PracticeUpdate: Dermatology - Winter 2018

EXPERT OPINION 22

Time for a Churchillian Approach to Idiopathic Guttate Hypomelanosis? By Warren R. Heymann MD

Dr. Heymann is Professor of Medicine and Pediatrics and Head of the Division of Dermatology at Cooper Medical School of Rowan University, and Clinical Professor of Dermatology at Perelman School of Medicine at the University of Pennsylvania in Philadelphia, Pennsylvania.

I was only 10 years old when Winston Churchill died; but, even as a child, I was aware of his inspirational abilities. I was reminded of his gift watching Gary Oldman portray the former prime minister in Darkest Hour , which recounted his fierceness in never giving in to the Germans, as the Brits were determining how to return their troops from Dunkirk. Although not in the movie, I recalled his quote: "Success consists of going from failure to failure with- out loss of enthusiasm." I lost my enthusiasm for treating idiopathic guttate hypomelanosis (IGH) long ago. Sir Winston would not have been proud. Perhaps it is time to reconsider some options for treating IGH. The following is a modified abstract from the excellent review of IGH by Juntongijin et al. 1 Idiopathic guttate hypomelanosis is a common acquired leukoderma characterized by multiple, discrete round or oval, porcelain-white macules on sun-exposed areas, especially on the extensor sur- face of forearms and pretibial areas. It usually affects individuals aged over 40 years and the likelihood of acquiring it increases with age. The exact patho- genesis remains controversial. However, there are several factors that are believed to be involved such as aging, ultraviolet exposure, trauma, genetic fac- tors [HLA-DQ3], autoimmunity, and local inhibition of melanogenesis. Despite the benign course of pro- gression, many patients visit medical centers owing to cosmetic concerns and to confirm the natural course of idiopathic guttate hypomelanosis. Because there is no standard therapy for this condition, numerous medical and surgical treatments including intral- esional corticosteroids, topical retinoids, topical calcineurin inhibitors, phenol peeling, cryotherapy, superficial dermabrasion, skin grafting, and ablative and non-ablative lasers have been tested with mixed results.

I have seen patients presenting with well-demarcated hypopigmented papules that may be considered as a hyperkeratotic variant of IGH. 2 Histologically, hyperkeratosis, an atrophic epidermis, flattened rete ridges, decreased melanin content, and reduced numbers of melanocytes have been reported. In a histopathologic study of 27 Korean patients with IGH, hyperkeratosis was frequently found (38%); however, the other “characteristic” findings such as epi- dermal atrophy (10.6%) and flattened rete ridges (14.9%) were relatively rare compared with normal skin. 3 Elec- tron microscopy demonstrates that melanocytes and melanosomes are normal in structure. In some areas, a reduced uptake of melanosomes by the keratino- cytes is observed. The authors contend that, because no significant structural abnormality of melanocytes is observed, IGH is due to a functional defect in the trans- fer of melanosomes frommelanocytes to keratinocytes. In the dermis, fibroblasts appear structurally normal, as do most elastic and collagen fibers, although there are focal elastotic changes. 4 Other features such as col- lagen bundle homogenization and inflammatory cell infiltration are unremarkable. 3 Histologic features of scars are not observed. 1

PRACTICEUPDATE DERMATOLOGY