Annales de dermatologie et de venereologie · 1997
[Enoxaparin-induced cutaneous necrosis localized on insulin lipodystrophies].
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Lefebvre I, Delaporte E, Dejobert Y, Catteau B, Piette F, Bergoend H
Аннотация
INTRODUCTION: Low-molecular weight heparin-induced cutaneous necrosis is exceptional. Pathogenesis remains unclear. We report an exceptional case with elective localization of the necrotic areas in insulin lipodystrophic tissue.
CASE REPORT: A 69-year old patient developed areas of skin necrosis after starting enoxaparin therapy. These areas were located far from the points of injection and focalized on skin areas where the patient had been injecting insulin daily for the last four years. These areas had an aspect of insulin lipodystrophy. Biopsy specimens showed leukocytoclastic vasculitis. There were no associated biological anomalies. One month later, prick-tests were made with different low-molecular weight heparins and calcium heparinate in a lipodystrophic area together with an enoxaparin control test in healthy skin. The only positive test was for enoxaparin in an insulin lipodystrophic area (hard erythema at 24 hours). Histology at 72 hours demonstrated leukocytoclastic vasculitis.
DISCUSSION: Six cases of cutaneous necrosis induced by low-molecular weight heparin have been reported, including three cases with enoxaparin. Two pathophysiological mechanisms could be involved: (i) localized heparin-dependent platelet aggregation, or (ii) vasculitis induced by type III hypersensitivity reaction. In our case, the leukocytoclastic aspect of the vasculitis was compatible with an immune complex hypersensitivity reaction. The localization of the necrotic areas would be explained by enoxaparin-induced preferential deposit of immune complexes in the vascular turbulences present in lipodystrophic areas.
CASE REPORT: A 69-year old patient developed areas of skin necrosis after starting enoxaparin therapy. These areas were located far from the points of injection and focalized on skin areas where the patient had been injecting insulin daily for the last four years. These areas had an aspect of insulin lipodystrophy. Biopsy specimens showed leukocytoclastic vasculitis. There were no associated biological anomalies. One month later, prick-tests were made with different low-molecular weight heparins and calcium heparinate in a lipodystrophic area together with an enoxaparin control test in healthy skin. The only positive test was for enoxaparin in an insulin lipodystrophic area (hard erythema at 24 hours). Histology at 72 hours demonstrated leukocytoclastic vasculitis.
DISCUSSION: Six cases of cutaneous necrosis induced by low-molecular weight heparin have been reported, including three cases with enoxaparin. Two pathophysiological mechanisms could be involved: (i) localized heparin-dependent platelet aggregation, or (ii) vasculitis induced by type III hypersensitivity reaction. In our case, the leukocytoclastic aspect of the vasculitis was compatible with an immune complex hypersensitivity reaction. The localization of the necrotic areas would be explained by enoxaparin-induced preferential deposit of immune complexes in the vascular turbulences present in lipodystrophic areas.