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Methotrexate treatment in cutaneous lupus erythematosus: subcutaneous application is as effective as intravenous administration

uloma formation and amastigotes. PCR identified these as L. donovani. Numerous milia were identified in the margin of the lesion prior to treatment with intralesional sodium stibogluconate. Milia are subepidermal keratin cysts and most commonly occur on the face. They can arise spontaneously or may occur following trauma including burns, radiotherapy and dermabrasion. Inflammatory dermatoses such as epidermolysis bullosa acquisita, porphyria cutanea tarda, bullous pemphigoid and bullous lichen planus can all result in milia formation. Prolonged use of topical corticosteroids leading to skin atrophy has been reported to cause milia and the nonsteroidal anti-inflammatory drug benoxaprofen causes milia formation. Primary milia are thought to derive from vellus hairs at the inferior portion of the infundibulum whereas secondary ones, as in our patients, are derived from eccrine sweat ducts, abnormal epidermis or hair follicles. Cutaneous leishmaniasis is caused by protozoal infection with one of the Leishmania species following the bite of a female sand fly. The Leishmania causes a granulomatous tissue response. There follows the development, usually at the site of the bite, of a papule or nodule which ulcerates after 1–3 months; however, this process may take considerably longer. Lesions self heal with scarring but this can take many months depending on the species involved. Treatment is advocated to accelerate resolution and to try to minimize scarring particularly in cosmetically sensitive sites. Infection with some species may lead to dissemination and mucosal disease. Milia have not previously been reported as sequelae of cutaneous leishmaniasis. Interestingly, milia have been reported following the resolution of type 1 reactions complicating borderline tuberculoid and mid-borderline leprosy. Mycobacterium leprae, like Leishmania species, causes granulomatous inflammation but in the two cases described there was no report of ulceration. Milia have not been reported following the use of sodium stibogluconate or allopurinol. We feel that the milia in these children formed as a consequence of the disruption of the epidermis and dermoepidermal junction due to the granulomatous inflammation and consequent ulceration caused by infection with Leishmania species. Milia are easily treated and should if necessary be dealt with to try to minimize the cosmetic and psychological impact of an already potentially disfiguring condition.