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PubMed1986

The effects of different doses of some acetylsalicylic acid formulations on platelet function and bleeding times in healthy subjects.

In an attempt to find the most appropriate dose and formulation(s) of acetylsalicylic acid (ASA) for thrombosis prophylaxis, healthy volunteers were given doses of ASA for 1 wk daily ranging from 50 to 3900 mg as either Aspro-Clear (soluble), Astrix (enteric coated pellets) or Ecotrin (enteric coated tablets). Platelet function and bleeding times were monitored. All doses of ASA significantly inhibited platelet function (p less than 0.05) and increased bleeding times (p less than 0.05) relative to control values. Irrespective of the formulation, maximum increases in bleeding time and platelet dysfunction were obtained with daily doses of about 100 mg, and no further changes were observed with higher doses.

Adult↗

PubMed2006

Usefulness of whole blood aggregometry and its comparison with thromboxane generation assay in monitoring acetylsalicylic acid effectiveness--a multiparametric study in rats.

BACKGROUND: There is a need for consensus concerning universal methodological criteria for detection of suboptimal response to acetylsalicylic acid (ASA) therapy. Therefore, animal models to test for ASA effectiveness remain of interest. Our objective was to verify the usefulness of multiparametric whole-blood impedance aggregometry and thromboxane A(2) generation, which are the most popular techniques used for monitoring of ASA treatment effectiveness. METHODS: Using multiparametric analysis of whole-blood impedance aggregometry, we examined which parameters of platelet aggregation or disaggregation allow for the best discrimination between ASA-treated (4 or 40 mg/kg for 60 days) and non-treated male rats. The effectiveness of ASA-mediated inhibition of platelet cyclooxygenase-1 was verified by determination of plasma thromboxane B(2) and urine 11-dehydro-thromboxane B(2), accepted as reference assays for monitoring of ASA-mediated platelet cyclooxygenase-1 inhibition. RESULTS: Two of the platelet agonists used, collagen (1 mg/L) and arachidonic acid (0.5 mmol/L), allowed discrimination of control and ASA-treated animals, whereas adenosine diphosphate (5 micromol/L) was not effective. It is noteworthy that only ASA-mediated changes in duration of the rising phase for platelet aggregation and the area under the curve for collagen-induced aggregation allowed significant discrimination between low and high ASA dose and remained correlated with the reference parameter, plasma thromboxane B(2). CONCLUSIONS: Analysis of aggregation curves, routinely based only on the amplitude and rate of platelet aggregation, may not be enough discriminative to distinguish between varying ASA doses and treatment schedules.

Adenosine Diphosphate↗

PubMed1981

Comparison of diflunisal and acetylsalicylic acid in patients with rheumatoid arthritis.

A double-blind comparison of the clinical efficacy and tolerance of varying doses of diflunisal (DFS) and acetylsalicylic acid (ASA) was carried out in 15 patients with rheumatoid arthritis who were given no other antirheumatic medication. An effort was made to select appropriate anamnestic, functional and sociofunctional tests and to optimize their validity by careful measurements performed by the same specialized physiotherapist and occupational therapist. In addition, the serum concentration of DFS and salicylic acid were monitored by high-pressure liquid chromatography. The therapeutic effects of DFS was at least as good as that of ASA. Moreover, DFS was better tolerated; all 7 patients on DFS could sustain the maximum dose (1g) of this drug, while that of ASA (4g) was tolerated by only one of 8 patients. All these experienced side effects, necessitating drug withdrawal in 3 cases, one being a serious hepatotoxic reaction. DFS treatment, on the other hand, was associated with only one minor side effect. The side effect difference was statistically significant (p less than 0.01). The analyses of drug concentrations in serum verified that all patients were exposed to DFS and ASA as planned, adding safety to the judgement of the therapeutic effects. The findings support the view that the novel salicylic acid derivative DFS may offer a therapeutic advantage in the treatment of rheumatoid arthritis; it seems to have at least the same therapeutic effect as ASA an may be better tolerated.

Adult↗

PubMed2003

Pharmacokinetics and plasma concentrations of acetylsalicylic acid after intravenous, rectal, and intragastric administration to horses.

