Abnormal Aspirin Metabolism in Patients with Cirrhosis and Its Possible Relationship to Bleeding in Cirrhotics

Menguy, René; Desbaillets, L.; Okabe, Susumu; Masters, Y. F.

doi:10.1097/00000658-197209000-00017

Cited by 30 publications

(14 citation statements)

References 18 publications

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“…These findings suggest that the pathogenic mecha nisms of the aggravated development of ASA-induced gastric lesions in cirrhotic rats involve gastric ionic changes (acid back diffusion) leading to mucosal damages and reduced activity of ASA metabolizing enzyme. Menguy et al (16), including one of the present authors (S.O. ), found that ASA-acyl-hydrolase, which metabolizes ASA to salicylate and acetic acid, is significantly lower in serum of cirrhotic patients than in normal subjects.…”

Section: Discussionsupporting

confidence: 51%

Effects of L-Glutamine on Acetylsalicylic Acid-Induced Gastric Lesions in Normal and Cirrhotic Rats

et al. 1975

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Abstract-Cirrhosis of the liver in rats was induced by the administration of carbon tetrachloride (0.1 ml/100 g of body weight, s.c.) biweekly for 13 weeks. In the pylorus ligation preparation, acetylsalicylic acid (ASA) 100 mg/kg p.o. Induced much more serious gastric damage in CCl4-induced cirrhotic rats as compared with rats with a normal liver. L-glutamine 750 mg/kg p.o. prevented the ASA-induced gastric lesions in both normal and cirrhotic rats, even though the degree of the inhibition was weaker in cirrhotic rats. Gastric analysis indicated that L-glutamine 750 mg, ,kg p.o. markedly inhibited the gastric ionic changes (acid back diffusion) in response to ASA in both cirrhotic and normal rats.Acetylsalicylic acid (ASA) is generally considered to be a hazardous agent on the stom ach in both man and experimental animals (1, 2). Thus, the compound should not be given to cirrhotic patients who are known to bleed from the gastrointestinal tract (3-5).A series of studies from this laboratory indicated that L-glutamine markedly suppresses the ASA induced gastric lesions in rats, possibly by preventing acid back diffusion caused by ASA (6-9). It was, therefore, of interest to examine whether or not, I) ASA induces more serious gastric lesions in cirrhotic rats, and 2) L-glutamine concomitantly given with ASA prevents the increased gastric damages in cirrhotic rats, as observed in normal rats.In this communication, we report the marked protection of gastric lesions and gastric ionic changes in response to ASA in both normal and cirrhotic rats by a concomitant ad ministration of L-glutamine. MATERIALS AND METHODSMale Donryu strain rats, 180-220 g at the beginning of the experiments, were used.

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Section: Discussionsupporting

confidence: 51%

Effects of L-Glutamine on Acetylsalicylic Acid-Induced Gastric Lesions in Normal and Cirrhotic Rats

et al. 1975

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“…This pattern of distribution agrees well with that reported by Menguy et ai. [5]. No significant change was noted in the distribution of the enzyme activ ity in various tissues of the acutely intoxicated rats (table I).…”

Section: Resultsmentioning

confidence: 82%

“…The assay of ASA esterase activity was carried out under the conditions of zero-order kinetics described by Menguy et al [5], and the amount of substrate hydrolyzed never exceeded 17%.…”

Section: Resultsmentioning

confidence: 99%

“…Serum ASA esterase activity was assayed by in cubating 0.5 ml of serum with 0.4 ml of 15 mmol/1 solution of ASA and 2.1 ml of 60 mmol/1 Tris buffer (pH 7.0) in a shaking water bath for 60 min at 25 C [5], Appropriate blanks without serum were included with each incubation. To measure the released SA, 5 ml of the color reagent as described by Trinder [9] were immediately added, with constant shaking, to 1 ml of the incubation mixture.…”

Section: Methodsmentioning

confidence: 99%

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Tissue Acetylsalicylic Acid Esterase Activity in Rats with Acute and Chronic Liver Damage from Carbon-Tetrachloride and Ethanol

Js¹

1975

Enzyme

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The hydrolysis of acetylsalicylic acid (ASA) in vivo by serum and various tissues of rats with experimentally produced acute and chronic toxic liver damage, was estimated by spectrophotometric measurement of salicylic acid (SA) appearance. It was inferred from the data obtained that the liver tissue helped to maintain normal ASA esterase activity in the blood which would otherwise be affected by liver damage.

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“…Aspi rin is of less importance in haemorrhages caused by other organic lesions. Cirrhotics are particu larly prone to gastrointestinal haemorrhage after aspirin ingestion (7). In those cirrhotics who bleed after aspirin taking there is a dif ferent pattern of lesions: ulcer and acute haemorrhagic gastritis are found more frequent ly than in the absence of aspirin ingestion.…”

Section: Discussionmentioning

confidence: 99%

Aspirin and Gastrointestinal Bleeding

Faivre¹,

Faivre²,

Léry³

et al. 1979

Digestion

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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 understanding of haemorrhagic lesions due to aspirin. Aspirin is responsible especially for haemorrhage from ulcers and acute gastritis or duodenitis. Aspirin is seen to be dangerous in a moderate number of susceptible individuals: those with peptic ulcer constitution or cirrhosis.

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Abnormal Aspirin Metabolism in Patients with Cirrhosis and Its Possible Relationship to Bleeding in Cirrhotics

Cited by 30 publications

References 18 publications

Effects of L-Glutamine on Acetylsalicylic Acid-Induced Gastric Lesions in Normal and Cirrhotic Rats

Effects of L-Glutamine on Acetylsalicylic Acid-Induced Gastric Lesions in Normal and Cirrhotic Rats

Tissue Acetylsalicylic Acid Esterase Activity in Rats with Acute and Chronic Liver Damage from Carbon-Tetrachloride and Ethanol

Aspirin and Gastrointestinal Bleeding

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