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PubMed1983

Public awareness of aspirin and sources of aspirin information in a rural Iowa community.

One hundren fifty households in a rural Iowa community were surveyed to determine the frequency and reasons for aspirin use, their awareness of aspirin effects, and their sources of aspirin information. Of those surveyed 82 percent used aspirin to some extent and 59 percent used it at least monthly. The frequency of aspirin use was indirectly associated with age. The number of correct aspirin effects mentioned was 1.8 +/- 1.1 with 89 percent mentioning analgesia as an effect of aspirin. Nineteen percent mentioned mental relaxation as an effect of aspirin. The number of correct effects mentioned was associated directly with education and indirectly with age but was not associated with the frequency of aspirin use. The number of information sources mentioned was 1.3 +/- 0.7 with 34 percent mentioning television and radio advertising as a source of aspirin information. Awareness of gastrointestinal irritation and antipyretic effects and the number of correct effects mentioned were each associated with mention of television and radio advertising as an information source. Use of aspirin for fever was associated with mention of physicians as an information source. Seventy-two percent of the respondents indicated a desire for more information with physicians mentioned as the desired source of additional information by 69 percent of respondents.

Aspirin↗
PubMed1982

Aspirin desensitization in aspirin-sensitive asthmatic patients: clinical manifestations and characterization of the refractory period.

Thirty aspirin-sensitive asthmatic patients underwent incremental, oral aspirin challenge until a "positive reaction" (delta FEV1 greater than or equal to 25%) occurred. After this reaction, aspirin was readministered in an attempt to achieve "desensitization." This was defined as the ability of the patient to ingest 650 mg of aspirin without experiencing upper or lower respiratory-tract symptoms or a decrease in lung function. To determine the "refractory period" following aspirin desensitization, patients were rechallenged after various intervals (days) without aspirin until a positive reaction recurred. All 30 aspirin-sensitive asthmatic patients were successfully desensitized to aspirin. Individual patient refractory periods ranged from less than 2 days to greater than 5 days, with most patients gradually returning to sensitivity between 2 to 4 days. Cross-densensitization with indomethacin and other nonsteroidal anti-inflammatory drugs was also demonstrated. These studies show that aspirin desensitization can be safely achieved in aspirin-sensitive asthmatic patients; however, this desensitization will gradually disappear over several days when additional aspirin is withheld.

Adolescent↗
PubMed1986

Abnormal responses to aspirin of leukocyte oxygenation of arachidonic acid in adults with aspirin intolerance.

The effect of 1 microM and 5 microM aspirin on oxygenation of arachidonic acid in vitro by basophils stimulated with anti-IgE was assessed with basophil-enriched suspensions of mononuclear leukocytes from five patients with asthma and hypertrophic allergic rhinitis and one patient with rhinitis alone who had recent adverse pulmonary reactions to aspirin, four aspirin-tolerant patients with asthma receiving therapy similar to that of the aspirin-sensitive patients, and eight normal subjects who resembled the patients with respect to sex and age. As quantified by the combined application of high-performance liquid chromatography and radioimmunoassays, the generation of the principal products prostaglandin E2 (PGE2) and leukotriene D4 was modified differently by aspirin but not sodium salicylate in the aspirin-sensitive patients. The alterations of PGE2 generation and of the ratio of leukotriene D4 to PGE2 generation by aspirin were much greater for basophil-containing leukocytes of aspirin-sensitive patients than those of the two control groups. Although the basic mechanism and relevance to pulmonary reactions of the observed effects of aspirin were not elucidated, aspirin clearly modifies the leukocyte oxygenation of arachidonic acid differently in aspirin-sensitive patients.

Adult↗
PubMed1989

Inhaled lysine-aspirin as a bronchoprovocation procedure in aspirin-sensitive asthma: its repeatability, absence of a late-phase reaction, and the role of histamine.

