Insulin-induced lipoatrophy: evidence for an immune pathogenesis.
Skin biopsy samples from 14 diabetic patients with lipoatrophy at injection sites and from five insulin-treated diabetic patients without such lipoatrophy (controls) were examined by immunofluorescence for the deposition of immunological components. Also sera from 13 of the patients with lipoatrophy and from all of the controls were assayed for insulin-binding capacity. Biopsy samples from the edge of lipoatrophic areas (eight cases) invariably showed abnormal deposition of immunological components in dermal vessel walls, whereas no such deposition was seen in the control samples. Mean serum insulin-binding capacity was 33.1 microgram/l in the patients with lipoatrophy compared with only 4.6 microgram/l in the controls. These findings suggest that insulin-induced lipoatrophy results from the local formation of immune complexes, complement fixation, and release of inflammatory mediators from the cellular infiltrate.
D000293:Adolescent; D000328:Adult; D000368:Aged; D003176:Complement C3 / Q000378:metabolism; D003920:Diabetes Mellitus / Q000188:drug therapy; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism; D007075:Immunoglobulin M / Q000378:metabolism; D007328:Insulin / Q000009:adverse effects* / Q000627:therapeutic use; D008060:Lipodystrophy / Q000139:chemically induced* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012867:Skin / Q000276:immunology
D003176:Complement C3; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007328:Insulin