[Functional assessment of posterior cordotomy in patients with bilateral vocal fold paralysis]. / Czynnosciowa ocena skutecznosci chordotomii tylnej u chorych z obustronnym porazeniem faldów glosowych.

UNLABELLED: Surgical treatment of bilateral vocal fold paralysis must be undertaken if such a condition lasts 6-12 months or longer and causes dyspnoea. The purpose of the procedures is to assure proper airflow through the glottis and to preserve good voice and unimpaired swallowing. Modern endoscopic surgery of the glottis is performed with CO2 laser. The following paper presents results of laser posterior cordotomy performed in 17 patients aged 19-73 years suffering from bilateral vocal fold paralysis. RESULTS AND CONCLUSIONS: In 7 patients the range of vocal fold resection had to be expanded. 3 individuals developed post-operative granulation in subglottal region. Spirometry and electroglottography were performed before and after the operation to assess the patients' laryngeal functions: respiration and voice quality. The results indicate that laser cordectomy was effective in the discussed group of patients.

Biochemical and clinical evidence that aspirin-intolerant asthmatic subjects tolerate the cyclooxygenase 2-selective analgetic drug celecoxib.

BACKGROUND: Subjects with aspirin-intolerant asthma (AIA) respond with bronchoconstriction and extrapulmonary adverse reactions to conventional nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit the cyclooxygenase (COX) step in the biosynthesis of prostaglandins. Recently, 2 isotypes of COX have been identified, and COX-2-selective NSAIDs have been developed for treatment of inflammatory disorders. OBJECTIVE: We investigated whether 33 subjects with a typical history of AIA tolerated the new COX-2-selective NSAID celecoxib. METHODS: All subjects displayed current aspirin sensitivity in oral or inhalation challenge tests. The subjects first underwent a double-blind, randomized, cross-over, increasing-dose challenge with placebo or celecoxib (10, 30, or 100 mg in suspension) on 2 occasions 7 days apart. Thereafter, all subjects were exposed to 400 mg of celecoxib administered during an open challenge session as two 200-mg doses 2 hours apart. Lung function, clinical symptoms, and urinary excretion of leukotriene E(4) (LTE(4)) were monitored, with the latter being a sensitive biochemical marker of aspirin intolerance. RESULTS: There were no changes in lung function or extrapulmonary symptoms during the double-blind sessions or in urinary excretion of LTE(4). Also, the highest recommended daily dose of celecoxib was well tolerated, with no symptoms, lung function changes, or alterations in urinary LTE(4) levels. CONCLUSIONS: A group of subjects with clinically well-documented AIA tolerated acute challenge with the selective COX-2 inhibitor celecoxib. The findings indicate that the intolerance reaction in AIA is due to inhibition of COX-1. Large long-term studies of COX-2 inhibitors in AIA should be undertaken.

A controlled study of 9alpha,11beta-PGF2 (a prostaglandin D2 metabolite) in plasma and urine of patients with bronchial asthma and healthy controls after aspirin challenge.

BACKGROUND: Prostaglandin D(2) (PGD(2)) is the predominant cyclooxygenase product of mast cells, the number of which is increased in bronchial asthma. Release of PGD(2) might reflect mast cell activation and disordered function of the asthmatic lung. OBJECTIVE: We sought to determine blood and urinary levels of 9alpha,11beta-PGF(2), a major stable PGD(2) metabolite in 2 well-defined phenotypes of asthma, aspirin-induced asthma (AIA) and aspirin-tolerant asthma (ATA), and in healthy control subjects and to study the effects of aspirin on PGD(2) release. METHODS: Using gas chromatography/mass spectrometry, we determined plasma and urinary concentrations of 9alpha,11beta-PGF(2) at baseline in 131 stable asthmatic patients, 65 of whom had AIA and 66 of whom had ATA. Fifty healthy nonatopic subjects served as the control group. The measurements were also performed after an aspirin challenge in 26 of 65 patients with AIA and in 24 of 50 control subjects. RESULTS: At baseline, patients with AIA had significantly higher plasma levels of 9alpha,11beta-PGF(2) than either patients with ATA or healthy subjects. A similar significant elevation of serum tryptase was observed in patients with AIA compared with patients with ATA and control subjects. Mean urinary 9alpha,11beta-PGF(2) values did not differ among the 3 groups. In patients with AIA, as opposed to healthy subjects, aspirin challenge invariably precipitated a clinical reaction, accompanied in most patients by a further rise in plasma levels of PGD(2) metabolite and tryptase. CONCLUSIONS: In stable AIA, though not in ATA, there is a steady release of PGD(2) into the blood, accompanied by the release of tryptase. Aspirin enhances this reaction in most patients. Release of bronchoconstrictive PGD(2) might contribute to the severe clinical course of AIA.

