Dear Editor:
Seborrheic melanosis (SM) is an interesting clinical entity, primarily of cosmetic concern, that afflicts dark skin with seborrhea. It presents in ethnic (African, Asian, Hispanic) skin and has gained recent attention in the literature coming from the Indian subcontinent.1 Its distinct distribution pattern, morphological features and associated clinical findings help distinguish it from its close differentials. It is important to recognize this distinct clinical entity since certain management considerations differ from other forms of facial melanosis.
A 25-year-old man presented with asymptomatic brownish-to-grayish hyperpigmented thin plaques over the centrofacial areas (alar creases, sides of nose, labio-mental crease and to a lesser extent transverse nasal crease and angles of mouth). The lesions appeared greasy and velvety with faint perilesional erythema. The surrounding skin had an oily texture and the nose was bulbous (Figures 1 and 2). The condition was present for two years with history of winter exacerbation. There was no involvement of the forehead, beard, retroauricular area or trunk.
FIGURE 1.
Brownish to grayish hyperpigmented thin plaques with greasy texture involving the nasal alar crease, sides of nose and transverse nasal crease.
FIGURE 2.
Brownish hyperpigmentation involving the alar creases, labio-mental crease and to a lesser extent angles of mouth.
He did not recall any history of preceding flakiness or redness at these sites. He gave a history of “dandruff” though not apparent at the time of examination. There was no history of atopy, rubbing or spectacle usage. Biopsy was deferred in view of poor cosmetic outcome. A diagnosis of SM was made based on the classic clinical presentation. He was treated with 2% ketoconazole cream once a day, tacrolimus 0.1% ointment at night, a bland emollient and sun-protection.
SM is an interesting morphological entity characterized by localized darkening in the seborrheic areas with variable erythema. Fitzpatrick Skin Type IV and above are affected.1 Pruritus may be mild or absent. Given its characteristic seborrheic distribution, greasy texture and winter exacerbation, an association with seborrheic dermatitis (SD) cannot be overlooked. In fact, some hypothesize it to be a form of post-inflammatory hyperpigmentation (PIH) to SD in individuals with darker skin tones. Hence a history of preceding erythema or scaling (“flakiness”) in the involved sites should be sought, though mild erythema may be imperceptible in darker skin.1 Evidence of seborrhea such as oily skin texture, greasy appearance of lesions, dyssebacia (follicular plugs with inspissated sebum), pityriasis capitis, etc. are supportive findings. In addition to the characteristic seborrheic distribution of lesions, these should incline the clinician towards making a diagnosis of SM.2 These characteristics also help distinguish SM from “frictional melanosis” which occurs over bony prominences, does not obey classic seborrheic pattern/morphology and has a history of repeated rubbing.3
It is interesting to note, however, that there are certain pointers against simply equating SM to a post-inflammatory sequala of SD.4 A history of frank SD may not be present; a relatively bulbous nose (as in this patient [Figure 1]) accentuates the alar and transverse nasal grooves allowing increased sebum accumulation in these areas without actual increase in sebum production.1,5 SM may often be completely asymptomatic.1 The labio-mental crease and angles of mouth are not typical sites for SD (but may be involved in perioral dermatitis, angular cheilitis etc.) and conversely, some classical sites of facial SD such as the eyelids, medial eyebrows are yet to be described for SM.1,4 Some authors speculate it to be a result of PIH due to multiple causes that have overlapping sites with SD.4
It is important for the dermatologist to recognize and identify SM as it is resistant to conventional lightening agents.3 Instead, topical anti-inflammatory/fungistatic agents effective in SD (topical calcineurin inhibitors, mild topical steroids and 2% ketoconazole cream) should be considered first, to allow any inflammatory component to subside. Topical lightening agents (e.g., kojic acid, azelaic acid, arbutin etc.) may be subsequently added at a later stage. It must be understood from a pathophysiological standpoint that while frictional melanosis, photo-melanosis and Riehl’s melanosis are different entities, triggers like sunlight/rubbing/cosmetics may work as additional components that contribute to/intensify the pigmentation of SM. Hence the holistic management of SM includes avoidance of these additional aggravating factors.1 The patient must be counseled regarding the slow treatment response, chronicity and innocuous nature of the condition.1,2
This is an attempt towards better describing SM which has till now been a rather ill-defined entity, especially since its histopathology is non-diagnostic and dermoscopy findings not well-established (the alar grooves and labiomental crease display variable degree of pigmentary, vascular and "seborrheic" dermoscopic changes even in normal individuals).2,4 Understanding the various considerations may help avoid a facial biopsy which may have cosmetic implications in dark-toned individuals. Though prima-facie facial melanoses of varied etiologies have considerable overlap in their clinical presentation, a suggestive distribution pattern and subtle morphological features guide the dermatologist towards a more specific diagnosis and help form a treatment strategy. While SM in ethnic skin has received special interest in the recent years, further studies may help to elucidate it further.
REFERENCES
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