Canine Multiple Myeloma

Canine multiple myeloma is a malignant plasma cell neoplasm affecting primarily middle-aged to older dogs, characterized by monoclonal gammopathy, osteolytic bone lesions, and Bence-Jones proteinuria. Neoplastic plasma cells proliferate in the bone marrow and secrete excessive immunoglobulins, often leading to hypercalcemia, renal impairment, and hyperviscosity syndrome.

Clinical signs include lethargy, bone pain, PU/PD, and bleeding or neurologic deficits. Diagnosis requires identification of a monoclonal spike on electrophoresis, plasmacytosis, and radiographic bone lysis. Treatment involves melphalan with corticosteroids, supportive care, and bisphosphonates. Remission is common, but long-term control depends on systemic involvement and therapeutic response.

🧬Canine Multiple Myeloma (Plasma Cell Myeloma)

Signalment / Predisposition

Accounts for < 8–10 % of canine hematopoietic malignancies. Predominantly affects older dogs, mean age ~8–9 years; no strong sex predilection.
Certain breeds like Labrador Retrievers, Golden Retrievers, and German Shepherds may be overrepresented.
Etiology is largely idiopathic; chronic immune stimulation and rare genetic predispositions have been suggested.

Pathophysiology

Neoplastic transformation of terminally differentiated B lymphocytes (plasma cells), leading to clonal proliferation in bone marrow and production of monoclonal immunoglobulins (M-protein).
Monoclonal proteins commonly IgG or IgA (less often IgM); may cause hyperviscosity, immunodeficiency, amyloidosis, or cryoglobulinemia.
Myeloma cells induce osteolytic lesions in flat bones and vertebrae → bone pain, pathologic fractures, hypercalcemia (via bone resorption).

Clinical Presentation & Physical Exam

Nonspecific signs: lethargy, anorexia, weight loss, intermittent lameness or pain, possible spinal pain.
Signs due to hyperviscosity syndrome: bleeding diatheses, neurologic deficits (e.g., visual changes, retinopathy).
Hypercalcemia consequences: PU/PD, vomiting, constipation, depression, weakness, seizures.
Possible organomegaly (splenomegaly), recurrent infections, bleeding tendency.

Laboratory Findings

Hy-perproteinemia with monoclonal ("M") spike on serum and/or urine protein electrophoresis (Bence-Jones proteins).
Bone marrow plasmacytosis > 20 % plasma cells supports diagnosis.
Frequent anemia, renal insufficiency, hypercalcemia.
Rarely, total calcium elevated with normal ionized calcium—due to protein-bound calcium from M-protein in absence of lytic lesions.

Diagnostic Imaging / Tests

Skeletal radiographs or CT: osteolytic lesions (“punched-out”) in vertebrae, pelvis, skull, ribs, long bones.
Bone marrow aspirate: confirms plasmacytic infiltration; cytology with eccentric nuclei and perinuclear clear zone; cell block + IHC (e.g., MUM1, CD20) helpful in atypical cases.
Protein electrophoresis (serum and urine) to detect monoclonal gammopathy; urinalysis for Bence‑Jones proteins.

Treatment

Chemotherapy backbone: melphalan plus corticosteroid (prednisone/prednisolone).
Alternatives or relapses: chlorambucil, cyclophosphamide, doxorubicin ± vincristine.
Radiation therapy may be used palliatively for focal bone pain or lesions.
Supportive: IV fluids, bisphosphonates (e.g., pamidronate) for hypercalcemia and bone pain; manage renal and electrolyte derangements.
In human medicine: advanced therapies include proteasome inhibitors, immunomodulators, monoclonal antibodies, and stem cell transplant—but their role in dogs is investigational.

Prognosis

Generally good initial response: 80–95 % dogs respond to chemotherapy within 3–6 weeks.
Median survival often ≈ 18 months, with remission common but relapse expected.
Complications (renal failure, infection, fractures, pain) are major determinants of survival and euthanasia.

NAVLE Relevance

NAVLE focuses on recognition of multiple myeloma as a differential for PU/PD, hypercalcemia, bone pain, protein spike, and understanding the role of bone marrow and imaging diagnostics.
Key diagnostic triad: monoclonal gammopathy (serum/urine), bone marrow plasma cell infiltration, lytic bone lesions.

Summary:

Feature	Key Points
Signalment	Older dogs (~8–9 yrs), certain breeds (Labrador, Golden, GSD)
Presentation	Lethargy, bone pain, PU/PD, neurological signs, infections
Lab Findings	Monoclonal gammopathy, marrow plasmacytosis, hypercalcemia, anemia, renal azotemia
Diagnosis	Imaging (osteolytic lesions), bone marrow aspirate/IHC, protein electrophoresis
Treatment	Melphalan + corticosteroids ± other chemo; supportive care; radiation for pain
Prognosis	Good initial response; median survival ~18 months; relapse expected

References & Further Reading

DVM360: Overview of multiple myeloma in dogs and cats; pathophysiology and signalment.
MSD/Vet Manual (professional): Manifestations including lytic lesions, hypercalcemia, diagnosis, treatment.
Merck Vet Manual: Hypercalcemia in dogs—malignancy-related, including multiple myeloma.
Veterinary Practice (2023): Clinical presentation, imaging, and breed predispositions in canine MM.
PubMed case reports: Hypercalcemia with normal ionized calcium; immunohistochemical diagnosis using cell block technique.