Inhalation of an aerosolized solution of lysine-aspirin has previously been described as a safer technique than oral challenge with aspirin for the diagnosis of aspirin-sensitive asthma. We describe a modification of this method that involves inhalation of serially doubling incremental concentrations of lysine-aspirin by a standardized technique and allows construction of concentration-response curves. In 11 subjects with asthma, mean (SEM) age 48.2 (2.9) years, the geometric mean (range) provocation concentrations of histamine and lysine-aspirin required to produce a 20% decrease in FEV1 from baseline were 0.6 (0.04 to 3.2) and 48.3 (15.5 to 219) mg/ml, respectively. No relationship was found between these values. In seven of nine subjects investigated on two consecutive occasions, bronchoconstriction with lysine-aspirin was repeatable to within a single doubling concentration difference. Bronchoconstriction provoked by lysine-aspirin was more rapid than with oral aspirin and was not followed by any late asthmatic reaction or increase in nonspecific airway hyperresponsiveness. In six subjects, premedication with the selective H1 histamine-receptor antagonist, terfenadine, had no significant effect on bronchoconstriction provoked by inhaled lysine-aspirin, indicating little role for release of histamine in the response. We conclude that inhalation of lysine-aspirin may be used as a bronchoprovocation procedure for the diagnosis and investigation of aspirin-sensitive asthma.

Aerosols↗
PubMed1994

Comparison of the effect of heparin and aspirin versus aspirin alone on transient myocardial ischemia and in-hospital prognosis in patients with unstable angina.

OBJECTIVES: This study compared the effects of heparin and aspirin versus aspirin alone on transient myocardial ischemia and in-hospital prognosis in patients with unstable angina. BACKGROUND: Transient myocardial ischemia occurring in patients with unstable angina is associated with an adverse prognosis. Heparin and aspirin are two drugs used frequently in the treatment of this condition, but the effect of combination therapy versus aspirin alone on transient myocardial ischemia is unknown. METHODS: Two hundred eighty-five consecutive patients with unstable angina were randomized to receive either intravenous heparin plus oral aspirin (150 mg once daily) (Group H + A) or aspirin alone (Group A). Patients also received a beta-adrenergic blocking agent, diltiazem and intravenous nitrates. ST segment monitoring was performed for the 1st 48 h of treatment. Patients were followed up for the duration of their in-hospital stay. RESULTS: One hundred fifty-four patients (30 women, mean [+/- SEM] age 58.3 +/- 0.8 years) received heparin and aspirin (Group H + A), and 131 patients (26 women, mean age 60.6 +/- 0.8 years) received aspirin only (Group A). ST segment monitoring (11,622 h) yielded 244 episodes of transient myocardial ischemia of a total duration of 7,819 min. There were no significant differences between the two treatment arms in the number of patients with transient myocardial ischemia (27 [18%] in Group H + A vs. 31 [24%] in Group A), number of episodes (96 in Group H + A vs. 148 in Group A) or total duration of transient myocardial ischemia (2,911 min in Group H + A vs. 4,908 min in Group A). The incidence of in-hospital myocardial infarction or death was significantly higher in patients with transient myocardial ischemia (53% vs. 22%, p < 0.0001). Five of the six deaths occurred in patients with transient myocardial ischemia. Event-free survival from myocardial infarction or death was similar in both treatment groups. Preadmission therapy with aspirin was associated with a lower in-hospital infarction rate (19% vs. 34%, p = 0.01). CONCLUSIONS: The presence of transient myocardial ischemia in patients with unstable angina is associated with a significantly higher incidence of myocardial infarction or death in hospital. Combined therapy with heparin and aspirin compared with aspirin alone makes no difference in the development of these events, nor does it reduce the development of transient myocardial ischemia.

Adult↗
PubMed2006

Failure to maintain an aspirin-desensitized state in a patient with aspirin-exacerbated respiratory disease.

BACKGROUND: Aspirin desensitization is a useful therapy in patients with aspirin-exacerbated respiratory disease. OBJECTIVE: To describe the clinical course of a man with aspirin-exacerbated respiratory disease who was unable to be desensitized to oral aspirin. METHODS: A standard aspirin desensitization protocol was used to achieve a maximum dose of 650 mg of oral aspirin. The patient initially tolerated this dose of aspirin. RESULTS: Within days of desensitization, the patient began to react to 650 mg of aspirin. Monitored challenge with this dose of aspirin led to marked decrease in forced expiratory volume in 1 second and pronounced nasal and ocular symptoms. CONCLUSIONS: We present a patient with classic aspirin-exacerbated respiratory disease, who despite undergoing a standard aspirin desensitization protocol was unable to maintain his desensitized state.

Administration, Oral↗
PubMed2003

Long-term treatment with aspirin desensitization in asthmatic patients with aspirin-exacerbated respiratory disease.

