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At least 73 records · Page 4Linked to original sources
PubMed1977

Comparative effects of tolfenamic acid and acetylsalicylic acid on human gastric mucosa. A double-blind crossover trial employing gastroscopy, extern gastrocamera and multiple biopsies.

A comparative study has been made of the effects of tolfenamic acid (Clotam) and acetylsalicyclic acid on the gastric mucosa in 10 healthy volunteers. The effects were evaluated by means of gastroscopy, photography of the gastric mucosa, and multiple biopsies. The schedule was for a randomized, double-blind crossover trial involving two drug-administered periods of one week's duration separated by an interval of at least 3 weeks. On each day of the drug-administration weeks either tolfenamic acid 600 mg or acetylsalicyclic acid 3 g was administered as three divided doses, taken with meals. Gastroscopy was performed prior to and after each week of drug administration. Subjective side effects were recorded during the therapy periods; haematemesis occurred in 2 volunteers taking acetylsalicyclic acid. The absence of gastritis in each subject during treatment with tolfenamic acid was confirmed both gastroscopically and histologically. In contrast, 6 out of 10 volunteers developed mild superficial acute gastritis after ingestion of acetylsalicyclic acid. The difference in effect between the two treatments on the gastric mucosa was statistically significant(p less than 0.05). The findings of this study are comparable to those of other studies and it is concluded that tolfenamic acid, in the relatively high dosage employed in this trial, is free from any irritant effect on the gastric mucosa.

Adult↗
PubMed1998

[Prevention of vascular complications following cerebral ischemia of arterial origin; the ESPRIT trial: mild anticoagulant therapy, combination treatment with acetylsalicylic acid plus dipyridamole or treatment with acetylsalicylic acid alone?].

The European and Australian Stroke Prevention in Reversible Ischaemia Trial (ESPRIT) is a randomised clinical trial in which patients with cerebral ischaemia of arterial origin will be randomised between oral anticoagulation (international normalized ratio (INR): 2.0-3.0), the combination of acetylsalicylic acid (in any dose between 30 and 325 mg per day) plus dipyridamole (400 mg daily) and acetylsalicylic acid only (in any dose between 30 and 325 mg per day). It is planned to enroll 4500 patients with a mean follow-up of three years. Primary outcome is the composite event of vascular death, stroke, myocardial infarction, or major bleeding complication; outcome assessment will be blinded. ESPRIT is an international, multicentre study in which 60-80 hospitals in the Netherlands and other countries in Europe and Australia will participate.

Adult↗
PubMed2005

Polymorphisms in genes encoding acetylsalicylic acid metabolizing enzymes are unrelated to upper gastrointestinal health in cardiovascular patients on acetylsalicylic acid.

BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid. The objective of this study was to assess whether polymorphisms in UGT1A6 and CYP2C9 genes are related to the prevalence of upper gastrointestinal symptoms in cardiovascular patients using acetylsalicylic acid for secondary prevention of ischaemic heart disease. METHODS: Blood samples were taken from acetylsalicylic acid using patients admitted to the Coronary Care Unit. Dyspepsia-related health was evaluated at week 2, using a validated upper gastrointestinal complaint questionnaire. A subset of 160 patients responded to a survey and were eligible to participate in this study. DNA was isolated and UGT1A6 and CYP2C9 genotypes were determined using polymerase chain reaction restricted fragment length polymorphism techniques. RESULTS: Seventy per cent of the patients returned the questionnaire. UGT1A6 and CYP2C9 variant polymorphisms were found in 103 (63%) and 56 (35%) patients, respectively. There was no association between gastrointestinal symptoms and UGT1A6 (OR = 0.80, 95% CI = 0.41-1.56) or CYP2C9 polymorphisms (OR = 0.85, 95% CI = 0.44-1.67). CONCLUSIONS: There was no association between polymorphisms in genes encoding for acetylsalicylic acid metabolizing enzymes on the prevalence of gastric complaints in cardiovascular patients on acetylsalicylic acid.

Aged↗
PubMed1983

Plasma levels of acetylsalicylic acid and salicylic acid after oral ingestion of plain and buffered acetylsalicylic acid in relation to bleeding time and thrombocyte function.

Buffered acetylsalicylic acid (Alka Seltzer, B-ASA) and plain aspirin (P-ASA) tablets were compared as to their effects on bleeding time and platelet function in eight healthy male volunteers. Two doses (500 and 1000 mg) of each preparation were investigated in a cross-over design, each volunteer being his own control in each dose group (n=4). Both preparations disturbed platelet aggregation to the same extent. Bleeding time increased after both preparations, though significantly more after the buffered preparation than after plain acetylsalicylic acid, irrespective of the dosage. The 1000 mg dose prolonged bleeding time significantly more than the 500 mg dose, irrespective of the preparation. Kinetic analysis showed that B-ASA gave higher peak plasma levels of acetylsalicylic acid (ASA) and accordingly salicylic acid peak levels were also higher after the buffered preparation. It is concluded that B-ASA in equi-analgesic doses prolongs bleeding time more than the plain preparation. Since it is less agressive on the gastro-intestinal mucosa, its use may be advantageous in situations where acetylsalicylic acid induced loss of platelet aggregation is desired. However, the risk of prolonged bleeding--e.g. after tooth extractions--is probably higher after the buffered preparation.

