Hyperglobulinemia
The most common cause of hyperglobulinemia with normal hydration status (i.e., without hemoconcentration) is inflammation resulting in increased production of numerous globulins, including many acute phase proteins (see the Acute Phase Response section later).
Chronic inflammation frequently results in a nonspecific increase in γ-globulins (polyclonal gammopathy) due to production of different immunoglobulins by plasma cells in response to chronic antigenic stimulation. A broad-based peak will be seen on SPE in the γ region and can extend into the β region due to production of IgM and/or acute phase β-globulins. An increase in both β- and γ-globulin fractions (β-bridging) can occur with intense antigenic stimulation, chronic active hepatitis, or lymphoma. Increased IgG in the γ-globulin fraction is termed hypergammaglobulinemia and can be seen in a range of chronic inflammatory diseases, including internal abscessation, chronic hepatitis, immune-mediated diseases (e.g., immune-mediated hemolytic anemia or thrombocytopenia), and lymphoma. Infection with the agent of epizootic bovine abortion triggered significant increases in IgG in clinically affected heifers.17Increased production of a single immunoglobulin by a clonal population of B lymphocytes/plasma cells is known as a monoclonal gammopathy. On SPE, the monoclonal peak is as narrow-based and sharp as the albumin peak due to the identical migration of the monoclonal immunoglobulins (also known as paraproteins). Monoclonal gammopathies are usually secondary to neoplasia of B lymphocytes or plasma cells, including B-cell lymphoma, multiple myeloma, and B-cell lymphocytic leukemia. Increased susceptibility to hemorrhage can occur with monoclonal gammopathy due to impaired platelet function caused by immunoglobulin coating and can be exacerbated by hyperviscosity syndrome.