BACKGROUND: Aspirin desensitization treatment is an option to decrease disease activity and reduce the need for systemic corticosteroids in patients with aspirin-exacerbated respiratory disease (AERD). OBJECTIVE: This study was designed to determine whether the clinical courses of patients with AERD improved as early as 6 months after starting aspirin desensitization and to compare this with follow-up evaluations after at least a year. METHODS: Between 1995 and 2000, 172 patients with AERD were admitted to our General Clinical Research Center, were desensitized to and treated with aspirin, were discharged to their home communities, and participated in follow-up interviews and written assessments of their clinical courses. RESULTS: By the first 6 months of aspirin treatment, there were significant reductions in sinus infections and numbers of short courses of prednisone and improvements in sense of smell and general assessment of nasal-sinus and asthma symptoms (P <.0001). These results persisted for 1 to 5 years (P <.0001). Mean prednisone doses decreased from 10.8 mg/d to 8.1 and 3.6 mg/d at 6 months and greater than 1 year, respectively. Of the 172 patients, 24 (14%) discontinued aspirin treatment because of side effects, and 115 (67%) responded to aspirin treatment. After eliminating those who discontinued aspirin treatment because of side effects, the improvement rate was 115 (78%) of 148 patients. Of the 126 patients who completed a year or more of aspirin treatment, 110 (87%) experienced improvement. CONCLUSION: Aspirin desensitization followed by daily aspirin is efficacious by at least the first 6 months of treatment and continues to be effective for up to 5 years of follow-up.

Administration, Inhalation↗
PubMed1994

Prospective evaluation of a prostacyclin-sparing aspirin formulation and heparin/warfarin in aspirin users with unstable angina or non-Q wave myocardial infarction at rest. The Antithrombotic Therapy in Acute Coronary Syndromes Research Group.

The aim of this trial was to compare the efficacy of combination antithrombotic therapy with a prostacyclin-sparing aspirin plus anticoagulation versus conventional aspirin plus anticoagulation, when added to antianginal therapy, in patients with unstable angina or non-Q wave myocardial infarction already being treated with aspirin. In a double-blind (for the aspirin) study, 144 prior aspirin users were randomized; 72 patients received controlled-release, prostacyclin-sparing aspirin 75 mg daily plus anticoagulation (intravenous heparin followed by warfarin to maintain the international normalized ratio at 2-3), and 72 patients received conventional aspirin 75 mg daily plus the same anticoagulation. Controlled-release aspirin was formulated to preserve endothelial cell prostacyclin synthesis. Trial therapy was begun by 13.2 +/- 12.3 h of qualifying pain, and continued for 12 weeks. The frequency of recurrent angina with electrocardiographic changes, myocardial infarction, or death, was analysed by intention to treat. At 12 weeks, events were: [table: see text] Twenty-six of the 42 (62%) recurrent ischaemic events occurred within 7 days of presentation. Four of the 144 patients (3%) experienced a major bleeding complication. It is concluded that in spite of maximal antithrombotic therapy, there is a significant failure rate of medical therapy in aspirin users presenting with unstable angina or non-Q wave myocardial infarction while at rest. Prostacyclin-sparing aspirin offers no clinical benefit over conventional aspirin.

Adult↗
PubMed1976

Immunological mechanisms in aspirin hypersensitivity. Studies on the immunogenicity of free aspirin.

Anti-aspiryl antibodies were produced in rabbits and guinea pigs by inoculation of aspirin incorporated in complete or incomplete Freund's adjuvant. These antibodies were readily detected by passive haemagglutination using rabbit erythrocytes incubated with aspirin at alkaline pH. Aspiryl conjugates with ovalbumin, human gamma-globulin, bovine gamma-globulin and rabbit serum were also prepared by incubating the proteins with aspirin at alkaline pH. Aspiryl conjugates prepared by this technique behaved, immunologically, identically with the conjugates prepared from aspirin chloride. By contrast, the molar absorbance at 305 nm of the conjugates prepared from aspirin was about 25 times lower than the molar absorbance of the conjugates prepared from aspirin chloride. Since the absorbance of salicylic acid is about eight times greater than that of aspirin, the conclusion is drawn that the aspiryl/salicylyl ratio is significantly higher in the conjugates prepared by incubating proteins with aspirin at alkaline pH than in the conjugates prepared from aspirin chloride. In parallel experiments, salicylic acid did not induce formation of specific antibodies capable of reacting with aspirin- or salicylic acid-treated red cells. Sera giving positive passive haemagglutination with aspirin-treated erythrocytes did not react with erythrocytes treated with salicylic acid or acetic anhydride.

