Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASPIRIN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1996

Aspirin desensitization treatment of aspirin-sensitive patients with rhinosinusitis-asthma: long-term outcomes.

BACKGROUND: Aspirin-sensitive patients with asthma experience continuous inflammation of their nasal and sinus tissues, complicated by recurrent sinusitis, which frequently leads to asthma attacks. Systemic corticosteroid therapy and sinus or polyp surgery are currently required to control underlying rhinosinusitis, and bursts of corticosteroids are used for asthma control. OBJECTIVE: After aspirin desensitization therapy, objective measures of respiratory disease activity, linked to the need for systemic corticosteroids and sinus surgery, were studied to determine whether any changes occurred. METHODS: Sixty-five aspirin-sensitive patients with asthma underwent aspirin challenge, followed by aspirin desensitization and daily treatment with aspirin over 1 to 6 years (mean, 3.1 years). Clinical outcome measurements before aspirin desensitization treatment and during follow-up were analyzed for the larger group of 65 patients and subgroups (29 patients receiving therapy for 1 to 3 years and 36 patients receiving therapy for 3 to 6 years). RESULTS: In the larger group of 65 patients, there were significant reductions in numbers of sinus infections per year (median, 6 to 2), hospitalizations for treatment of asthma per year (median, 0.2 to 0), improvement in olfaction (median, 0 to 2), and reduction in use of systematic corticosteroids (mean, 10.2 to 2.5 mg) with p values less than 0.0001. Numbers of sinus and polyp operations per year were significantly reduced (median, 0.2 to 0; p = 0.004), and doses of nasal corticosteroids (in micrograms) were significantly reduced (mean dose, 139 to 106 micrograms, p = 0.01). Emergency department visits and use of inhaled corticosteroids were unchanged. CONCLUSIONS: The results support a role for aspirin desensitization treatment of aspirin-sensitive patients with rhinosinusitis-asthma.

Adult↗
PubMed1998

Nasal provocation test with lysine-aspirin for diagnosis of aspirin-sensitive asthma.

Nasal provocation tests (NPTs) with lysine-aspirin (L-ASA) have been recently introduced for assessment of aspirin-induced asthma (AIA). They differ in dose and means of aspirin instillation, duration of observation period, and criteria for positivity. Thus far they have not become a routine part of clinical diagnosis. Fifty-one patients with AIA, confirmed by oral challenge test, were recruited to undergo diagnostic NPTs with L-ASA. In 10 of these patients (19.6%), NPTs could not be performed because of total obstruction of at least one nostril or marked fluctuations in nasal flows, leaving 41 patients with AIA for the study. Control groups consisted of 13 aspirin-tolerant asthmatic patients and 10 healthy subjects. L-ASA at a total dose of 16 mg of acetylsalicylic acid applied bilaterally into the inferior nasal conchae caused significant fall in inspiratory nasal flow in at least one nostril (>40%), which was measured by anterior rhinomanometry, and clinical symptoms of watery discharge and nasal blockage in 35 of 41 patients with AIA, one of 10 healthy subjects, and none of 13 aspirin-tolerant asthmatic patients. No relationship was found between the baseline nasal flow values and the intensity of response to L-ASA. No systemic reactions, including bronchospasm, were noticed, even in patients whose initial FEV1 was lower than 70% of predicted value. This test is highly specific (95.7%) and sensitive (86.7%), but negative results do not exclude possible intolerance to aspirin (predictive value of a negative result 78.6%). In conclusion, the NPT described is a simple, safe, and quick test for diagnosis of AIA. It can be used in patients with unstable asthma. It may be a method of choice to confirm hypersensitivity to aspirin manifested only by symptoms from the upper respiratory tract. Patients suspected of aspirin intolerance who have negative NPT results should undergo bronchial or oral challenge tests with aspirin.

Adult↗
PubMed1998

Butyrylcholinesterase-catalysed hydrolysis of aspirin, a negatively charged ester, and aspirin-related neutral esters.