Analgesics and asthma.

The incidence of asthma is increasing throughout the world, which presents both public health and economic concerns. It is widely recognized that in some adult patients with asthma, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX)-1 exacerbate the condition. This is a distinct clinical syndrome called aspirin-induced asthma (AIA). The disease develops according to a characteristic pattern of symptoms. Persistent eosinophilic rhinosinusitis precedes development of nasal polyposis, aspirin hypersensitivity, and asthma. There is no in vitro test, and diagnosis can only be established by provocation tests with aspirin. At the biochemical level, AIA is characterized by a chronic overproduction of cysteinyl leukotrienes. The key enzyme, leukotriene C4 synthase, is overexpressed in bronchi, and its messenger RNA is upregulated in peripheral blood eosinophils. This can be partly related to the genetic polymorphism of the enzyme. The disease runs a protracted course, even if COX-1 inhibitors are avoided. The course of AIA is often severe, and at least half of the patients need systemic corticosteroids to control their asthma. To prevent life-threatening reactions, patients with AIA should avoid aspirin and other analgesics that inhibit COX-1. The incidence of cross-sensitivity to paracetamol in AIA patients is low and, when a reaction does occur, the symptoms experienced are shorter and milder than if the reactions were evoked by an NSAID. Rapidly growing evidence indicates that highly specific COX-2 inhibitors, known as coxibs, are well tolerated and can be safely used by AIA patients.

Improvement of aspirin-intolerant asthma by montelukast, a leukotriene antagonist: a randomized, double-blind, placebo-controlled trial.

Leukotriene antagonists block the proinflammatory actions of leukotrienes (LT) and have been introduced as new treatments for asthma. Conventional therapy with glucocorticosteroids does not inhibit the biosynthesis of leukotrienes. We therefore tested whether addition of the leukotriene receptor antagonist montelukast was of therapeutic benefit in a group of aspirin-intolerant patients with asthma of whom 90% already were treated with moderate to high doses of glucocorticosteroids. Under double-blind conditions, 80 aspirin-intolerant patients with asthma were randomized to receive 4 wk oral treatment of either 10 mg of montelukast or placebo once daily at bedtime. Pulmonary function was measured as forced expiratory volume in 1 s (FEV(1)) once a week in the clinic and daily as morning and evening peak expiratory flow rate (PEFR). Asthma symptoms and use of rescue bronchodilator were also recorded daily. Asthma specific quality of life (QoL) was assessed before and after the treatments. The group receiving montelukast showed a remarkable improvement of their asthma, whereas the group given placebo showed no change. Thus, from equal baseline values, the mean difference between the groups over the 4-wk treatment period was 10.2% for FEV(1) and 28.0 L for morning PEFR (p for both < 0.001). The improved pulmonary function in the group receiving montelukast occurred at the same time as 27% less bronchodilator was used (p < 0.05), and it was associated with fewer asthma symptoms than in the group given placebo, including 1.3 nights more of sleep per week and 54% fewer asthma exacerbations (p < 0.05). There was also an improvement in asthma-specific QoL (p < 0.05). The therapeutic response to montelukast was consistent across patients with different baseline characteristics and did not correlate with baseline urinary LTE(4). Addition of a leukotriene receptor antagonist such as montelukast improves asthma in aspirin-intolerant patients over and above what can be achieved by glucocorticosteroids.