Relationship of inhibition of prostaglandin biosynthesis by analgesics to asthma attacks in aspirin-sensitive patients.

Szczeklik, Andrzej; Gryglewski, Ryszard J.; Czerniawska-Mysik, G

doi:10.1136/bmj.1.5949.67

Cited by 458 publications

(225 citation statements)

References 11 publications

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“…2,3 The underlying mechanisms of aspirin-intolerance appear to be related to inhibition of cyclo-oxygenase with subsequent release of leukotrienes and other mediators. 4 Our previous study, using the leukotriene D 4 receptor antagonist montelukast, confirmed the evidence that leukotrienes play an important role in the development of nasal polyps in patients with aspirin-intolerant asthma. 5 Trials of desensitisation, using aspirin, have been reported in patients with aspirin-intolerant asthma.…”

Section: Introductionsupporting

confidence: 61%

“…This is thought to cause an exacerbation of asthma and the formation of nasal polyps. 4 Intranasal therapy with lysine-aspirin has been reported to be effective in both aspirin-sensitive and aspirin-tolerant nasal polyps. 9,14 -16 Nucera et al 15 showed, in an open study, that the relapse rates of nasal polyps after medical or surgical polypectomy were significantly lower than those for a non-randomised control group, in patients receiving a low (sub-desensitising) dose of lysine-aspirin once weekly.…”

Section: Discussionmentioning

confidence: 99%

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Intranasal lysine-aspirin administration decreases polyp volume in patients with aspirin-intolerant asthma

Ogata

Darby

2007

J. Laryngol. Otol.

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Introduction: Nasal polyposis associated with aspirin-intolerant asthma tends to be difficult to control, with frequent recurrences. We examined the effect of intranasal lysine-aspirin administration on resistant nasal polyps of asthmatic, aspirin-intolerant patients, when used in addition to routine therapy.Patients and methods: Thirteen patients with asthma and intolerance to aspirin were recruited. All but one had undergone numerous polypectomies and were uncontrolled on standard therapy with intranasal corticosteroids, leukotriene receptor antagonists and nasal douching. Aspirin treatment involved one drop (100 ml) of 30 mg/ml lysine-aspirin solution to each nostril, initially daily, increased every two or three days up to a maximal of 18 drops (54 mg lysine-aspirin) a day. Nasal symptoms, nitric oxide level, nasal inspiratory peak flow rate, peak expiratory flow rate and nasendoscopic grading were assessed prior to therapy and three months later. We also compared the change in endoscopic polyp scores during three months of lysine-aspirin administration with the changes which had occurred during the three months prior to administration (during which time other therapies had been identical).Results: Nasal blockage symptoms tended to decrease; other nasal symptoms were unchanged. Significant changes were seen in nasal inspiratory peak flow rate (103.3 + 18.9 and 140.0 + 16.7 l/ min before and after aspirin, respectively; p ¼ 0.014), but not in peak expiratory flow rate (438.7 + 33.4 and 440.0 + 28.4 l/min before and after aspirin, respectively; p ¼ 0.700). Nasal nitric oxide levels rose significantly (in both sides, p ¼ 0.028). Expired chest nitric oxide levels did not change. Nasal polyp scores on nasendoscopic examination were significantly reduced (right side, p ¼ 0.027; left side, p ¼ 0.018). Compared with the preceding three months, adding intranasal lysine-aspirin application had the effect on decreasing nasal polyp volume (right side, p ¼ 0.031; left side, p ¼ 0.016).Conclusion: This open study suggests that intranasal lysine-aspirin administration reduces nasal polyp volume in aspirin-intolerant patients, without any adverse affect on concomitant asthma. This was a preliminary study and should be followed by a placebo-controlled, double-blind trial.

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Section: Introductionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Intranasal lysine-aspirin administration decreases polyp volume in patients with aspirin-intolerant asthma

Ogata

Darby

2007

J. Laryngol. Otol.

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“…Moreover, there was a clear correlation between the potency of a drug to inhibit COX in vitro and its ability to precipitate a clinical reaction. We presented these results at an international conference in London in 1974 and published them in British Medical Journal in 1975 [7], expanding the results to other NSAIDs in the following two years. These results were confirmed by several other laboratories and led to the development of the cyclooxygenase theory of AIA.…”

Section: Mechanisms Of the Diseasementioning

confidence: 99%

Aspirin-induced asthma: a tribute to John Vane as a source of inspiration

Szczeklik

2010

Pharmacological Reports

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Abstract:Aspirin-induced asthma is a distinct clinical syndrome consisting of inflammation, characterized by chronic eosinophilic rhinosinusitis with asthma and often nasal polyposis. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) exacerbate asthma, resulting in violent attacks. This is the hallmark of the clinical syndrome as explained by the cyclooxygenase theory. This theory, which is now generally accepted, states that asthma attacks precipitated by aspirin and other NSAIDs have no allergic background; instead, they occur due to the inhibition of cyclooxygenase-1 in sensitive patients. This paper describes how the discoveries of John Vane inspired the authors of the cyclooxygenase theory and led to further insight into the biology of eicosanoid metabolism in this relatively common type of asthma.

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“…Other analgesic and/or anti-inflammatory agents, such as mefenamic acid, indomethacin, paracetamol and phenylbutazone may also produce asthmatic episodes in man (Samter & Beers, 1968;Smith, 1971;Szczeklik, Gryglewski & Czerniawska-Mysik, 1975;Delaney, 1975). Paradoxically, most of these agents counteract bronchoconstriction induced in experimental animals by slow reacting substance of anaphylaxis (SRS-A) or bradykinin (Berry & Collier, 1964).…”

Section: Introductionmentioning

confidence: 99%

“…Samter & Beers (1968) have postulated that altered responses of peripheral chemoreceptors initiate a series of reflexes in which mild analgesics act as agonists rather than antagonists. Lately, inhibition of biosynthesis of prostaglandins by aspirin and other mild analgesics has been associated with their ability to induce asthmatic episodes (Szczeklik et al, 1975).…”

Section: Introductionmentioning

confidence: 99%

Dual Effects of Aspirin in Guinea‐pig Lungs

Mielens

Rosenberg

1976

British J Pharmacology

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Dual effects of aspirin were demonstrated in guinea‐pig lungs: (a) aspirin (3.3 mg/kg i.v.) antagonized bronchoconstriction induced by slow reacting substance of anaphylaxis (SRS‐A); (b) aspirin produced bronchoconstriction when injected in the presence of propranolol into guinea‐pigs in vivo at 330 mg/kg, or into guinea‐pig isolated lungs in vitro as a 4% solution (40 mg/ml). The severity of bronchoconstriction following administration of aspirin was directly related to the degree of β‐adrenoceptor blockade and to the age of the guinea‐pigs. Aspirin‐induced bronchoconstriction was prevented in vivo and in vitro by atropine and it could be reversed in vivo by atropine. Aspirin‐induced bronchoconstriction was not inhibited by vagotomy or phenoxybenzamine. These data suggest that the mechanism involved in aspirin‐induced bronchoconstriction may be local cholinergic stimulation and that reduced β‐adrenergic drive may be a predisposing factor.

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Relationship of inhibition of prostaglandin biosynthesis by analgesics to asthma attacks in aspirin-sensitive patients.

Cited by 458 publications

References 11 publications

Intranasal lysine-aspirin administration decreases polyp volume in patients with aspirin-intolerant asthma

Intranasal lysine-aspirin administration decreases polyp volume in patients with aspirin-intolerant asthma

Aspirin-induced asthma: a tribute to John Vane as a source of inspiration

Dual Effects of Aspirin in Guinea‐pig Lungs

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