Adult↗
PubMed1988

Thermal, ventilatory, and gluco-regulatory responses during exercise following short-term acetylsalicylic acid ingestion.

Acetylsalicylic acid and exercise combined produce perturbations in thermal, respiratory and carbohydrate metabolism. However, the therapeutic implications of these therapies are antithrombotic and fibrinolytic respectively. In a double-blind, counterbalanced cross-over design of eight men, salicylate ingestion in combination with 60 min of moderate intensity exercise (50% VO2 max) significantly increased respiratory rate and oxygen consumption (p less than 0.05) both at rest and during the exercise protocol. The effect of acetylsalicylic acid ingestion on gluco-regulatory and counter-regulatory hormones was not significant compared to the placebo. These data suggest a safe prophylactic role for a combined short-term acetylsalicylic acid ingestion and exercise therapy in the development of coronary artery disease when exercising in a thermal neutral environment.

Adult↗
PubMed1994

Spectrofluorimetry at zero angle: determination of salicylic acid in an acetylsalicylic acid pharmaceutical formulation.

In this work, a solid-state spectrofluorimetric method for drug assays was developed. In particular, we report the determination of salicylic acid (SA), as a hydrolysis product, in solid pharmaceutical formulations containing acetylsalicylic acid (ASA). Recently, we described a sensitive and accurate fluorescence method that provided, through a mathematical application, the simultaneous determination of ASA and SA. By means of the spectrofluorimetric method reported herein it was possible to carry out the SA determination, without any mathematical calculation and with a sensitivity 100 times that of our previous method. The intra- and inter-day reproducibility of the spectrofluorimetric method, expressed as the relative standard deviation, ranged from 0.1 to 0.3%. The present method requires a fluorescence apparatus with the excitation and detection systems in-line (zero angle). The detection system was not sensitive to the excitation wavelength, but was highly sensitive to emission wavelengths from 350 to 800 nm. The results obtained were compared with those of our previous spectrofluorimetric method, together with those of a high-performance liquid chromatography method and a US Pharmacopeia method. The sensitivity of the method was of the order of 10(-8) g.

Aspirin↗
PubMed2006

A new effect of acetylsalicylic acid? Significantly lower prevalence of nasal carriage of Staphylococcus aureus among patients receiving orally administered acetylsalicylic acid.

We aimed to evaluate effect of acetylsalicylic acid on the prevalence of nasal carriage of Staphylococcus aureus. Patients were orally administered a prophylactic dose of acetylsalicylic acid and then were compared with control subjects. The prevalence of nasal carriage of S. aureus was significantly lower among patients who received acetylsalicylic acid than among the control subjects (P<.001).

Administration, Oral↗
PubMed1976

Application of gas-liquid chromatography and high-performance liquid chromatography to the analysis of trace amounts of salicylic acid, acetylsalicylic anhydride and acetylsalicylsalicylic acid in aspirin samples and aspirin formulations.

The gas-liquid chromatographic (GLC) determination of salicylic acid (SA) in 12 commercial acetylsalicylic acid (aspirin, ASA) samples and 12 ASA formulations is reported. The GLC determination of SA as an impurity in ASA, utilising methylation with methyl iodide in the presence of potassium carbonate, requires a column chromatographic separation of SA prior to derivatization. Trace amounts of SA in ASA have also been determined by high-performance liquid chromatography (HPLC) on a Sil-X-I adsorption column using light petroleum-ethyl acetate-acetic acid as the mobile phase. Acetylsalicylic anhydride (ASN) and acetylsalicylsalicylic acid (ASSA) were determined by HPLC on a reversed-phase C18 column with water-methanol mixtures as the mobile phase. GLC was also applied to the determination of ASN as an impurity in ASA formulations.

Anhydrides↗
PubMed1993

Nasal secretions in response to acetylsalicylic acid.

BACKGROUND: Acetylsalicylic acid (ASA) induces rhinorrhea in a subset of patients with asthma or chronic rhinosinusitis or both and nasal polyps. The underlying mechanism of the reaction is obscure. METHODS: To assess the nasal response to ASA challenge, four groups of patients were challenged orally with ASA: group A (10 ASA-sensitive patients); group B (nine patients with nasal polyps and histories of tolerance to ASA); group C (nine ASA-tolerant patients with chronic allergic rhinitis); and group D (eight healthy nonatopic subjects). RESULTS: Nasal lavages obtained before and after ASA challenge were assayed for proteins (total protein, lactoferrin, lysozyme, albumin) and inflammatory mediators (histamine, prostaglandin D2, and leukotriene C4). ASA challenges induced severe rhinorrhea and congestion and significant increases in mean concentrations of all measured nasal proteins in group A. Histamine and prostaglandin D2 rose, but not significantly. In the two control groups with chronic rhinitis, ASA induced increases in the concentration of proteins and histamine. Leukotriene C4 concentrations were significantly elevated in nasal lavages after ASA challenge in groups A and C only. In group D no symptoms or changes in nasal proteins were observed after aspirin challenge. CONCLUSIONS: These observations suggest that production of lipoxygenase products of arachidonate may induce glandular secretions that may participate in the clinical changes associated with ASA sensitivity.

