Introduction

• Accounts for 8% of all hematopoietic tumors.
• Cause: proliferation of neoplastic plasma cells in bone marrow.
• Signs: non-specific, hyperviscosity.
• Diagnosis: laboratory results, bone marrow cytology, radiographic lesions.
• Treatment: chemotherapy (melphalan and prednisolone).
• Prognosis: may be controlled with treatment.

Pathogenesis

Etiology

• Unknown.
• Possible causes - genetic predisposition, viral infection (but not FeLV or FIV), chronic immune stimulation, exposure to carcinogens.

Pathophysiology

• Proliferation of neoplastic plasma cells usually → secretion of monoclonal immunoglobulin (paraprotein) → hyperviscosity and other clinical signs.

• Neoplastic plasma cells proliferate in bone marrow.
• In most cases these cells secrete an abnormal immunoglobulin (paraprotein) (usually IgA or IgG heavy or light chain fragments) → excretion of immunglobulin leads to renal tubular damage.
• The paraprotein may be a cryoglobulin.
• Hyperproteinemia or monoclonal gammopathy affects platelet function and may interfere with clotting mechanisms.
• Increased serum viscosity (particularly with IgA secreting myelomas) → circulatory impairment with cardiovascular, respiratory, neurological and ocular signs (hyperviscosity syndrome).
• Some non-secretory myelomas have been reported.
• Antibody coating of red blood cells → hemolysis (Coomb's positive anemia).
• Increased percentage of plasma cells in marrow → anemia, leukopenia and thrombocytopenia.
• Abnormal plasma cells → reduced immune function.
• Hypercalcemia seen in 20% of cases.
• Anemia due to reduced marrow synthesis and increased RBC fragility.

Timecourse

• Insidious onset.

Diagnosis

Treatment

Outcomes