Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient, an 80-year-old female, had complained of a cough for 20 weeks, and was not cured by cough medicine. Gastroesophageal reflux was considered as the cause of the cough because of her symptoms and gastrointestinal fiberscopy (GIF) and barium meal studies. She made favorable progress on a histamine H2 blocker and cysapurid for 4 weeks. Therefore we diagnosed her cough as caused by gastroesophageal reflux. We also studied the incidence of chronic persistent cough in patients suspected of gastroesophageal reflux because of symptoms and GIF results. Among 676 cases examined by GIF at Niigata-kenritsu Myoko Hospital, we detected 7 cases who complained of heartburn and in whom we observed hiatal hernia and reflux esophagitis by GIF. Only one of them, the present case, complained of a cough. CPC caused by gastroesophageal reflux is not seen frequently, but the possibility of GER as the cause of CPC should be considered.
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PMID:[A case of chronic persistent cough (CPC) caused by gastroesophageal reflux (GER) (including a study of CPC caused by suspected GER)]. 157 43

The purpose of this study was to ascertain whether in patients with persistent cough the presence of bronchial hyperresponsiveness (BH) and development of asthma could be speculated based on clinical data. Only patients who met strict criteria excluding exogenous factors that influence BH, especially smoking or respiratory infection, were included in this study. The study group included 15 males and 50 females aged 18 to 62 years (mean +/- S.D. of 44 +/- 12 years) whose physical findings, chest X-rays, spirometry results and peripheral leukocyte counts were within normal limits. Duration of cough was at least one month. The patients had no history of wheezing, dyspnea or previous bronchodilator therapy. None of them had ever been smokers. In addition, there was no history of upper respiratory tract infection in the preceding month. BH was assessed by "Astograph" using methacholine. Cmin and Dmir or SGrs/Grs cont. were measured as the indexes of bronchial sensitivity or reactivity respectively. A methacholine Cmin of 3, 125 micrograms/ml or less was taken as a positive indication of BH. The evaluated clinical data were age, pulmonary function (spirogram or flow volume curve), atopic factors (serum total IgE and family or personal history of atopic diseases), peripheral eosinophil count, bronchial sensitivity or reactivity, and clinical features of cough (induction by exercise or cold air and nocturnal worsening). The results were as follows. (1) Twenty-nine (45%) of 65 patients were BH-positive (BH-positive group). (2) There was no significant difference in age, %FVC, IgE, and family or personal history of atopic diseases between the BH-positive and negative group. However, the BH-positive group had significantly lower FEV1.0%, %FEV1.0, PEFR, (p less than 0.05) and V25/H (p less than 0.01) and a higher peripheral eosinophil count (p less than 0.05) than the BH-negative group. (3) Seventeen (85%) of 20 BH-positive patients prescribed bronchodilators (beta 2 agonist/theophylline) responded to therapy within a month. (4) Seven (29%) of 24 BH-positive patients available for 2 years follow-up developed clinical asthma. (5) There was no significant difference in %FVC, FEV1.0%, V25/H and peripheral eosinophil count between the patients who developed asthma (Group A) and those who did not (Group N-A). However, The patients in Group A were older than those in Group N-A.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical study on bronchial hyperresponsiveness and development of bronchial asthma in patients with persistent cough]. 174 66

The prevalence and severity of cough during long-term enalapril treatment were examined by comparing a cohort of 136 hypertensive patients who started treatment with enalapril with consecutive age and sex-matched patients who commenced nifedipine therapy during the same period. Cough and other symptoms were assessed by a questionnaire designed to avoid bias towards reporting cough. After a mean of 27 months' treatment patients on enalapril had an excess of persistent cough (16 per cent, 95 per cent CI 7-25, p less than 0.01), voice change (14 per cent, 95 per cent CI 2-27, p less than 0.05) and sore throat (10 per cent, 95 per cent CI -0.1 to 20.3 per cent, p less than 0.01) when compared to nifedipine-treated patients. The cough was usually dry, moderate or severe, paroxysmal, and troublesome at night. Cough tended to be more common in women (23 per cent vs. 7.2 per cent), non-smokers, and at higher doses of enalapril, but was not related to age, duration of treatment, or chronic respiratory disease. Dry cough commonly persists as a troublesome side-effect during long-term enalapril treatment, and is often associated with voice change and sore throat.
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PMID:Prevalence of persistent cough during long-term enalapril treatment: controlled study versus nifedipine. 175 76