Adult↗
PubMed2006

Biological basis and clinical implications of acetylsalicylic acid resistance.

Acetylsalicylic acid (ASA) is effective in preventing strokes, heart attacks and vascular-related events associated with cardiovascular disease (CVD). Notwithstanding, many patients suffer recurrent events while on ASA therapy. During the past decade, a number of investigators have suggested that these patients are unresponsive to ASA or are 'ASA-resistant'. In the past, this view was met with wide skepticism. Although there is mounting evidence that ASA resistance is a real phenomenon, an understanding of its biological basis and how to measure it is still unclear. The complexity of the problem is discussed below in an attempt to stimulate clinicians and CVD researchers to give serious thought to the ASA resistance problem. It is anticipated that a better understanding of ASA resistance will help us to appreciate its relative importance and its implications in the clinical setting.

Acetylation↗
PubMed1989

Drug interactions involving aspirin (acetylsalicylic acid) and salicylic acid.

Aspirin (acetylsalicylic acid) is metabolically converted to salicyclic acid by the action of carboxylesterases. Although metabolic drug interactions involving aspirin are theoretically possible, there appear to have been no studies to date which have shown conclusively that aspirin hydrolysis is altered by coadministered drugs. However, a number of treatments are known to affect the rate or extent of aspirin absorption, including activated charcoal, antacids, cholestyramine and metoclopramide. Caffeine and metoprolol have been reported to increase peak salicylic acid concentration following aspirin administration, and coadministration of dipyridamole and aspirin results in higher plasma aspirin concentrations. The mechanism(s) responsible for these latter observations remains unknown. Salicylic acid is extensively bound to plasma albumin, and many of the reported drug interactions involve displacement of the coadministered drug from plasma protein. Protein binding displacement appears to be the basis of salicylic acid interactions with diclofenac, flurbiprofen, ibuprofen, isoxicam, ketoprofen, naproxen, phenytoin and tolmetin. Following displacement of these agents increased clearance of total drug occurs, and consequently the plasma concentration of total drug decreases. Although generally not measured, unbound concentration of the interacting drug should not be markedly altered. Salicylic acid also increases total plasma clearance of fenoprofen but, unlike the interactions with the other propionic acid non-steroidals, plasma protein binding displacement does not appear to be involved. Induction of fenoprofen metabolism is a possibility, although there is no firm evidence from other studies that salicylate is able to induce the metabolism of coadministered drugs. Since salicylic acid is extensively metabolised, it is not surprising that it is able to inhibit the metabolism of certain coadministered drugs and chemicals, an effect which has been reported for salicylamide, valproic acid, m-xylene, and zomepirac. The interactions with salicylamide, m-xylene and zomepirac are probably competitive in nature since mutual inhibition of salicylic acid metabolism occurs. There is an additional component of protein binding displacement in the interactions with valproic acid and zomepirac, resulting in increased unbound drug concentration. Certain coadministered drugs (or chemicals) may alter the metabolism of salicylic acid; inhibition of its metabolism has been demonstrated following treatment with benzoic acid, salicylamide, m-xylene, zomepirac and possibly cimetidine. In contrast, salicylic acid elimination is enhanced in oral contraceptive steroid users and by corticosteroid treatment. Oral contraceptive steroids induce both salicylic acid glucuronidation and salicylurate formation. Induction of metabolism has also been proposed to account for the effects of corticosteroids, but this is still to be proven.(ABSTRACT TRUNCATED AT 400 WORDS)

Antacids↗
PubMed1983

[Distribution of salicylic acid and hydrolysis of acetylsalicylic acid in the human fetus in early pregnancy].

The materno-fetal transfer of salicylic acid and its distribution in the fetal organism was investigated in women of early pregnancy. Acetylsalicylic acid (Acesal) was administered orally in a single dose or in repeated doses at different times before legal interruption. The mean passage rates were about 6-15%. They were independent of the maternal serum concentrations of salicylic acid. The distribution of salicylic acid on the fetal liver, intestine, kidneys, lungs and brain was different. All fetal organs (9th to 15th week of gestation) studied exhibit an acetylsalicylic acid-splitting esterase activity. The esterase activity of the fetal liver was about 30% of the hydrolytic activity of the adult liver. The esterase activity was mainly located in the 105 000 X g-supernatant of cell homogenates.

Aspirin↗