Although aspirin (acetylsalicylic acid) is negatively charged, it is hydrolysed by butyrylcholinesterase (BuChE). Catalytic parameters were determined in 100 mM Tris buffer, pH 7.4, in the presence and absence of metal cations. The presence of Ca2+ or Mg2+ (<100 mM) in buffer did not change the Km, but accelerated the rate of hydrolysis of aspirin by wild-type or D70G mutant BuChE by 5-fold. Turnover numbers were of the order of 5000-12000 min-1 for the wild-type enzyme and the D70G and D70K enzymes in 100 mM Tris, pH 7.4, containing 50 mM CaCl2 at 25 degreesC; Km values were 6 mM for wild-type, 16 mM for D70G and 38 mM for D70K. People with 'atypical' BuChE have the D70G mutation. The apparent inhibition seen at high aspirin concentration was not due to inhibition by excess substrate but to spontaneous hydrolysis of aspirin, causing inhibition by salicylate. The wild-type and D70G enzymes were competitively inhibited by salicylic acid; the D70K enzyme showed a complex parabolic inhibition, suggesting multiple binding. The effect of salicylate was substrate-dependent, the D70K mutant being activated by salicylate with butyrylthiocholine as substrate. Km value for wild-type enzyme was lower than for D70 mutants, suggesting that residue 70 located at the rim of the active site gorge was not the major site for the initial encounter aspirin-BuChE complex. On the other hand, the virtual absence of affinity of the W82A mutant for aspirin indicated that W82 was the major residue involved in formation of the Michaelis complex. Molecular modelling of aspirin binding to BuChE indicated perpendicular interactions between the aromatic rings of W82 and aspirin. Kinetic study of BuChE-catalysed hydrolysis of different acetyl esters showed that the rate limiting step was acetylation. The bimolecular rate constants for hydrolysis of aspirin by wild-type, D70G and D70K enzymes were found to be close to 1x106 M-1 min-1. These results support the contention that the electrostatic steering due to the negative electrostatic field of the enzyme plays a role in substrate binding, but plays no role in the catalytic steps, i.e. in the enzyme acetylation.

Acetylation↗
PubMedDate not supplied

Prior aspirin use in unstable angina predisposes to higher risk: the aspirin paradox.

BACKGROUND: Aspirin is the most widely prescribed agent used in prevention of coronary thrombosis. Thus, many patients presenting with acute coronary syndromes have a history of aspirin usage. METHODS: To assess response to medical therapy in patients taking aspirin prior to admission with an acute coronary syndrome, we reviewed outcomes data from the Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-wave Coronary Events (ESSENCE) and Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) studies. RESULTS: Patients with acute coronary syndromes who had taken aspirin prior to enrollment were less likely to have non-Q-wave myocardial infarction on admission (ESSENCE: 16.0% vs. 29.2%, p<0.001; PRISM-PLUS: 34.2% vs. 57.7%, p<0.001). However, prior aspirin users were more likely to be failed by standard medical therapy with unfractionated heparin than non-prior aspirin users (ESSENCE: 21.5% vs. 16.5%, p=0.017; PRISM-PLUS: 23.5% vs. 12.1%, p<0.001). Prior aspirin users received greater benefit from both enoxaparin (21.5% vs. 16.8%, p=0.009) and tirofiban with unfractionated heparin (23.5% vs. 16.0%, p=0.007) than from unfractionated heparin alone. Non-prior aspirin users presented with higher rates of non-Q-wave myocardial infarction. CONCLUSIONS: Prior aspirin users admitted with acute coronary syndromes may have a more benign presentation, but are more likely to be failed by medical therapy with unfractionated heparin and should be considered as a high-risk group. Enoxaparin or the combination of tirofiban and unfractionated heparin are both more effective than unfractionated heparin in this group.

Aged↗
PubMed2005

The blocking effect of essential controller medications during aspirin challenges in patients with aspirin-exacerbated respiratory disease.

