The alpha-chain of high-affinity receptor for IgE (FcepsilonRIalpha) gene polymorphisms and serum IgE levels.

Background: The high-affinity receptor for immunoglobulin-E (IgE) (FcepsilonRI) plays a major role in the pathogenesis of allergy, but there are only two published studies on its alpha subunit (FcepsilonRIalpha) genetic variability in allergic diseases.

Aims Of The Study: Mutational screening in the region of the FcepsilonRIalpha gene promoter and the first exon with subsequent genetic variability assessment in allergic patients and a random population sample.

Methods: Allergic subjects were individuals with asthma or urticaria.

[Functional assessment of posterior cordotomy in patients with bilateral vocal fold paralysis].

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.

Plasma 9alpha,11beta-PGF2, a PGD2 metabolite, as a sensitive marker of mast cell activation by allergen in bronchial asthma.

Background: Prostaglandin D(2) (PGD(2)) is a major cyclooxygenase product generated by activated mast cells during an allergic response. Assessment of PGD(2) and its metabolites in patients with asthma has mostly been performed in urine, bronchoalveolar lavage fluid and induced sputum, whereas human plasma determinations have been performed only sporadically.

Methods: In 32 patients with allergic asthma and 50 healthy non-allergic controls, baseline plasma and urinary levels of 9alpha,11beta-PGF(2), a primary PGD(2) metabolite, were assessed by gas chromatography/mass spectrometry.

Diagnosis, prevention and treatment of aspirin-induced asthma and rhinitis.

Bronchial asthma is not a homogenous disease. Several variants of asthma can be distinguished. One of them is aspirin-induced asthma.

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.

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.

Clinical and genetic features underlying the response of patients with bronchial asthma to treatment with a leukotriene receptor antagonist.

Background: Treatment with antileukotriene drugs results in clinical improvement in many, though not all, patients with asthma. It can be hypothesized that the subpopulation of asthmatic patients, characterized by aspirin intolerance and cysteinyl-leukotriene overproduction, might profit most from antileukotriene treatment.

Materials And Methods: We compared the clinical response to montelukast in two well-matched groups of patients with mild asthma: 26 aspirin-intolerant asthmatics (AIAs) and 33 aspirin-tolerant asthmatics (ATAs).

Protection against exercise-induced bronchoconstriction by montelukast in aspirin-sensitive and aspirin-tolerant patients with asthma.

Background: Montelukast, a cysteinyl-leukotriene receptor antagonist, was reported to have a protective effect against exercise-induced bronchoconstriction (EIB). Aspirin-induced asthma (AIA) is characterized by overproduction of cysteinyl-leukotrienes.

Objective: The aim of the study was to compare the response to exercise and the effect of montelukast on EIB in AIA as compared to aspirin-tolerant asthma (ATA).

Mutations C677T and A1298C of the 5,10-methylenetetrahydrofolate reductase gene and fasting plasma homocysteine levels are not associated with the increased risk of venous thromboembolic disease.

Mild hyperhomocysteinemia is associated with homozygosity for the thermolabile variant of 5,10-methylenetetrahydrofolate reductase (MTHFR) and could increase the risk of venous thromboembolic disease (VTD). Recently, the second A1298C mutation of the MTHFR gene was described. The present study aimed to analyze both mutations of the MTHFR gene and plasma homocysteine levels in subjects with VTD.

Aspirin-induced rhinitis and asthma.

Interesting findings relating to aspirin-induced asthma recently emerged. In this distinct clinical syndrome, aspirin and most other nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase precipitate rhinitis and asthma attacks. Aspirin-induced asthma affects 5-10% of adult asthmatics, but remains largely underdiagnosed.

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).

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.

[Selective cyclooxygenase 2 inhibitors (COX-2)].

Cyclooxygenase is key enzyme in the prostaglandin synthesis. It exists in two isoforms, which have distinct functions in the organism. Cyclooxygenase-2 (COX-2) participates in the pathophysiology of inflammation.

Safety of a specific COX-2 inhibitor in aspirin-induced asthma.

In a subset of patients with asthma, aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) that inhibit simultaneously cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) precipitate dangerous asthmatic attacks. We tested the hypothesis that in patients with aspirin-induced asthma the attacks are triggered by inhibition of COX-1 and not COX-2. In twelve asthmatic patients (seven men, five women, average age 39 years) oral aspirin challenge precipitated symptoms of bronchial obstruction with fall in FEV1 > 20%, and a rise in urinary leukotriene E4 (LTE4) excretion; also in five patients the stable metabolite of PGD2, 9alpha11betaPGF2, increased in urine.

[Coincidence of 20210A prothrombin variant and factor V Leiden predisposing to venous thromboembolism].

Coexistence of inherited and environmental risks leads to the high hazard of venous thromboembolism. In such cases, there might be difficulties in the diagnosis and treatment of recurrent episodes. The importance of Factor V Leiden and prothrombin variant 20210A in the pathogenesis of venous thromboembolic disease, is widely accepted, but the carriership of thrombophilic genes' variants is usually not sufficient for the development of the disease.

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.

[Asthma and aspirin intolerance].

Undesirable reactions to aspirin and other non-steroidal antiinflammatory drugs compose a diverse group of clinical manifestations with different pathogenic mechanisms. In this review we describe one particular type of manifestation: aspirin-induced asthma. This syndrome describes a straightforward situation with typical clinical signs.

Oral and bronchial provocation tests with aspirin for diagnosis of aspirin-induced asthma.

In 35 asthmatic patients with acetylsalicylic acid (aspirin; ASA) intolerance (AIA) and 15 asthmatics tolerating ASA well, the authors compared the diagnostic value of the placebo-controlled oral ASA versus inhaled L-lysine (L) ASA challenges. All AIA subjects gave a history of asthmatic attacks following ingestion of ASA and in all of them the intolerance was confirmed by oral challenge test over the past 10 yrs. Doses of ASA increasing in geometric progression were used in oral tests 10-312 mg (cumulative dose 500 mg); in bronchial tests 0.