Anhydrides↗
PubMed2006

Risk of upper gastrointestinal ulcer bleeding associated with selective cyclo-oxygenase-2 inhibitors, traditional non-aspirin non-steroidal anti-inflammatory drugs, aspirin and combinations.

BACKGROUND: The risks and benefits of coxibs, non-steroidal anti-inflammatory drugs (NSAIDs), and aspirin treatment are under intense debate. OBJECTIVE: To determine the risk of peptic ulcer upper gastrointestinal bleeding (UGIB) associated with the use of coxibs, traditional NSAIDs, aspirin or combinations of these drugs in clinical practice. METHODS: A hospital-based, case-control study in the general community of patients from the National Health System in Spain. The study included 2777 consecutive patients with endoscopy-proved major UGIB because of the peptic lesions and 5532 controls matched by age, hospital and month of admission. Adjusted relative risk (adj RR) of UGIB determined by conditional logistic regression analysis is provided. RESULTS: Use of non-aspirin-NSAIDs increased the risk of UGIB (adj RR 5.3; 95% confidence interval (CI) 4.5 to 6.2). Among non-aspirin-NSAIDs, aceclofenac (adj RR 3.1; 95% CI 2.3 to 4.2) had the lowest RR, whereas ketorolac (adj RR 14.4; 95% CI 5.2 to 39.9) had the highest. Rofecoxib treatment increased the risk of UGIB (adj RR 2.1; 95% CI 1.1 to 4.0), whereas celecoxib, paracetamol or concomitant use of a proton pump inhibitor with an NSAID presented no increased risk. Non-aspirin antiplatelet treatment (clopidogrel/ticlopidine) had a similar risk of UGIB (adj RR 2.8; 95% CI 1.9 to 4.2) to cardioprotective aspirin at a dose of 100 mg/day (adj RR 2.7; 95% CI 2.0 to 3.6) or anticoagulants (adj RR 2.8; 95% CI 2.1 to 3.7). An apparent interaction was found between low-dose aspirin and use of non-aspirin-NSAIDs, coxibs or thienopyridines, which increased further the risk of UGIB in a similar way. CONCLUSIONS: Coxib use presents a lower RR of UGIB than non-selective NSAIDs. However, when combined with low-dose aspirin, the differences between non-selective NSAIDs and coxibs tend to disappear. Treatment with either non-aspirin antiplatelet or cardioprotective aspirin has a similar risk of UGIB.

Adult↗
PubMed1996

Aspirin related gastrointestinal bleeders have an exaggerated bleeding time response due to aspirin use.

BACKGROUND: Gastrointestinal bleeding is related to non-steroidal anti-inflammatory drug (NSAID) use, especially aspirin, but only a small subset of users bleed. AIM: To look for risk factors or mechanisms whereby aspirin may promote gastrointestinal bleeding. PATIENTS: Sixty one patients with previous aspirin related upper gastrointestinal bleeding and 61 matched controls. METHODS: Patients and controls were given 375 mg of aspirin and sequential skin bleeding time and blood aspirin levels were measured. Additional studies included platelet lumiaggregation, von Willebrand factor, Factor VIII, and coagulation studies. RESULTS: Baseline skin bleeding time was similar in bleeders and controls, but bleeders had a more prolonged skin bleeding time after aspirin use. Hyper-response was more frequent in bleeders (30% v 9.3%; p < 0.01) and was associated with more than one previous separate bleeding event and a lower packed cell volume during the preceding bleeding episode. No differences were found in other factors studied. Logistic regression analysis identified prolonged skin bleeding time after aspirin use as an independent factor contributing to aspirin related gastrointestinal bleeding (RR = 5.4; 95% CI: 1.8 to 17.1). CONCLUSIONS: 30% of patients with a history of aspirin related gastrointestinal bleeding have an exaggerated prolongation of skin bleeding time in response to aspirin, which may be a risk factor for bleeding. This intrinsic defect or to subclinical von Willebrand disease or different aspirin metabolism.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

The effect of aspirin desensitization on urinary leukotriene E4 concentrations in aspirin-sensitive asthma.

