Occupational contact dermatitis from methyl-ter-pyridine in a chemistry laboratory technician.
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Biomedical subjects
Publications and source records attributed to P Caussade.
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BACKGROUND: Electron microscopy examination of scalp biopsies from a patient with chloroquine achromotrichia gave elements concerning the pathogenesis of chloroquine-induced achromotrichia. CASE REPORT: A 21-year old light brown-haired patient developed achromotrichia after four months of treatment with chloroquine for subacute lupus erythematosus. Hair bleaching completely regressed 5 months after discontinuing chloroquine despite replacement with hydroxychloroquine. During the achromatrichia phase, many ultrastructural anomalies were observed in the hair root melanocytes: the nuclei were small and densified, and there was an accumulation of immature melanosomes in the cytoplasm; these melanosomes, mainly in stage II, were rarely transferred to keratinocytes. After recovery from the achromotrichia, melanocytes displayed a normal aspect. DISCUSSION: Pathophysiological disturbances leading to chloroquine induced achromotrichia are still unclear. The ultrastructural study of hair follicles in our patient show that under chloroquine action melanocytes become unable to perform complete melanin synthesis and to produce normally melanized melanosomes which may be transferred to keratinocytes. Non-melanized or poorly melanized melanosomes accumulate in the melanocytes which finally become inactive cells. These findings suggest that achromotrichia is induced by a toxic effect of chloroquine on the melanocyte.
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Natural killer activity of peripheral blood mononuclear cells against the human cell line K 562 was evaluated in 11 patients with mycosis fungoides and simultaneously in 10 age- and sex-matched controls. In the patient group, nine had no previous treatment and in two topical therapy had been discontinued more than 3 months before. None had any associated disease or concurrent therapy that could interfere with the immune system. Patients with early disease showed a mean specific lysis and a range of individual data similar to the controls whereas patients with advanced disease had a significant defect of natural killer activity at effector: target ratios of 100 : 1, 50 : 1, and 25 : 1, as shown by the Mann-Whitney test. Preincubation of effector cells with alpha-interferon for 1 h in a single patient with low natural killing capacity led to a clear increase of the specific lysis, suggesting reduced functional activity rather than depletion of effector cells.
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