The author studied the characteristics of ACE inhibitor-induced cough in 41 non-smoking hypertensive patients. For at least 6 months, 20 patients (10 males and 10 females) were treated with enalapril, and 21 (11 males and 10 females) with aracepril. The results were as follows. 1) ACE inhibitor-induced cough was induced in 7 cases (1 male and 6 females). The incident rate of cough was 17.1%. ACE inhibitor-induced cough was not significantly related to past allergic history or to the beta-adrenergic blocker therapy. The laboratory findings of the cough sufferers--such as eosinophil percent in venous blood, serum GOT and GPT, urea nitrogen, creatinine, renal function (PSP excretion test and creatinine clearance), and pulmonary function (%FVC, FEV1.0% and %V25)--were not significantly different from those of the non-coughers. 2) Inhibitory effects of ipratropium bromide inhalation of ACE inhibitor-induced cough were noted in 83.3% of the patients, but their coughs did not completely disappear. From these findings, the pathogenesis of this cough may be related to be as follows. The cough seems to be related to the release of acetylcholine from vagal nerve terminals or to the stimulation of irritant receptors and vagal reflex. 3) Chronic persistent cough or bronchial asthma did not occur after stopping the treatment with ACE inhibitors. The mean follow-up period was 15.6 months.
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PMID:[Angiotensin converting enzyme (ACE) inhibitor-induced cough in non-smoking hypertensive patients]. 183 7

Chronic cough persisting for two months or more that remains unexplained after extensive investigations is a common clinical problem. The purpose of this study was to determine whether such cough is associated with otherwise asymptomatic gastro-oesophageal reflux. Thirteen patients with chronic persistent cough that was unexplained after a standard diagnostic assessment were identified. All were non-smokers. The mean (SE) duration of cough was 17.8 (8.0) months. Ten had never had reflux symptoms and three had had mild symptoms only after the onset of the cough. All the patients completed standardised cough diary cards for eight weeks and underwent 24 hour ambulatory oesophageal pH monitoring. A reflux episode was defined as a fall in oesophageal pH to below 4.0. Nine control subjects were matched for age, lung function, and body mass index. The patients experienced significantly more episodes of reflux per 24 hours than the controls (115.8 (SE 31.7) versus 4.7 (1.4) and longer reflux episodes (15.5 (5.8) versus 1.7 (0.5) minutes), and the oesophageal pH was below 4.0 considerably longer (84.5 (20.2) versus 3.8 (1.3) minutes). Cough occurred simultaneously with 13% (2.2%) of reflux episodes and within five minutes in another 35% (5.8%) of episodes, whereas gastro-oesophageal reflux occurred simultaneously with 78% (5.5%) of cough episodes and within five minutes in another 12% (2.3%) of episodes. It is concluded that chronic persistent cough that remains unexplained after a standard diagnostic assessment is associated with otherwise asymptomatic gastro-oesophageal reflux. It is suggested that a self perpetuating mechanism may exist whereby acid reflux causes cough via a local neuronal oesophageal-tracheo-bronchial reflex, and the cough in turn amplifies reflux via increased transdiaphragmatic pressure or by inducing transient lower oesophageal sphincter relaxation. Further study of this mechanism and the role of specific antireflux treatment in chronic persistent cough is warranted.
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PMID:Chronic persistent cough and gastro-oesophageal reflux. 187 35

Although rarely considered in series of lower airway foreign bodies, endobronchial sutures can cause chronic cough or hemoptysis years after thoracic surgery. Eight endobronchial sutures were found in six patients who had undergone surgery four to 30 years prior to admission. Symptoms began two to 25 years after surgery and lasted from two to six years prior to diagnosis. Cough had been attributed to chronic bronchitis or bronchiectasis in five patients and to tracheal narrowing secondary to surgical repair of tracheomalacia in the sixth. Bronchoscopy was diagnostic in all cases. Suture removal was performed with either forceps or endoscopic suture scissors to cut the suture followed by extraction with forceps. Symptoms resolved within three days and granulation tissue by two to four weeks after suture removal. This series suggests that endobronchial suture should be considered in patients with a history (even remote) of previous thoracic surgery who present with chronic, persistent cough unresponsive to specific therapy for any underlying pulmonary disease.
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PMID:Endobronchial suture. A foreign body causing chronic cough. 142 24