Patients with aspirin sensitive asthma (ASA) can be desensitized to aspirin but the mechanisms by which this happens are unknown. To test the hypothesis that there may be a reduction in aspirin-induced leukotriene release following aspirin desensitization, we studied nine patients with ASA, 37 +/- 2.3 yr of age (mean +/- SEM) with a baseline FEV1 of 94 +/- 3.5%. Urinary leukotriene E4 (LTE4) and FEV1 were measured before and after ingestion of a threshold dose of aspirin leading to a 15% decrease in FEV1, and then at intervals following desensitization, when a maintenance dose of 600 mg aspirin was ingested. Prior to desensitization, the maximum decrease in FEV1 following ingestion of a threshold dose of aspirin was 15.3 +/- 3.9%, and urinary LTE4 rose from a baseline value of 235 +/- 79.4 pg/mg creatinine to 1,714 +/- 783 pg/mg creatinine at 3 h. Immediately after acute desensitization, which was performed over several days, 600 mg aspirin provoked a maximum decrease in FEV1 of only 3.3 +/- 2.4%, and urinary LTE4 increased from a baseline of 645 +/- 223 pg/mg creatinine to 1,256 +/- 456 pg/mg creatinine. Following ingestion of 600 mg aspirin for 9 +/- 3.2 mo (n = 5; chronic desensitization), urinary LTE4 rose from a basal level of 432 +/- 127 pg/mg creatinine to 749 +/- 257 pg/mg creatinine at 3 h after 600 mg aspirin, and this was accompanied by a maximum decrease in FEV1 of 7.4 +/- 4.5%. Although there was significantly less aspirin-induced LTE4 excretion after acute desensitization, substantial amounts of LTE4 were still produced without any significant change in lung function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Effects of ticlopidine or ticlopidine plus aspirin on platelet aggregation and ATP release in normal volunteers: why aspirin improves ticlopidine antiplatelet activity.

Aspirin and ticlopidine are used to prevent arterial thrombosis. In some clinical settings ticlopidine is administered with aspirin for improving antithrombotic effect. We administered aspirin (100 mg/day), ticlopidine (500 mg/day), or ticlopidine and aspirin for 7 days to healthy volunteers. Platelet aggregation and ATP release induced by sodium arachidonate, ADP, or a combination of both were measured. Sodium arachidonate (0.25 mmol/L), which produces no platelet aggregation, combined with adenosine diphosphate (1 mumol/L), which produced a reversible platelet aggregation of 20% after ticlopidine, resulted in a synergistic platelet aggregation response in normal (74.6 +/- 9.2%) and in ticlopidine platelet-rich plasma (59.1% +/- 14.9%, p < 0.0001). Synergism after sodium arachidonate (0.75 mmol/L) plus adenosine diphosphate (4 mumol/L) fell from 75.8% +/- 11.0% and 59.1% +/- 15.6% after ticlopidine or aspirin, respectively, to 14.8% +/- 18.0% (p < 0.0001) after ticlopidine plus aspirin. Aspirin and ticlopidine alone did not inhibit adenosine triphosphate release as thoroughly as did aspirin plus ticlopidine. Aspirin or ticlopidine does not adequately prevent platelet activity as ticlopidine plus aspirin do. Addition of aspirin to treatment with ticlopidine improves their antiplatelet activity and better results could be obtained in arterial thrombotic prevention strategies.

Adenosine Triphosphate↗
PubMed1999

Comparative safety and tolerability of clopidogrel and aspirin: results from CAPRIE. CAPRIE Steering Committee and Investigators. Clopidogrel versus aspirin in patients at risk of ischaemic events.

