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PubMed1997

[Cost-effectiveness analysis of prevention of reinfarction using low-dose acetylsalicylic acid; model calculation].

The purpose of this study is to estimate the potential of savings which can be achieved by prophylaxis of myocardial reinfarction with low-dose acetylsalicylic acid (ASA) at 75 mg per day over a treatment period of two years. After secondary analysis of published data, the effectiveness of low-dose ASA is compared to placebo by a model calculation. The difference in the effectiveness between the prophylaxis with ASA and placebo is taken from an international meta-analysis. The economic valuation of this difference is carried out by a cost-effectiveness analysis applying disease costs per case. According to the model calculation, 5535 DM can be saved per patient with a history of myocardial infarction with 75 mg ASA a day over a treatment period of two years. In 1991 there were around 740,000 patients with a history of myocardial infarction in the age group of 25-64 in the Old Bundesländer of the Federal Republic of Germany. The application of the results of the model calculation would lead to considerable savings. Even in the sensitivity analysis with different assumptions regarding costs incurred by hospital treatment and costs incurred by premature retirement, the cost advantage of the ASA-prophylaxis remains. Due to the cautious and conservative assumptions in the model calculation the potential of savings is likely underestimated. Nevertheless, there is a distinct advantage for the prophylaxis with low-dose ASA which already occurs in direct costs thus leading to advantages also for cost carriers.

Adult↗
PubMed2005

Dual effects of acetylsalicylic acid on mast cell degranulation, expression of cyclooxygenase-2 and release of pro-inflammatory cytokines.

Several studies have demonstrated that nonsteroidal anti-inflammatory drugs, such as acetylsalicylic acid (ASA), can have inhibitory or enhancing effects on inflammatory cell function. These effects seem independent of cyclooxygenase activity and prostaglandin synthesis inhibition. Here, we examined the effect of ASA on bone marrow-derived mast cells in more detail. ASA blocked the expression of cyclooxygenase-2, the production of tumor necrosis factor-alpha and interleukin-6, and the release of granule mediators from mast cells in a concentration-dependent fashion. Concomitantly, ASA inhibited nuclear factor (NF)-kappaB activity, as well as the phosphorylation and breakdown of the inhibitory protein IkappaB-alpha. We thus propose that the anti-inflammatory effects of ASA in mast cells are due to suppression of IkappaB kinase activity, thereby inhibiting subsequent phosphorylation and degradation of IkappaB-alpha, activation of NF-kappaB, and transcription of proinflammatory cytokines. The inhibition of BMMC degranulation was independent of NF-kappaB activation, however. Interestingly, the expression of cyclooxygenase-2 was not inhibited at 1mM ASA, but was even enhanced significantly. The latter might contribute to the adverse effects of ASA in ASA-sensitive asthmatics.

Animals↗
PubMed1980

Comparison of intravenous acetylsalicylic acid and dipyrone in postoperative pain: an interim report.

1 In 17 gynaecological patients with postoperative pain the analgesic efficacy of intravenous lysine salicylate 1.8 g (corresponding to acetylsalicylic acid (ASA) 1.0 g) and dipyrone 1.0 g were compared in a double-blind randomized study. 2 In the ASA group, mean pain relief and pain intensity difference scores reached a maximum 30 min after drug administration and remained at this level for the next 90 minutes. 3 In the dipyrone group, these scores reached their peak 60 min after drug administration and seemed to fall off during the next hour. 4 The mean pain relief and intensity difference scores were greater following aspirin than dipyrone. However, firm conclusions cannot be drawn from the results of this small study.

Adult↗
PubMed2002

Low dose acetylsalicylic acid in prevention of pregnancy-induced hypertension and intrauterine growth retardation in women with bilateral uterine artery notches.

