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At least 19 recordsLinked to original sources
PubMed2001

[The study of 18 cases of aspirin urticaria at dermatology of Yodogawa Christian Hospital--on the difference between aspirin asthma and aspirin urticaria].

Aspirin intolerance manifests itself as two clinical symptoms, urticaria/angioedema and asthma. However, there is seldom patient of aspirin intolerance who has the both symptoms, urticaria and asthma. So we suspect that the pathogenic mechanism for aspirin urticaria differs from that for aspirin asthma. We examined 18 patients of aspirin urticaria at dermatology of Yodogawa Christian Hospital, especially as to oral aspirin challenge test. All patients had no symptom of asthma. Threshold dose evoke urticaria/angioedema after ingesting 100 to 500 mg of aspirin (average, 311 mg). Urticaria/angioedema occurred within 50 minutes to 14 hours (average, 3 hours 16 minutes) after ingesting aspirin. The dose and the time of oral aspirin challenge test for these 18 patients were more spent than those for reported patients of aspirin asthma. These results support the opinion that aspirin urticaria has the different pathogenic mechanism from aspirin asthma. In addition, we experienced one patient of aspirin intolerance which caused hyperemia and edema of the bulbar conjunctiva. She had no symptom of urticaria and asthma, and had the both character of aspirin urticaria and asthma as to aspirin challenge test. We propose that aspirin intolerance is classified in reaction of the skin (urticaria/angioedema) and reaction of the mucosa (asthma), and it has an intermediate type.

Adolescent↗
PubMed1994

Effects of low dose aspirin (50 mg/day), low dose aspirin plus dipyridamole, and oral anticoagulant agents after internal mammary artery bypass grafting: patency and clinical outcome at 1 year. CABADAS Research Group of the Interuniversity Cardiology Institute of The Netherlands. Prevention of Coronary Artery Bypass Graft Occlusion by Aspirin, Dipyridamole and Acenocoumarol/Phenprocoumon Study.

OBJECTIVES: This study was performed to compare the efficacy and safety of aspirin, aspirin plus dipyridamole, and oral anticoagulant agents in the prevention of internal mammary artery graft occlusion. BACKGROUND: Antithrombotic drugs increase vein graft patency after coronary artery bypass surgery. Their benefit after internal mammary artery grafting has not been established. METHODS: Angiographic internal mammary artery graft patency at 1 year was assessed in 494 patients who received both internal mammary artery and vein grafts. These patients were a subgroup of a prospective, randomized vein graft patency study in 948 patients assigned to treatment with aspirin, aspirin plus dipyridamole, or oral anticoagulant agents. The design was double-blind for both aspirin groups and open for oral anticoagulant treatment. Dipyridamole (5 mg/kg body weight per 24 h intravenously, followed by 200 mg twice daily) and oral anticoagulant agents (prothrombin time target range 2.8 to 4.8 international normalized ratio) were started before operation, and low dose aspirin (50 mg/day) after operation. Clinical outcome was assessed by the incidence of myocardial infarction, thrombosis, major bleeding or death. RESULTS: Occlusion rates of distal anastomoses were 4.6% in the aspirin plus dipyridamole group and 6.8% in the oral anticoagulant group versus 5.3% in the aspirin group (p = NS). Overall clinical event rates were 23.3% and 13.3% in the aspirin plus dipyridamole group and the aspirin group, respectively (relative risk 1.75, 95% confidence interval 1.09 to 2.81, p = 0.025), and 17.1% in the oral anticoagulant group. CONCLUSIONS: Internal mammary artery graft patency at 1 year is not improved by aspirin plus dipyridamole or oral anticoagulant agents over that obtained with low dose aspirin alone. However, there is evidence that the overall clinical event rate increases if dipyridamole is added to aspirin.

Acenocoumarol↗
PubMed1995

Direct Comparison of Aspirin Plus Hirudin, Aspirin Plus Heparin, and Aspirin Alone Among 12,000 Patients with Acute Myocardial Infarction Not Receiving Thrombolysis: Rationale and Design of the First American Study of Infarct Survival (ASIS-1).

