It is, therefore, essential to consider IE when evaluating a patient with cryoglobulinemia. Despite not being commonly observed in this setting, cryoglobulinemic vasculitis LGD-6972 has been documented as the presenting symptom of IE [6-7]. to 90% of cases, cryoglobulinemia has been linked to many other infections, such as the hepatitis B virus and HIV, and autoimmune conditions like Sjogrens syndrome, systemic lupus erythematosus, and rheumatoid arthritis [1]. Since most cases of cryoglobulinemia have an underlying cause, definitive treatment typically attempts to correct the underlying disorder once it is identified. Therefore in patients found to have cryoglobulinemic vasculitis, accurate identification of the cause of the disorder is crucial to developing a treatment plan. We present a case of cryoglobulinemic vasculitis observed with infective endocarditis (IE). Case presentation A 56-year-old male with no prior medical history except for chronic low back pain was admitted to the hospital for a painful rash over his legs, feet, and hands with associated malaise for five weeks. The patient stated his rash became more prominent when he was cold. The patient denied any history of drug use. He denied any fever or arthralgias. A punch biopsy performed by a dermatologist three weeks prior revealed only mild spongiosis with a superficial perivascular lymphocytic infiltrate. The dermatology service was consulted for the rash. His physical examination included a toxic-appearing man breathing room air with subtle palpable purpura and scattered 1-3 mm ulcers mainly on the acral surfaces of his hands and feet but LGD-6972 also bilateral lower legs (Figure ?(Figure1).1). The patient was suspected to have leukocytoclastic vasculitis which was subsequently confirmed by histological examination. His labs were pertinent for methicillin-sensitive Staphylococcus aureus positive blood cultures x2, significantly elevated?immunoglobulin G (IgG) and?immunoglobulin M (IgM) cryoglobulins, and one small vegetation on the aortic valve found on transthoracic echocardiogram. Urinalysis showed trace proteinuria. Erythrocyte sedimentation rate (ESR) was 92 mm/hr, C-reactive protein (CRP) was 44 mg/L, complete blood count (CBC), and liver function tests (LFTs) were unremarkable. Hepatitis panel, HIV, Coccidioidomycoses titers, anti-nuclear antibody, and anti-neutrophil cytoplasmic antibodies were negative, and protein electrophoresis was Rabbit polyclonal to SHP-1.The protein encoded by this gene is a member of the protein tyrosine phosphatase (PTP) family. within normal limits. Creatinine was 1.6 mg/dL, elevated from a baseline of 0.9 mg/dL, and glomerular filtration rate (GFR) was 56 mL/min. Urine output was adequate. Extensive coagulopathy studies found no abnormalities. Venous and arterial Doppler ultrasound studies performed in bilateral lower extremities had no significant findings. Two punch biopsies of separate lesions showed vasculitis in small capillaries (Figure ?(Figure2).2). No septic or thrombotic emboli were appreciated. The patient was diagnosed with cryoglobulinemic vasculitis. He?was LGD-6972 started on intravenous (IV) cefazolin, but the cutaneous lesions persisted for weeks after beginning antibiotic therapy. After coordination with infectious disease and dermatology services, the patient was started on 60 mg of IV methylprednisolone every six hours for four days. The patient reported significant improvement regarding his rash and overall well-being after two days of initiating corticosteroid therapy. He was given a two-week course of prednisone, tapering from 40 mg to 5 mg, topical triamcinolone 0.1% ointment, and was instructed to continue cefazolin for a total course of eight weeks. Open in a separate window Figure 1 Purpuric lesion on the right foot (A) and ulcer on dorsal right second toe (B) Open in a separate window Figure 2 Histological staining with hematoxylin and eosin reveals leukocytoclasia and mild lymphocytic infiltrate of the small capillaries (10x magnification) Discussion Cryoglobulinemia entails LGD-6972 the presence of abnormal antibodies that are water-soluble in warm environments yet precipitate in colder conditions. Immune complexes produced from precipitation cause inflammation that affects the small vessels, most notably in the skin and joints [2]. The most typical symptoms are fatigue, purpura, and arthralgia. Renal and nervous system involvement is also commonly seen, presenting as proteinuria, microscopic hematuria, and mononeuritis multiplex. Diagnosis is made based on clinical, laboratory, and histological evidence, and typically relies on the identification of cryoglobulins in the serum [1]. Type III cryoglobulinemia, involving polyclonal IgG and IgM, results from hepatitis C infection in the majority of cases. However, it can also be caused by autoimmune disorders, lymphoproliferative disease, and.