OBJECTIVE: To evaluate the efficacy of low-dose acetylsalicylic acid in the prevention of pregnancy-induced hypertension and intrauterine growth retardation in high-risk pregnancies as determined by transvaginal Doppler ultrasound study of the uterine arteries at 12 to 14 weeks of gestation. DESIGN: Randomised, double blind and placebo-controlled trial. SETTING: The Department of Obstetrics and Gynaecology, Tampere University Hospital, Finland. POPULATION: One hundred and twenty pregnant women considered to be at high risk of pre-eclampsia or intrauterine growth retardation were screened by transvaginal Doppler ultrasound at 12 to 14 weeks of gestation. METHODS: Ninety pregnant women with bilateral notches in the uterine arteries were randomised to receive acetylsalicyclic acid 0.5mg/kg/day (n = 45) or placebo (n = 45) from 12 to 14 weeks of gestation. MAIN OUTCOME MEASURES: Hypertensive disorders of pregnancy and intrauterine growth retardation. RESULTS: Forty-three women on acetylsalicyclic acid and 43 on placebo were successfully followed up. The use of acetylsalicyclic acid was associated with a statistically significant reduction in the incidence of pregnancy-induced hypertension (11.6% vs 37.2%, RR = 0.31, 95% CI 0.13-0.78) and pre-eclampsia (4.7% vs 23.3%, RR = 0.2, 95% Cl 0.05-0.86). The incidence of hypertension before 37 weeks of pregnancy was also significantly reduced (2.3% vs 20.9%, RR = 0.22, 95% CI 0.05-0.97). The reduction in the incidence of intrauterine growth retardation (2.3% vs 7%) was not statistically significant. Acetylsalicyclic acid was not associated with excess risk of maternal or fetal bleeding. CONCLUSION: In women rated in Doppler velocimetry waveform analysis to be at high risk of pre-eclampsia, low-dose acetylsalicyclic acid reduces the incidence of pregnancy-induced hypertension and especially proteinuric pre-eclampsia.

Adult↗
PubMed1999

Underuse of acetylsalicylic acid in individuals with myocardial infarction, ischemic heart disease or stroke: data from the 1995 population-based Nova Scotia Health Survey.

OBJECTIVE: To determine current patterns of acetylsalicylic acid (ASA) use in Nova Scotia for individuals with self-reported myocardial infarction, stroke or ischemic heart disease. DESIGN: Descriptive, cross-sectional, population-based study using data from the 1995 Nova Scotia Health Survey (NSHS). The NSHS was based on a probability sample and was representative of the Nova Scotia adult population by age, sex and region. Survey data were obtained by standardized home interviews conducted by trained public health nurses. SETTING: The province of Nova Scotia in 1995. PARTICIPANTS: Survey respondents who reported having a myocardial infarction, stroke or ischemic heart disease were assessed. RESULTS: Among those who reported a history of myocardial infarction, stroke or ischemic heart disease, 55% (95% CI 47% to 63%), 49% (95% CI 38% to 61%) and 54% (95% CI 39% to 68%), respectively, reported using ASA at the time of the survey. Overall, only 53% of those with cardiovascular disease were using ASA. Exclusion of persons with potential contraindications to ASA did not significantly increase these proportions. CONCLUSIONS: ASA appears to be underused in those at high risk for future vascular events. Further research is required to investigate determinants of ASA use and to increase appropriate use of ASA.

Adolescent↗
PubMed1975

Acetylsalicylic acid and gastrointestinal bleeding measurement of blood loss using a modified radioactive chromium method.

A comparative study of the gastrointestinal blood loss during intake of a new buffered acetylsalicylic acid (ASA) preparation and plain ASA tablets has been performed. A modified radioactive chromium method was used. The 51Cr activity was considerably less than that used in previous methods, and no feces homogenization was necessary. The study was performed in 18 volunteers using a randomized crossover design. A significant reduction in gastrointestinal bleeding was registered during ingestion of the buffered ASA in comparison with the plain ASA tablets.

Administration, Oral↗
PubMed1984

Suppressive effect of acetylsalicylic acid on erythropoietin-responsive cells in mice.

The time-response curve for RBC-59Fe uptake following i.p. injections of 3 doses of 5 mg of acetylsalicylic acid (ASA) at 4 hour interval into normal, nonpolycythemic mice, shows a maximal depression (35% of normal) at 3 days after ASA with return to almost normal values by 7 days. The effect is dose-related, showing a plateau with doses of ASA above 5 mg/4 hr. The shape of the time-response curve indicates that the more mature cells in the erythron are not affected by ASA and that the major effect of the drug must be on earlier erythroid cells. Administration of ASA prior to administration of erythropoietin (Epo) into post-hypoxic polycythemic mice depresses the incorporation of 59Fe into erythrocytes. The depression of radioiron uptake is similar when ASA is given prior to or simultaneously with Epo. When ASA is given 24 hr after injection of Epo, suppression is less marked. These results suggest a suppressive effect of the drug on the erythropoietin-responsive cells (ERC).

Animals↗
PubMed1982

Influence of acetylsalicylic acid on acute circulatory effects of the beta-blocking agents pindolol and propranolol in humans.

