Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to ascertain whether the modern effective anti-ulcer drugs have had any influence on the natural history of hemorrhagic peptic ulcer disease and other acid-related gastroduodenal bleeding disorders. In the prospective part of the study the anamnestic data of all 73 patients admitted to our hospital with a bleeding ulcer or related disease during the year 1989 were compared with the data of 73 patients subjected to elective upper GI tract endoscopy for abdominal symptoms other than bleeding, paying special attention to potential risk factors. There were no differences in previous ulcer history or operations for ulcer disease between these two groups. Cigarette smoking and coffee consumption were not different, but the bleeders consumed alcohol more often, and, in particular, they used ulcerogenic drugs or other hemorrhagic diathesis-provoking agents significantly more frequently than controls. In the retrospective part of the study these 73 patients were compared with the medical records of all 87 patients admitted to our hospital in 1976 for a bleeding peptic ulcer disease, to ascertain whether introduction of H2-blocking agents had had any influence on the nature of the patient population, characteristics of the disease, and severity of bleeding. The patients had become slightly older, and male preponderance was seen in both groups. The proportion of gastric ulcer had decreased, and duodenal ulcer had increased. In general, the bleeding seemed to become less severe but was more severe among women in both groups. In 1989 almost all patients were treated with H2 antagonists, and seven patients received additional medical therapy (vasopressin, somatostatin, or tranexamic acid).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peptic ulcer bleeding today: risk factors and characteristics of the disease. 168 92

An acquired hemorrhagic disorder developed in two patients in association with postsplenectomy thrombocytosis and leukocytosis during the course of the myeloproliferative syndrome. The presence of acquired von Willebrand's disease in these individuals was demonstrated by a decrease or absence of the larger von Willebrand factor (vWF) multimers, alteration of the repeating vWF multimeric "triplet," decreased ristocetin cofactor activity (vWF:RCo), and prolonged bleeding time. The bleeding stopped in both patients after treatment with either 1-deamino-[8-D-arginine]-vasopressin (DDAVP) or Cohn fraction I. Treatment with thrombocytapheresis and azathioprine or busulfan resulted in reduction of the elevated platelet and white cell counts and was associated with partial correction of the vWF abnormalities and remission of the hemostatic abnormalities. In five additional patients with the myeloproliferative syndrome, but without bleeding symptoms, large multimers of plasma vWF were diminished also. These findings suggest that acquired von Willebrand's disease should be considered when a bleeding diathesis develops during the course of the myeloproliferative syndrome.
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PMID:Acquired von Willebrand's disease in the myeloproliferative syndrome. 633 59

We report a quite rare case of acquired type 3-like von Willebrand syndrome (vWS) that preceded full-blown systemic lupus erythematosus (SLE). A 16-year-old woman with no previous disease history and no family history of hemorrhagic diathesis was referred to our hospital because of recurrent epistaxis and gingival bleeding. She was diagnosed as having atypical type 3 von Willebrand disease because of prolonged bleeding time with normal platelet count and prolonged activated partial thromboplastin time (aPTT), and an almost complete absence of von Willebrand factor (vWF) antigen, ristocetin cofactor activity (vWF:RCo) and ristocetin-induced platelet agglutination (RIPA). Furthermore, electrophoretic analysis of plasma vWF revealed a trace amount of vWF and an absence of the multimeric form of vWF. Infusions of either vasopressin or factor VIII/vWF concentrates improved bleeding symptoms and corrected the aPTT and RIPA. However, she complained of low-grade fever, general fatigue and polyarthralgia 5 months later, and leukocytepenia and hypo-complementemia developed. Anti-double-stranded DNA antibodies and lupus erythematosus cells became positive. These findings were compatible with SLE. Mixing the patient's platelet-poor plasma (PPP) with normal platelet-rich plasma (PRP) (PPP/PRP = 2/1) resulted in a complete inhibition of RIPA, suggesting the presence of vWF inhibitor in her plasma. Treatment with prednisolone (40 mg/day) started and the bleeding tendency gradually improved. One month later, all of the laboratory data including aPTT, bleeding time, RIPA and vWF:RCo became normal. These findings indicate that she has an acquired type 3-like vWS associated with SLE.
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PMID:Acquired type 3-like von Willebrand syndrome preceded full-blown systemic lupus erythematosus. 1203 3

We studied the effect of vasopressin analogue desglycinamide-arginine-vasopressin on changes in platelet hemostasis produced by intragastric administration of Ticlid or clopidogrel (inhibitors of ADP-induced platelet aggregation). Intranasal administration of the peptide under conditions of hemorrhagic diathesis produced a hemostatic effect and normalized some parameters of blood coagulation.
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PMID:Correction of changes in ADP-induced platelet aggregation with vasopressin analogue desglycinamide-arginine-vasopressin. 1628 90