Sixteen asthmatic children completed a double blind placebo controlled crossover study of controlled release salbutamol (CRS) to assess its efficacy in controlling night time cough. Children with asthma were enrolled into the study on the basis of a history of persistent cough confirmed by two overnight tape recordings at home. Outcome was measured by two overnight tapes on each medication. Other treatment was unaffected. There was no significant fall in cough counts on CRS. Median scores were 14.5 and 12.0 coughing episodes per night for CRS and placebo respectively. Mean overnight oxygen saturation was identical in both treatment periods but morning peak flow showed a trend towards improvement on CRS. Treatment with CRS does not have a significant effect in control of night cough although it may improve objective measurements of lung function.
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PMID:Effect of controlled release salbutamol on nocturnal cough in asthma. 195 4

A newly recognized chlamydial species, Chlamydia pneumoniae causes acute respiratory infections including pneumonia, bronchitis and pharyngitis. In this paper, eight cases of bronchitis and tonsillitis associated with C. pneumoniae are presented. Three cases came to the clinic because of persistent cough and productive sputum. C. pneumoniae was isolated from sputum of a patient and cultured in HeLa 229 cells. Other two patients were diagnosed serologically; Antibodies were measured by microimmunofluorescence using formalized elementary bodies of C. pneumoniae. A titer of 512 in the IgG class was detected. Four patients had sore throat. C. pneumoniae was isolated and cultured from tonsillar swabs in all of them. A patient with sore throat and cough diagnosed as pharyngolaryngitis was sero-positive. Antibodies to C. pneumoniae in IgG and IgM class were 128 and 32, respectively. All the patients were treated with macrolide antibiotics (erythromycin and rokitamycin), and clinical symptoms subsided. In five patients from whom the organism was isolated, the agents were eradicated by the treatment. However, clinical courses of those patients revealed that patient takes a long time to recover from the illness, if diagnosis and first choice of antimicrobial agent are not appropriate.
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PMID:[Respiratory tract diseases due to Chlamydia pneumoniae]. 204 Sep 12

Cough is a symptom frequently encountered by the otolaryngologist--head and neck surgeon. Although most coughs are self limited, chronic cough often proves to be a frustrating problem. Seventy-two infants and children under age 16 with a normal chest radiogram have now been evaluated for chronic cough persisting for longer than 4 weeks. Cough-variant asthma was the most common cause of cough, followed by sinusitis, gastroesophageal reflux, aberrant innominate artery, psychogenic cough, and subglottic stenosis. Chronic cough is best managed by first following an individualized diagnostic protocol designed to determine the etiology of the cough. This is followed by specific therapy to treat the underlying disorder. Children with persistent cough and normal chest radiograph are best served when referred promptly for evaluation by an otolaryngologist when the primary physician's initial efforts at diagnosis and treatment are not effective. Endoscopy is underutilized in practice and its importance understated in the literature. It is particularly helpful in establishing a precise diagnosis in infants under 18 months of age.
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PMID:Chronic cough in infants and children: an update. 204 39

Angiotensin-converting enzyme inhibitors sometimes cause cough; the mechanism is unknown. We therefore studied the effects of ambulatory treatment with captopril on pulmonary function and on nonspecific bronchial responsiveness to methacholine in 15 hypertensive subjects. Lung volumes, expiratory flows and nonspecific bronchial responsiveness to methacholine using doses up to 64 g/L were measured before and four and eight weeks after captopril treatment was started. Throughout the study the subjects recorded respiratory symptoms and peak expiratory flow rates. In four subjects a persistent cough developed related to the use of captopril, but this was not associated with the development of airflow obstruction or bronchial hyperresponsiveness. The mean provocative concentration of methacholine that resulted in a 20% fall in the forced expiratory volume in 1 s was 43.6 +/- 1.8 g/L after eight weeks of captopril treatment compared with 61.6 +/- 1.2 g/L at the baseline evaluation. We concluded that there was no significant change in lung function during treatment with captopril. The development of a cough related to this medication is not associated with the development of airflow obstruction or airway hyperresponsiveness.
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PMID:Pulmonary function and airway responsiveness during long-term therapy with captopril. 265 33


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