Lymphocyte infiltration of the upper and middermis that can extend into the epidermis characterizes the erythematous plaque (Bircher et al., 1990). Dermal and epidermal edema (spongiosis) is observed in lesions that appear eczematous. The T lymphocytes of helper-suppressor (CD4+) phenotype predominate, together with

FIGURE 14 (See color insert) Heparin-induced skin lesions. (A) Heparin-induced erythematous plaques: UFH injections into the lower abdomen resulted in painful erythematous plaques beginning on day 7 of sc UFH treatment; at this time, the platelet count fell only by 9% from 340 to 311 x 109/L. HIT antibody seroconversion from a negative baseline was shown using the serotonin release assay (from 0% to 84% serotonin release). (B) Heparin-induced skin necrosis: UFH injections into the right anterior thigh led to skin necrosis: a large black eschar with irregular borders is surrounded by a narrow band of erythema. The platelet count fell to 32 x 109/L; despite stopping heparin, the patient developed symptomatic proximal deep vein thrombosis 10 days later. Abbreviations: HIT, heparin-induced thrombocytopenia; UFH, unfractionated heparin. Source: (B) From Warkentin 1996a.

CD1+/DR+ dendritic (Langerhans) cells, are consistent with a type IV delayed hypersensitivity immune response. Cytokine synthesis by activated CD4 cells could explain the peripheral blood eosinophilia that has been reported in a few patients (Bircher et al., 1994). In contrast, histopathology of lesions associated with cutaneous necrosis usually shows intravascular thrombosis of dermal vessels, with or without perivascular inflammation and red cell extravasation of variable degree (Hall et al., 1980; Kearsley et al., 1982; Cohen et al., 1988; MacLean et al., 1990; Balestra et al., 1994).

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