Concerning the nature of intolerance to aspirin

Samter, Max; Beers, Ray F.

doi:10.1016/0021-8707(67)90076-7

Cited by 294 publications

(147 citation statements)

References 15 publications

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“…Soon after the finding of aspirin-sensitivity in asthmatic patients (Samter & Beers, 1967) it was reported that in addition to aspirin, other anti-inflammatory drugs were also associated with an acute asthmatic attack in a patient with intrinsic bronchial asthma. These drugs include indomethacin, aminopyrine, tartrazine (a yellow dye frequently present as a food additive), acetoaminophen and mefenamic acid (Vanselow & Smith, 1967;Smith, 1971;Szczeklik, Gryglewski & Czerniawska-Mysik, 1975).…”

Section: Discussionmentioning

confidence: 99%

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Spontaneous Activity in the Trachea of Dogs Treated With Indomethacin: An Experimental Model for Aspirin‐related Asthma

Ito

Tajima

1981

British J Pharmacology

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1 Electrical and mechanical properties of smooth muscle cells or of neuro-effector transmission in the smooth muscle layer of the dog trachea, were studied after treatment with indomethacin, by means of the double sucrose gap, microelectrode or tension recording methods. 2 After several subcutaneous injections of indomethacin (1.0 mg/kg daily), 6 out of 12 dogs were coughing and wheezing. 3 Smooth muscle tissues dissected from the trachea of the coughing dog showed spontaneous electrical and mechanical activities at the frequency of 8-15 per min. These spontaneous electrical and mechanical activities were completely suppressed by treatment with atropine (10-6 M), isoprenaline (5 x 10-7 M) or prostaglandin E2 (10-9 M) but not by tetrodotoxin (1.5 x 10-6 M). 4 Direct muscle stimulation induced oscillatory potential changes followed by tension development in the trachea of the indomethacin-treated dog. 5 In the indomethacin-treated dog, mean membrane potential of the tracheal smooth muscle cells was -52.4 mV, and in the control trachea, the potential was -59.0 mV. 6 In the trachea from control dogs, the amplitude of test e.j.ps after conditioning e.j.ps was always smaller than the conditioning e.j.p., at any time interval between the two stimuli. In the trachea from indomethacin-treated dogs, facilitation phenomena were observed. 7 In the trachea from the indomethacin-treated dog, prostaglandin E, (PGE,) or PGE2 (10-")'-10-9 M) markedly suppressed the amplitude of the e.j.p. but did not affect the facilitation phenomenon. 8 These results indicate that endogenous prostaglandins play important physiological roles in the feed-back inhibitory mechanisms for acetylcholine release from the nerve terminals during the resting and active states. 9 The results are also discussed in relation to the genesis of aspirin-induced asthma in man.

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Section: Discussionmentioning

confidence: 99%

“…It has been reported that in some patients with bronchial asthma, aspirin induces acute asthmatic attacks (Samter & Beers, 1967). It has also been reported that ingestion of indomethacin is associated with an acute asthmatic attack in some patients with intrinsic bronchial asthma (Vanselow & Smith, 1967).…”

Section: Introductionmentioning

confidence: 99%

Spontaneous Activity in the Trachea of Dogs Treated With Indomethacin: An Experimental Model for Aspirin‐related Asthma

Ito

Tajima

1981

British J Pharmacology

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“…This syndrome is characterized by aspirin hypersensitivity, bronchial asthma, and chronic rhinosinusitis with nasal polyposis, commonly named the "aspirin triad" (Samter and Beers 1967). AIA affects about 5%-10% of adult asthmatics and is found more often in women (Szczeklik and Stevenson 2003).…”

Section: Introductionmentioning

confidence: 99%

Leukotriene-related gene polymorphisms in ASA-intolerant asthma: an association with a haplotype of 5-lipoxygenase

et al. 2004

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A recent study has demonstrated the possible involvement of a leukotriene C4 synthase (LTC4S) gene polymorphism in ASA-intolerant asthma (AIA) in a Polish population, whereas no significant association was noted in other populations. To investigate the role of genetic polymorphism in AIA development, we screened single nucleotide polymorphisms (SNPs) of the key enzymes involved in arachidonate metabolism, and the cysteinyl leukotriene receptor 1 (CYSLTR1) in a large Korean population with AIA: 93 AIA and 181 ASA-tolerant asthma (ATA) patients, and 123 normal controls. The single-base extension method was used to genotype SNPs in 5-lipoxygenase (ALOX5, -1708G→A, 21C→T, 270G→A, 1728G→A), ALOX5-activating protein (ALOX5AP, 218A→G), prostaglandin-endoperoxide synthase 2 (PTGS2, COX2, -162C→G, 10T→G, R228H, V511A), LTC4S (-444A→C), and CYSLTR1 (927T→C). Haplotype analyses were undertaken for the SNPs in ALOX5. No significant differences in allele and genotype frequencies of single SNPs were observed between the patient groups (P>0.05). However, the frequency of the ALOX5-ht1 [G-C-G-A] haplotype in the AIA group was significantly higher than its frequency in the ATA group with a probability (P) of 0.01, odds ratio (OR) of 5.0, and 95% confidence interval (95%CI) of 1.54-17.9, and in the normal controls (P=0.03, OR=4.5, 95%CI=1.1-18.4), by using a dominant model. These results suggest a lack of association between the ALOX5AP, PTGS2, LTC4S, and CYSLTR1 gene polymorphisms and the AIA phenotype in the Korean population. However, the possible involvement of ALOX5-ht1 [G-C-G-A] in AIA development is suggested.

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“…Although there is currently considerable controversy regarding the incidence and pathogenesis of fungal sinusitis, [3][4][5] most sinus surgeons would agree that, in at least some patients with CRS and polyposis, reactivity to commensal fungal organisms or some similar disease process is occurring. The typical findings with allergic fungal sinusitis include polypoid mucosa and tenacious allergic mucin with abundant eosinophils and eosinophil breakdown products.…”

Section: A a B Bmentioning

confidence: 99%