BACKGROUND: The blocking effect of controller medications for asthma could have an effect on the outcome of aspirin challenges in patients suspected of having aspirin-exacerbated respiratory disease (AERD). OBJECTIVE: To evaluate whether there was any blocking effect of long-acting beta2-agonists, systemic corticosteroids, and/or inhaled corticosteroids alone or as co-therapy with leukotriene modifier drugs (LTMDs). METHODS: Between 1981 and 2004, 678 patients with suspected AERD were admitted for aspirin challenge and desensitization. All patients had asthma, chronic sinusitis, nasal polyposis, and at least 1 historical reaction to a nonsteroidal anti-inflammatory drug. Asthma controller medications taken during aspirin challenge were recorded and analyzed with respect to their potential effects on 4 possible outcomes of aspirin challenge, namely, naso-ocular reaction, lower airway reaction, classic upper and lower airway reaction, or a negative challenge result. RESULTS: When compared with AERD patients who received no controller medications, the combined use of LTMDs, inhaled corticosteroids, and long-acting beta2-agonists led to a statistically significant change in aspirin challenge outcomes (P = .009), mainly shifting the reaction from a classic upper and lower respiratory tract reaction to naso-ocular reactions only. LTMDs appeared to have the strongest effect (P < .001) in blocking lower respiratory tract reactions. Systemic corticosteroids did not have the same effects. Blocking of both upper and lower respiratory tract reactions to aspirin as a result of taking controller medications did not occur. CONCLUSION: Controller medications are frequently needed to stabilize airways of patients with AERD. LTMDs alone or in combination with other controllers blocked lower respiratory tract reactions during aspirin challenge in some patients with AERD but did not change the overall rate of positive aspirin challenge results and did not lead to false-negative challenges.

Administration, Oral↗
PubMed2000

Natural history of aspirin-induced asthma. AIANE Investigators. European Network on Aspirin-Induced Asthma.

There is a subset of patients with bronchial asthma who are susceptible to disease exacerbation upon receiving aspirin and other nonsteroidal anti-inflammatory drugs. This is a clinical syndrome, called aspirin-induced asthma (AIA), associated with alterations in arachidonate metabolism and cysteinyl-leukotriene overproduction. The natural history and clinical characteristics of this type of asthma were studied. Sixteen clinical centres in 10 European countries provided standardized information to the specially developed patient-oriented database regarding: medical history, physical examination, diagnosis, and treatment. Diagnosis of AIA was based on a typical history, confirmed by positive aspirin provocation tests, carried out in 91% of the patients. A total of 500 patients were enrolled in the study. AIA developed according to a pattern, characterized by a sequence of symptoms. First, persistent rhinitis, appearing at a mean age of 29.7+/-12.5 yrs, then asthma, aspirin intolerance and nasal polyposis appear. The clinical presentation in different European countries was remarkably similar. In females, who outnumbered males by 2.3:1, the onset of symptoms occurred significantly earlier and the disease was more progressive and severe than in males. Atopy, present in approximately a third of patients, led to earlier manifestation of rhinitis and asthma, but not of aspirin intolerance or nasal polyposis. A family history of aspirin intolerance, recorded in 6% of patients, had a less evident effect on the course of the disease than sex or atopy. Fifty one per cent of patients, in addition to inhaled steroids, required chronic systemic corticosteroid therapy at a mean dose of 8 mg prednisone x day(-1). Surprisingly, 15% of patients were unaware of intolerance to aspirin and learnt about it only after having provocation tests performed. All over Europe, aspirin-induced asthma develops in a similar characteristic way. Its course is influenced by sex and the presence of atopy. In half of the patients, asthma is severe, and steroid-dependent. The uniform natural history of aspirin-induced asthma might suggest a common underlying principle.

Adolescent↗
PubMed1997

Aspirin and platelets: the antiplatelet action of aspirin and its role in thrombosis treatment and prophylaxis.