In ten hospitalized, hypertensive male patients (WHO stage I or II) an acetylsalicylic acid (ASA) pretreatment (p.o. 5.0 g/24 h) prevented the acute blood pressure (BP) lowering effect of pindolol (1 mg i.v.) as compared with a placebo pretreatment. Similarly in six other hospitalized male patients (four normotensive, two slightly hypertensive) a single dose of ASA (1.0 or 1.5 g orally), which alone tended to raise the BP, reduced the decrease in systolic BP and led to an increase in diastolic BP following propranolol (5 mg i.v.). The ASA pretreatment did not affect the decrease in heart rate and cardiac contractility (measured by systolic time intervals) after the application of pindolol and propranolol, respectively. In conformity with data in the literature, the results suggest a possible connection between endogenous prostaglandins and the hypotensive, but not negative chronotropic and inotropic activity of the beta-blocking agents investigated.

Adult↗
PubMed1988

[Effect of acetylsalicylic acid on uric acid metabolism in patients with rheumatism].

Concentrations of uric acid (UA) in the blood, saliva, circadian urine and serum xanthinoxidase activity were studied in 150 rheumatic fever patients during acetylsalicylic acid (ASA) therapy. UA concentrations were also studied in the organs (myocardium, mitral cusp, liver and kidneys) of the dead. Low salicylemia in nonreactive rheumatic fever and therapeutic salicylemia in recurrent rheumatic carditis produced a normalizing effect on uric acid metabolism but in limited renal and salivary gland excretory capacity ASA therapy aggravated uric acid metabolic disorder.

Adult↗
PubMed1996

[Acetylsalicylic acid as an augmentation factor in food allergy].

A 39-year-old female patient presented with an intense allergic reaction and shock after ingesting sunflower seeds and simultaneously acetylsalicylic acid (ASA). Skin tests and CAP specific. IgE demonstrated an IgE-mediated sensibilization to sunflower seeds. When sunflower seeds were eaten alone, only discrete paresthesia of the oral mucosa occurred. Surprisingly, an oral challenge with ASA was well tolerated. The supplementary contribution of ASA to the allergic reaction was dose-dependent. The quantity of the allergen also modified the intensity of the symptoms. This surprising effect of ASA may be attributed to increased gastric resorption of the allergens. During the course of this reaction, eosinophil-cationic-protein was released.

Adult↗
PubMed1987

Influence of acetylsalicylic acid (1.0 g/day) on platelet survival time, beta-thromboglobulin and platelet factor 4 in patients with peripheral arterial occlusive disease.

In this study we investigated the influence of acetylsalicylic acid (ASA) 1.0 g/day on 111-In-platelet survival time (PST) and on plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) in 37 patients (median age: 63.4 years) with arteriographically proven peripheral arterial occlusive disease (PAOD) in a chronic stable phase. We found a slight but significant increase of PST during therapy with ASA (weighted mean (WM): 184.3----193.2 [median] hours, p less than 0.05; multiple hit (MH): 182.4----192.8 hours, p less than 0.005) for the total group of patients. Concerning the influence of risk factors of PAOD on PST during ASA-therapy, there was a significant increase of PST only in the nondiabetics (WM: 180.3----204.6 hours, p less than 0.01; MH: 176.8----195.3 hours, p less than 0.01). There was a negative correlation between the baseline values of PST and their increase following ASA therapy (WM: r = -0.63; p less than 0.0001; MH: r = -0.61, p less than 0.0001). The pretreatment levels of beta-TG--but not PF 4--were significantly (p less than 0.001) elevated compared to healthy controls. Therapy with ASA caused a significant decrease in the plasma levels of beta-TG (median: 30.4----26.6 ng/ml, p less than 0.001) and PF 4 (2.95----2.2 ng/ml, p less than 0.01).

Adult↗
PubMed1987

The effect of acetylsalicylic acid and indomethacin on the catecholamine- and oxytocin-induced contractility and prostaglandin (6-keto-PGF1 alpha, PGF2 alpha)-production of human pregnant myometrial strips.