Six healthy adult horses (5 mares and 1 stallion) were given a single dose of acetylsalicylic acid (ASA), 20 mg/kg of body weight, by intravenous (IV), rectal, and intragastric (IG) routes. Serial blood samples were collected via jugular venipuncture over a 36-h period, and plasma ASA and salicylic acid (SA) concentrations were determined by high-performance liquid chromatography. After IV administration, the mean elimination rate constant of ASA (+/- the standard error of the mean) was 1.32 +/- 0.09 h(-1), the mean elimination half-life was 0.53 +/- 0.04 h, the area under the plasma concentration-versus-time curve (AUC) was 2555 +/- 98 microg x min/mL, the plasma clearance was 472 +/- 18.9 mL/h/kg, and the volume of distribution at steady state was 0.22 +/- 0.01 L/kg. After rectal administration, the plasma concentration of ASA peaked at 5.05 +/- 0.80 microg/mL at 0.33 h, then decreased to undetectable levels by 4 h; the plasma concentration of SA peaked at 17.39 +/- 5.46 microg/mL at 2 h, then decreased to 1.92 +/- 0.25 microg/mL by 36 h. After rectal administration, the AUC for ASA was 439.4 +/- 94.55 microg x min/mL and the bioavailability was 0.17 +/- 0.037. After IG administration, the plasma concentration of ASA peaked at 1.26 +/- 0.10 microg/mL at 0.67 h, then declined to 0.37 +/- 0.37 microg/mL by 36 h; the plasma concentration of SA peaked at 23.90 +/- 4.94 microg/mL at 4 h and decreased to 0.85 +/- 0.31 microg/mL by 36 h. After IG administration, the AUC for ASA was 146.70 +/- 24.90 microg x min/mL and the bioavailability was 0.059 +/- 0.013. Administration of a single rectal dose of ASA of 20 mg/kg to horses results in higher peak plasma ASA concentrations and greater bioavailability than the same dose given IG. Plasma ASA concentrations after rectal administration should be sufficient to inhibit platelet thromboxane production, and doses lower than those suggested for IG administration may be adequate.

Absorption↗

PubMed1988

The absorption of acetylsalicylic acid from an enteric-coated formulation and the inhibition of thromboxane formation.

To compare conventional (CT) and enteric-coated (ECT) tablets of acetylsalicylic acid (ASA) six healthy adult subjects ingested one 0.5-g tablet of these formulations daily for fifteen days in a cross-over study. Significant amount of ASA was detected in peripheral blood of every subject after the ingestion of CT or ECT. The rate of absorption of ASA was faster and its peak plasma concentration was higher after the ingestion of CT. The formation of thromboxane B2 (TXB2) decreased during blood clotting concomitantly with the absorption of ASA from both formulations. The formation of TXB2 was equally and completely inhibited by CT and ECT as it decreased to 1% of the control value one day after the first dose. During treatment with a single daily dose of 0.5 g of CT or ECT, the serum level of TXB2 remained at this low level and returned to the control level gradually in two weeks after the last dose. The present study indicates that significant amount of unchanged ASA is absorbed also from ECT and that the formation of TXB2 is equally and completely inhibited with a 0.5-g daily dose of both formulations.

Adult↗

PubMed1983

Preventing acetylsalicylic acid damage to human gastric mucosa by use of prostaglandin E2.

To determine the lowest dose of prostaglandin E2 (PGE2) capable of preventing the acetylsalicylic acid (ASA)-induced fall in the gastric transmucosal potential difference, six healthy men (mean age 24 years) were studied on 5 separate days, in random sequence. In the control experiment, 100 ml of 140 mM hydrochloric acid was instilled five times into the stomach for 15 minutes each time, during which the transmucosal potential difference was measured continuously. In the test experiments, 20 mM ASA plus PGE2 in doses of 0, 0.1, 0.5, or 1.0 mg were added to the control solution during the second and third instillations. The mean control potential difference (+/- standard error) was -50 +/- 2 mV. During the administration of ASA there was a 25% reduction in the potential difference; this change was statistically significant (p less than 0.01). With all three doses of PGE2 the fall in potential difference was prevented. The results demonstrate that ASA damage to human gastric mucosa can be prevented entirely by concurrent administration of as little as 100 micrograms of PGE2. This supports the view that mucosal protection is a physiologic function of PGE2.