The antithrombotic action of aspirin (acetylsalicylic acid) is due to inhibition of platelet function by acetylation of the platelet cyclooxygenase (COX) at the functionally important amino acid serine529. This prevents the access of the substrate (arachidonic aid) to the catalytic site of the enzyme at tyrosine385 and results in an irreversible inhibition of platelet-dependent thromboxane formation. Aspirin is an approximately 150- to 200-fold more potent inhibitor of the (constitutive) isoform of the platelet enzyme (COX-1) than the (inducible) isoform (COX-2) which is expressed by cytokines, inflammatory stimuli, and some growth factors. This explains the different dosage requirements of aspirin as an antithrombotic (COX-1) and an anti-inflammatory drug (COX-2), respectively. Aspirin is the "gold standard" antiplatelet agent for prevention of arterial thromboses. The optimum dose of aspirin as an antithrombotic drug can differ in different organ circulations. While 100 mg/day is sufficient for prevention of thrombus formation in the coronary circulation, higher doses may be required for the prevention of vascular events in the cerebral and peripheral circulation. However, any effective antiplatelet dose of aspirin is associated with an increased risk of bleeding. Therefore, the individual benefit/risk ratio determines the administration of the compound. There are no known prostaglandin-independent mechanisms for the antithrombotic action of aspirin in clinical use. Thus, platelet activation caused by other factors remains unchanged and might result in a resistance against inhibition of platelet function by aspirin. This involves platelet activation by shear stress and ADP. Additionally, there is no "sparing" of endothelial prostacyclin synthesis in clinical conditions of atherosclerotic endothelial injury. In this case, inhibition of COX-1 by aspirin will also reduce the amount of precursors for vascular prostacyclin synthesis, provided, for example, from adhering platelets.

Anti-Inflammatory Agents↗
PubMed2005

Intranasal lysine-aspirin in aspirin-sensitive nasal polyposis: a controlled trial.

OBJECTIVES/HYPOTHESIS: Intranasal lysine-aspirin has been used as a method of desensitization in patients with aspirin-sensitive nasal polyps to control their recurrence and prevent frequent surgical intervention. However, the studies are limited in number, and their design is open to criticisms. Thus, we conducted a controlled trial to study the clinical effectiveness of topical lysine-aspirin in patients with aspirin-sensitive nasal polyposis. STUDY DESIGN: Prospective, randomized, double blind, placebo controlled, crossover trial. METHODS: Aspirin-sensitive patients confirmed by intranasal challenge were enrolled and randomized to receive 16 mg of topical lysine-aspirin every 48 hours or placebo for 6 months before crossover. Polyp growth and nasal and chest symptoms were monitored using acoustic rhinometry, nasal inspiratory peak flow, peak expiratory flow rate, and a daily diary of symptom scores. RESULTS: Twenty-two patients were enrolled. After withdrawals and drop outs, data were available on 11 patients for analysis. Multivariate analysis of measured parameters did not reveal a significant clinical benefit to patients receiving topical lysine-aspirin compared with placebo. Deterioration was similar while on lysine-aspirin or placebo. CONCLUSIONS: This is the first controlled clinical trial of topical desensitization in aspirin-sensitive nasal polyp patients. Despite the failure to demonstrate clinical benefit, tissue studies have shown a significant improvement at the microscopic level. Further work with larger numbers of patients along with conventional treatment may show a clinical improvement in these patients.

Administration, Intranasal↗
PubMed2000

Intranasal challenge with aspirin in the diagnosis of aspirin intolerant asthma: evaluation of nasal response by acoustic rhinometry.

BACKGROUND: Nasal provocation tests with lysine-aspirin have recently been introduced for assessment of aspirin intolerant asthma. A study was undertaken to evaluate the usefulness of acoustic rhinometry, a new non-invasive technique, in the diagnosis of aspirin intolerant asthma/rhinitis. METHODS: Fifteen patients with aspirin intolerant asthma/rhinitis (nine women, mean (SD) age 54.7 (14) years), eight patients with aspirin tolerant asthma/rhinitis (three women, mean (SD) age 52.6 (7.8) years), and eight healthy subjects (two women, mean (SD) age 32.5 (9.7) years) were studied. All subjects were challenged with saline (0.9% NaCl) and 25 mg lysine acetylsalicylic acid (L-ASA) instilled into each nostril of the nose on two separate days. The clinical response was evaluated based on nasal symptoms (sneezes, itching, secretion and blockage). The nasal response was measured by acoustic rhinometry. Symptoms and rhinometry curves were recorded at 10 minute intervals for three hours, one hour before challenge and two hours after challenge. RESULTS: L-ASA challenge induced a significant increase in symptoms in patients with aspirin intolerant asthma/rhinitis. No differences in the clinical response were detected in those with aspirin tolerant asthma/rhinitis or healthy subjects. L-ASA challenge induced a significant decrease in nasal volume measured by acoustic rhinometry in aspirin intolerant patients. No differences were detected between the challenges in aspirin tolerant patients. If a 25% decrease in nasal volume is taken as the cut off point, the specificity of the test was 94% and the sensitivity reached 73%. The nasal challenge was well tolerated by all subjects. CONCLUSION: Acoustic rhinometry may be used to study the nasal response to L-ASA. Nasal challenge with L-ASA is safe and can be used as a diagnostic test even in asthmatic patients with severe bronchial obstruction.

