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Lipodermatosclerosis: a clinicopathologic study of 17 cases and differential diagnosis from erythema nodosum.
Journal of Cutaneous Pathology 2009 April
BACKGROUND: The clinical manifestations of lipodermatosclerosis (LDS) may mimic cellulitis and various panniculitides.
METHODS: To better characterize the histopathologic changes of LDS, we reviewed the clinicopathologic findings of 26 cases with a pathologic diagnosis consistent with LDS. A final diagnosis of LDS was made in 17 cases based on the clinicopathological correlation. As some cases manifested erythema nodosum (EN)-like lesions, 14 specimens of EN were reviewed to identify features for differential diagnosis.
RESULTS: Microscopically, the acute LDS lesions were characterized by patchy hemorrhage, ischemic fat necrosis with lipophages or hyalinization in the fat lobules. As the disease progressed to the subacute and chronic stages, lipomembranous or membranocystic fat necrosis, septal fibrosis and background venous stasis in the dermis became more pronounced. In contrast, EN typically displayed minimal venous stasis and membranocystic fat necrosis.
CONCLUSIONS: LDS may manifest as EN-like lesions. Therefore LDS should be included in the differential diagnosis of EN. Clinicopathologic correlation is essential for diagnosis. Differentiating the acute LDS from the early EN is more difficult. A constellation of the findings of septal/lobular panniculitis, hemorrhage in the subcutaneous tissue, and lipophages and/or ischemic fat necrosis in the fat lobules favors the diagnosis of acute LDS.
METHODS: To better characterize the histopathologic changes of LDS, we reviewed the clinicopathologic findings of 26 cases with a pathologic diagnosis consistent with LDS. A final diagnosis of LDS was made in 17 cases based on the clinicopathological correlation. As some cases manifested erythema nodosum (EN)-like lesions, 14 specimens of EN were reviewed to identify features for differential diagnosis.
RESULTS: Microscopically, the acute LDS lesions were characterized by patchy hemorrhage, ischemic fat necrosis with lipophages or hyalinization in the fat lobules. As the disease progressed to the subacute and chronic stages, lipomembranous or membranocystic fat necrosis, septal fibrosis and background venous stasis in the dermis became more pronounced. In contrast, EN typically displayed minimal venous stasis and membranocystic fat necrosis.
CONCLUSIONS: LDS may manifest as EN-like lesions. Therefore LDS should be included in the differential diagnosis of EN. Clinicopathologic correlation is essential for diagnosis. Differentiating the acute LDS from the early EN is more difficult. A constellation of the findings of septal/lobular panniculitis, hemorrhage in the subcutaneous tissue, and lipophages and/or ischemic fat necrosis in the fat lobules favors the diagnosis of acute LDS.
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