| Gammopathies are conditions in which serum immunoglobulin levels are greatly increased. Using electrophonetic patterns, they can be classified either as polyclonal (increases in all major immunoglobulin classes) or monoclonal (increases in a single homogeneous immunoglobulin). |
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Polyclonal gammopathies in animals are seen in chronic pyodermas; chronic viral, bacterial, or fungal infections; granulomatous diseases; abscessation; chronic parasitic infections; chronic rickettsial diseases, such as tropical canine pancytopenia; chronic immunologic diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and myositis; or with neoplasia. They also may be idiopathic. In some animals, the gammopathy may appear initially to be monoclonal
because of a predominance of 1 immunoglobulin class (usually IgG). Examples of this phenomenon have been seen in cats with noneffusive feline infectious peritonitis and in dogs with chronic tropical canine pancytopenia. |
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Monoclonal gammopathies are characterized by the presence of a homogeneous serum immunoglobulin protein. Uninvolved immunoglobulin classes are usually depressed. Monoclonal gammopathies are either benign (ie, associated with no underlying disease), or potentially associated with immunoglobulin-secreting tumors. In humans, benign gammopathies may become malignant at a later date; in other animals, they are rare and are not associated with a demonstrable tumor or clinical illness. |
| Tumors that secrete monoclonal antibodies originate either from plasma cells (myeloma) or lymphoblasts (lymphosarcoma). Plasma-cell myelomas can secrete intact proteins of any immunoglobulin class or immunoglobulin subunits (light chains or heavy chains). Myeloma proteins in dogs are commonly IgG or IgA types and less commonly IgM. Myelomas of the IgA type are particularly common in Doberman Pinschers. Monoclonal immunoglobulin produced by lymphosarcoma are often of the IgM class,
regardless of species. Myeloma proteins in cats and horses usually are IgG and, uncommonly, IgM, IgG (T) (horses), or IgA. |
| Clinical signs depend on the location and severity of the primary neoplasm and on the amount and type of immunoglobulin secreted. Plasma-cell myelomas frequently develop in marrow cavities of flat bones of the skull, ribs, and pelvis, and in the vertebrae. Pathologic fractures of diseased bone can lead to CNS or spinal disorders or to pain and lameness. Lymphosarcomas frequently involve parenchymatous organs; therefore, clinical signs are more diverse. |
| Clinically evident illness can result from the presence of the monoclonal protein itself. Amyloidosis (
Amyloidosis: Introduction) can be due to increased immunoglobulin catabolism. Hyperviscosity syndrome appears in 20% of dogs with monoclonal gammopathy, especially with IgM or IgA monoclonal proteins, and can occur if the protein levels in blood are high. In this syndrome, plasma viscosity can be many times normal, which leads to profound vascular disturbances, thrombosis,
and bleeding diathesis. Depression, blindness, and neurologic manifestations can be due to hemorrhage in the nervous system and retina. Some IgM monoclonal proteins act as cryoglobulins and aggregate in vitro and in vivo when the plasma is cooled. Animals with cryoglobulinemia often develop gangrenous sloughs of the ear tips, eyelids, digits, and tip of the tail, especially during cold weather. (See also
cold hemolytic disease under autoimmune hemolytic anemia and thrombocytoeenia,
Autoimmune Hemolytic Anemia and Thrombocytopenia.) Myelomas that produce autoantibodies to various tissues have been identified in humans, but not in other animals. Finally, animals with monoclonal gammopathies may have greatly depressed levels of normal immunoglobulins and, therefore, may develop serious secondary infections. |
| Immunoglobulin-secreting tumors usually are treated with glucocorticoids and alkylating drugs. The prognosis for remission after therapy is much better in dogs than cats. Even in dogs, however, the longterm prognosis is poor and relapse is common after 6-12 mo. Plasmapheresis may be needed to lower serum viscosity in animals with clinical signs of hyperviscosity syndrome. Antibiotics and globulin injections may help prevent secondary infections. |
