Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of a dry, nonproductive cough during ACE inhibitors therapy has been described in several reports. However, the mechanism of this effect is still unknown. In order to clarify whether ACE inhibitor-induced cough is a symptom of an asthmatic disturbance, six patients (age 54-68) with cough related to captopril or enalapril were rechallenged with ACE inhibitors after an adequate washout period. Baseline airway function and bronchial reactivity to metacholine were measured at the end of the washout period and on the fourth day of rechallenge which was accompanied by the reappearance of cough without wheezing. Rechallenge did not cause changes in dynamic lung function; a low and not significant (p less than 0.1) increase in metacholine dose causing a 15% and a 20% reduction in baseline FEV 1 was observed. It is concluded that cough and bronchoconstriction are likely to be mediated through different nervous pathways and that ACE inhibitor-induced cough is not a variant of asthmatic cough.
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PMID:[Bronchial reactivity and cough due to ACE inhibitors]. 207 84

Steroids are used in progressive lung sarcoid despite arguments that spontaneous remission occur and therapy may not alter outcome. We studied a unique group of 6 patients with dyspnea and advancing pulmonary sarcoid, who had documented untreated progressive disease for 6.8 +/- 2.4 years. Raised SACE, Ga 67 lung uptake, and lymphocyte counts in lung lavage fluid indicated continued active alveolitis. After 3-6 months on steroid, MRC dyspnea grade fell from 2.5 to 0.3 and FVC, FEV, and DLCO increased by 36%, 27% and 16% respectively. This was associated with a fall in small opacity profusion scores on x-ray lung uptake of Ga 67 and serum ACE. These improvements were sustained for the duration of follow up (mean 22 months). These data show that steroids can alter the natural history of progressive sarcoid and reversible alveolitis may coexist with established fibrosis.
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PMID:Evidence that steroids alter the natural history of previously untreated progressive pulmonary sarcoidosis. 357 16

Quadriceps muscle weakness is an important contributor to exercise limitation in patients with chronic obstructive pulmonary disease. The deletion allele of the angiotensin converting enzyme gene polymorphism has previously been associated with a greater response to strength training in healthy subjects and might, therefore, protect against detraining in these patients. In 103 stable outpatients (mean [SD] FEV(1) 34.4 [16.5] % predicted), the angiotensin deletion allele was associated with greater isometric quadriceps strength; mean (SD) 31.4 (10.8) kg for insertion homozygotes, 34.1 (13.0) kg for heterozygotes, and 38.3 (11.6) kg for deletion homozygotes (p = 0.04 linear trend). Adjusted for fat-free mass, the relationship was stronger (linear trend p = 0.007). There was no correlation between strength and genotype in a group of 101 age-matched healthy control subjects. Twitch quadriceps force in response to magnetic femoral nerve stimulation, measured in 39 patients, was also genotype dependent; 8.3 (2.6) kg for insertion homozygotes, 10.1 (3.6) kg for heterozygotes, and 12.4 (3.5) kg for deletion homozygotes (p = 0.002 linear trend). Body mass index and fat-free mass did not differ significantly between genotypes in either group. There was no association in either patients or control subjects between genotype and inspiratory muscle strength. In chronic obstructive pulmonary disease the deletion allele is associated with greater quadriceps strength independent of confounding factors.
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PMID:Angiotensin converting enzyme genotype and strength in chronic obstructive pulmonary disease. 1533 91