While antithrombotic therapy of acute myocardial infarction is clearly beneficial, substantial controversy exists regarding the optimal regimen. In particular, while aspirin alone has proven highly effective in reducing rates of reinfarction, stroke, and death following acute coronary occlusion, heparin has not clearly been shown to have additional benefit when added to aspirin but is associated with increased rates of hemorrhagic stroke and major bleeding. At the same time, available data for newer specific thrombin inhibitors such as hirudin suggest greater benefits than aspirin alone or aspirin plus heparin in terms of maintaining coronary flow, but possibly higher risks of hemorrhagic stroke and major bleeding. Since no completed or ongoing large-scale clinical trial has directly compared aspirin plus hirudin, aspirin plus heparin, and aspirin alone, it is not currently possible to decide which of these three antithrombotic regimens provides the optimal bmefit-to-risk ratio. The First American Study of Infarct Survival (ASIS-1) is directly comparing aspirin alone, aspirin plus heparin, and aspirin plus hirudin among 12,000 patients presenting with signs and symptoms of acute myocardial infarction who are not felt by their responsible physicians to be appropriate candidates for thrombolytic therapy. Such patients comprise almost two thirds of all U.S. subjects presenting with acute myocardial infarction and are a group at substantial risk of death, reinfarction, and stroke. Thus, the ASIS-I trial will provide importantly relevant data regarding the optimal antithrombotic regimen for the majority of patients presenting with acute myocardial infarction. In this manuscript we provide the rationale and design for the First American Study of Infarct Survival (ASIS-1), a randomized, double-blind, placebo-controlled trial directly comparing aspirin alone, aspirin plus intravenous heparin, and aspirin plus intravenous hirudin in the treatment of acute myocardial infarction patients not receiving thrombolytic therapy.

Journal Article↗
PubMed1981

Salicylate-aspirin interaction in the rat. Evidence that salicylate accumulating during aspirin administration may protect vascular prostacyclin from aspirin-induced inhibition.

Aspirin inhibits cyclooxygenase, thus preventing thromboxane A2 production in blood platelets and prostacyclin in vascular cells. Aspirin is rapidly hydrolyzed to salicylate in the circulation. The objectives of this study were (a) to evaluate whether administration of salicylate, though ineffective by itself, prevents the inhibitory effect of aspirin on platelet and/or vascular cyclooxygenase activity; (b) to verify whether salicylate accumulating in blood after aspirin administration interferes with the pharmacological activity of further doses of aspirin. Pretreatment of rats with sodium salicylate (25-100 mg/kg i.p.) resulted in dose-related prevention of the effect of a subsequent dose of aspirin (2.5-10 mg/kg i.v.) on both platelet and vascular cells. Sodium salicylate appeared to amplify the greater response of platelets to aspirin compared with vessel wall. Pretreatment of rats with repeated high doses of aspirin (200 mg/kg) resulted after 24 h in blood salicylate levels (150-200 microgram/ml) that significantly prevented the inhibitory effect of a subsequent dose of aspirin on newly synthesized vascular prostacyclin. Blood salicylate levels obtained after 36 or 48 h (less than 50 microgram/ml) were too low to blunt aspirin's effect. The interference with aspirin of its major endogenous metabolite should be borne in mind when interpreting results obtained with high dose aspirin or during repeated administration of this drug.

Animals↗
PubMed1981

The bioavailabilities of aspirin from an aspirin aluminum and an aspirin tablet and the effects of food and aluminum hydroxide gel.

The bioavailability of aspirin from an aspirin aluminum tablet was compared with that from an aspirin tablet in humans by determining total salicylate excreted in the urine. The effects of concomitant intakes of antacid or food on the bioavailability of aspirin were also investigated. The bioavailability of aspirin from an aspirin aluminum tablet was nearly 60% of that from an aspirin tablet. The low bioavailability of aspirin from an aspirin aluminum tablet was caused by slow release of aspirin from the aluminum complex, and not increased by concomitant intake of food. Intake of food, however, reduced both rate and extent of bioavailability of aspirin from an aspirin tablet, but dried aluminum hydroxide gel granules had no effect on the bioavailability of it.

Adult↗
PubMed2004

Lack of aspirin effect: aspirin resistance or resistance to taking aspirin?