OBJECTIVE: The objective of this study was to provide a comprehensive comparison of the long term safety and tolerability of clopidogrel, a new adenosine diphosphate (ADP) receptor antagonist that inhibits platelet activation induced by ADP, and aspirin (acetylsalicylic acid). PATIENTS AND METHODS: The study population comprised 19,185 patients with symptomatic atherosclerosis manifested as recent ischaemic stroke, recent myocardial infarction or symptomatic peripheral arterial disease. Patients were randomised to receive clopidogrel 75 mg/day or aspirin 325 mg/day for a minimum of 1 year and a maximum of 3 years. RESULTS: Compared with aspirin, clopidogrel reduced the combined risk of ischaemic stroke, myocardial infarction or vascular death by 8.7% (p = 0.043). The incidence of early permanent discontinuations of the study drug due to adverse events was almost identical in both treatment groups (11.94% for clopidogrel vs 11.92% for aspirin). Reported neutropenia was similar in the clopidogrel and aspirin groups (0.10 vs 0.17%, respectively) with corresponding rates (0.05 vs 0.04%, respectively) for severe neutropenia. Thrombocytopenia was identical in the clopidogrel and aspirin groups (0.26%), with the rates of severe thrombocytopenia being 0.19 vs 0.10%, respectively. None of these observed differences was statistically significant. The overall incidence of haemorrhagic events did not differ statistically significantly between treatment groups (9.27% for clopidogrel vs 9.28% for aspirin; p = 0.98). There was a trend towards a lower incidence of intracranial haemorrhage in the clopidogrel group (0.31%) compared with the aspirin group (0.42%). Any reported gastrointestinal haemorrhage was significantly less frequent with clopidogrel (1.99%) than with aspirin (2.66%) [p < 0.002]. The corresponding data for severe gastrointestinal bleeding were 0.49 vs 0.71%; p < 0.05. Overall, there were significantly fewer gastrointestinal adverse events with clopidogrel than with aspirin (27.1 vs 29.8%; p < 0.001), with less abdominal pain, dyspepsia, constipation, or peptic, gastric, or duodenal ulceration with clopidogrel. Diarrhoea was significantly more common in the clopidogrel group (4.46 vs 3.36%; p < 0.001), although the incidence of severe diarrhoea (0.23 vs 0.11%) was low and was not significantly different between groups. There were significantly more patients with rash in the clopidogrel group (6.0%) compared with the aspirin group (4.6%) [p < 0.001]. However, these events were generally mild and transient in nature. CONCLUSION: Given the favourable benefit/risk ratio, clopidogrel represents a clinically important advance in the treatment of patients with manifest atherosclerotic disease.

Arteriosclerosis↗
PubMed1995

Aspirin modulates interleukin-3 production: additional explanation for the preventive effects of aspirin in antiphospholipid antibody syndrome.

OBJECTIVE: The granulocyte macrophage colony stimulating factors (GMCSF) and interleukin-3 (IL-3) are defined as positive signals for pregnancy, since they support the process of trophoblast invasion and expansion and induce placental growth and development. Aspirin and IL-3 were shown to be effective in preventing the manifestations of experimental antiphospholipid antibody syndrome (APS). Aspirin inhibits the activity of the enzyme cyclooxygenase in macrophages, which leads to a shift in the arachidonic acid metabolism toward the lipoxygenase pathway, and results in overproduction of leukotrienes. Our data indicated that leukotrienes are capable of stimulating IL-3 production in vitro. Our aim was to examine whether aspirin may exert its beneficial effect in APS not only by its ability to prevent thromboxane A2 production and prostaglandin I2 (PGI2) formation, but also by stimulating IL-3 production. METHODS: Splenocytes and macrophages from naive mice were cultured in vitro with low dose aspirin. Nordihydroguaiaretic acid (NDGA), an inhibitor of 5-lipoxygenase, was added to mixed cultures of splenocytes and macrophages containing low dose aspirin. IL-3 production was observed. RESULTS: When splenocytes and macrophages were cultured in vitro with low dose aspirin (10 micrograms/ml), a marked stimulation of IL-3 production was noted. When NDGA was added to mixed cultures of splenocytes and macrophages containing low dose aspirin, it decreased the IL-3 production. Higher dose of aspirin did not affect the cytokine production. When splenocytes were incubated without the addition of exogenous macrophages, no stimulation of IL-3 production was noted. However, when purified leukotriene B4 or leukotriene C4 was added, there was an increase of 71 and 261%, respectively, in the stimulation of IL-3 production (p < 0/01). These results were supported by in vivo studies, in which a higher serum IL-3 level was detected in mice fed low dose aspirin, compared to the control group and to mice fed a higher dose of aspirin. CONCLUSION: Aspirin acts as a potent stimulator of IL-3 through its ability to raise leukotriene production, which induces production of IL-3 both in vitro and in vivo.

Animals↗
PubMed1991

Caffeine as an analgesic adjuvant. A double-blind study comparing aspirin with caffeine to aspirin and placebo in patients with sore throat.

