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PubMed1983

Oral analgesic efficacy of suprofen compared to aspirin, aspirin plus codeine, and placebo in patients with postoperative dental pain.

The purpose of this study was to evaluate the analgesic efficacy and safety of single oral doses of suprofen 200 and 400 mg, compared with aspirin 650 plus codeine 60 mg, aspirin 650 mg, and placebo in the relief of moderate to severe pain resulting from the surgical removal of impacted third molars. 157 patients completed a randomized, double-blind, single-dose, stratified, parallel-groups trial, and were observed for at least 4 h. Based upon each of the summary efficacy measures, sum pain intensity difference (SPID), percent SPID, TOTPAR and a global evaluation, all four active treatments were approximately equally effective and all were statistically superior to placebo. In addition, suprofen at both dose levels was significantly more effective than placebo beginning at the 0.5-hour observation for mean pain intensity, whereas the two aspirin treatments were not superior to placebo until the 1-hour observation. Side effects were minimal; there was one in the suprofen 200 mg, three in the aspirin 650 mg, and one in the placebo treatment group. Thus, it appears that suprofen at 200 and 400 mg is a safe and effective oral analgesic for the relief of moderate or severe postoperative dental pain, and it is possible that compared to aspirin 650 mg and aspirin 650 mg plus codeine 60 mg, it has a more rapid onset of action.

Adolescent↗
PubMed1984

Effect of the calcium ionophore A23187 and aspirin on histamine release in vitro from leukocytes of aspirin-intolerant donors.

In vitro histamine release from leukocytes of 10 aspirin-intolerant donors in response to the calcium ionophore A23187 and aspirin was compared to that of controls. Incubation with A23187 induced a concentration-dependent histamine release from leukocytes of all donors. At 0.1 and 0.2 micrograms/ml A23187, release from leukocytes of aspirin-intolerant donors was significantly less (p less than 0.01) than that of controls. Preincubation with aspirin failed to alter spontaneous or A23187-stimulated histamine release. Leukocytes of aspirin-intolerant donors do not demonstrate an enhanced sensitivity to histamine release stimulated by aspirin or A23187.

Adult↗
PubMed2004

Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

The majority of patients who suffer peri-operative thromboembolic complication while undergoing vascular procedures do so despite taking aspirin. This study examined the antiplatelet effect of aspirin during surgery in patients undergoing carotid endarterectomy (CEA). Fifty patients undergoing CEA were standardised to 150 mg aspirin daily for > or =2 weeks. Platelet aggregation in response to arachidonic acid (AA) was measured in platelet rich plasma prepared from blood taken prior to, during, and at the end of surgery. Spontaneous platelet aggregation was also studied, as was the role of physiological agonists (ADP, collagen, thrombin, and epinephrine) in mediating the in vivo and in vitro responses to AA. Eighteen patients undergoing leg angioplasty, also on 150 mg aspirin, without general anaesthesia, served as a control group. In the CEA patients aggregation induced by AA (5 mM) increased significantly from 7.6 +/- 5.5% pre-surgery to 50.8 +/- 29.5% at the end of surgery (p <0.0001). Aggregation to AA was even greater in samples taken mid-surgery from a sub-set of patients (73.8+/-7.2%; p = 0.0001), but fell to 45.9 +/- 7.4% by the end of surgery. The increased aggregation in response to AA was not due to intra-operative release of physiological platelet agonists since addition of agents that block/neutralise the effects of ADP (apyrase; 4 micro g/ml), thrombin (hirudin; 10 units/ml), or epinephrine (yohimbine; 10 micro M/l) to the samples taken at the end of surgery did not block the increased aggregation. The patients undergoing angioplasty also showed a significant rise in the response to AA (5 mM), from 5.6 +/- 5.5% pre-angioplasty to 32.4 +/- 24.9% at the end of the procedure (p <0.0001), which fell significantly to 11.0 +/- 8.1% 4 hours later. The antiplatelet activity of aspirin, mediated by blockade of platelet arachidonic acid metabolism, diminished significantly during surgery, but was partially restored by the end of the procedure without additional aspirin treatment. This rapidly inducible and transient effect may explain why some patients undergoing cardiovascular surgery remain at risk of peri-operative stroke and myocardial infarction.