The effects of acetylsalicylic acid (ASA) and indomethacin (IND) on the epinephrine and oxytocin stimulated contractility and prostaglandin (6-keto-PGF1 alpha, PGF2 alpha) production of superfused myometrial strips from the pregnant human uterus at term are reported. Without preincubation in ASA or IND epinephrine dose-dependently (10 ng/ml to 1 microgram/ml) stimulated the contractility and significantly increased the PG-release of the myometrial strips. The epinephrine induced increase in contractility was correlated to a higher increase in PGF2a production and a decreased 6-keto-PGF1 alpha/PGF2 alpha ratio (5.4 to 1.8). Superfusion of oxytocin increased myometrial contractions and PGF2 alpha release according to dose (3-12 microU/ml). However, 6-keto-PGF1 alpha production was not affected by oxytocin. Myometrial strips preincubated with ASA (100 micrograms/ml) or IND (10 micrograms/ml) demonstrated little spontaneous activity and the PG production was below the detection limit of the RIA. The stimulating effect of epinephrine and oxytocin on the contractility and PGF2 alpha release of the myometrial strips was inhibited significantly. During continuous superfusion of the ASA and IND preincubated myometrial strips with Tyrode's solution the inhibitory effect on spontaneous, epinephrine-, and oxytocin-stimulated contractility and PGF2 alpha release gradually declined over a period of 2 hours. This decrease of the inhibitory effect was more significant in ASA preincubated specimens. Our results demonstrate that spontaneous, epinephrine-, and oxytocin-stimulated contractility and PG release of human myometrial strips can be inhibited by ASA and IND and that this inhibitory effect is reversible. Furthermore our results suggest that in pregnant human myometrium the inhibition of PGF2 alpha production by ASA and IND is more pronounced than that of 6-keto-PGF1 alpha (PGI2).

Aspirin↗
PubMed2004

Clinical, double-blind, placebo-controlled study investigating the combination of acetylsalicylic acid and pseudoephedrine for the symptomatic treatment of nasal congestion associated with common cold.

It was the aim of this clinical study to demonstrate the efficacy of 1000 mg acetylsalicylic acid (ASA, CAS 50-78-2) in combination with 60 mg pseudoephedrine (PSE, CAS 90-82-4), compared with placebo, in the symptomatic treatment of nasal congestion associated with the common cold. A further aim was to demonstrate the efficacy of 500 mg ASA + 30 mg PSE and of 1000 mg paracetamol (CAS 103-90-2) + 60 mg PSE (active control) in the symptomatic treatment of nasal congestion. The study was designed as a randomized, two-center, double-blind, double-dummy, placebo-controlled, parallel-group, single-dose efficacy and safety trial over 6 h and was carried out in the USA. In total, at two centers, 643 patients who had a history and diagnosis of acute upper respiratory tract infection (URTI), were included; they showed symptoms such as nasal congestion, scratchy/sore throat, headache, generalized muscle ache, earache, runny nose, fever, sneezing etc. The investigational drugs ASA and PSE were both provided as granules in sachets and the granules were dissolved in water before administration; the combined preparation of paracetamol + PSE was administered as commercially available tablets encapsulated for blinding. For all preparations, matching placebos were provided. The primary efficacy variable was the area under the curve for differences from baseline on a nasal congestion scale in the first 2 h after treatment. To be eligible for the study, otherwise healthy volunteers were to present with nasal stuffiness of recent onset that reached a score of at least 6 on the 11-point scale for nasal congestion (0 = not stuffy, 10 = very stuffy). The primary analysis of the primary efficacy variable was calculated by analysis of variance including treatment group, severity (moderate/severe) and center as main strata. The analysis was performed using the intent-to-treat population. All active treatments proved to be statistically significantly superior to placebo with regard to the primary efficacy variable. Significant superiority of active treatment compared with placebo could also be demonstrated for an interval of up to 6 h after intake of the drug and for the relief of nasal congestion. The lower dose did not reveal significant different results compared with placebo for relief of nasal congestion in patients with a severe nasal congestion score at baseline. As well in patients with moderate nasal congestion score (NCS) at start of the study the difference from baseline in the NCS compared with placebo was not statistically significant. Thus a trend towards better efficacy in the higher dose could be assumed. No difference was found between 1000 mg ASA + 60 mg PSE and the active control. There were no differences between the two centers. The treatment proved to be safe and well tolerated, without relevant differences between the four treatment groups. Main adverse events were found to be related to the upper respiratory tract infection or were of gastrointestinal nature. In conclusion, the combination of ASA with PSE can be considered as an effective and safe remedial for the symptomatic treatment of the nasal congestion during URTI.

Acetaminophen↗
PubMed1984

Influence of sex, blood group, secretor character, smoking habits, acetylsalicylic acid, oral contraceptives, fasting and general health state on blood coagulation variables in randomly selected young adults.

