Based on our case study, and a review of the literature, we suggest that markedly elevated level of serum globulin in a patient with cerebral infarction requires measurement of blood viscosity, especially in patients with multiple myeloma.. the right anterior cerebral artery territory. On admission, routine blood tests showed a slight decrease in hemoglobin and a marked increase in erythrocyte sedimentation rate. Peripheral blood smear, serum protein electrophoresis, serum visocity, and bone marrow aspiration showed that she had IgG multiple myeloma with hyperviscosity. She was treated by chemotherapy with cyclophosphamide and discharged with the improved clinical condition. strong class=”kwd-title” Keywords: Multiple Myeloma, Immunoglobulin G, Cerebral Infarction, Hyperviscosity INTRODUCTION Multiple myeloma (MM) is usually a human B-cell neoplasm characterized by the clonal expansion of malignant plasma cells in the bone marrow. The cause of this disease is only partially comprehended, but the production of soluble factors by the myeloma cells is likely to be involved. The most important complications are hypercalcemia associated with rapid skeletal dissolution, acute or chronic renal insufficiency, and infection. All these, along with less common complications such as the hyperviscosity syndrome, hyperuricemia, and neurologic involvement, must be recognized and managed Sotrastaurin (AEB071) appropriately to achieve optimal results from primary therapy. The serum hyperviscosity syndrome has been described clinically as the triad of bleeding, visual signs and symptoms, and neurologic manifestations (1, 2). This oncologic emergency occurs in patients with IgM, IgG, and IgA monoclonal gammopathies as well as in some patients with polyclonal immunoglobulin disorders (3). We reported a patient with hyperviscosity-induced cerebral infarction as the first sign of IgG multiple myeloma based on clinical, laboratory, brain MRI, and bone marrow biopsy. CASE REPORT A 68-yr-old right-handed woman was admitted to Chonnam National University Hospital on 6 March, 2002 due to hypesthesia and monoplegia in the left Sotrastaurin (AEB071) Sotrastaurin (AEB071) leg. She also complained of headache and dizziness. Mild anemia had been discovered three months before admission, but was not treated. The patient had no risk factors of stroke except old age. On admission, physical examination revealed an anemic conjunctiva without icteric sclera. She had no lymphadenopathy, and no palpable mass on her abdomen. Vital signs were normal. Dilated fundoscopic examination revealed no abnormalities. There was no abnormality in EKG and echocardiography. Her mental status was alert. Other neurological examinations were normal except monoplegia, hypesthesia, increased deep tendon reflex (3+) with ankle jerks, and up-going Babinski in the left leg. Diffusion- and T2-weighted MRI revealed a hyperintense lesion in the callosomarginal territory of the right anterior cerebral artery, and MR angiography did not show significant stenosis around the intra- and extracranial artery (Fig. 1). Open in a separate window Fig. 1 T2-weighted (A) and diffusion-weighted (B) axial MRI scans show acute cerebral infarction around the callosomarginal territory of right anterior cerebral artery. MR angiography (C) has no stenosis on intracranial arteries. Laboratory data were as follows: hematocrit 26.6% (normal, 37-52), hemoglobin 8.2 g/dL (normal, Mouse monoclonal antibody to PA28 gamma. The 26S proteasome is a multicatalytic proteinase complex with a highly ordered structurecomposed of 2 complexes, a 20S core and a 19S regulator. The 20S core is composed of 4rings of 28 non-identical subunits; 2 rings are composed of 7 alpha subunits and 2 rings arecomposed of 7 beta subunits. The 19S regulator is composed of a base, which contains 6ATPase subunits and 2 non-ATPase subunits, and a lid, which contains up to 10 non-ATPasesubunits. Proteasomes are distributed throughout eukaryotic cells at a high concentration andcleave peptides in an ATP/ubiquitin-dependent process in a non-lysosomal pathway. Anessential function of a modified proteasome, the immunoproteasome, is the processing of class IMHC peptides. The immunoproteasome contains an alternate regulator, referred to as the 11Sregulator or PA28, that replaces the 19S regulator. Three subunits (alpha, beta and gamma) ofthe 11S regulator have been identified. This gene encodes the gamma subunit of the 11Sregulator. Six gamma subunits combine to form a homohexameric ring. Two transcript variantsencoding different isoforms have been identified. [provided by RefSeq, Jul 2008] 12-18), erythrocyte sedimentation rate 127 mm/hr (normal, below 20), leukocyte 4.6103/L (normal, 4.3-10.8) and platelet counts 190103/L (normal, 130-400). A peripheral blood smear showed extensive rouleaux formation. The prothrombin time was 80.8% (13.3/80.8/1.13; sec/%/INR) of that of control; partial thromboplastin time was 27.1 sec (normal, 26.5-41). The plasma level of Protein C and S activity were in the normal range. Serum creatinine was 0.6 mg/dL (normal, 0.6-1.5), serum sodium 137 mEq/L (normal, 135-153), potassium 4.1 mEq/L (normal, 3-5), total calcium 7.1 mg/dL (normal, 8.6-10.6), ionized calcium 2.4 mEq/L (normal, 2.0-2.4), and uric acid 1.5 mg/dL (normal, 2.4-7). The total serum protein concentration was 9.6 g/dL (normal, 6.0-8.0), albumin was 1.8 g/dL (normal, 3.5-5.5), and globulins were 7.8 g/dL. Serum protein electrophoresis (SPEP) revealed hyperproteinemia, hypoalbuminemia and a prominent spike at the gamma-globulin region (Fig. 2). Levels of immuno-globunins were as follows: IgG 6,060 mg/dL (normal, 700-1,600), IgA 23.1 mg/dL (normal, 70-400), IgM 55.4 mg/dL (normal, 40-230), IgE 17.8 mg/dL (normal, 0.0-100) and 2-microglobulin 1.08 mg/L (normal, 0.7-3.4). Her relative serum viscosity at 37 was 5.2 (normal, 1.4 to 1 1.8). Random urine protein was 23 mg/dL (normal, 1.0-14.0), but Bence-Jones protein.