A case of primary lymphoma of the prostate is reported in a nine‐year‐old crossbred dog. The lesion was treated with cytotoxic drugs, however, the dog was euthanased because of inadequate response. This is the first recorded case of primary prostatic lymphoma in the dog.
Hairy cell leukaemia (HCL) is a rare lymphoproliferative disorder associated with pancytopenia, splenomegaly and the presence of typical hairy B lymphocytes in the bone marrow and/or peripheral blood. The most significant complication relates to opportunistic infections that arise as a consequence of neutropenia and monocytopenia. HCL is occasionally associated with systemic autoimmune disorders including polyarteritis nodosa and rheumatoid disease. Secondary autoimmune haemolytic anaemia (AIHA) appears to be rare. We report on two cases of HCL complicated by fatal cold anti‐i AIHA. Fulminant haemolysis causing death is rare in cold AIHA and only a few individual cases have been reported, none having anti‐i specificity.
We present the case of a patient diagnosed as having presumed idiopathic thrombocytopenic purpura (ITP) who subsequently developed chronic myelomonocytic leukaemia (CMML) after an interval of 16 months. A variety of peripheral cytopenias are commonly seen in myelodysplastic disorders (MDS), and autoimmune phenomena, including secondary ITP, are well described, especially in cases of CMML. We would advocate evaluation for possible MDS/CMML by morphological examination of the peripheral blood/bone marrow in adult patients presenting with isolated thrombocytopenia, especially if there is subsequent development of additional peripheral cytopenias, monocytosis or hepatosplenomegaly.
We report the case of a 71-year-old man on warfarin for chronic atrial fibrillation presenting with a massive spontaneous soft tissue bleed. Despite reversing the effects of warfarin with large doses of intravenous vitamin K and fresh frozen plasma, bleeding continued, and his prothrombin time and activated partial thromboplastin time remained prolonged. The prothrombin time and activated partial thromboplastin time failed to correct with 50% normal plasma. Further investigations confirmed a lupus inhibitor with low levels of factors II, V, VII and XI. Factor II, V and XI levels normalized, however, when the patient's plasma was diluted 1:16 in buffer, suggesting the lupus inhibitor may have been interfering with these factor assays causing artefactual low results. Factor VII levels remained consistently low at all dilutions. The patient subsequently died following a massive left haemothorax despite surgical intervention and treatment with activated recombinant factor VII concentrate. We presumed the primary problem was bleeding from a local vascular lesion but the patient was never well enough to undergo confirmatory angiography. This case highlights the fact that patients with lupus inhibitors can develop severe haemorrhagic complications, and illustrates the complexities involved in both the investigation and treatment of abnormal bleeding in these patients.
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