Biomedical subjects
Publications and source records attributed to L T Nesbitt.
We observed 11 cases of fixed drug eruption to tetracyclines. Two cases were in a mother and her adult son, and two patients experienced fading of their lesions while continuing to take 1 g of the drug per day. Several patients were cross-reactive to different salts.
In a 12-year-old boy with clinical and histologic features of Mikulicz disease, systemic lupus erythematosus (SLE) developed two years later. Atrophic plaques and nodules in the skin along with substantial increase in salivary gland enlargement characterized the onset of SLE. There was lack of renal and joint manifestations, and no evidence of keratoconjunctivitis sicca or xerostomia was seen. Histopathologic changes in the skin lesions included mucinous infiltrates, chronic vasculitis, and dermal-epidermal junction findings typical of SLE. Direct immunofluorescene studies of skin lesions and normal-appearing skin showed granular deposition of immunoglobulins and complement at the dermal-epidermal junction zone. Level of anti-DNA antibodies was noticeably elevated, and the serum C3 value was depressed. The patient's response to systemic corticosteroid therapy was dramatic.
Seventy-one children with the diagnosis of systemic lupus erythematosus (SLE) (39 cases), dermatomyositis (25 cases), or scleroderma (7 cases) were studied retrospectively. The children with SLE were much sicker than those with the other two diseases and were found to have a poorer prognosis than adults with SLE. In general, the earlier the age of onset, the poorer the prognosis. Early gastrointestinal bleeding, abnormal renal findings, and cardiac abnormalities heralded early death from SLE. The peak incidence of SLE near the time of puberty suggests hormonal influence on this disorder in children. Survival rates and morbidity improved as the treatment improved. Corticosteroids were the main therapeutic agents. The patients with scleroderma also received varying doses of vitamin E, penicillamine, chloroquine hydrochloride, and salicylates. The antimetabolites were used to treat SLE starting in the late 1960s.
Eleven patients with a skin disorder in which clinical, histopathologic, and immunofluorescent findings showed overlap features of both lupus erythematosus (LE) and lichen planus (LP) were observed for several years. Clinical lesions were extremely long-term and consisted primarily of livid red to violaceous atrophic patches and plaques, most common on acral aspects of the extremities. Nails were also commonly involved, often showing anonychia. Histologic changes combined cell-rich and cell-poor lichenoid patterns in the papillary dermis, suggesting both LP and LE. The major immunofluorescent finding in all patients was the presence of ovoid bodies at the dermal-epidermal (D-E) junction and in the upper dermis. Most patients showed both a linear arrangement and a clustering pattern of these bodies. Four patients also had coexistant but poorly developed linear deposits of immunoglobulins and complement at the D-E junction.
Three siblings displayed an unusual form of keratoderma characterized by diffuse and striate hyperkeratosis of the palms and soles, hyperkeratotic plaques over the dorsum of the hands and toes, and linear hyperkeratotic lesions over the Achilles tendon area, ankles, elbows, and knees. The predominant location of these lesions led to the term acral keratoderma for this disorder. Histologically, besides thickening of all epidermal layers with that of the stratum corneum being most notable, various dyskeratotic changes were evident in the epidermis. Pedigree analysis of the family suggested an autosomal recessive inheritance pattern. There were similarities and differences between the type of keratoderma displayed by these three patients and that of patients described previously with the disorder known as keratoma hereditarium mutilans.