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)

The clinical and physiologic effects of bronchopulmonary lavage of both lungs at separate times in 14 patients with alveolar proteinosis proved by biopsy were followed for 2 to 96 months. Before lavage, all patients had moderate to severe dyspnea on exertion. Twelve had a nonproductive cough, and 2 had a productive cough; both were smokers. Nine had generalized fatigue, and 4 had weight loss. Twelve of 14 had fine inspiratory rales. All of the patients had abnormal chest roentgenograms, and 13 of 14 had an increased lactate dehydrogenase concentration. After lavage, all patients had loss of fatigue and improved exercise tolerance, with most returning to normal activity. Cough cleared in 12 of 14 and remained only in the cigarette smokers. Inspiratory rales cleared completely in most patients (11 of 12) and partially in one. The rales usually returned during exacerbations. Physiologic measurements that changed significantly after bilateral lavage included: vital capacity, total lung capacity, resting room air PO2, exercise PO2, PO2 while breathing 100 per cent O2, and DLCO. Because all measurements were made within 5 days of the second lavage, one must attribute the acute improvement to the removal of proteinaceous material from the alveoli. The long-term effects varied; some patients required annual or semiannual lavages, wherease others remained in remission after lavage for 36 to 96 months. Exacerbations were accompanied by increased dyspnea, reappearance of rales, and deterioration of the gas-exchange parameters noted previously. Repeat lavage reversed the clinical symptoms and physiologic abnormalities in patients who had recurrences.
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PMID:Physiologic effects of bronchopulmonary lavage in alveolar proteinosis. 69 76

The objective of the study was to determine if residual pleural thickening after treatment for pleural tuberculosis could be predicted from the pleural fluid findings at the time of the initial thoracentesis. Forty-four patients initially diagnosed as having pleural tuberculosis between January 1986 and January 1988 were separated into two groups: the 23 patients in group 1 had residual pleural disease, while the 21 patients in group 2 had no residual pleural disease after treatment for their pleural tuberculosis was completed. The clinical characteristics of the two different groups did not differ significantly, but the patients in group 1 tended to be a little sicker in that the duration of their symptoms was longer, their hemoglobin values were lower, and weight loss and cough were more frequent. There were no significant differences in the pleural fluid findings in the two different groups. The mean pleural fluid protein level was 5.40 +/- 0.58 g/dl for group 1 and 5.17 +/- 0.80 g/dl for group 2, while the mean pleural fluid glucose level was 78.6 +/- 19.5 mg/dl for group 1 and 79.5 +/- 20.1 mg/dl for group 2. The mean pleural fluid lactate dehydrogenase (LDH) level in group 1 was 593 +/- 498 IU/L, while the mean level for group 2 was 491 +/- 198 IU/L. The presence of residual pleural thickening was not related to the chemotherapeutic regimen or the performance of a therapeutic thoracentesis. From this study we conclude that approximately 50 percent of patients with pleural tuberculosis will have residual pleural thickening when their therapy is completed, but that one cannot predict which patients will have residual pleural thickening from either their clinical characteristics or their pleural fluid findings.
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PMID:The relationship between pleural fluid findings and the development of pleural thickening in patients with pleural tuberculosis. 816 80

The pharmacology, toxicity, and therapeutic effectiveness of etoposide (VP-16) given by the intrapleural route were examined in a phase I trial. Ten patients with malignant pleural effusion received 100, 150, or 225 mg/m2 VP-16 infused over 2 h into the pleural space after drainage of pleural fluid. The administration of VP-16 was tolerated well, with no local pain, increase in cough, dyspnea, or infection. Myelosuppression was mild at doses of 150 mg/m2 or less but severe at 225 mg/m2. Drug levels were followed in both plasma and pleural fluid for up to 12 h. Clearance of VP-16 from the pleural cavity was low at 2 ml/min m2. Peak pleural-fluid drug levels in patients receiving 225 mg/m2 exceeded 300 micrograms/ml, whereas peak drug concentrations in corresponding plasma samples obtained at the same time amounted to less than 10 micrograms/ml. Serial chest X-rays showed no disappearance of pleural effusion in nine evaluable patients. However, follow-up investigation of pleural fluid characteristics [carcinoembryonic antigen (CEA), lactic dehydrogenase (LDH), and cytologic examination] suggested some evidence of local therapeutic benefit.
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PMID:Intrapleural etoposide for malignant effusion. 218 91