Administration, Intranasal↗
PubMed1992

Ticlopidine versus aspirin for the prevention of recurrent stroke. Analysis of patients with minor stroke from the Ticlopidine Aspirin Stroke Study.

BACKGROUND AND PURPOSE: Ticlopidine has not been formally compared with aspirin in patients with a completed stroke. We therefore performed an analysis on a subgroup of patients from the Ticlopidine Aspirin Stroke Study (TASS) with a recent minor completed stroke as the qualifying ischemic event. METHODS: This was a multicenter, double-blind, randomized trial of patients with a recent history of cerebral ischemia. Eligible patients had a qualifying minor stroke within 3 months of study entry. All patients received either 650 mg aspirin twice daily or 250 mg ticlopidine twice daily for up to 5.8 years. The primary study end point was the first occurrence of nonfatal stroke or death from any cause. A secondary end point was the first occurrence of a fatal or nonfatal stroke. RESULTS: Minor stroke was the qualifying ischemic event in 927 patients (463 received ticlopidine and 464 received aspirin). The cumulative event rate at 1 year for nonfatal stroke or death was 6.3% for patients receiving ticlopidine and 10.8% for patients receiving aspirin, a 42% risk reduction in favor of ticlopidine. For fatal or nonfatal stroke, the cumulative event rate at 1 year was 4.8% for patients receiving ticlopidine and 7.5% for those receiving aspirin, a risk reduction of 36% for ticlopidine relative to aspirin. The overall risk reductions were 22.1% for nonfatal stroke or death and 19.9% for fatal or nonfatal stroke. Adverse reactions were reported in 58% of the ticlopidine patients and 51% of the aspirin patients. CONCLUSIONS: The results in this subgroup are consistent with the overall TASS results and show that ticlopidine is somewhat more effective than aspirin for reducing the risk of stroke in patients with a completed minor stroke.

Adult↗
PubMed2006

Antithrombotic properties of aspirin and resistance to aspirin: beyond strictly antiplatelet actions.

Aspirin is effective in the prevention of cardiovascular events in high-risk patients. The primary established effect of aspirin on hemostasis is to impair platelet aggregation via inhibition of platelet thromboxane A(2) synthesis, thus reducing thrombus formation on the surface of the damaged arterial wall. Growing evidence also indicates that aspirin exerts additional antithrombotic effects, which appear to some extent unrelated to platelet thromboxane A(2) production. Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as factor XIII activation. Aspirin also acetylates lysine residues in fibrinogen resulting in increased fibrin clot permeability and enhanced clot lysis as well as directly promoting fibrinolysis with high-dose aspirin. The variable effectiveness of aspirin in terms of clinical outcomes and laboratory findings, which has been termed aspirin resistance, may be related to these additional antithrombotic effects that are altered when associated with common genetic polymorphisms such as the Leu33Pro beta(3)-integrin or Val34Leu factor XIII mutations. However, the clinical relevance of these observations is still unclear. Elucidation of the actual impacts of aspirin other than antiaggregation effects could be important in view of the widespread use of this drug in the prevention of thrombotic manifestations of atherosclerosis.

Aspirin↗
PubMed1974

Influence of L-glutamine on aspirin-induced gastric lesions and absorptions as well as antipyretic, analgesic and anti-inflammatory effects of aspirin in rats and mice.

