Leukocytoclastic vasculitis secondary to erysipelas: An unusual case of noncryoglobulinemic vasculitis in a hepatitis C patient

摘要

Leukocytoclastic vasculitis (LCV) is a type of small vessel vasculitis caused by immune complex deposition, characterized clinically by palpable purpura and pathologically by polymorphonuclear leukocyte infiltrate, nuclear dust, and fi-brinoid change in the small dermal vessels. Drugs, infections, and collagen vascular diseases account for the majority of cases. Extensive literature review suggests that although LCV is a known complication of streptococcal infection of the throat, LCV secondary to erysipelas is exceedingly rare and has been reported only once previously. We describe a 42-year-old, hepatitis C-positive man who developed LCV following erysipelas of the face. CASE A 42-year-old Hispanic man with history of hepatitis C and intravenous drug abuse was admitted to the Medicine Unit of the Montefiore Medical Center for evaluation of high fever (101°F), cough, sore throat, facial swelling, erythema, and tenderness for 1 week. Physical examination revealed a sharply demarcated erythematous patch on the central face with indurated advancing borders (Fig. 1), cervical lymphadenopathy, and splenomegaly. Petechial rash developed on bilateral lower extremities 1 day before admission and rapidly progressed to palpable purpuric lesions on day 2 of hospitalization (Fig. 2). Complete blood cell count showed mild leukocytosis (white blood cell count, 15,800/muL) with a left shift, and the chemical panel was within normal limits. Other relevant laboratory values included erythrocyte sedimentation rate 50 mm/h, antistreptolysin antibody titer 3410 IU/L, positive streptozyme, positive anti-hepatitis C virus (HCV) antibody, HCV viral load 1,932,918 IU/mL, HCV genotype-type 1, absence of monoclonal protein, negative antineutrophil antibody and antineu-trophil cytoplasmic antibody, low complement levels (C3 was 48 mg/dL, C4 was 2 mg/dL), normal rheumatoid factor (RF) levels (20 IU/mL), and negative cryoglobulins. The patient was treated with intravenous cefazolin, which yielded improvement in his general condition, leukocytosis, and simultaneous involution of the facial erysipelas and purpuric lesions.