The clinical presentation of 60 consecutive Pneumocystis carinii pneumonias in 58 HIV-infected patients (48 men, 10 women, mean age 34 [22-53] years) was prospectively evaluated from April to August 1989 and compared with 60 consecutive P. carinii pneumonias in 59 HIV-infected patients (55 men, 4 women, mean age 37.5 [22-60] years) between 1981-88. Mortality rates within 14 days after diagnosis of P. carinii pneumonia were 50% (8 of 16 patients) until 1985, 20.5% (9 of 44) between 1986 and August 1988, and 1.7% (one of 60) in 1989. The degree of severity of the pneumonias at time of diagnosis was markedly lower in 1989, as shown by following parameters (averages of 1989, compared with averages of 1981-88): lactate dehydrogenase 540 (250-1419) U/l versus 680 (235-1920) U/l (not significant); alveolo-arterial difference of partial oxygen tension (pA-aO2) 22.9 (0.5-73.5) mmHg versus 39.7 (19-70) mmHg (P less than 0.001); score of radiological findings 1.4 (0-3) versus 2.7 (0-4) (P less than 0.001). In 1989, mainly clinical symptoms (dry cough: 57 of 60 cases, dyspnea: 44 of 60 cases, fever: 43 of 60 cases) initiated the diagnostic procedure: chest radiographs, lactate dehydrogenase and pA-aO2 were normal in 13, 25 and 33 episodes, respectively. The lower mortality rate of P. carinii pneumonia could not primarily be explained by therapeutical progress since the treatment of choice did not change fundamentally since 1981. Above all, early diagnosis fundamentally determined the probability of survival.
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PMID:[Pneumocystis carinii pneumonia in HIV infection: better prognosis because of early diagnosis]. 222 63

Allergic alveolitis due to mold dust inhalation in farmers is a severe but rare disease in Scandinavia. In this report 38 cases of the disease are presented. There were 31 men and 7 women, with mean ages of 46 and 38 years respectively. Strict diagnostic criteria were used, resulting in 21 definite, 12 probable and 5 possible cases. None of the patients were current smokers, but 10 of the men were ex-smokers. The great majority of the patients fell ill between October and April. The symptoms were dyspnea, cough, fatigue, episodes of fever, and in some cases loss of weight. The average duration of the disease was 6 months. The moldy material most commonly associated with the disease was straw, followed by hay, grain, and wood chips. For those tested serum lactate dehydrogenase was raised in 80% and the mean value for PaO2 was 7.8 kPa. Precipitating antibodies to mold antigens were positive in 68%. In general, pulmonary function tests showed a restrictive pattern. Over half of the patients still had dyspnea on exercise after recovery. Three fourths of the patients were treated with antibiotics and thus clearly had been misjudged as having an infection.
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PMID:Allergic alveolitis in Swedish farmers. 260 70

A traditional Chinese remedy, Qing-Fei-Tang (Seihai-to, T90), has been used for treatment of chronic respiratory diseases with long-lasting cough and sputum, e.g. chronic bronchitis. We examined the effect of T90 and its main component flavonoid, baicalein, on the lucigenin-dependent chemiluminescence (CL) and leukotriene B4 (LTB4) synthesis of human alveolar macrophages (AM). AM were obtained by bronchoalveolar lavage from patients with various respiratory diseases, including sarcoidosis, idiopathic pulmonary fibrosis, bronchial asthma, chronic bronchitis and lung cancer. CL were observed by stimulating 1 x 10(5) AM with phorbol myristate acetate in the presence of lucigenin. LTB4 were generated by incubating 1 x 10(6)/ml AM with Ca ionophore A23187 for 30 min and determined by reverse phase high performance liquid chromatography and radioimmunoassay. T90 (0.2-2.0 mg/ml) and baicalein (0.1-100 microM) inhibited both CL and LTB4 production of AM in a dose-dependent fashion. These inhibitory effects were not due to cytotoxic effects of the procedure because neither 2 mg/ml T90 nor 100 M baicalein affected the viability of AM nor lactate dehydrogenase release from AM. These results suggest that T90 exerts its effect on inflammatory lung diseases through the anti-inflammatory action, i.e. inhibiting the oxidative and arachidonate metabolism of local inflammatory lung cells.
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PMID:Effects of qing-fei-tang (seihai-to) and baicalein, its main component flavonoid, on lucigenin-dependent chemiluminescence and leukotriene B4 synthesis of human alveolar macrophages. 285 72