Blood samples were drawn from 129 randomly selected young adults. Intake of acetylsalicylic acid (ASA), contraceptive drugs, smoking habits and health state were registered. Males had significantly higher systolic blood pressure, shorter bleeding time and lower VIII:C. Smoking was only correlated to some variables assessed in the female group. Users of oral contraceptives smoked more, had a shorter bleeding time and higher fibrinogen levels. Factor VIIIR;Ag was elevated only in female smokers with blood group non-O. Non-secretors had shorter bleeding times and a tendency towards higher VIIIR:Ag.

Adult↗
PubMedDate not supplied

High-dose acetylsalicylic acid after cerebral infarction. A Swedish Cooperative Study.

Within 3 weeks of the event, 505 patients with cerebral infarction, minor or major stroke, were randomly assigned to treatment with acetylsalicylic acid (ASA) 1.5 g/day or placebo in a double-blind clinical trial with a follow-up of 2 years in all patients. Primary events were considered to be recurrent stroke or death; secondary events, myocardial infarction and transient ischemic attack. There was no difference in stroke recurrence rate in the ASA and placebo groups (12 and 13%, respectively), nor was there any significant difference in the rate of recurrent stroke or death, first event counted (23% in the ASA and 22% in the placebo group). The risk of transient ischemic attack and myocardial infarction was not reduced in the ASA group. In the present study there was no prophylactic effect of high-dose ASA after cerebral infarction. A compilation of the major trials of ASA after transient ischemic attack and cerebral infarction is presented.

Adult↗
PubMed1992

Interaction between heparin and acetylsalicylic acid on gastric mucosal and skin bleeding in humans.

The haemorrhagic effect of unfractionated heparin and of the low molecular weight heparin, enoxaparin, on gastric mucosal bleeding induced by acetylsalicylic acid (ASA) and on skin bleeding induced by the Simplate technique was investigated in healthy human volunteers. Endoscopic estimation of gastric bleeding by visual analogue scores was more sensitive than biochemical quantitation of blood in the gastric washing by a modified HaemoQuant method. Contrary to what was expected, the ASA-induced gastric mucosal bleeding was not increased by heparin pretreatment, whereas heparin in combination with ASA, but not ASA alone, significantly increased the skin bleeding time. In the interaction with ASA, enoxaparin and unfractionated heparin appeared to act similarly.

Adult↗
PubMed1994

Antiaggregative therapy with acetylsalicylic acid and diclofenac in patients with acute myocardial infarction.

A total of 109 male patients with acute transmural myocardial infarction (MI) were studied. 26 patients received a dose of acetylsalicylic acid (aspirin, ASA) 500 mg/d and 29 patients of 50 mg/d. 27 patients were given diclofenac (25 mg/d). 27 patients received no antiplatelet therapy. We observed thrombocyte hyperaggregation on the 1st MI day, a rapid increase in platelet activity by the 7th day and a considerable decrease in platelet aggregation during the 3rd and 4th weeks of illness in the group without antiaggregative treatment. The present study clearly demonstrated high antiaggregatory efficacy of ASA in dose of 50 mg/d which was significantly higher than that in daily dose of 500 mg ASA. Low-dose aspirin had fewer side-effects than aspirin 500 mg/d. However, although daily dose of 50 mg aspirin significantly inhibited platelet hyperaggregation on 7th day of MI, the hyperactivity of thrombocytes was not abolished. Diclofenac 25 mg daily had only a moderate antiaggregative efficacy in acute MI patients.

Adult↗
PubMed1992

Influence of buffered and unbuffered acetylsalicylic acid on dental enamel and dentine in human teeth: an in vitro pilot study.

An in vitro study was conducted to investigate the erosive effect of buffered and unbuffered acetylsalicylic acid (ASA) on dental enamel and dentine in human teeth by scanning electron microscopy. In order to standardize the specimens and to improve comparability the dental enamel and dentine were superficially abraded. The enamel and dentine specimens were therefore particularly sensitive to the influences of acid agents. Concentrated solution of buffered chewable ASA tablets (500 mg ASA and 300 mg calcium carbonate in 5 ml water) showed no changes in the enamel surface structure after exposure times of 1 min, 5 min and 60 min. In contrast, minimal corrosive effects were already seen after exposure of the enamel surface to the unbuffered ASA solutions for 1 min. After exposure times of 5 min and 60 min erosion of the enamel was more pronounced. Immersion in the unbuffered ASA solution led to clearly visible micromorphological changes on the dentine surfaces even after exposure for 1 min. Exposure of the dentine specimens to the buffered ASA solutions led to only very slight changes in the surface morphology. Therefore, the scanning electron micrograph after exposure to buffered ASA is comparable to the picture of untreated dentine.

Aspirin↗