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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

Observation of Reduction of Nocturnal Asthma by an Inhaled Anticholinergic Drug

There is now considerable evidence that nocturnal asthma represents an exaggeration of the normal diurnal variation in airway caliber. There is a degree of resting cholinergic tone present in human airways. Since asthmatic subjects show an exaggerated bronchoconstrictor response to cholinergic agonists, it is possible that increased cholinergic tone at night might contribute to nocturnal asthma . There may be several possible mechanisms for the increase in cholinergic effects at night. There may be an increase in

Details of Nocturnal Asthma by an Inhaled Anticholinergic Drug

With placebo, there was a difference between morning and evening PEF of 61.0±45.0 L/min (mean ±SEM; p<0.01; n = 18), or a fall in morning PEF of 17.3 ±2.0 percent (expressed as a percentage of evening PEF). The percentage fall in PEF after 200μg of oxitropium bromide was not significantly different from that after placebo (15.6±3.1 percent), but there was a significant reduction in the percentage of morning fell after 400μg (10.3 ± 3.3 percent;

Reduction of Nocturnal Asthma by an Inhaled Anticholinergic Drug

The mechanism of nocturnal asthma is still uncer-tain. In both normal and asthmatic subjects, anticholinergic drugs cause bronchodilatation, thus indicating a degree of resting cholinergic tone in human airways. There is some evidence that vagal tone may be greater in asthmatic subjects than in normal subjects, since the sinus arrhythmia gap, which reflects cardiac vagal tone, is more prolonged. There is no direct evidence for circadian variation in cholinergic regulation of airway tone, but several

Considerations of Passive Smoking on Lung Function and Airway Reactivity in Asthmatic Subjects

Involuntary smoking produces unpleasant symptoms in many individuals. These subjective complaints may be sufficient cause to regulate smoking in confined public places. However, it remains controversial whether acute passive smoking is associated with important pulmonary physiologic hazards. The present study was designed to investigate whether involuntary smoking presents an acute respiratory risk to asymptomatic asthmatic individuals. Our data demonstrate that one hour of passive cigarette smoke inhalation by young, clinically stable asthmatics produced no change

Outcomes of Passive Smoking on Lung Function and Airway Reactivity in Asthmatic Subjects

Results obtained in individual subjects are shown in Table 2. Mean data and statistical comparisons between groups of paired data are provided in Table 3. Symptoms and Signs Marked eye irritation was a universal finding. Most individuals opted to wear the protective goggles after spending several minutes in the chamber. Three subjects experienced mild, transient, self-limiting cough. Except for eye and nasopharyngeal irritation, the subjects were comfortable and spent the time in the chamber reading