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Immune-Mediated Hemolytic Anemia

Liaison: Patti Emmett, MS, RN, CIC
Email: sunfiresams@bigfoot.com

Decreased numbers of red blood cells (RBCs) due to destruction by the immune system.

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Signs and Symptoms

weakness and/or loss of energy
decreased interest in food
dark urine
pale gums
jaundice (yellow tinge in the whites of the eyes)
enlarged spleen
aslight fever may be present.

Causes

In many cases (60-70%), a cause isn't found. In some cases, a primary reaction by the immune system precedes the act of red blood cell destruction.

The immune system (lymphocytes) begins to attack the body's own RBCs with destructive antibodies. RBCs normally carry oxygen to tissues, and carry away waste. Iron and bilirubin are sent to the liver in larger amounts than normal causing jaundice and impaired liver function.

Altered liver function, lack of adequate tissue oxygen, and complications of blood clot formation can be life-threatening.

Risk Factors

Cancer (e.g. hemangiosarcoma) and drugs can trigger the immune system to overreact. (The immune system starts targeting proteins that resemble the drug; RBCs are destroyed as "innocent bystanders"). Examples of implicated drugs include trimethoprim-sulfa and methimazole.

Diagnostic Tests

Blood cell counts can determine if the numbers of red blood cells are normal or too low (anemia). Anemia can occur from bleeding or from increased RBC destruction (IMHA).

The bone marrow tries to make more RBCs to replace the destroyed, mature RBCs. Because the bone marrow can't keep up with the destruction, immature forms of RBCs ("reticulocytes" and "nucleated RBCs") may be released into the blood.

Additional testing can determine if the bone marrow is not responding. This may be temporary and resolve, or persist.

Treatment Guidelines

Note: Treatment of animals should only be performed by a licensed veterinarian. Veterinarians should consult the current literature and current pharmacological formularies before initiating any treatment protocol.

Prednisone and dexamethasone for immunosuppression.
Azathioprine if no response to above.
Transfusion when a crisis occurs.

References

Barlough,J.E., Pedersen, N.C, 1995. "The immune system and disorders" in UC Davis School of Vet Med book of dogs. Siegal, M. Ed., p.331-333. Harper Collins, New York.
http://merckvetmanual.com/mvm/htm/bc/60205.htm p. 1-3.
http://www.marvistavet.com/html/body_imha.html
Kohn, B., 2003. Evans’ syndrome: immune-mediated hemolytic anemia in Immune-mediated thrombocytopenia-current approach. 28^th World Congress of World Small Animal Veterianry Assoc., Thailand. P. 1-3.
Trepanier, L.A., Danhof, R., Toll, J., and Watrous, D. 2003. Clinical findings in 40 dogs with hypersensitivity associated with administration of potentiated sulfonamides. J Vet Int Med 9; 17(5):p. 647-652. Link to abstract
Holloway, S.A., Meyer, D.J, and Mannella, C. 1990. Prednisolone and danazol for treatment of immune-mediated anemia, thrombocytopenia, and ineffective erythroid regeneration in a dog. J Am Vet Med Assoc 197 (8):1045-1048. Link to abstract

Conclusions supported by anecdotal evidence, an individual breeder’s opinion or experience, and non-affiliated (personal) websites with credible information backed by affirmation of website owners.

Information based on material published in general dog magazines, breed publications, breed websites or published books about dogs or specific breeds having a general consensus among reputable breeders and/or veterinarians but lacking supporting scientific research.

Information based on preliminary peer-reviewed findings but still in a theoretical phase of understanding.

Information based on an established body of peer-reviewed research in science/veterinary journals and information contained in contemporary veterinary textbooks that reflect a general consensus of the scientific and/or veterinary community.

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