BACKGROUND: A lack of aspirin effect on platelets after a myocardial infarction (MI) is associated with poor health outcome. This lack of effect may be due to biological resistance to aspirin or due to nonadherence (the patient is not taking the aspirin, hence it has no effect). Determining which of these factors predicts poor outcome would inform potential intervention strategies. METHODS: Aspirin effect on platelets was assessed in a cohort of MI survivors who were divided into three groups: group A ("adherent"), patients whose platelets were affected by aspirin; group B ("nonadherent"), patients whose platelets showed no aspirin effect and who admitted in an interview that they were not taking their medications; and group C (potentially biologically resistant to aspirin), patients whose platelets showed no aspirin effect but maintained that they were taking their aspirin. Two health outcome measures (death, reinfarction, or rehospitalization for unstable angina; or admission for any cardiovascular causes) were assessed 12 months after enrollment. RESULTS: Seventy-three patients were enrolled and classified into groups A ("adherent," 52 patients), B ("nonadherent," 12 patients), and C ("potentially aspirin resistant," 9 patients). Adverse events and readmission were more common in the nonadherent group (B)-42% and 67%, respectively, when compared with the adherent group (A)-6% and 11%, and with the potentially biologically resistant group (C)-11% and 11%. CONCLUSIONS: Nonadherence is a significant mediator of poor outcome. It is important to evaluate whether or not patients are taking their medications in clinical settings and in studies that evaluate the effect of prescribed medications.

Aspirin↗
PubMed1997

Platelet responses to several agonists and combinations of agonists in whole blood: a placebo controlled comparison of the effects of a once daily dose of plain aspirin 300 mg, plain aspirin 75 mg and enteric coated aspirin 300 mg, in man.

Platelet responses to several agonists and combinations of agonists have been measured in whole blood from healthy volunteers. We have determined the effects of once daily treatment for five days with plain aspirin 300 mg, plain aspirin 75 mg, enteric coated aspirin 300 mg or placebo. Measurements were made of platelet aggregation (using a platelet counting technique) and the release reaction (14C-5HT release from pre-labelled platelets). The extents of these responses before aspirin administration depended on the agonist used. ADP, adrenaline and PAF failed to induce any 14C-5HT release in most subjects, but combinations of these agonists acted synergistically to produce extensive 14C-5HT release. All three aspirin preparations reduced the extent of the platelet responses to most agonists: platelet aggregation induced by collagen, ristocetin and arachidonate and 14C-5HT release induced by collagen, streptokinase, and various combinations of ADP, adrenaline and PAF. None of the preparations had any effect on the aggregation that occurred in the absence of an agonist (spontaneous aggregation), but they all reduced streptokinase-induced aggregation to control (spontaneous) levels, and abolished the 14C-5HT release induced by arachidonate and by ristocetin. All three aspirin preparations were equally effective after two daily doses. No further inhibition of platelet responses was obtained after five daily doses. Plain aspirin 300 mg achieved its maximal effect after only a single dose, but enteric coated aspirin 300 mg (and sometimes plain aspirin 75 mg) produced sub-maximal inhibition after only a single dose. Parallel investigations on the effects of these aspirin regimes on gastric mucosal prostaglandin E2 synthesis and gastroduodenal mucosal injury were performed. These results will be reported separately.

Adenosine Diphosphate↗
PubMed1977

A comparison of a new slow release aspirin ("slow aspirin") with plain aspirin in the treatment of rheumatoid disease.

In a single centre double-blind crossover study in eighteen patients with established rheumatoid disease, a new slow release aspirin ("slow aspirin") was compared with plain aspirin with respect to patient tolerability and gastric mucosal damage as observed at gastroscopy. "Slow aspirin" was significantly better than plain aspirin with regard to gastroscopic findings. With "slow aspirin", the gastric mucosal appearances were definitely better in eight patients, worse in two, and eight showed no difference. There was a high incidence of gastric ulceration or erosions in the groups as a whole (39%) but few patients complained of dyspepsia. There was little difference in the ability of both plain and "slow aspirin" in controlling the patients' joint symptoms. Evidence has been provided to suggest that "slow aspirin" is less injurious to the gastric mucosa. In an attempt to reduce gastric mucosal damage due to prolonged aspirin treatment it is therefore concluded that "slow aspirin" merits consideration in the management of chronic rheumatoid disease.