Aged↗
PubMed1985

Warfarin versus dipyridamole-aspirin and pentoxifylline-aspirin for the prevention of prosthetic heart valve thromboembolism: a prospective randomized clinical trial.

In a prospective, randomized, parallel study, two regimens of platelet-suppressant therapy (PST)--dipyridamole-aspirin and pentoxifylline-aspirin--were compared with standard oral anticoagulation with warfarin in the prevention of prosthetic heart valve thromboembolism. In the entire group of 254 patients followed for 395.6 patient-years, the thromboembolic rate was significantly less in the warfarin group (warfarin vs dipyridamole-aspirin, p less than .005; warfarin vs pentoxifylline-aspirin, p less than .05). Subgroup analysis disclosed that, in patients with isolated mitral valve replacement, warfarin was superior to both of the PSTs with respect to the prevention of thromboembolism (warfarin vs dipyridamole-aspirin, p = .005; warfarin vs pentoxifylline-aspirin, p less than .05). Furthermore, a significant number of our patients could not tolerate the antiplatelet agents. However, in the rare situation in which repeated significant bleeding occurs despite careful adjustment of the dosage of warfarin, PST may be an acceptable alternate method of thromboembolism prophylaxis.

Adult↗
PubMed1997

Results of a consecutive series of patients receiving only antiplatelet therapy after optimized stent implantation. Comparison of aspirin alone versus combined ticlopidine and aspirin therapy.

BACKGROUND: Previous studies have shown that stents can be inserted in coronary arteries of patients who are subsequently treated safely with antiplatelet therapy only (ticlopidine and/or aspirin) with a low incidence of stent thrombosis, provided that stent expansion is adequate and there are no other flow-limiting lesions present. However, it is unknown whether ticlopidine combined with aspirin is superior to aspirin alone in preventing stent thrombosis. METHODS AND RESULTS: From March 1993 through July 1995, 801 consecutive patients assigned to receive either aspirin therapy alone (ASA, 264 patients, 348 lesions) or a combination of ticlopidine and aspirin (TIC-ASA, 537 patients, 737 lesions) after a successful stent insertion, in most accomplished with intravascular ultrasound guidance, were evaluated retrospectively. At 1 month, there was no difference in the ASA group compared with the TIC-ASA group in the rate of any stent thrombosis (1.9% versus 1.9%; P = 1), subacute stent thrombosis (1.9% versus 1.3%; P = .5), cumulative major adverse clinical events (1.9% versus 2.0%; P = 1), and peripheral vascular complications (0.5% versus 0.2%; P = .3). Medication side effects that required termination of antiplatelet therapy occurred only in 1.9% of patients in the TIC-ASA group (P = .04). CONCLUSIONS: At 1-month clinical follow-up, stent thrombosis and other adverse clinical outcomes were not significantly different between the ASA and TIC-ASA groups. Medication side effects occurred only in patients treated with ticlopidine. These results provide further evidence of the safety of treatment with antiplatelet therapy only after optimal stent implantation and support the efficacy of aspirin alone in preventing stent thrombosis.

Angioplasty, Balloon↗
PubMed1994

Eicosanoids in bronchoalveolar lavage fluid of aspirin-intolerant patients with asthma after aspirin challenge.

We have recently shown that oral aspirin provocation leads to an increase in LTE4 and a reduction in 11-dehydro-TXB2 levels in urine of patients with aspirin induced-asthma (AIA). To test the hypothesis that cyclooxygenase inhibition and an enhancement of cysteinyl-leukotriene production occurs in the lungs of patients with AIA, we examined the eicosanoid levels in bronchoalveolar lavage fluid obtained 30 min after lysine-aspirin or placebo inhalation in 10 patients with AIA. Eosinophil cationic protein (ECP) levels were determined to evaluate eosinophil activation. Six asthmatics nonsensitive to aspirin (NA) underwent challenge with placebo. The dose of lysine-aspirin inhaled by patients with AIA was equal to that which had produced > or = 20% fall in FEV1. Compared with NA, patients with AIA had: (1) eicosanoid levels, particularly PGE2 and TXB2, elevated and (2) higher number of eosinophils and ECP. The overproduction of eicosanoids could be related to a distinct eosinophilic inflammation in airways of patients with AIA. Inhalation of lysine-aspirin had no effects on 12-HETE and 15-HETE levels, but it markedly depressed cyclooxygenase products and significantly enhanced leukotriene production in the lungs of patients with AIA.

