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Hemangiosarcoma, lymphoma, and adenocarcinoma may be associated with consumptive
thrombocytopenia due to disseminated intravascular coagulation. Immunologic and inflammatory
mechanisms cause increased platelet consumption and decreased platelet survival. However, bleeding
tendencies without thrombocytopenia occasionally exist. Altered platelet function due to an acquired
membrane defect has been associated with hyperglobulinemia. Vasculitis also may contribute to the
hemostatic disorder.
Vaccine‐induced Thrombocytopenia:
Dogs vaccinated repeatedly with modified‐live adenovirus and paramyxovirus vaccines may develop
thrombocytopenia 3–10 days after repeat vaccination. The thrombocytopenia is usually transient and
may be sufficiently mild that a bleeding tendency will not be evident unless superimposed on another
platelet or coagulation disorder. Studies have failed to confirm an association between recent
vaccination and development of idiopathic thrombocytopenic purpura; however, it might still occur
rarely.
Drug‐induced Thrombocytopenia:
Thrombocytopenia associated with administration of certain drugs has been reported in dogs, cats, and
horses. One mechanism is marrow suppression of megakaryocytes or generalized marrow stem cell
suppression (after administration of estrogen, chloramphenicol, phenylbutazone, diphenylhydantoin,
and sulfonamides). Another mechanism is increased platelet destruction and consumption (after
administration of sulfisoxazole, aspirin, diphenylhydantoin, acetaminophen, ristocetin, levamisole,
methicillin, and penicillin). Drug reactions are idiosyncratic and therefore unpredictable. Platelets
usually return to normal shortly after the drug is discontinued. Drug‐induced bone marrow suppression
may be prolonged. The chemotherapy drug lomustine has sometimes caused prolonged
thrombocytopenia that persists after the drug is stopped.
Other:
Quantitative platelet disorders have been reported in liver disease with or without coagulation protein
deficiencies. In two studies of cats with thrombocytopenia, 29%–50% had infectious diseases, including
feline leukemia, feline infectious peritonitis, panleukopenia, or toxoplasmosis. The mechanism of
thrombocytopenia has not been identified in many cases. Feline leukemia virus replicates and
accumulates in megakaryocytes and platelets; aplasia or hypoplasia of marrow stem cells, immune
destruction of infected platelets, or extravascular sequestration of platelets within lymphoid tissues may
contribute to thrombocytopenia in this disease."
https://www.ncbi.nlm.nih.gov/pubmed/6976036