Introduction

Cryoglobulins are immunoglobulins that reversibly precipitate at temperatures below 37°C and redissolve on rewarming [1]. According to the Brouet classification, type I consists of a single monoclonal immunoglobulin and is linked to lymphoproliferative disorders, whereas types II and III constitute mixed cryoglobulinemia: type II combines a monoclonal IgM with rheumatoid factor activity and polyclonal IgG, and type III contains only polyclonal immunoglobulins [1]. Mixed cryoglobulins can deposit in small vessels and trigger an immune complex-mediated vasculitis affecting skin, joints, peripheral nerves, and kidneys [2,3]. Chronic HCV infection is identified in the large majority of patients with mixed cryoglobulinemia and is regarded as the principal etiologic driver [3,4]. Almost a quarter of patients with mixed cryoglobulinemia have nephropathy at the time of their diagnosis, and renal involvement follows the diagnosis of cryoglobulinemia after a mean of 2.6-4 years [5,6]. Late diagnosis can allow for the progression of complications such as membranoproliferative glomerulonephritis and renal failure [6].

Cutaneous involvement is the most common feature, and the prototypical lesion is palpable purpura over the dependent lower extremities; weakness and arthralgia complete the classic clinical triad [2]. Because the eruption is erythematous, sometimes warm, and may be accompanied by edema, it is frequently misinterpreted as cellulitis, particularly when unilateral, leading to repeated antibiotic courses and diagnostic delay [7]. We present a patient whose recurrent lower-limb purpura was managed as cellulitis for over a year before serologic testing revealed HCV-associated type III mixed cryoglobulinemic vasculitis, and we discuss the diagnostic approach, key mimics including levamisole-adulterated cocaine vasculopathy, and the clinical course following HCV-directed therapy.