Practice and Educational Gaps in Abnormal Pigmentation




Dyschromia refers to abnormal pigmentation and is one of the most common diagnoses in dermatology. However, there are many educational and practice gaps in this area, specifically in melasma, postinflammatory hyperpigmentation, and vitiligo. This article aims to review the gold standard of care for these conditions as well as highlight common educational and practice gaps in these areas. Finally, possible solutions to these gaps are addressed.


Key points








  • Dyschromia is one of the most common diagnoses in dermatology, yet there are significant educational and practice gaps in this area.



  • The main educational and practice gaps in melasma and postinflammatory hyperpigmentation include alternative or adjunct therapies to hydroquinone and lack of exposure to a variety of skin tones.



  • The main educational and practice gaps in vitiligo include underutilization and customization of phototherapy, use of agents for stabilization of progressive disease, and surgical treatment of vitiligo.



  • Residency programs need to address educational gaps in disorders of pigmentation to prevent educational gaps from becoming practice gaps.






Introduction


Dyschromia refers to abnormal pigmentation of the skin or nails, including numerous conditions that cause both hyperpigmentation and hypopigmentation. It is one of the most common diagnoses in dermatology, especially in individuals with skin of color. From 1993 to 2010, there were approximately 24.7 million office visits made to dermatology practices for the management of dyschromia. Despite the high prevalence of dyschromia in the general population, there is a disconnect between the occurrence of this condition and the resources directed toward its management. As such, it is important to define the standard of care for abnormal pigmentation, more specifically, postinflammatory hyperpigmentation (PIH), melasma, and vitiligo, as well as address clinical and educational gaps that may lead to substandard practices.




Introduction


Dyschromia refers to abnormal pigmentation of the skin or nails, including numerous conditions that cause both hyperpigmentation and hypopigmentation. It is one of the most common diagnoses in dermatology, especially in individuals with skin of color. From 1993 to 2010, there were approximately 24.7 million office visits made to dermatology practices for the management of dyschromia. Despite the high prevalence of dyschromia in the general population, there is a disconnect between the occurrence of this condition and the resources directed toward its management. As such, it is important to define the standard of care for abnormal pigmentation, more specifically, postinflammatory hyperpigmentation (PIH), melasma, and vitiligo, as well as address clinical and educational gaps that may lead to substandard practices.




Gold standard


Melasma/Postinflammatory Hyperpigmentation


Melasma is a condition characterized by irregularly shaped hyperpigmented patches most commonly located in a centrofacial, malar, or mandibular pattern. Depending on the location of pigment deposition, melasma can be characterized as epidermal, dermal, or mixed type, with worse prognosis associated with dermal pigmentation. Pigment location can be determined by examination under a Wood lamp, with epidermal pigment becoming accentuated under illumination. Melasma is often associated with UV exposure, genetic predisposition, and hormonal changes, such as pregnancy or the initiation of oral contraceptive pills (OCPs). PIH occurs when cutaneous inflammation leads to increased pigmentation in the dermis or epidermis. Several conditions are capable of inducing PIH, such as atopic dermatitis, acne, medication reactions, and procedure-related inflammation. Hyperpigmentation develops in the same area as preceding inflammation and occurs more commonly in skin types III–VI.


Evaluation of melasma is performed using the Melasma Area and Severity Index, or MASI, score. This evaluation involves adding the severity ratings for darkness and homogeneity, which are then multiplied by the numerical value given for 4 facial areas, including the forehead, chin, and left and right malar regions, and the percentage involvement of each area. A modified MASI score, which removes the homogeneity parameter, has subsequently been created. Clinical photography is also important in following this condition over time. The MelasQoL is a scale that assesses the impact of melasma on quality of life (QoL). The only validated outcome measure for evaluation of PIH is the Postacne Hyperpigmentation Index. Scoring is based on median lesion size, intensity, and number of lesions. A PIH Investigator’s Global Assessment scale has also been developed at Henry Ford Hospital to characterize the intensity of hyperpigmentation. Serial photography is also important in monitoring progression and treatment response. Currently, no validated quality-of-life measure specific to PIH exists.


The first step in treatment of both melasma and PIH is the avoidance of causative factors. In patients with melasma, those currently taking OCPs should switch to an alternate form of birth control. With regards to PIH, treatment of the underlying condition causing cutaneous inflammation is imperative. In both instances, photoprotection is critical because UV exposure can exacerbate hyperpigmentation. Although most broad-spectrum chemical sunscreens provide protection against both UV-A and UV-B wavelengths, they are not effective against visible light. Visible light has been shown to induce production of reactive oxygen species (ROS) in addition to proinflammatory cytokines, and matrix metalloproteinase 1. A study performed by Mahmoud and colleagues showed that exposure to visible light induced pigmentation in skin types IV–VI, which was darker and more sustained than pigmentation caused by UV exposure. Physical sunscreens, such as iron oxide, provide coverage against the visible light spectrum and are often present in commercially available make-up products. Use of tinted sunscreen containing iron oxide in patients with melasma showed a smaller increase in MASI scores over time compared with patients using the same sunscreen without iron oxide. Another study comparing the use of a visible light-UV sunscreen and hydroquinone to UV-only sunscreen with hydroquinone showed greater increases in MASI scores with the UV-only sunscreen and hydroquinone combination. There is a paucity of literature regarding the effect of physical sunscreens in PIH, which is an area that needs to be addressed in future studies.