Adult↗

PubMed1996

Simultaneous determination of acetylsalicylic acid and salicylic acid in human plasma by high-performance liquid chromatography.

A high-performance liquid chromatographic (HPLC) method is described for the simultaneous determination of acetylsalicylic acid (ASA) and its main metabolite salicylic acid (SA) in human plasma. Acidified plasma is deproteinized with acetonitrile which is separated from the aqueous layer by adding sodium chloride. ASA and SA are extracted into the acetonitrile layer with high yield, and determined by reversed-phase HPLC (column: Novapak C18 4 microns silica, 150 x 4 mm I.D.; eluent: 740 ml water, 900 microliters 85% orthophosphoric acid, 180 ml acetonitrile) and photometric detection (237 nm). 2-Methylbenzoic acid is used as internal standard. The method allows the determination of ASA and SA in human plasma as low as 100 ng/ml with good precision (better than 10%). The assay was used to determine the pharmacokinetic parameters of ASA and SA following oral administration of 100-500 mg ASA in healthy volunteers.

Analgesics, Non-Narcotic↗

PubMed1999

Simultaneous determination of paracetamol, caffeine and acetylsalicylic acid by means of a FI ultraviolet pls multioptosensing device.

A simple and rapid analytical procedure is proposed for the simultaneous determination of caffeine (CF), acetylsalicylic acid (ASA) and paracetamol (PCT) in pharmaceutical preparations by partial least-squares (PLS) treatment of a flow-through multisensor based on the integration of the retention and UV detection of the analytes on a solid support. Diode-array spectrophotometry has been used to obtain spectra (240-350 nm) of the analytes retained on C18 bonded phase beads packed in a flow cell. By using a 0.5% pH 1 HClO4 solution as the carrier, the multisensor responds linearly in the measuring range without requiring additional reagents or derivatization processes and the active microzone is regenerated by using methanol as eluting agent. Spectra of the corresponding analytes were used to provide multivariate data for the multivariate procedure. The statistical parameters obtained by the application of PLS methods at different reaction times were analysed, from which the optimum reaction time for the simultaneous determination of the analytes was selected. In the analysis of real and synthetic samples, precise and accurate values were obtained.

Acetaminophen↗

PubMed1979

Oral acetylsalicylic acid (aspirin) challenge in asthmatic children.

Thirty-two asthmatic children, mean age 9.6 years (range: 6-14 years), were studied by oral challenge with acetylsalicylic acid (Aspirin), and their PEFR was recorded at 30 min intervals for 3 hr. They had been asthmatic for a mean of 7.1 years. Other allergic symptoms (urticaria, rhinitis or atopic dermatitis), were present in 81% of the patients, and a family history of atopy in 94%; the mean blood eosinophilia was 590 cells per mm3. In three children aspirin induced a fall in PEFR values less than 8% which was non-significant. In the group as a whole there was an increase in the PEFR values of 13.9%, 150 min after aspirin challenge. These values where subjected to statistical analysis (Kolmogorov-Smirnov, Student's and Wilcoxon tests), which showed this increase to be significant at a level of P = 0.001. Possible mechanisms involving prostaglandin synthetase inhibition by aspirin are discussed as an explanation for this increase.

Adolescent↗

PubMed1981

Oral and inhaled sodium cromoglycate in challenge test with food allergens or acetylsalicylic acid.

The prophylactic effect of oral and inhaled sodium cromoglycate (SCG) in challenge tests of patients with IgE-mediated food allergy or sensitivity towards acetylsalicylic acid (ASA) was investigated. In food allergic patients SCG administered orally protected against an asthmatic reaction whereas inhaled SCG was without effect. In ASA sensitivity neither oral nor inhaled SCG protected the patients against bronchospasms. SCG seems to act on mucosal surfaces and may inhibit uptake of macromolecular antigens but not affect the absorption of ASA.

Administration, Oral↗

PubMed1983

Propranolol and acetylsalicylic acid in migraine prophylaxis. Double-blind crossover study.

