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Hemostatic defect in endoscoped upper gut bleeding.

W H Hall·T Q My·J D Welsh·J W Hamptom
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Abstract

In an effort to assess the role of salicylate ingestion in upper gastrointestinal bleeding, one observer obtained a blood specimen for salicylate determination, performed a Duke bleeding time, and obtained a detailed drug history at the time of diagnostic endoscopy. Although a salicylate ingestion history was common, other variables did not correlate with it. Prolonged bleeding time occurred in 21 of the 81 patients, versus 1 of 22 controls. It was strongly associated with liver disease, with the alcohol habit by history, and with endoscopically severe gastritis, but was not correlated with plasma salicylate levels or evidence of salicylate ingestion by history, or with thrombocytopenia. Additional relationships linked liver disease and gastritis with prolonged bleeding time. There was no direct evidence from this study that salicylate ingestion occurred more frequently among gastrointestinal bleeders than among controls, and there was no evidence that the hemostatic defect increased the magnitude of bleeding.

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AlcoholismAspirinBlood Coagulation TestsGastritisGastrointestinal HemorrhageHumansLiver DiseasesThrombocytopeniaJournal Article

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W H Hall, T Q My, J D Welsh, J W Hamptom. 1978. Hemostatic defect in endoscoped upper gut bleeding.. https://pubmed.ncbi.nlm.nih.gov/305713/

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Long-term mortality after transfusion-associated non-A, non-B hepatitis. The National Heart, Lung, and Blood Institute Study Group.

BACKGROUND: Acute non-A, non-B hepatitis after blood transfusion often progresses to chronic hepatitis and sometimes culminates in cirrhosis or even hepatocellular carcinoma. However, the frequency of these sequelae and their effects on mortality are not known. METHODS: We traced patients with transfusion-related non-A, non-B hepatitis who had been identified in five major prospective studies conducted in the United States between 1967 and 1980. We matched each patient with two control subjects (identified as the first and second controls) who received transfusions but who did not have hepatitis. The mortality rates in the three groups were determined with use of data from the National Death Index and Social Security Death Tapes. Cause-specific mortality was determined by reviewing death certificates. RESULTS: Vital status was established for over 94 percent of the 568 patients who had had non-A, non-B hepatitis and the two control groups (526 first controls and 458 second controls). After an average follow-up of 18 years, the estimate by life-table analysis of mortality from all causes was 51 percent for those with transfusion-associated non-A, non-B hepatitis, as compared with 52 percent for the first controls and 50 percent for the second controls. The survival curves for the three groups were virtually the same. Mortality related to liver disease was 3.3, 1.1, and 2.0 percent, respectively, among the three groups (P = 0.033 for the comparison of the group with non-A, non-B hepatitis with the combined control group). Seventy-one percent of the deaths related to liver disease occurred among patients with chronic alcoholism. CONCLUSIONS: In this long-term follow-up study, there was no increase in mortality from all causes after transfusion-associated non-A, non-B hepatitis, although there was a small but statistically significant increase in the number of deaths related to liver disease.

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