Adult↗
PubMed2004

Co-administration of nitric oxide-aspirin (NCX-4016) and aspirin prevents platelet and monocyte activation and protects against gastric damage induced by aspirin in humans.

OBJECTIVES: The goal of this study was to test the hypothesis that NCX-4016 may have broader anti-inflammatory and antithrombotic effects as well as better gastric tolerability than aspirin in humans. BACKGROUND: NCX-4016 is an aspirin derivative containing a nitric oxide-releasing moiety that prevents platelet activation and modulates tissue factor (TF) expression and cytokine release from lipopolysaccharide (LPS)-stimulated monocytes. METHODS: This was a blind-observer, placebo-controlled, parallel-group study in which 48 healthy subjects were randomized to receive NCX-4016 800 mg twice a day, NCX-4016 800 mg twice a day plus aspirin 325 mg, aspirin 325 mg, or placebo for 21 days. RESULTS: Similar to aspirin alone, NCX-4016 effectively inhibited platelet aggregation induced by 0.6 mmol/ arachidonic acid, clot-stimulated thromboxane (TX) B2 generation in whole blood, and urinary excretion of 11-dehydro-TXB2. Unlike aspirin alone, the administration of NCX-4016 significantly inhibited TF expression in monocytes stimulated ex vivo with 10 micromol/l LPS (determined by flow-cytometry analysis of TF on CD14 positive cells). NCX-4016 also inhibited the rapid TF expression induced in monocytes by a proteinase activated receptor agonist (thrombin receptor activator protein, 2 micromol/l) as well as LPS-induced expression of CD11b . Ex vivo, release of MCP-1 and interleukin-6 were significantly inhibited by NCX-4016, but not by aspirin. NCX-4016 was not associated with gastric damage, and significantly reduced gastric injury when co-administered with aspirin, although both drugs reduced gastric PGE2 production to the same extent. CONCLUSIONS: NCX-4016 is equally effective as aspirin in inhibiting cyclooxygenase activity. However, NCX-4016 causes less gastric damage and prevents monocyte activation. Larger multicenter trials are warranted to establish clinical efficacy and safety of NCX-4016.

Administration, Oral↗
PubMed1999

Aspirin absorption rates and platelet inhibition times with 325-mg buffered aspirin tablets (chewed or swallowed intact) and with buffered aspirin solution.

Large clinical trials such as the second International Study of Infarct Survival routinely gave patients with myocardial infarction a chewed aspirin, yet there are no data to show whether chewing of aspirin is better, or worse, than swallowing a whole tablet. We performed a randomized, placebo-controlled study to determine whether chewing aspirin or administering it in solution accelerates its absorption and antiplatelet activity. On separate days, 12 fasting volunteers ingested 325 mg of buffered aspirin, either by chewing a tablet for 30 seconds before swallowing it with 4 ounces of water, swallowing a whole tablet with 4 ounces of water, or drinking 4 ounces of Alka Seltzer. Frequent blood samples were obtained for serum aspirin, salicylate, and thromboxane B2 (TxB2) concentrations. With all formulations of aspirin, serum TxB2 decreased 50% when the plasma aspirin concentration reached approximately 1,000 ng/ml. A 50% and 90% decrease in serum TxB2 occurred more quickly after chewing a tablet than after a tablet was swallowed whole. For example, the t 50% for serum TxB2 inhibition was 5.0 +/- 0.6 minutes with the chewed tablet versus 12.0 +/- 2.3 minutes when the tablet was swallowed (p = 0.01). A 50% decrease in serum TxB2 occurred 7.6 +/- 1.2 minutes after Alka Seltzer solution (p = 0.04 vs chewing a tablet; p = 0.13 vs swallowing a whole tablet). Chewing an aspirin tablet is the most effective way of accelerating absorption of aspirin into the blood and shortening the time required for an antiplatelet effect.

Absorption↗
PubMed1980

Aspirin-sensitive asthma: tolerance to aspirin after positive oral aspirin challenges.