The aim of this double-blind crossover study was to compare the prophylactic effect of acetylsalicylic acid (ASA) with that of propranolol (PRP) in the treatment of migraine. Plasma concentrations of the two drugs were measured in order to investigate a possible relationship to the clinical effect. Compared to the pretreatment period, PRP and ASA reduced migraine index, frequency, duration, severity of attacks and headache days. Due to the limited number of patients, our results should be cautiously interpreted, however relevant the clinical improvement seemed. Improvement of migraine index was not related to different plasma levels of the two drugs.

Adolescent↗

PubMed1988

Effects of triflusal and acetylsalicylic acid on platelet aggregation in whole blood of diabetic patients.

A study was made on the inhibitory effect of triflusal (600 mg/d X 15) and acetylsalicylic acid (ASA, 400 mg/d X 15) on platelet aggregation in whole blood (WB) and platelet-rich plasma (PRP) induced by ADP (2.5 mumol/l), adrenaline (50 mumol/l), collagen (1 microgram/ml) and arachidonic acid (0.8 mmol/l), in 30 insulin-dependent diabetic patients without vascular complications. Determination was also made of the serum levels of thromboxane B2 (TxB2) and of the plasma levels of 6-keto-PGF1-alpha and of beta-thromboglobulin (B-TG). Both drugs exhibited higher inhibitory effects in WB than in PRP. In WB, a significant difference between triflusal and ASA was observed against ADP-induced aggregation (67% and 46% inhibition respectively, p less than 0.01). Both drugs strongly inhibit the formation of TxB2 in serum (85% and 99%, respectively). Triflusal does not significantly change the plasma levels of 6-keto-PGF1-alpha; ASA, by contrast, causes reduction of over 95% in those plasma levels. The plasma levels of B-TG were not modified by either of the drugs.

Adult↗

PubMed2006

Does Ginkgo biloba special extract EGb 761 provide additional effects on coagulation and bleeding when added to acetylsalicylic acid 500 mg daily?

OBJECTIVE: The aim of this study was to determine whether Ginkgo biloba special extract EGb 761 amplifies the known effects of acetylsalicylic acid (ASA) on platelet aggregation, bleeding time or other coagulation parameters in healthy subjects. METHODS: In a double-blind, double-dummy procedure, 50 healthy male subjects (20-44 years) were randomly allocated in equal numbers to one of two possible treatment sequences, i.e. ASA followed by ASA + EGb 761 or ASA + EGb 761 followed by ASA. Each treatment lasted 7 days; the washout period between treatments was 3 weeks. Study medication was taken twice daily (ASA group: ASA 500 mg tablet + placebo-coated tablet in the morning and placebo tablet + placebo-coated tablet in the evening; ASA + EGb 761 group: ASA 500 mg tablet + EGb 761 120 mg-coated tablet in the morning and placebo tablet + EGb 761 120 mg-coated tablet in the evening), resulting in a daily dose of ASA 500 mg in the ASA group and 500 mg ASA + 240 mg EGb 761 in the ASA + EGb 761 group. Bleeding time, coagulation parameters and platelet activity in response to various agonists were determined. In addition, adverse events, laboratory variables and vital signs were measured. The primary variable bleeding time was assessed in confirmatory analysis, all other variables were evaluated descriptively. The coagulation variables were analysed by ANOVA under the crossover model. RESULTS: ASA given alone clearly prolonged bleeding time. ASA and the combination of ASA + EGb 761 exerted quite similar effects on all coagulation parameters measured, including bleeding time (ASA alone: 4.1 min before therapy, 6.2 min after therapy; ASA + EGb 761: 4.2 min before therapy, 6.3 min after therapy; ratio of means: 1.01, 90% CI 0.86, 1.19) and agonist-induced platelet aggregation (collagen-induced platelet aggregation - ASA: 84.5% before therapy, 81.0% after therapy; ASA + EGb 761: 86.6% before therapy, 81.0% after therapy; ratio of means: 1.00, 90% CI 0.95, 1.05; adenosine diphosphate-induced platelet aggregation - ASA: 72.6% before therapy, 47.2% after therapy; ASA + EGb 761: 71.7% before therapy, 44.8% after therapy; ratio of means: 0.95, 90% CI 0.85, 1.06). Both treatments were well tolerated, and both the number and nature of adverse events in the two groups were similar. CONCLUSIONS: Our findings suggest that co-administration of ASA and EGb 761 does not constitute a safety risk, including in an elderly patient population undergoing treatment with EGb 761.

