Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma VIII:von Willebrand factor antigen (VIII:vWF) levels were elevated approximately two- to eightfold in seven patients (three adults and four children) during acute episodes of thrombocytopenia, renal failure, and hemolytic anemia (the hemolytic-uremic syndrome, HUS). In all seven patients, there was an alteration in plasma VIII:vWF patterns during these acute HUS episodes, so that the largest VIII:vWF forms were relatively decreased. Plasma VIII:vWF multimer patterns returned to normal, or nearly to normal, as platelet counts returned to preexisting levels, even in the patients whose recovery of renal function was incomplete and whose plasma VIII:vWF antigen level remained above normal. The sister of one of the HUS patients had a similar clinical prodrome (gastroenteritis) that was not followed by thrombocytopenia or renal failure and was not accompanied by an elevated level or abnormal forms of plasma VIII:vWF. These results suggest that an alteration in VIII:vWF metabolism, distribution, or interaction with platelets is associated with acute HUS episodes. In contrast to patients with chronic relapsing thrombotic thrombocytopenic purpura, none of the HUS patients (either during or after the acute HUS episodes) had a defect in the conversion of unusually large VIII:vWF multimers derived from endothelial cells to the VIII:vWF forms found in normal plasma.
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PMID:Abnormal VIII: von Willebrand factor patterns in the plasma of patients with the hemolytic-uremic syndrome. 643 74

We describe a previously healthy 9-year-old girl who had multiple purpura several days after acute adenovirus gastroenteritis and mycoplasma pneumonia. Initial laboratory evaluation revealed a prolonged prothrombin time (PT) and APTT, low complement levels (C4, CH50), and positive immune complex (C1q) in her serum. Platelet count, fibrinogen, and other routine blood chemistry tests were normal. The prolonged APTT was not corrected by mixture of the patient's plus normal plasma. Clotting activities of factors II, V, VIII, IX, X, XI, and XII reduced. Further examinations revealed the presence of lupus anticoagulant (LA), phosphatidylserine-dependent anti-prothrombin antibodies (aPS/PT), and anticardiolipin antibodies. Mycoplasma pneumonia was treated by minocycline and the patient's skin lesions disappeared spontaneously within a week. During follow-up, she showed no other bleeding symptoms, and no signs of SLE or other autoimmune diseases. Four weeks after admission to our hospital, blood coagulation tests and serum complements normalized. Clotting activities of factors and antiphospholipid antibodies were not detected, half year later. The bleeding in this case was associated with acquired hypoprothrombinemia caused by antiphospholipid antibodies following acute adenovirus gastroenteritis and mycoplasma pneumonia.
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PMID:[A case of lupus anticoagulant hypoprothrombinemia syndrome following adenovirus gastroenteritis and mycoplasma pneumonia]. 2459 69