L-glutamine markedly suppressed the development of the gastric lesions induced by aspirin in pylorus-ligated rats. In non-ligated normal rats, aspirin was absorbed rapidly after administration and was maintained in the blood in high salicylate concentration thereafter. When aspirin was administered in combination with L-glutamine, the absorption of aspirin was at nearly the same level as when aspirin had been given alone. In pylorus-ligated rats, administration of aspirin was followed by slow increment in blood salicylate concentration. Blood salicylate level in these rats was higher when aspirin was administered in combination with L-glutamine than when it had been given alone. Combined administration of aspirin and L-glutamine produced little influence on the antipyretic, analgesic and anti-inflammatory effects of aspirin in non-ligated normal rats.

Administration, Oral↗
PubMed1991

Swedish Aspirin Low-Dose Trial (SALT) of 75 mg aspirin as secondary prophylaxis after cerebrovascular ischaemic events. The SALT Collaborative Group.

The efficacy of aspirin in daily doses of 300 mg and more as secondary prophylaxis after cerebrovascular events is well established. Since much lower doses of aspirin can inhibit platelet function, and carry a lower risk of adverse effects, the Swedish Aspirin Low-dose Trial (SALT) was set up to study the efficacy of 75 mg aspirin daily in prevention of stroke and death after transient ischaemic attack (TIA) or minor stroke. 1360 patients entered the study 1-4 months after the qualifying event: 676 were randomly assigned to aspirin treatment and 684 to placebo treatment. The median duration of follow-up was 32 months. Compared with the placebo group, the aspirin group showed a reduction of 18% in the risk of primary outcome events (stroke or death; relative risk 0.82, 95% confidence interval 0.67-0.99; log-rank analysis p = 0.02), and reductions of 16-20% in the risks of secondary outcome events (stroke; stroke or two or more TIAs within a week of each other necessitating a change of treatment; or myocardial infarction). Adverse drug effects were reported by 147 aspirin-treated and 123 placebo-treated patients Gastrointestinal side-effects were only slightly more common in the aspirin-treated patients, but that group had a significant excess of bleeding episodes (p = 0.04). Thus, we have found that a low dose (75 mg/day) of aspirin significantly reduces the risk of stroke or death in patients with cerebrovascular ischaemic events.

Aspirin↗
PubMedDate not supplied

[Aspirin tolerance in individuals with aspirin-induced urticaria-edematous lesions].

The study involved 22 individuals with aspirin-produced urticaria-edematous skin lesions. Hypersensitivity to aspirin was established with anamnesis showing such lesions on aspirin intake and oral test with aspirin. Threshold, provocative dose of aspirin was determined in all patients at the beginning of the study. Moreover, threshold provocative indomethacin dose was additionally determined in 12 patients. Tolerance to aspirin was produced by the oral administration of aspirin in increasing doses upto total dose 600 mg at a 24-hour intervals. Twelve patients were given 25 mg of indomethacin after 24 hours, and 50 mg of this drug after 48 hours. The patients tolerated indomethacin well during aspirin tolerance stage. The authors suggest that both urticaria-edematous and bronchial type of aspirin hypersensitivity are of the same pathogenetic origin.

Adult↗
PubMed1994

CLASP: a randomised trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) Collaborative Group.

Pre-eclampsia is a common and serious complication of pregnancy that affects both mother and child. Review of previous small trials of antiplatelet therapy, particularly low-dose aspirin, suggested reductions of about three-quarters in the incidence of pre-eclampsia and some avoidance of intrauterine growth retardation (IUGR), but larger trials have not confirmed these results. In our multicentre study 9364 women were randomly assigned 60 mg aspirin daily or matching placebo. 74% were entered for prophylaxis of pre-eclampsia, 12% for prophylaxis of IUGR, 12% for treatment of pre-eclampsia, and 3% for treatment of IUGR. Overall, the use of aspirin was associated with a reduction of only 12% in the incidence of proteinuric pre-eclampsia, which was not significant. Nor was there any significant effect on the incidence of IUGR or of stillbirth and neonatal death. Aspirin did, however, significantly reduce the likelihood of preterm delivery (19.7% aspirin vs 22.2% control; absolute reduction of 2.5 [SD 0.9] per 100 women treated; 2p = 0.003). There was a significant trend (p = 0.004) towards progressively greater reductions in proteinuric pre-eclampsia the more preterm the delivery. Aspirin was not associated with a significant increase in placental haemorrhages or in bleeding during preparation for epidural anaesthesia, but there was a slight increase in use of blood transfusion after delivery. Low-dose aspirin was generally safe for the fetus and newborn infant, with no evidence of an increased likelihood of bleeding. Our findings do not support routine prophylactic or therapeutic administration of antiplatelet therapy in pregnancy to all women at increased risk of pre-eclampsia or IUGR. Low-dose aspirin may be justified in women judged to be especially liable to early-onset pre-eclampsia severe enough to need very preterm delivery. In such women it seems appropriate to start low-dose aspirin prophylactically early in the second trimester.

