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 24-year-old man who had had bronchial asthma between the ages of 10 and 12 years was admitted to our hospital on October 10, 2000. In May 1999, he had received antituberculosis therapy for left upper lobe infiltrate, which resolved two months later. Chest radiography on admission showed recurrence of the left upper lobe infiltrate. He complained of cough and low grade fever. Thoracic CT demonstrated gloved-finger shadows in the left upper lung field, as well as central bronchiectasis. Wheeze was not ausculated, and flow volume curve revealed no obstructive changes. Total IgE was markedly increased (6,084 IU/ml), and IgE RAST was positive for multiple allergens including Aspergillus species and precipitating antibody test against Aspergillus fumigatus was also positive. Bronchofiberscopy revealed mucoid impaction at the left B1 + 2, and culture of lavage fluid demonstrated Aspergillus fumigatus. A bronchial biopsy at the orifice of the left upper lobe bronchus revealed thickening of the basement membrane, eosinophil infiltration, and marked hypertrophy of the mucus glands. The diagnosis was allergic bronchopulmonary aspergillosis (ABPA), and 30 mg prednisolone was initiated and tapered. The infiltrate detected on chest radiography was resolved. Eight months later, asthmatic symptoms were observed, and Fluticasone dipropionate administration was started. However, the infiltration seen in the chest radiographs have not recurred until now. Asthmatic inflammation of the bronchial mucosa was demonstrated in a case of ABPA without clinical asthma.
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PMID:[Bronchial biopsy in allergic bronchopulmonary aspergillosis without clinical asthma]. 1283 48

We studied 223 outpatients who presented between October 2001 and June 2003 with persistent cough of more than 3 weeks' duration. Eosinophilic airway disorders (EAD), including atopic cough and cough variant asthma, were clinically diagnosed in 119 patients, on the basis of the following factors: history of atopic disease, duration of cough, history of previous prolonged cough, or presence of forced expiration wheeze. Since eosinophils are frequently found in the sputum of patients with EAD, a positive test strongly suggests the presence of EAD. In this study, the test was positive in 86% of the patients with EAD. The patients with clinically diagnosed EAD, including those with no eosinophils in the sputum, were treated with inhaled fluticasone 400 or 800 microg/day. Fluticasone was effective in 97% of the patients with EAD and was more effective than bronchodilators or antiallergic drugs. When we compared the results of fluticasone 400 microg/day with those of 800 microg/day doses, the cough disappeared within 1 week in 28% of the patients who received 400 microg/day, whereas in 76% with 800 microg/day. Among the patients with diagnosed EAD, bronchial asthma developed in 6 patients during the observation period. Most of these patients had forced expiration wheeze and lower FEV 1 at the initial visit. This study showed that EAD could be diagnosed in the early stage on the basis of thorough history-taking, the presence of forced expiration wheeze and detection of eosinophils in the sputum. It is important to diagnose and treat EAD as early as possible since inhaled steroid is highly effective.
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PMID:[Eosinophilic airway disorders: important causes of prolonged cough in Japan]. 1556 1