With respect to topical therapies, hydroquinone is the mainstay of treatment. Inhibition of tyrosinase, the enzyme responsible for converting dihydrophenylalanine to melanin, is its main mechanism of action. It can be used alone, but is more effective when used in combination with a retinoid and corticosteroid, which is known as Kligman’s formula. However, caution is advised because use of hydroquinone has been associated with ochronosis, a blackish discoloration of the skin that is difficult to reverse. Currently, there are several other lightening agents that can be used as an alternative or adjunct to hydroquinone. Examples include soy, ellagic acid, niacinamide, licorice extract, kojic acid, vitamin C, and arbutin ( Table 1 ). These compounds have been shown to cause statistically significant reductions in pigmentation. Most of these alternative therapies are available as over-the-counter products.



Table 1

Agents for treatment of hyperpigmentation








































































































Ingredient Mechanism Products Comments
Hydroquinone


  • Inhibits tyrosinase



  • Inhibits synthesis of melanocyte DNA and RNA

Nadinola


  • Risk of ochranosis with overuse



  • May require prescription depending on percentage

HQ/retinoid/CS


  • Retinoid:




    • Inhibits tyrosinase



    • Increases turnover of keratinocytes



    • Increases dispersal of keratinocyte pigment granules




  • Corticosteroid:




    • Anti-inflammatory


Triluma


  • First-line treatment for hyperpigmentation



  • Requires prescription

Azelaic acid


  • Inhibits tyrosinase




  • PCA Skin Pigment Bar (combination of kojic acid and azelaic acid)




  • Also used in many acne and rosacea products



  • Available in OTC products and as a prescription product

Mequinol


  • Competitive inhibitor of tyrosinase

Solage (combination product of mequinol/retinoid)


  • Less irritating than hydroquinone

Kojic acid


  • Inhibits tyrosinase by binding copper



  • Scavenger of ROS




  • La Roche-Posay Mela-D Pigment Control (combination of kojic acid, LHA, and glycolic acid)




  • Chelation agent produced by fungi



  • Can be combined with glycolic acid to improve penetration and LHA to increase cellular turnover

Soy


  • PAR-2 inhibitor



  • Suppresses melanosome transfer



  • Suppresses ROS




  • Aveeno Active Naturals Positively Radiant



  • Neutrogena Visibly Even Daily Moisturizer




  • Also has surfactant activity

N -acetylglucosamine


  • Inhibits conversion of protyrosinase to tyrosinase




  • Olay Total Effects Tone Correcting Moisturizer (combination product with niacinamide)




  • Monomeric unit of chitin, which makes up the exoskeleton of insects and crustaceans

Licorice extract


  • Inhibits tyrosinase



  • Suppresses ROS




  • Lancôme Bright Expert Dark Spot Corrector



  • The Body Shop Moisture White Shiso Moisture Cream




  • Obtained from the root of Glycyrrhiza glabra

Arbutin


  • Competitive inhibitor of tyrosinase




  • Timeless Skin Care Skin Lightening Cream (combination of arbutin, vitamin C, kojic acid)



  • Skinceuticals Phyto + Botanical Gel for Hyperpigmentation (combination of arbutin, kojic acid)




  • Derivative of HQ found in pears, blueberries, cranberries, and wheat

Vitamin C


  • Inhibits tyrosinase through interaction with copper




  • Garnier Skin Renew Clinical Dark Spot Corrector



  • Shiseido White Lucent Intensive Spot Targeting Serum




  • Rapidly oxidized and unstable; drug delivery is important limiting factor

Niacinamide


  • Inhibits melanosome transfer to keratinocytes




  • L’Oreal Youth Code Dark Spot Serum Corrector



  • Philosophy Miracle Worker Dark Spot Corrector




  • Active derivative of vitamin B3

Emblica


  • Inhibits tyrosinase



  • Suppresses ROS




  • Skinceuticals Pigment Regulator Daily High Potency Brightening Treatment (combination of emblica extract, kojic acid)




  • Derived from Indian gooseberries

Lignin peroxidase


  • Depolymerizes melanin




  • Elure Advanced Lightening Lotion




  • Enzyme derived from tree fungus

Glutathione


  • Inhibits tyrosinase




  • Available as OTC supplement




  • Endogenously produced antioxidant

Ellagic acid


  • Inhibits tyrosinase




  • In combination with salicylic acid




  • Also has antioxidant properties

Tumeric


  • Antioxidant




  • Ole Henriksen Visual Truth Eye Cream




  • Also has wound-healing properties

Mulberry


  • Inhibits tyrosinase




  • Docteur Renaud (Paris)

Aloesin


  • Inhibits tyrosinase




  • Jan Marini Transformation Cream




  • Derived from aloe vera

Green tea


  • Antioxidant




  • MD formulations Moisture Defense Antioxidant Hydrating Gel

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Feb 11, 2018 | Posted by in Dermatology | Comments Off on Practice and Educational Gaps in Abnormal Pigmentation

Full access? Get Clinical Tree

Get Clinical Tree app for offline access