Adult↗
PubMedDate not supplied

Tolerance to aspirin in aspirin-sensitive asthmatics. Methods of inducing the tolerance state and its influence on the course of asthma and rhinosinusitis.

Aspirin-sensitive asthma is a serious clinical problem, frequently involving dramatic exacerbation and sometimes even death after the accidental ingestion of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). The majority of such asthmatics usually suffer from chronic rhinosinusitis and nasal polyps as well, and almost half of them from headaches. Widal et al. in 1922, and later, Zeiss and Lockey were able to elicit tolerance to aspirin (ASA). In all the studies performed so far, tolerance to ASA was achieved by giving double threshold ASA doses every day or every few hours. This method elicited severe dyspnea and sometimes pronounced extrabronchial sensitivity symptoms. From our previous studies, it appeared that the smaller the aspirin dose, the weaker the sensitivity symptoms, and that it is possible to induce tolerance after eliciting only very slight sensitivity reactions. Based on this observation, we elaborated a new method of eliciting aspirin tolerance by the daily administration of gradually increasing doses of aspirin starting with subthreshold doses. Applying this method, we achieved tolerance to aspirin without any adverse reactions. The patients in a tolerance state to ASA also tolerated well other NSAIDs, i.e. indomethacin and diclofenac. It is possible to maintain a tolerance state for a long time by the administration of ASA at proper intervals. It was shown that such a procedure may have a beneficial influence on the course of asthma and rhinitis. In our opinion, inducing and maintaining aspirin tolerance in aspirin-sensitive asthmatics is indicated in the following situations: 1) the need to treat coexisting rheumatic diseases; 2) the need to treat coexisting intractable headaches; and 3) the need for symptomatic treatment of ASA-sensitive asthma and rhinitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗
PubMed1998

Effect of nitric oxide-releasing aspirin derivative on gastric functional and ulcerogenic responses in rats: comparison with plain aspirin.

The effects of a nitric oxide (NO)-releasing derivative of aspirin, NCX-4016, on gastric functional and ulcerogenic responses in rat stomachs were examined in comparison with those of aspirin. Topical application of aspirin (80 mM) to the stomach markedly decreased transmucosal potential difference and slightly increased luminal pH (acid back-diffusion) with minimal effect on mucosal blood flow, whereas NCX-4016 caused a marked increase in mucosal blood flow with no effect on potential difference and pH. Aspirin itself was ulcerogenic, causing damage in the mucosa when administered p.o., and it markedly potentiated gastric ulcerogenic response to hypothermic stress (28 degrees C-30 degrees C) with no effect on acid secretion when given s.c. NCX-4016, however, was not ulcerogenic by itself, did not modify the ulcerogenic response to stress and even showed a dose-dependent protection against HCl/ethanol-induced gastric lesions. When NCX-4016 was given intragastrically to pylorus-ligated rats, a large amount of NO was detected in both gastric contents and serum. NCX-4016 administered either p.o. or s.c. produced an equipotent inhibition of mucosal PGE2 generation in the stomach, as compared with aspirin. In addition, both aspirin and NCX-4016 suppressed carrageenan-induced rat paw edema. These results suggest that, unlike aspirin, the NO-releasing derivative of aspirin NCX-4016 neither had a topical irritating action on the stomach nor exerted a worsening effect on gastric ulcerogenic response to stress, but rather provided gastric protection against ethanol, despite inhibiting cyclo-oxygenase activity and showing anti-inflammatory action much as aspirin does. NCX-4016, probably by releasing NO, exerted protective effects that counteracted the potential damaging effects of cyclo-oxygenase inhibition.

Animals↗