Adult↗
PubMed1986

Biochemical selectivity of oral versus intravenous aspirin in rats. Inhibition by oral aspirin of cyclooxygenase activity in platelets and presystemic but not systemic vessels.

In rats intravenous aspirin was only slightly more effective an inhibitor of platelet thromboxane B2 (TxB2) than of aorta 6-keto-prostaglandin (PGF)1 alpha generation (1.9 versus 2.1 mg/kg). In contrast, oral aspirin was about five times more effective on platelet than on aorta cyclooxygenase activity. The "biochemical selectivity" of aspirin as an inhibitor of platelet and vascular cyclooxygenase thus was not apparent after intravenous administration of the drug. However, this could be achieved by relatively low doses of oral (or intraduodenal) aspirin, on account of "presystemic" acetylation of platelet cyclooxygenase. Even in this condition, though, aspirin selectivity was relative to "systemic" peripheral vessels but not to the vessels of the enterohepatic circulation. Indeed after an oral or intraduodenal dose of 5 mg/kg aspirin, generation of portal vein 6-keto-PGF1 alpha was inhibited to much the same extent as platelet TxB2, while inferior vena cava 6-keto-PGF1 alpha formation was spared.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

Aspirin and warfarin versus aspirin monotherapy after myocardial infarction.

OBJECTIVE: To review data concerning combined aspirin/warfarin versus aspirin alone for secondary prevention after myocardial infarction (MI). DATA SOURCES: Literature was accessed through MEDLINE (1966-September 2002). Search terms included aspirin, warfarin, secondary prevention, and myocardial infarction. DATA SYNTHESIS: Despite use of low-dose aspirin after an MI, risk of subsequent death and ischemic events remains high, making strategies for secondary prevention imperative. Relevant, large, long-term studies focusing on dual aspirin/warfarin versus aspirin alone in post-MI patients were evaluated. CONCLUSIONS: Aspirin 75-325 mg/d should remain first-line therapy for secondary prevention after MI. Combining aspirin 75-81 mg with warfarin to maintain the international normalized ratio at 2.0-2.5 may provide added benefit, but should be considered only for patients at high risk for thromboembolic events.

Aspirin↗
PubMed2000

Comparison of sibrafiban with aspirin for prevention of cardiovascular events after acute coronary syndromes: a randomised trial. The SYMPHONY Investigators. Sibrafiban versus Aspirin to Yield Maximum Protection from Ischemic Heart Events Post-acute Coronary Syndromes.

BACKGROUND: Aspirin lowers risks of death and myocardial infarction in patients with acute coronary syndromes. Intravenous glycoprotein IIb/IIIa receptor antagonists further reduce the rates of ischaemic events in these patients, but the efficacy of long-term oral glycoprotein IIb/IIIa receptor blockade has not been established. We tested whether the oral glycoprotein IIb/IIIa receptor antagonist sibrafiban would prevent more cardiovascular events than aspirin, when given within 7 days of, and sustained for 90 days after, an acute coronary syndrome event. METHODS: 9233 patients who had stabilised after an acute coronary syndrome event were randomly assigned aspirin (80 mg orally twice daily) or low-dose or high-dose sibrafiban. Sibrafiban doses (3.0 mg, 4.5 mg, or 6.0 mg) were based on a model accounting for weight and serum creatinine and designed to achieve at least 25% steady-state inhibition of platelet aggregation (low dose) or at least 50% inhibition (high dose). The primary endpoint was the composite of death, non-fatal infarction or reinfarction, or severe recurrent ischaemia at 90 days. Analysis was by intention to treat. FINDINGS: The 90-day rate of the primary endpoint did not differ significantly between the groups assigned aspirin (302 [9.8%]), low-dose sibrafiban (310 [10.1%]; odds ratio 1.03 [95% CI 0.87-1.21]), and high-dose sibrafiban (303 [10.1%]; 1.03 [0.87-1.21]). The groups did not differ significantly in the rates of the component events or secondary efficacy endpoints. Major bleeding was more common with high-dose sibrafiban (171 [5.7%]) than with aspirin (120 [3.9%]) or low-dose sibrafiban (159 [5.2%]). INTERPRETATION: Sibrafiban showed no additional benefit over aspirin for secondary prevention of major ischaemic events after an acute coronary syndrome, and was associated with more dose-related bleeding.

