Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathological findings in 87 cases of canine splenic abnormality recognised clinically by abdominal palpation or radiography, or at exploratory laparotomy, are presented. The most common diagnosis was of splenic neoplasia (n = 38) and the most frequently recognised canine splenic neoplasm was haemangiosarcoma (17 of 38 cases). Benign splenic enlargement secondary to nodular hyperplasia (n = 6), haematoma (n = 16) or non-specific changes including congestion, haemorrhage, extramedullary haemopoiesis and haemosiderin deposition (n = 14) was also recognised. A diagnosis of non-specific pathology was more frequently recorded when portions of spleen, as opposed to the entire organ, were submitted for assessment. Splenic infarction, with (n = 3) or without (n = 7) torsion, abscessation (n = 2) and focal mast cell proliferation (n = 1) accounted for the remainder of the cases. Clinical follow-up was available for 35 cases and revealed good long-term survival in cases of splenic haematoma or haemangioma, with relatively poor survival with a diagnosis of splenic haemangiosarcoma or anaplastic sarcoma. A range of splenic disorders was recognised in dogs of the labrador breed (16 of 87 cases) and three of 17 cases of haemangiosarcoma occurred in German shepherd dogs. The possible predisposition of dogs of these breeds to splenic disorders is discussed.
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PMID:A review of pathological diagnoses made from 87 canine splenic biopsies. 858 57

An autopsy case of systemic mast cell disease (SMCD) without primary skin lesions in a 57-year-old Japanese male is described. Initially the patient was suspected of having liver cirrhosis or malignant lymphoma because of hepatomegaly and lymph node enlargement on admission. However, a lymph node biopsy and bone marrow aspiration conducted on his third admission indicated a SMCD because of the existence of metachromatic cell aggregates stained with toluidine blue. At autopsy, the diagnosis was confirmed because the proliferating cells were histochemically proven to be mast cells by naphthol AS.D chloroacetate esterase, Giemsa and alcian blue, in addition to toluidine blue staining. The intra-abdominal and retroperitoneal lymph nodes were replaced by mast cell aggregates, which caused the splenic infarction and bilateral hydronephrosis, with infiltration of mast cells into the spleen and kidneys also being apparent. Mast cell infiltration was similarly found in the bone marrow, liver, ileum and ascending colon. Immunohistochemically, the mast cells were positive for antibodies of alpha 1-antichymotrypsin, CD45 (LCA), CD43 (MT-1), CD45R (MB-1) and the oncoprotein c-kit. Electron microscopic examination using formalin-fixed tissue gave supportive evidence of a mast cell origin for the lesions.
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PMID:Systemic mast cell disease with splenic infarction: a case report. 970 48