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Research of Montelukast on Exhaled Leukotrienes and Quality of Life in Asthmatic Patients

All patients were recruited from asthma clinics in a primary care practice (Table 1). Accurately interpreted spirometry in primary care at asthma and COPD in clinics – https://onlineasthmainhalers.com/spirometry-can-be-done-in-family-physicians-offices-and-alters-clinical-decisions-in-management-of-asthma-and-copd.html . Patients had been receiving a stable dose of inhaled steroids for at least 2 months. All patients used short-acting P-agonists as needed, and 26 of 50 patients were also receiving a long-acting p2-agonist. After an initial visit and baseline measurements, all patients received 4 weeks of treatment

Effect of Montelukast on Exhaled Leukotrienes and Quality of Life in Asthmatic Patients

Asthma is a chronic inflammatory disease of the airways characterized by an infiltration of the airways by inflammatory cells including eosinophils , mast cells, and T lymphocytes. Inhaled corticosteroids remain a first-line therapy for the control of inflammation in patients with asthma. However, it appears that suppression of inflammation may not be complete, and the effect of inhaled corticosteroids on cysteinyl-leukotriene (cys-LT) biosynthesis is lim-ited. cys-LTs are important inflammatory mediators of asthma produced by the 5-lipoxygenase

Considerations of Anticholinergic Drug, Ipratropium Bromide (Sch 1000), as an Aerosol in Chronic Bronchitis and Asthma

Atropine has been administered parenterally and by inhalation to prevent and curtail asthmatic attacks. Gold and associates showed that procedures decreasing vagal stimulation, including intravenous or aerosol treatment with atropine, could prevent increases in airway resistance caused by several different antigens in dogs. Pretreatment of asthmatic patients with atropine can block their shortterm response to methacholine and certain antigens. Intravenous administration of atropine to dogs prevented bronchospasm induced by intravenous or aerosol administration of serotonin

Data of Anticholinergic Drug, Ipratropium Bromide (Sch 1000), as an Aerosol in Chronic Bronchitis and Asthma

In the group with bronchial asthma, all doses of ipratropium and isoproterenol produced significant (P < 0.05) improvements in the FEVi, compared with the placebo, within five minutes of administration. The duration of significant improvement in FEVi was less than 15 minutes after the lO^g dose of ipratropium bromide; it was 30 minutes after the 20/xg dose of ipratropium bromide and after 75/xg of isoproterenol, one hour for 150/ig of isoproterenol, and up to four hours after the

Bronchodilator Action of the Anticholinergic Drug, Ipratropium Bromide (Sch 1000), as an Aerosol in Chronic Bronchitis and Asthma

Ipratropium bromide (N-isopropyl-notropine-tropic acid ester methylbromide), also known as Sch 1000, is an atropine-like agent which has been developed as an aerosol bronchodilator drug. This compound is believed to produce bronchodilata-tion by inhibiting increases in levels of cyclic guano-sine monophosphate mediated by cholinergic receptors, as contrasted with the action of adrenergic receptor stimulants in raising levels of cyclic adenosine monophosphate . Previous investigations have shown effective bronchodilation by ipratropium in asthmatic patients. This study was undertaken to establish

Deliberations of Studies Concerning Patients with Asthma, Aspirin Intolerance, and Nasal Polyps

Afzelius has suggested that the ultrastructural abnormalities seen in cilia can be separated into two groups: those with the specific defects he associates with the immotile cilia syndrome and those regarded as nonspecific. The occasional morphologic changes we have seen in our “triad” asthmatics and normal subjects would all be classified under his nonspecific category. Indeed, even most of the ultrastructural abnormalities noted in our patient with situs inversus and sinusitis were of this nonspecific

Outcomes of Studies Concerning Patients with Asthma, Aspirin Intolerance, and Nasal Polyps

Of the seven patients with “triad” asthma, five had nasal biopsy specimens showing ciliated epithelium. One of the male patients with a nasal biopsy revealing only squamous metaplasia provided us with a semen sample. An additional patient had squamous metaplasia of the biopsied nasal mucosa, with rare ciliated cells identified only by light microscopy. Scanning and transmission electron microscopy of those specimens with ciliated epithelium obtained from these “triad” asthmatics all showed ultrastructurally normal cilia.

Ultrastructural and Functional Studies of Cilia from Patients with Asthma, Aspirin Intolerance, and Nasal Polyps

Recently, much attention has been focused on ultra-structural abnormalities of cilia and their association with respiratory disease, infertility, and Kar-tageners syndrome ( http://www.sciencedirect.com/science/article/pii/S0012369216382708 ). Although generally referred to as the immotile cilia syndrome, other observers, have identified motion in some of the cilia and suggested the use of the term “ciliary dysldnesis.” Sleigh has noted that at present, “primary ciliary dyskinesia” is the preferred term. This would encompass the previously described syndromes including Kartagener s syndrome

Observations of Coronary Arterial Spasm in the Aspirin-induced Asthma Syndrome

Aspirin-induced asthma is a distinct clinical syndrome. It starts with vasomotor rhinitis which leads to chronic nasal congestion and later to the formation of nasal polyps. Bron-chospasm follows with the development of intrinsic asthma. Rhinitis and asthma often precede the appearance of aspirin or other nonsteroidal anti-inflammatory drug (NSAID) sensitivity which is the hallmark of the syndrome. The diagnosis of the AIA syndrome was made in our patient because of the history of precipitation of acute asthma after

Is Coronary Arterial Spasm Part of the Aspirin-induced Asthma Syndrome

Aspirin will precipitate asthmatic attacks in some patients. This distinct clinical syndrome, called aspirin-induced asthma (AIA) includes vasomotor rhinitis, nasal polyps, intrinsic asthma, and aspirin sensitivity. Aspirin may also aggravate angina attacks in patients with Prinzmetal’s variant angina (PVA). There have been no reports describing the occurrence of coronary ischemic abnormalities in patients with AIA during acute attacks precipitated by aspirin. We report a case of coronary artery spasm during an episode of bronchial asthma induced by