salicylate/hemorrhage

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Coagulopathy and bleeding associated with salicylate toxicity.

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Salicylate toxicity is a common cause of morbidity and hospitalization. Animal and human studies suggest that salicylates cause a dose-dependent inhibition of the activation of factors 2, 7, 9, and 10. However, limited reports of coagulopathy or major bleeding from salicylate toxicity

Aspirin and gastrointestional bleeding. Interest of plasma salicylate determination.

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From history-taking and from analysis of plasma salicylate levels it is shown that a link exists between aspirin and gastrointestinal bleeding in 68% of cases. Salicylate levels alone indicate that aspirin has been taken in 22% of cases. Plasma salicylate measurement and endoscopy allow a better

Salicylate-induced gastrointestinal bleeding: comparison between soluble buffered, enteric-coated, and intravenous administration.

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Serum salicylate levels and blood loss in stools were compared in 94 patients after intake of various forms of acetylsalicylate. Four different oral soluble forms, an enteric-coated variety and an intravenous form were evaluated. Analysis of the results of blood loss measurement in stools showed

Comparison of serum salicylate levels and gastro-intestinal blood loss between salsalate (Disalcid)and other forms of salicylates.

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In a first stage the effect of a single dose of 3 g of salsalate on serum salicylate level was compared with a single intake of 3 g of soluble or enteric-coated acetylsalicylates in 12 healthy subjects. Salsalate seems to resorb faster than the enteric-coated forms but more slowly than the soluble

Aspirin-induced gastric bleeding stops despite rising plasma salicylate.

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In 7 subjects, 100-ml successive portions of buffered acid (pH between 3.5 and 2.9) solutions of aspirin (1 g/liter) were instilled into the stomach and recovered after 10 min. Blood in the recoveries was estimated chemically. After there had been three successive increases in the rate of blood loss

Salicylate-induced bleeding problem in ophthalmic plastic surgery.

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A 54-year-old woman with clinically asymptomatic PCV underwent eyelid surgery. Twenty-four hours after an uncomplicated procedure she had a severe bleeding diathesis following the ingestion of a small amount of aspirin. Treatment of her bleeding disorder and a review of the effects of salicylates on

Fecal blood loss and plasma salicylate study of salicylsalicylic acid and aspirin.

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Using a placebo-controlled methodology, 20 healthy volunteers housed in a clinical research facility for 23 days were studied for fecal blood loss and plasma salicylate levels after taking salsalate (salicylsalicylic acid) or aspirin. Daily dosages were 3000 mg salsalate or 3900 mg aspirin. Aspirin

Hemorrhagic shock as a sequela of splenic rupture in a patient with infectious mononucleosis: focus on the potential role of salicylates.

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Despite the fact that the vast majority of splenic ruptures are traumatic, infectious mononucleosis has been incriminated as a major predisposing factor that affects the integrity of the spleen, thus causing atraumatic ruptures and life-threatening hemorrhages. Herein we present a case of a

Whole blood viscosity issues VI: Association with blood salicylate level and gastrointestinal bleeding.

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BACKGROUND This series on whole blood viscosity issues has been trying to elucidate the sensitivity, specificity and usefulness of the laboratory parameter in clinical practice. The postulation has been that since antiplatelet is used in the management of stasis, of which blood viscosity is an

The aspirin metabolite sodium salicylate causes focal cerebral hemorrhage and cell death in rats with kainic acid-induced seizures.

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Aspirin (acetylsalicylic acid), and its main metabolite sodium salicylate, have been shown to protect neurons from excitotoxic cell death in vitro. The objective of our study was to investigate the possible neuroprotective effects of sodium salicylate in vivo in rats with kainic acid-induced

Interactions between sodium salicylate and acetyl salicylic acid evaluated using ADP induced platelet aggregation and bleeding time.

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1 g acetyl salicylic acid orally significantly enhanced the initial rate of platelet aggregation induced by 1 mumol/l and 2.5 mumol/l ADP. Sodium salicylate was without effects on the platelet aggregation and specifically it did not prevent acetylsalicylic acid from inhibiting the secondary

Salicylate-induced occult gastrointestinal blood loss: comparison between different oral and parenteral forms of acetylsalicylates and salicylates.

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Gastrointestinal fecal blood loss, determined by injecting 51Cr-labelled autologous red blood cells, was measured in 191 orthopaedic patients after oral or parenteral intake of different forms of acetylsalicylates or salicylates. Oral or parenteral administration of non-acetylated salicylates caused

Fatal hemorrhage from minor trauma following massive salicylate ingestion.

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The anticoagulant property of aspirin has long been appreciated. Recently, the physiologic mechanism has been identified and documented extensively. Despite the long-lasting inhibition of platelet function and clinically significant postoperative hemorrhage following aspirin use, few serious

Reduction of indomethacin-induced gastrointestinal blood loss by sodium salicylate in man.

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The gastrointestinal bleeding during treatment with indomethacin, aspirin, phenylbutazone and sodium salicylate in healthy human subjects was determined. Gastrointestinal blood loss was determined by the Cr51-labelled erythrocyte method. The method was modified by us. Collected stool was incinerated

Moderate anticoagulation by salicylate prevents thrombosis without bleeding complications. An experimental study in rats.

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It has previously been shown that salicylate (S) acts as a vitamin K (vit K)-antagonist inducing a decrease in plasma levels of vit K-dependent clotting factors and inhibiting the vit K-dependent carboxylation reaction in the liver. In this study we evaluated whether this biochemical effect had a

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