Adult↗

PubMed2000

[Acetylsalicylic acid effects on pain sensitivity to myocardial ischemia and skin sensitivity in patients with angina pectoris].

AIM: To clarify if pain-relieving action of acetylsalicylic acid (ASA) is associated with lowered sensitivity of anginal patients to pain due to myocardial ischemia. MATERIALS AND METHODS: A double blind randomized placebo-controlled trial enrolled 10 males aged 42-69 years with stable effort angina (EA) of functional class II-III. When exposed to exercise tolerance test (treadmill, stress-system Sicard 460S, computed ECG), the patients developed EA attack with at least 1 mm decline of ST segment on ECG. The exercise test was made before, 2 and 4 hours after administration of ASA and placebo. Sensitivity to ischemia was estimated by the total depth of the ST segment decline in 11 ECG leads (sigma ST) registered at the attack onset. Tactile and pain thresholds (TT and PT) were studied with a highly reproducible technique. TT and PT were measured before, 2 and 4 hours after ASA and placebo administration. RESULTS: 2 and 4 hours after intake of 100 mg of ASA, sigma ST and TT significantly rose compared to the baseline level and placebo. PT significantly rose vs the baseline level. CONCLUSION: ASA deteriorates sensitivity of anginal patients to myocardial ischemia, skin tactile and pain sensitivity and thus can deprive the EA patient of the pain attack signal. This leads to the risk of overexercising and emergence of painless myocardial ischemia.

Adult↗

PubMed2004

[Endothelium and platelets in pregnant women with chronic glomerulonephritis and therapeutic efficacy of acetylsalicylic acid and dipiridamol].

AIM: To estimate platelet and endothelial condition in pregnant women with chronic glomerulonephritis (CGN), prognostic value of these changes and efficacy of acetylsalicylic acid (ASA) and dipiridamol in prevention of unfavourable outcomes of pregnancy in CGN. MATERIAL AND METHODS: The examination covered 74 CGN pregnant patients, 14 non-pregnant CGN patients, 11 pregnant women with preeclampsia, 19 healthy pregnant women. The levels of fibronectin, endothelin-1,2, 6-keto-PGF1a, thromboxane B2 (TxB2) secretory beta-thromboglobulin in the blood, activity of intrathrombocytic lactate dehydrogenase (LHG), platelet aggregation. ASA (125 mg/day) was given to 33 CGN pregnant women in combination with dipiridamol (150-225 mg/day). Control group consisted of 32 CGN pregnant women. RESULTS: Content of fibronectin, endothelin, TxB2 and beta-thromboglobulin in blood plasm, aggregation with ADP in CGN pregnant women were higher than in healthy pregnant women and nonpregnant CGN patients. Plasmic 6-keto-PGF1a was low. Preeclampsia was accompanied with elevated fibronectin, TxB2 and beta-thromboglobulin, hyperactive LDH. Platelet aggregation was suppressed. Blood beta-thromboglobulin directly correlated with systolic and diastolic arterial pressure, 24-h proteinuria and blood creatinine. Reverse Correlation was seen in blood beta-thromboglobulin with albuminemia, glomerular filtration rate, body mass of the newborn and term of labor. A direct correlation was found between the activity of intrathrombocytic LDH and systolic and diastolic arterial pressure, a weak reverse correlation--between platelet count in capillary blood and systolic pressure, platelet aggregation with ADP and terms of labor. Of the highest prognostic value were the level of beta-thromboglobulin and fibronectin, the activity of intrathrombocytic LDH and platelet aggregation in response to ADP. ASA and dipiridamol reduced the risk of fetal retardation and fetal loss. CONCLUSION: Pregnant women with CGN have endothelial-thrombocytic dysfunction because of unidirectional influence of both CGN and pregnancy. We think that endothelial-platelet dysfunction connects renal impairment and placental failure in pregnant women with CGN deteriorating a gestational CGN and pregnancy complications. Correction of endothelial-platelet state with ASA and dipiridamol is effective in prevention of fetal retardation and fetal loss in pregnant women with CGN.