Two aspirin-sensitive asthmatic patients underwent oral aspirin challenges for investigative purposes. Folowoing the expected respiratory reaction to aspirin, the patients became refractory to the further adverse effects of aspirin. Additionally they began taking 325 mg aspirin per day, and after 6 and 8 mo aspirin dosage was increased to 650 mg per day. We have noted an improvement in their rhinitis and asthma during this open drug trial. Furthermore, maintenance systemic corticosteroids have been reduced in one patient and discontinued in the other without a decline in lung function values. If these intitial observations are found in a larger number of aspirin-sensitive asthmatic patients, changes in our understanding of the pathogenesis of rhinosinusitis-asthma-aspirin syndrome would follow, and treatment for such asthmatic patients might be improved.

Administration, Oral↗
PubMed1991

[Neutrophil chemotactic activity after administration of aspirin during aspirin tolerance in patients with asthma and aspirin hypersensitivity].

The increase of neutrophil chemotactic activity (NCA) is related to degranulation of mast cells. In aspirin asthma following aspirin bronchial provocation NCA increases in 50% to 100% of the studied patients. The authors studied NCA after aspirin in patients with aspirin asthma during a state of induced tolerance. If NCA would not increase that would imply that in the state of induced tolerance degranulation of mast cells does not occur. Out of 22 subjects NCA was increased in 11. In these patients tolerance to aspirin was induced and NCA was once more studied. The authors found that in these patients after a dose of 600 mg of aspirin NCA was not increased. This could impose that in patients with aspirin asthma that developed tolerance to aspirin degranulation of mast cells does not occur.

Adult↗
PubMed1985

Bronchial hyperreactivity to histamine in aspirin sensitive asthmatics: relationship to aspirin threshold and effect of aspirin desensitisation.

Twenty seven aspirin sensitive asthmatic patients were studied to determine the relationship between non-specific bronchial responsiveness to inhaled histamine and the degree of sensitivity to aspirin (aspirin threshold dose). No correlation was found between provocative concentration of histamine (PC20H) and aspirin threshold dose. In 11 patients the influence of aspirin desensitisation on bronchial reactivity to inhaled histamine was examined. Mean PC20H measured the day after the patients were desensitised to 600 mg of aspirin did not change significantly from the values before desensitisation. These observations suggest that sensitivity to aspirin and non-specific bronchial hyperreactivity in asthmatic patients are independent phenomena.

Adult↗
PubMed2000

Double-blind study of the safety of clopidogrel with and without a loading dose in combination with aspirin compared with ticlopidine in combination with aspirin after coronary stenting : the clopidogrel aspirin stent international cooperative study (CLASSICS).

BACKGROUND: Combination therapy with the ADP receptor antagonist ticlopidine plus aspirin has emerged as standard care after coronary stenting. Clopidogrel, a new ADP receptor antagonist, has greater molar potency than ticlopidine and better safety/tolerability. METHODS AND RESULTS: Patients (n=1020) were randomized after successful stent placement and initiated on a 28-day regimen of either (1) 300-mg clopidogrel loading dose and 325 mg/d aspirin on day 1, followed by 75 mg/d clopidogrel and 325 mg/d aspirin; (2) 75 mg/d clopidogrel and 325 mg/d aspirin; or (3) 250 mg BID ticlopidine and 325 mg/d aspirin. The primary end point consisted of major peripheral or bleeding complications, neutropenia, thrombocytopenia, or early discontinuation of study drug as the result of a noncardiac adverse event during the study-drug treatment period. The primary end point occurred in 9.1% of patients (n=31) in the ticlopidine group and 4.6% of patients (n=31) in the combined clopidogrel group (relative risk 0.50; 95% CI 0.31 to 0.81; P=0.005). Overall rates of major adverse cardiac events (cardiac death, myocardial infarction, target lesion revascularization) were low and comparable between treatment groups (0.9% with ticlopidine, 1.5% with 75 mg/d clopidogrel, 1.2% with the clopidogrel loading dose; P=NS for all comparisons). CONCLUSIONS: The safety/tolerability of clopidogrel (plus aspirin) is superior to that of ticlopidine (plus aspirin) (P=0.005). The 300-mg loading dose was well tolerated, notably with no increased risk of bleeding. Secondary end point data are consistent with the hypothesis that clopidogrel and ticlopidine have comparable efficacy with regard to cardiac events after successful stenting.