Administration, Oral↗
PubMed2000

A low dose of aspirin (75 mg/day) lowers thrombin generation to a similar extent as a high dose of aspirin (300 mg/day).

This randomized, double-blind, parallel-group study was performed to assess the effect of 1-week treatment with 75 and 300 mg aspirin on thrombin generation. Eighteen healthy men, aged 20-25 years, entered the study. After 1 week of aspirin treatment with a daily dose of 75 mg, bleeding time became prolonged by 102 s (P = 0.02), and it was prolonged by 165 s with 300 mg (P = 0.0005). None of the doses of aspirin affected peripheral blood concentrations of prothrombin fragment 1+2 and fibrinopeptide A. At the site of microvascular injury, 75 mg aspirin led to a marked, about 60%, reduction in the total amount of thrombin generated (P = 0.04). A similar decrease was observed after 7-day treatment with 300 mg aspirin (P = 0.009). We conclude that the thrombin-lowering action of aspirin in the range between 75 and 300 mg daily given for 7 days is not dose dependent.

Adult↗
PubMed2002

[Tolerability of Asacard--controlled-release aspirin and aspirin-induced asthma].

Asacard is a microcapsulated, controlled-release form of acetylsalicylic acid, which delivers very low but constant amount of the drug directly into the intestine. The dose 162.5 mg Asacard, used in prevention of cardiovascular diseases, is thus sufficient to block platelets in the portal vein from synthesizing thromboxane but not high enough to enter the systemic circulation and block the formulation of prostacyclin and other prostaglandins. It is generally accepted that in aspirin-induced asthma (AIA) the bronchospasm is provoked by inhibition of prostaglandin synthesis with overproduction of cysteinyl leukotrienes. The aim of our study was to verify the hypothesis if Asacard, as a form of aspirin, which theoretically does not block prostacycline synthesis in systematic circulation, would be well tolerated by patients with AIA. We thus studied in an open study the tolerability of three single, increasing doses of Asacard in 10 patients with confirmed by oral challenge test aspirin intolerance (4 males, 6 females, mean age 40 years). Initially, the patients received 40 mg of Asacard and FEV1 and clinical symptoms were assessed every 30 minutes for 8 hours. A positive reaction was defined as a > or = 20% decline in FEV1 from baseline. Patients with negative reaction received 75 mg Asacard 7 days later. In absence of the reaction, the last dose 162.5 mg was administered a week later. In 5 out of 10 patients studied, Asacard given at single doses up to 162.5 mg was tolerated well. In the remaining 5, it provoked bronchospasm, a fall in FEV1 > or = 20% and other extrabronchial symptoms of aspirin intolerance. No correlation was found between the doses of regular aspirin, which provoked a fall in FEV1 > or = 20% during baseline oral provocation test and Asacard doses. In conclusion, any form of aspirin, even controlled-release, should not be prescribed for patients with AIA, because it may provoke symptoms of intolerance to this drug.

Adult↗
PubMed2006

[Aspirin resistance in patients taking small dose of aspirin].

