Case Presentation: A 66-year-old man presented with several days of fevers, arthralgias, fatigue, and a progressive non-blanching purpuric rash of the face, abdomen, and extremities. One month earlier, biopsy had shown IgM and C3-positive leukocytoclastic vasculitis (LCV), and a course of prednisone had not improved his symptoms. Infectious and autoimmune evaluations, including lumbar puncture, were unrevealing. CBC demonstrated a normocytic anemia, and inflammatory markers (ESR and CRP) were elevated.CT imaging revealed a destructive right iliac lesion. Biopsy demonstrated 5–10% κ-restricted plasma cells, and serum studies showed monoclonal IgG κ with M-spike 0.4 g/dL, κ/λ ratio 5.32, and monoclonal urine protein. Cryoglobulin testing detected monoclonal IgG κ type I cryoglobulinemia. Additional imaging revealed scattered small lytic lesions.He was diagnosed with IgG κ multiple myeloma presenting with paraneoplastic type I cryoglobulinemia–associated LCV. He began chemotherapy with interval improvement in myeloma markers and near resolution of his rash.
Discussion: LCV is a common small-vessel vasculitis with a broad differential including infection, autoimmune disease, medications, and malignancy.¹ Most cases are self-limited or respond to supportive care. However, systemic features such as anemia, inflammation, or constitutional symptoms should prompt evaluation for less common etiologies, including plasma cell dyscrasias.Type I cryoglobulinemia is caused by monoclonal immunoglobulins that precipitate at low temperatures, leading to vascular occlusion, ischemia, or vasculitis.² It is most often linked to MGUS or Waldenström macroglobulinemia but can occur with other plasma cell dyscrasias. Although it also occurs in multiple myeloma, its presentation primarily as LCV is rare.³ In this patient, the combination of constitutional symptoms, destructive bone lesion, monoclonal IgG κ paraprotein, and cryoglobulin positivity established the diagnosis of myeloma-associated type I cryoglobulinemic vasculitis.This case highlights a key teaching point: a common presentation may be the first indication of a rare and serious underlying malignancy. Recognizing when LCV deviates from its usual benign course, and integrating systemic symptoms, paraprotein studies, and imaging, can facilitate early identification of plasma cell disorders and therefore better treatment outcomes.
Conclusions: Atypical or persistent LCV should raise suspicion for malignant causes. This case demonstrates multiple myeloma presenting initially as LCV through type I cryoglobulinemia and emphasizes the importance of maintaining diagnostic breadth when common conditions follow an unexpected trajectory.