Administration, Oral↗

PubMed1991

[The effect of glycine on the gastroduodenal tolerability of acetylsalicylic acid. An endoscopic, controlled double-blind study in healthy subjects].

In a randomized double-blind study the gastroduodenal tolerability of daily 500 mg acetylsalicylic acid (ASA, CAS 50-78-2) in combination with 250 mg glycine (CAS 56-40-6) (Godamed) and 500 mg ASA without addition of glycine were evaluated in 20 healthy volunteers giving upper GI-endoscopy. Both ASA-preparations have been taken over a period of 4 weeks. Endoscopic controls were performed at entry, and repeated after 7, 14 and 28 days of treatment. Both ASA-preparations induced comparable gastroduodenal damages during the whole test period: The lesions score of both groups on day 7, 14 and day 28 was almost identical. In contrast to plain ASA, where 9 of 10 volunteers reported gastrointestinal side effects, all subjects receiving ASA in combination with glycine did not complain from any dyspeptic symptoms, i.e. epigastric pain etc. The reasons for the apparent better tolerability of ASA in combination with glycine are discussed.

Adult↗

PubMed1990

[Endoscopic studies on the gastric tolerance of paracetamol and acetylsalicylic acid. A placebo-controlled, double-blind study in healthy volunteers].

Endoscopic Studies on the Gastric Tolerance Following 6 Days Treatment of Paracetamol and Acetylsalicylic Acid/A placebo-controlled double-blind-study in healthy volunteers. In placebo-controlled randomized double-blind cross-over-fashion the gastric and duodenal tolerance of a 6 day treatment with 3000 mg acetylsalicylic acid (ASA; as a commercially available preparation) and 3000 mg paracetamol (Tylenol) were directly compared in 12 healthy volunteers. An endoscopic evaluation of the gastric and duodenal mucosa was performed. 3000 mg ASA daily evoked significant more gastro-duodenal lesions than 3000 mg paracetamol daily and placebo. Difference between Paracetamol and placebo did not reach statistical significance. Based on the comparable analgetic potency of both compounds and the apparently better gastro-duodenal tolerability paracetamol is the drug of choice when a non-inflammatory problem requires an analgesic.

Acetaminophen↗

PubMed1989

[Acetylsalicylic acid in the treatment of arterial thromboembolytic diseases. 2. Clinical documentation].

A review of the literature is undertaken to account for the current status of acetylsalicylic acid (ASA) in the treatment of patients with arterial thrombo-embolic conditions. Employment of ASA monotherapy has been documented to be effective in clinically controlled investigations in patients with unstable angina pectoris, transient cerebral ischaemia, coronary by-pass and femoro-popliteal endarterectomy and introduction of vascular prostheses and, in addition, in primary and secondary prophylaxis of acute myocardial infarction (AMI). In combination with dipyridamol, ASA has been found to be effective in secondary AMI prophylaxis, coronary by-pass operation and in peripheral arteriosclerosis. In patients with cardiac valvular prostheses, conventional anticoagulation therapy must still constitute the basic treatment but dipyridamol may be employed to increase the antithrombotic efficacy of the treatment. The dosage of ASA in the majority of works has been about 1,000 mg daily while isolated investigations have shown good effect from doses as low as 60 mg daily. It appears to be important for the efficacy of the treatment with platelet inhibitors in the above-mentioned conditions that treatment is instituted rapidly and, in connection with operative intervention, preferably preoperatively. In other clinical conditions such as preeclampsia, hypertension in pregnancy, diabetic angiopathy and nephropathy, membranoproliferative glomerulonephritis and arterio-venous shunts with haemodialysis, treatment with ASA appears to be effective but documentation in extensive clinically-controlled investigations is not yet available. The duration of treatment with ASA in arterial thrombo-embolic disease does not appear to be illustrated unanimously in the articles published but, as the atherosclerotic lesion is not influenced by ASA, there are indications for life-long therapy.

Aspirin↗