population it is intended for: those with rosacea, or with inflamed or sensitive skin.
Azelaic acid is a dicarboxylic acid produced by Pityrosporum ovale. It inhibits the synthesis of cellular proteins and is bactericidal against Propionibacterium acnes and Staphylococcus epidermidis. Azelaic acid is both keratolytic and comedolytic by decreasing keratohyalin granules and reducing filaggrin in the epidermis. It not only scavenges free oxygen radicals, thereby reducing inflammation, but is also a tyrosinase inhibitor – making it a safe, non–hydroquinone-based alternative to skin lightening.
Azelaic acid has little toxicity, it is ingested regularly as it is found in wheat, barley, and rye. Topical side effects are usually mild and can subside with increased use. The most common side effects include erythema, local stinging, pruritus, scaling, and a burning sensation. It is considered safe in pregnancy and a great alternative to medications for acne in pregnant or nursing patients.
The largest constraint with azelaic acid preparations on the market – and most likely the reason it has not been more widely used for acne, rosacea, antiaging, and hyperpigmentation – is the formulation. The foam and gel preparations are irritating and difficult to use on dry or sensitive skin. The 20% cream preparations are slightly better tolerated; however, in vitro skin-penetration studies have shown that cutaneous penetration of azelaic acid is greater after application of a 15% gel (aqueous-based vehicle) and 15% foam (hydrophilic oil-in-water emulsion) as compared with the 20% cream formulations.
In my clinical experience, azelaic acid can only be used in rosacea patients with oily or nonsensitive skin. The majority of my rosacea patients cannot tolerate the burning sensation, albeit transient and mild. Acne patients who do not have dry skin and pregnant patients with mild acne are a great population for integrating azelaic acid into an acne regimen. I also use azelaic acid as an alternative for mild melasma and lentigines in patients who are tapering off hydroquinone or cannot use hydroquinone. In the future, we need better, creamier, nonirritating formulations to be developed and more studies of higher concentrations of this acid for both prescription/patient at-home use, as well as more elegant in-office localized peel systems using azelaic acid.
Dr. Talakoub and Dr. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
Fitton A and Goa KL. Drugs. 1991 May;41(5):780-98.
Del Rosso JQ. J Clin Aesthet Dermatol. 2017 Mar;10(3):37-40.
Breathnach AC et al. Clin Dermatol. Apr-Jun 1989;7(2):106-19.
Acid series: Lactic acid
One of the most commonly used organic acids used on the skin, lactic acid, has been used for over 3 decades. Originally derived from milk or plant-derived sugars, this gentle exfoliating acid can be used in peels, serums, masks, and toners, and has the additional benefit of hydrating the skin. Lactic acid is formulated in concentrations from 2% to 50%; however, because of its large molecular size, it doesn’t penetrate the deeper layers of the dermis to the same extent as the other alpha-hydroxy acids (AHAs), such as glycolic acid. Thus, it is one of the gentler exfoliants and one that can be used in sensitive skin or darker skin types.
Despite its mild peeling effects, lactic acid is best used to treat xerotic skin because of its function as a humectant, drawing moisture into the stratum corneum. Similar to the other AHAs, lactic acid has also been shown to decrease melanogenesis and is a gentle treatment for skin hyperpigmentation, particularly in skin of color. Side effects include peeling, stinging, erythema, photosensitivity, and hyperpigmentation when improperly used.
Very little clinical research has been reported in the last 20 years as to the uses and benefits of lactic acid in skincare. In my clinical experience, daily use of lactic acid is more effective and has more long-term benefits for hydration and rejuvenation of the skin than the other AHAs. Concentrations of 10%-15% used daily on the skin as a mild exfoliant and humectant have shown to improve texture, decrease pigmentation and improve fine lines – without thinning of the skin seen with the deeper dermal penetrating acids.
Confusion in the market has also risen as many over-the-counter brands have included ammonium lactate in their portfolio of moisturizers. Ammonium lactate is a combination of ammonium hydroxide and lactic acid, or the salt of lactic acid. A comparative study evaluating the difference between 5% lactic acid and 12% ammonium lactate for the treatment of xerosis showed that ammonium lactate was significantly more effective at reducing xerosis. It is widely used in the treatment of keratosis pilaris, calluses, xerosis, and ichthyosis.
Widespread use of lactic acid has not gotten as much glory as that of glycolic acid. However, in clinical practice, its functions are more widespread. It is a much safer acid to use, and its added benefit of increasing hydration of the skin is crucial in its long-term use for both photoaging and the prevention of wrinkles. With any acid, the exfoliating properties must be treated with adequate hydration and barrier repair.
The intrinsic moisturizing effect of lactic acid makes it a much more well-rounded acid and that can be used for longer periods of time in a broader spectrum of patients.