Despite its frequent clinical use in analgesic agents, caffeine has not been accepted unequivocally as an analgesic adjuvant. To evaluate this activity of caffeine, we used new study methods in a randomized controlled trial on patients with acute sore throat due to tonsillopharyngitis. Patients were randomly assigned to receive a single dose of one of three treatments: 800 mg of aspirin with 64 mg of caffeine (n = 70), 800 mg of aspirin (n = 68), or placebo (n = 69). Under double-blind conditions, during a 2-hour evaluation period, patients used different rating scales to assess pain intensity, change in pain, relief, and two qualities of throat pain, how swollen the throat felt, and difficulty swallowing. Aspirin with caffeine and aspirin alone were significantly more effective than placebo for all efficacy measurements from 30 minutes through 2 hours and overall. The aspirin-caffeine combination also showed evidence of activity at 15 minutes on the relief scale. Aspirin with caffeine was more effective than aspirin alone after 30 minutes and over the entire study period. For patients with fever, both active treatments were equally effective antipyretic agents. We conclude, therefore, that 800 mg of aspirin, given alone or with 64 mg of caffeine, is an effective analgesic and antipyretic agent. Because the aspirin-caffeine combination is significantly more effective than aspirin alone as an analgesic, we also conclude that 64 mg of caffeine is an analgesic adjuvant.

Adult↗
PubMed2004

Use of aspirin and ibuprofen compared with aspirin alone and the risk of myocardial infarction.

BACKGROUND: Laboratory investigations suggest that the simultaneous use of aspirin and ibuprofen may attenuate the antiplatelet effect of aspirin, making it less useful for cardioprotection. To determine if there is clinical evidence of this potentially harmful interaction, we conducted a retrospective matched case-control study. METHODS: All patients issued outpatient prescriptions for aspirin or ibuprofen from January 1, 1990, to December 31, 2000, at the Durham Veterans Affairs Medical Center pharmacy were included in the study. Patients who used aspirin and ibuprofen concurrently were matched against those who used aspirin only by race, sex, age within 10 years, and cholesterol levels (either low-density lipoprotein or total cholesterol) to within 30 mg/dL (0.78 mmol/L). The rate ratio of experiencing a myocardial infarction per patient-month of drug exposure was then determined. RESULTS: Some 3859 patients received both aspirin and ibuprofen, for a total of 52 139 patient-months of medication use. This group experienced 138 infarctions. The 10 239 patients receiving aspirin only, for a total of 156 417 patient-months of use, experienced 684 infarctions. The rate ratio of having an infarction was 0.61 (95% confidence interval, 0.50-0.73) (P <.001), favoring the group that took aspirin and ibuprofen simultaneously. An analysis of diabetic patients found a rate ratio of 0.48 (95% confidence interval, 0.34-0.66) (P <.001). An examination of patients who spent time in both groups at different times resulted in a rate ratio of infarction during combined use of 0.70 (95% confidence interval, 0.59-0.83) (P <.001). CONCLUSION: There does not seem to be an increased risk of myocardial infarction among patients simultaneously consuming aspirin and ibuprofen compared with aspirin alone.

Aged↗
PubMed1993

Comparative trial of prednisone plus aspirin versus aspirin alone in the treatment of anticardiolipin antibody-positive obstetric patients.

OBJECTIVE: We compared the use of aspirin alone with combined therapy (prednisone plus aspirin) in antiphospholipid antibody-positive obstetric patients with prior adverse pregnancy outcome. STUDY DESIGN: Thirty-nine patients meeting specific laboratory and clinical inclusion criteria were randomized to receive either combined therapy (prednisone plus low-dose aspirin, n = 17) or aspirin alone (n = 22). The daily aspirin dose was 81 mg; prednisone was begun at 20 mg/day and increased or decreased on the basis of observed changes in serial antibody levels. Perinatal outcomes were compared between groups. Evaluation of treatment-related maternal complications and serial antibody titers was also accomplished. RESULTS: Thirty-four randomized subjects were evaluable (prednisone plus low-dose aspirin, n = 12 vs aspirin only, n = 22); no perinatal losses were observed in the study cohort. Preterm delivery was experienced by significantly more patients receiving prednisone plus low-dose aspirin than aspirin only (8/12 vs 3/22, respectively; p = 0.003), and prednisone exposure appeared to be an independent risk factor for preterm birth. CONCLUSIONS: The use of prednisone therapy in conjunction with low-dose aspirin does not appear to improve outcome and may provoke obstetric complications in antiphospholipid antibody-positive patients.

Adult↗