A 71-year-old woman with psoriasis-associated rheumatoid arthritis had for 15 months been treated with methotrexate (5 mg/week orally). Four weeks before admission she had developed dyspnoea and cough. On admission her axillary temperature was 38.2 degrees C, the white cell count was normal. Erythrocyte sedimentation rate (50/90 mm), lactate dehydrogenase activity (449 U/l) and the creatinine level (1.33 mg/dl) were all elevated. Blood gas analysis revealed partial respiratory impairment (pO2 52 mm Hg), and the chest X-ray demonstrated bilateral interstitial-alveolar changes. Despite antibiotics the temperature continued to rise, and on the 11th day a blood eosinophilia of 4% was noted. The bronchial mucosa was normal on bronchoscopy, and transbronchial biopsy showed only minor interstitial fibrosis, occasional macrophages and lymphocytes. Cultures of the lavage-fluid were negative. As methotrexate pneumonitis was suspected the drug was discontinued and prednisolone administered (50 mg daily for 3 days, gradually reducing over 7 days). The symptoms quickly improved, and blood gas analysis and the X-rays became normal. The patient was discharged symptom-free after 30 days.
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PMID:[Severe pneumonitis as a complication of low-dose methotrexate therapy in psoriasis-associated polyarthritis]. 773 58

A 51-year-old man, known to have chronic-aggressive hepatitis B, HIV infection and exertional dyspnoea, was hospitalized because of acute physical deterioration, cough with whitish exudate and dyspnoea at rest. Despite a CD4/CD8 ratio of 0.16 no prophylactic measures against Pneumocystis carinii had been taken. On examination the lungs were unremarkable, but the liver was enlarged and there were petechiae over all parts of the body. Laboratory tests showed impaired liver functions and a rise in lactate dehydrogenase activity (538 U/l). Chest radiogram demonstrated small to very small infiltrates in the lung. As Pneumocystis carinii pneumonia was suspected but bronchoscopy was too risky, he was at first treated with trimethoprim/sulphamethoxazole (four times 320/1600 mg/24 h intravenously). When this failed, he received pentamidine (4 mg/kg, after 4 days 2 mg/kg intravenously), and finally cefotiam (twice 2 g daily), tobramycin (three times 40 mg daily) and corticoids (100 mg). Despite this treatment he died after 10 days from respiratory failure. Autopsy revealed interstitial pneumonia throughout the lung as well as focal mucor infiltrations in the wall of middle-calibre lung veins. Mucor is a ubiquitous, facultatively pathogenic mold fungus.
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PMID:[Pulmonary mucormycosis in an HIV-infected patient]. 783 42

The authors present the results of a ten year retrospective analysis about amiodarone-induced pulmonary toxicity. Only cases without any etiology (after complete explorations made in hospital), and judged probably imputable to amiodarone treatment were kept. This work finds all characteristics usually described with amiodarone pulmonary toxicity: dyspnea, cough, weight loss, restrictive lung disease and interstitial infiltration in the chest roentgenogram. It shows three another points: pulmonary disease is more frequent during first and fourth years of amiodarone treatment, pneumopathy occurs more rapidly in patients with a previous history of pulmonary disease, and patients with amiodarone lung toxicity may have elevation in lactate dehydrogenase activity.
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PMID:[Amiodarone-induced pleuropneumopathies: experience 1983-1993 in a drug vigilance Regional Center]. 785 56

A 69-year-old man with coronary heart disease complained of pain in his right flank. He had dyspnoea, cough and fever up to 38.8 degrees C. In addition to various positive indicators of inflammatory disease he had a creatinine concentration of 1.8 mg/dl and an increased activity of lactate dehydrogenase (1655 U/l). The chest radiograph demonstrated pneumonia and computed tomography showed an infarct in the right kidney. The ECG indicated atrial fibrillation with an irregular ventricular rate and left bundle branch block. Echocardiography demonstrated dilatation of the left ventricle and a thrombus adherent to the wall. Transoesophageal echocardiography additionally recorded spontaneous type I echo-contrast, which disappeared after therapeutic heparinization. Cerebral infarctions were shown by computed tomography, undertaken because of neurological symptoms. There were also signs of silent myocardial ischaemia. As a coronary artery bypass operation was contraindicated, percutaneous transluminal balloon angioplasty was attempted but dissection occurred, causing irreversible cardiogenic shock of which the patient died.
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PMID:[Spontaneous echo contrast in the left ventricle as an indicator for an increased risk of thromboembolism]. 792 30


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