REVERSIBLE PROLONGED SKIN BLEEDING-TIME IN ACUTE GASTROINTESTINAL-BLEEDING PRESUMED DUE TO NSAIDS

Citation
Jp. Day et al., REVERSIBLE PROLONGED SKIN BLEEDING-TIME IN ACUTE GASTROINTESTINAL-BLEEDING PRESUMED DUE TO NSAIDS, Journal of clinical gastroenterology, 22(2), 1996, pp. 96-103
Citations number
37
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
01920790
Volume
22
Issue
2
Year of publication
1996
Pages
96 - 103
Database
ISI
SICI code
0192-0790(1996)22:2<96:RPSBIA>2.0.ZU;2-X
Abstract
The purpose of this research was to look for a possible mechanism wher eby NSAIDs, and particularly ASA, might cause gastrointestinal bleedin g. A total of 34 hospitalized GI bleeders and 29 age- and sex-matched controls were studied. Skin bleeding time (SET) was measured within 6 h of coming to hospital and before any blood products were given. All patients and controls were questioned regarding current NSAID use. Thi s history was supplemented by estimation of serum salicylate and of pl atelet cyclooxygenase activity to detect unreported current aspirin (A SA) use. Various aspects of platelet function were also tested by lumi aggregation in 28 controls and, after recovery, in 27 of the bleeders. Of 34 bleeders, 26 bled from the upper GI tract, (13 from peptic ulce r) and eight from the lower GI tract, 30 (88%) had a current intake of NSAIDs and of these 22 (73%) used ASA, some in combination with other NSAIDs, whereas 12 of 29 controls were using NSAID's, 11 of which wer e ASA. SET in the bleeders was 9.0 +/- 1.02 min versus 4.8 +/- 0.42 mi n in the controls (p < 0.001). SET measured 6.6 days later in 28 bleed ers was 4.7 +/- 0.22 min (p < 0.0006), and of those tested after recov ery all but one had fallen to 6.5 min or less. None had any residual c onstitutional platelet abnormalities as tested by lumiaggregation. By logistic regression, NSAID intake was strongly associated with prolong ed SET to > 6 min (odds ratio [OR], 16.7; p < 0.0002), whereas NSAID i ntake (OR 14.6; p < 0.0003) and SET > 6 min (OR 1.8; p < 0.005) contri buted to a bleeding outcome. Almost 90% of GI bleeders had recently co nsumed NSAIDs, mostly ASA, on an average 15 h before onset of bleeding . Although most of the nonbleeders who had used NSAIDs did not have a prolonged SET, most of the bleeders who used NSAIDs had an abnormal el evation of SET, suggesting a possible mechanism for GI bleeding. Retes ting similar to 7 days after recovery from bleeding showed normalizati on of the SET, indicating that the defect was transient and spontaneou sly reversible.