OBJECTIVE: To investigate the phenomenon and influencing factors of aspirin resistance (AR) in patients taking small dose of aspirin. METHODS: Three hundred and twenty-eight patients with stable cardiac and cerebral vascular diseases, diabetes mellitus, et al taking aspirin 100 mg/d for > or =14 days, and then their blood samples were collected for determination of optical platelet aggregation index using arachidonic acid (AA) and adenosine diphosphate (ADP). AR was defined as a state in which aggregation of > or =20% with AA and that > or =70% with ADP was found. Aspirin semi-resistance (ASR) was defined as meeting one of the above criteria. If both above criteria were not met, the condition was defined as aspirin sensitive. The difference in clinical characteristics among the groups and independent risk factors associated with AR and ASR were analyzed. RESULTS: Of 328 patients, 4.9% were AR, 27.4% were ASR. Among AR+ASR group, female, elderly, diabetic and hypertensive patients were predominant, but less common in smokers. Logistic regression analysis showed that diabetes mellitus was an independent risk factor of AR and ASR [odds ratio (OR)=0.953, 95% confidence interval (CI) 0.323-0.876, P=0.013], and hypertension was independently associated with AR and ASR (OR=0.610, 95%CI 0.376-0.991, P=0.046). The risk of AR and ASR was increased in non-smokers (OR=2.231, 95%CI 1.182-4.210, P=0.013). CONCLUSION: The incidence rate of AR in patients taking small dose of aspirin was 4.9%. Diabetes mellitus and hypertension are relative risk factors of AR and ASR. The risk of AR and ASR in the no-smoking patients is increased.

Adult↗
PubMed1989

Glucocorticosteroids attenuate aspirin-precipitated adverse reactions in aspirin-intolerant patients with asthma.

We evaluated the effects of corticosteroid pretreatment on the intensity of adverse reactions to aspirin during carefully controlled aspirin challenges in 13 aspirin-sensitive asthmatics. Two studies were performed. First, using a double-blind crossover design, we administered to five patients 75 mg prednisone daily or placebo for two days preceding the challenge. No consistent protection against adverse reactions was achieved. In the second study, a 10-day pretreatment with 15 mg oral prednisolone and topical intrabronchial and intranasal beclomethasone offered total clinical protection against bronchospasm produced by threshold doses of aspirin in five of eight patients. In two others, the bronchospasm provoked was less severe, and only in one patient did its intensity remained unchanged. There was a significant reduction in fall of mean pulmonary function tests following the second aspirin challenge, which was performed after ten days of steroid treatment. Steroids given for ten days also prevented significantly nasal discharge and nasal blockade. When diagnostic challenge tests with aspirin are carried out in asthmatic patients on long-term corticosteroid therapy, there is an increased possibility of false negative results.

Adult↗
PubMed1987

Fibrinolysis, blood coagulation, and platelet function during aspirin-induced bronchoconstriction in aspirin-intolerant asthmatics.

Nineteen asthmatic patients, 11 with and eight without aspirin (ASA) intolerance were studied in order to test possible platelet and coagulation system involvement in the pathogenesis of aspirin-induced bronchoconstriction (AIB). Aspirin-intolerant asthmatics were challenged with a previously established ASA threshold dose and, in nine of them, a positive asthmatic reaction occurred (mean fall in FEV1 39.4%). Seven out of nine patients with a positive reaction had a significant decrease in euglobulin lysis time (P less than .01) during AIB. A positive reaction after ASA was accompanied by an increase in the plasma recalcification time in five of these patients. There were no concomitant statistically significant changes in the platelet count, circulating platelet aggregates, and platelet factor 4 activity. In a control group of ASA-tolerant asthmatics, aspirin at a 200-mg dose did not evoke any respiratory reaction and, during two hours after ASA, no significant variation was found in any of the laboratory parameters studied. We conclude that activation of fibrinolysis accompanying AIB results from intrinsic pharmacologic properties of aspirin, and may contribute to the pathogenesis of aspirin intolerance through a more generalized activation of plasma proteolytic activity.

Adult↗
PubMed1986

Peripheral venous plasma aspirin concentrations and platelet aggregation inhibition produced by enteric-coated aspirin formulations.

