Vitiligo delimiting dermatophyte infection.

Sir,

Dermatophyte infection, a common superficial fungal disease is precipitated by many factors such as advanced age, collagen vascular disease, systemic corticosteroid therapy or Cushing's disease, hematologic malignancy, chronic mucocutaneous candidiasis, diabetes mellitus, atopy, underlying peripheral vascular disease, and disorders of keratinization. In these patients the infection is often less symptomatic or even asymptomatic. The local defence against the infection may involve factors like the epidermal Langerhans cells, antifungal property of sebum, role of T lymphocytes, and synthesis of metalloproteases associated with infection. Chronic dermatophyte infection was found to be associated with poor T-lymphocyte-mediated response to specific fungal antigens, suggesting that depression of responses is responsible for the poor clinical response. Langerhans cells can act as antigen-presenting cells for dermatophyte antigens.

Vitiligo is documented to be associated with many autoimmune diseases. There is enough evidence that epidermal dendritic cells (Langerhans cells and intermediate cells) are absent in patients with vitiligo. The epidermal cells derived from vitiliginous skin, show a lower stimulatory effect in the allogeneic mixed skin cell lymphocyte culture reaction than those from normal skin suggesting a possibility of functional impairment of Langerhans cells in vitiliginous skin.[1] It has been suggested that defective keratinocyte metabolism and biosynthesis of tetrahydrobiopterin and catecholamine have been put forward in the pathogenesis of vitiligo.

We report a female in whom tinea corporis was limited to the patch of vitiligo. A 70-year-old hypothyroid, diabetic woman presented with huge patch of vitiligo over the trunk which showed erythematous scaly plaque that was strictly limited to the depigmented patch. There was no sign of scaling over the pigmented skin [Figures 1 and 2]. Scraping for fungus was positive over the depigmented skin. All the three consecutive specimens from the pigmented, normal-appearing skin close to the scaly margin and culture on Sabouraud dextrose phosphate (SDP) agar were negative. She responded well to clotrimazole cream and griseofulvin.

Figure 1

Patch of tinea corporis with scaling and peripheral extension towards the depigmented, vitiliginous patch sparing the pigmented skin over the abdomen and chest

Figure 2

Same patient showing tinea corporis delimited by vitiligo over the back

Psoriasis and lichen planus[2] have been reported to occur over vitiligo patch. Absence of melanin may play a role in inflammatory reactions following sun exposure according to Baghestani et al., who have reported familial colocalization of lichen planus and vitiligo on sun-exposed areas where lichen planus began from depigmented areas and then extended to normal skin.[3] The altered expression of antigens identified by infiltrating T-cells due to photo damage over a vitiliginous patch, has been suggested as a factor in colocalization of lichen planus and vitiligo.[4] Chhabra et al., have described pleomorphic cutaneous sarcoidosis confined to lesions of vitiligo vulgaris.[5]

The occurrence of dermatophyte infection limiting to the vitiliginous patch may be due to the local immune defect either directly to reduced or absent melanocyte or indirectly to the reduced number of Langerhans cells in a vitiligo patch. The role of altered T-cells in delimiting the extent of dermatophyte infection within the vitiliginous patch cannot be ruled out. To the best of the authors’ knowledge, vitiligo delimiting dermatophyte infection has so far not been reported.