Dr. Lily Talakoub and Dr. Naissan O. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
One of the most commonly used organic acids used on the skin, lactic acid, has been used for over 3 decades. Originally derived from milk or plant-derived sugars, this gentle exfoliating acid can be used in peels, serums, masks, and toners, and has the additional benefit of hydrating the skin. Lactic acid is formulated in concentrations from 2% to 50%; however, because of its large molecular size, it doesn’t penetrate the deeper layers of the dermis to the same extent as the other alpha-hydroxy acids (AHAs), such as glycolic acid. Thus, it is one of the gentler exfoliants and one that can be used in sensitive skin or darker skin types.
Despite its mild peeling effects, lactic acid is best used to treat xerotic skin because of its function as a humectant, drawing moisture into the stratum corneum. Similar to the other AHAs, lactic acid has also been shown to decrease melanogenesis and is a gentle treatment for skin hyperpigmentation, particularly in skin of color. Side effects include peeling, stinging, erythema, photosensitivity, and hyperpigmentation when improperly used.
Very little clinical research has been reported in the last 20 years as to the uses and benefits of lactic acid in skincare. In my clinical experience, daily use of lactic acid is more effective and has more long-term benefits for hydration and rejuvenation of the skin than the other AHAs. Concentrations of 10%-15% used daily on the skin as a mild exfoliant and humectant have shown to improve texture, decrease pigmentation and improve fine lines – without thinning of the skin seen with the deeper dermal penetrating acids.
Confusion in the market has also risen as many over-the-counter brands have included ammonium lactate in their portfolio of moisturizers. Ammonium lactate is a combination of ammonium hydroxide and lactic acid, or the salt of lactic acid. A comparative study evaluating the difference between 5% lactic acid and 12% ammonium lactate for the treatment of xerosis showed that ammonium lactate was significantly more effective at reducing xerosis. It is widely used in the treatment of keratosis pilaris, calluses, xerosis, and ichthyosis.
Widespread use of lactic acid has not gotten as much glory as that of glycolic acid. However, in clinical practice, its functions are more widespread. It is a much safer acid to use, and its added benefit of increasing hydration of the skin is crucial in its long-term use for both photoaging and the prevention of wrinkles. With any acid, the exfoliating properties must be treated with adequate hydration and barrier repair.
The intrinsic moisturizing effect of lactic acid makes it a much more well-rounded acid and that can be used for longer periods of time in a broader spectrum of patients.
Dr. Lily Talakoub and Dr. Naissan O. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
One of the most commonly used organic acids used on the skin, lactic acid, has been used for over 3 decades. Originally derived from milk or plant-derived sugars, this gentle exfoliating acid can be used in peels, serums, masks, and toners, and has the additional benefit of hydrating the skin. Lactic acid is formulated in concentrations from 2% to 50%; however, because of its large molecular size, it doesn’t penetrate the deeper layers of the dermis to the same extent as the other alpha-hydroxy acids (AHAs), such as glycolic acid. Thus, it is one of the gentler exfoliants and one that can be used in sensitive skin or darker skin types.
Despite its mild peeling effects, lactic acid is best used to treat xerotic skin because of its function as a humectant, drawing moisture into the stratum corneum. Similar to the other AHAs, lactic acid has also been shown to decrease melanogenesis and is a gentle treatment for skin hyperpigmentation, particularly in skin of color. Side effects include peeling, stinging, erythema, photosensitivity, and hyperpigmentation when improperly used.
Very little clinical research has been reported in the last 20 years as to the uses and benefits of lactic acid in skincare. In my clinical experience, daily use of lactic acid is more effective and has more long-term benefits for hydration and rejuvenation of the skin than the other AHAs. Concentrations of 10%-15% used daily on the skin as a mild exfoliant and humectant have shown to improve texture, decrease pigmentation and improve fine lines – without thinning of the skin seen with the deeper dermal penetrating acids.
Confusion in the market has also risen as many over-the-counter brands have included ammonium lactate in their portfolio of moisturizers. Ammonium lactate is a combination of ammonium hydroxide and lactic acid, or the salt of lactic acid. A comparative study evaluating the difference between 5% lactic acid and 12% ammonium lactate for the treatment of xerosis showed that ammonium lactate was significantly more effective at reducing xerosis. It is widely used in the treatment of keratosis pilaris, calluses, xerosis, and ichthyosis.
Widespread use of lactic acid has not gotten as much glory as that of glycolic acid. However, in clinical practice, its functions are more widespread. It is a much safer acid to use, and its added benefit of increasing hydration of the skin is crucial in its long-term use for both photoaging and the prevention of wrinkles. With any acid, the exfoliating properties must be treated with adequate hydration and barrier repair.
The intrinsic moisturizing effect of lactic acid makes it a much more well-rounded acid and that can be used for longer periods of time in a broader spectrum of patients.
Dr. Lily Talakoub and Dr. Naissan O. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.