In a random cross-over design, six healthy consenting adult volunteers were given on separate occasions single doses of 300-650 mg of 3 different formulations of enteric-coated aspirin. Over various intervals for 48-54 h following dosage, plasma aspirin and salicylate concentrations were measured together with percentage inhibition of platelet aggregation activated by threshold concentrations of sodium arachidonate alone and combined with ADP and collagen. In all subjects each formulation delivered measurable quantities of aspirin to the peripheral circulation, the unchanged drug being detected at various times up to and including 28 h after dosage. Moreover, low aspirin concentrations were found to co-exist with unimpaired platelet aggregation. All 3 formulations yielded statistically significant (P less than 0.01) inhibition of platelet aggregation activated both by arachidonate and by the combination of aggregants when tested 24-29 and 48-54 h after dosage; there were no significant differences (P greater than 0.05) between the 3 formulations in this regard. Two different patterns of delivery of unchanged aspirin to the systemic circulation from these enteric-coated formulations were apparent. These patterns may be important when considering which aspirin formulation might be most appropriate in chronic use for an antiplatelet effect. None of the enteric-coated formulations used in this study may be optimal in this regard.

Adenosine Diphosphate↗
PubMed1984

Effects of chronic aspirin ingestion in aspirin-intolerant asthmatic patients.

The effects of regular aspirin ingestion after aspirin-desensitization were evaluated in 10 aspirin-intolerant asthmatic patients. Chronic aspirin ingestion was not observed to be associated with either a significant improvement of mean FEV1 values or with a decrease in daily corticosteroid requirements. This study suggests that regular aspirin ingestion in aspirin-intolerant asthmatic patients does not induce a measurable improvement of the respiratory status.

Administration, Oral↗
PubMed1994

[A case of aspirin-induced cough without bronchoconstriction. A new type of aspirin hypersensitivity].

A 54-year-old woman was admitted to our hospital because of an asthmatic attack. Her first asthma attack occurred when she was 53 years old. It was followed by a flu-like infection, and was preceded for one year perennial rhinitis and loss of the sense of smell. Symptoms were perennial, and unrelated to the seasons. Because these clinical findings resembled those of aspirin-induced asthma (AIA), an aspirin-DL-lysine i.v. challenge test was done. Cough, perspiration, and flushing was provoked within 15 min after aspirin-DL-lysine injection, but FEV1 did not change. Respiratory sounds were normal and no wheezing was audible. Other cyclooxygenase inhibitors (ketoprofen, sulpyrine and acetaminophen) provoked the same symptoms. Successively increasing doses of injected aspirin-DL-lysine resulted in complete tolerance to this stimulus. We propose that aspirin-induced cough without bronchoconstriction is a new type of aspirin hypersensitivity.

Aspirin↗
PubMed1993

The differential effect of aspirin on human platelet activation in aspirin-sensitive asthmatics and normal subjects.

1. The in vitro effect of aspirin on platelet aggregation and ATP release induced by platelet activating factor (PAF), arachidonic acid (AA) and collagen (COL) was assessed in 10 aspirin-sensitive (ASP+) asthmatic patients and 10 normal subjects. 2. For PAF, but not AA or COL, both the baseline EC50 and minimum concentration required to produce a maximum response for aggregation were significantly increased in ASP+ asthmatics compared with normal subjects (P < 0.05). Maximum ATP released was greater in ASP+ patients for all agonists but the difference was most significant for PAF (P < 0.025). 3. In ASP+ asthmatics COL induced, but not AA induced, aggregation was less sensitive to inhibition by aspirin compared with normals (P < 0.01). Similarly, analysis of the area under the percent inhibition concentration-response curve showed aspirin to be less effective in inhibiting platelet aggregation induced by PAF in ASP+ asthmatics than in normal subjects (normal subjects: 155 +/- 11 mg% ml-1, ASP+ asthmatics: 115 +/- 19 mg% ml-1; P < 0.05). 4. Regression analysis showed a poor correlation (r = 0.25, P < 0.4933) between the degree of aspirin induced inhibition of ATP release and platelet aggregation induced by PAF in ASP+ asthmatics. 5. The significant differences observed in platelet responses to PAF, COL and to aspirin in ASP+ asthma patients further suggests an abnormality in platelet function exists in this syndrome.

Adenosine Triphosphate↗