Aged↗
PubMed1986

Comparison of effects of lysine aspirin, soluble aspirin and conventional aspirin on buccal potential difference in healthy volunteer subjects.

The effects of aspirin, soluble aspirin and lysine aspirin on buccal mucosal potential difference (p.d.) were compared in a double-blind trial. Placebo and three doses of each preparation containing 150, 300 and 600 mg of aspirin were allocated according to a latin square design. Six volunteer subjects were studied; each received a total of 10 treatments at least 24 h apart. All doses of each preparation considered, a significant treatment effect was seen [F (d.f. = 2,306) = 6.2, P less than 0.003]. Lysine aspirin showed the least effect of the active treatments on buccal p.d. with a change from baseline of +8.5 mV compared with +13.3 for soluble aspirin +14.4 for conventional aspirin and -5.2 mV for placebo.

Aspirin↗
PubMed1989

Rioprostil heals pre-existing aspirin-induced gastric lesions in dogs during daily aspirin administration without altering the anti-inflammatory or analgesic efficacy of aspirin.

Rioprostil (3-100 micrograms/kg/day p.o.), but not cimetidine (30 mg/kg/day p.o.), healed pre-existing aspirin (1950 mg)-induced gastric lesions in dogs despite daily aspirin (975 mg) administration. Gastric antisecretory doses of rioprostil (10 and 100 micrograms/kg/day) decreased lesion scores by 71 to 77 and 90 to 93% after 7 and 11 days, respectively. A nonantisecretory dose of rioprostil (3 micrograms/kg/day) decreased lesion scores by 80% after 14 days. In contrast, lesion scores in dogs receiving either vehicle or a maximal gastric antisecretory dose of cimetidine (30 mg/kg/day) remained unchanged during the 28-day course of treatment. In addition, rioprostil prevented the weight loss which accompanied daily administration of aspirin (975 mg) in vehicle- or cimetidine-treated dogs. When cimetidine-treated dogs were switched to daily rioprostil (100 micrograms/kg/day) and aspirin (975 mg/day) therapy, lesions healed within 6 days. In separate studies, rioprostil had no effect on the sensitivity of the gastric mucosa to subsequent aspirin administration. In addition, discontinuation of maintenance therapy during rioprostil treatment was of no increased benefit (i.e., lesions did not heal faster). Finally, in a model of urate-induced knee-joint synovitis, rioprostil treatment did not inhibit the anti-inflammatory or analgesic efficacy of aspirin, or have any proinflammatory effect of its own.

Analgesia↗
PubMed1979

Modified USP assay for simultaneous determination of aspirin and nonaspirin salicylates in aspirin and buffered aspirin tablets.

Modified USP procedures are described for the simultaneous determination of nonaspirin salicylates and aspirin in aspirin and buffered aspirin tablets. The existing USP procedures are not stability indicating for intact aspirin when significant levels of nonaspirin salicylates are present, as is often the case in short-term, high temperature stability programs. The modified procedures yeld considerably shorter analysis times and stability-indicating assays for intact aspirin without the need for sophisticated equipment other than that presently required by USP XIX.

Aspirin↗
PubMed1980

Aspirin--a national survey III: Determination of impurities in bulk aspirin and aspirin formulations by high-pressure liquid chromatography and spectrophotometry.

A quantitative high-pressure liquid chromatographic method, using a reversed-phase column and an aqueous acetic acid-methanol solution as the mobile phase, was employed for the determination of O-acetyl-O-salicylsalicylic acid and O-salicylsalicylic acid in pharmaceutical aspirin preparations. The aspirin was dissolved, filtered, and injected into the chromatograph. The absorbance of the impurities was measured at 254 nm. Acetylsalicylic anhydridge was determined by a spectrophotometric method. The aspirin was dissolved in pH 11.3 buffer and extracted with benzene. An aliquot of the benzene was evaporated, and the residue was dissolved in alpha-benzamidocinnamate-pyridine reagent. The acetylsalicylic anhydride was measured using the difference between the absorbance at 362 and 372 nm. Possible interference of aspirin with the procedure is discussed. Thirty-four bulk aspirin and 172 tablet formulations were examined. Results for O-acetyl-O-salicylsalicylic acid, O-salicylsalicylic acid and acetylsalicylic anhydride are given.

Aspirin↗