Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic cough may be the sole presenting manifestation of bronchial asthma (reference 3; Corrao et al, 1979), and "cough variant asthma (CVA)" has been used to categorize such patients. In order to clarify the clinical picture of CVA, we evaluated the clinical history, laboratory data, sputum cytology and pulmonary function in 14 subjects (5 males and 9 females, aged 14 to 65 years) compatible with the following diagnostic criteria: (1) chronic cough persistent for more than 8 weeks, (2) no wheeze nor dyspnea, (3) no rales, (4) no past history of asthma, (5) bronchial hyperreactivity to methacholine proven by Takishima's method (reference 13), (6) effectiveness of bronchodilators against cough, (7) normal chest X-ray film, (8) afebrile and negative CRP, (9) absence of sinusitis and postnasal drip, or if present, they are proved not to be responsible for the cough, and (10) no other causes of cough such as heart disease, prescription of ACE inhibitors, current smoking. The results were as follows. 1) Many of the subjects were atopic, with positive skin tests to one or more common allergens in 10 subjects, elevated serum IgE in 4 subjects, and past history and family history of atopy in 4 and 7 subjects, respectively. 2) Respiratory infection preceded the onset of CVA in 3 subjects. 3) Cough was generally nocturnal, but 2 subjects coughed only in the daytime. 4) FEV1.0% was decreased (less than 70%) in only 2 subjects, whereas V25 was decreased (less than 80% of predicted value) in 11 out of 12 evaluable subjects, which suggested peripheral airway obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical study on cough variant asthma]. 150 83

Physicians should suspect ACE inhibitors as the cause of cough in patients whose symptom begins soon after the institution of therapy with this class of drugs. This is particularly important in patients without a personal or family history of atopy, with normal physical findings, chest radiographs, and lung function tests. Rather than subjecting the patient to an extensive workup, substitution of a different antihypertensive agent is an inexpensive way to show whether the ACE inhibitor is the cause of the chronic cough.
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PMID:Chronic cough caused by angiotensin converting enzyme inhibitors. 229 44

As a symptom of an underlying condition, cough is one of the most common reasons patients see physicians. To the majority, a cough means that 'something is wrong' and it causes exhaustion and/or self-consciousness. Patients find these reasons as well as effects on lifestyle, fear of cancer and/or AIDS or tuberculosis to be the most troublesome concerns for which they seek medical attention. The treatment of cough can be divided into two main categories: (a) therapy that controls, prevents or eliminates cough (i.e. antitussive); and (b) therapy that makes cough more effective (i.e. protussive). Antitussive therapy can be either specific or nonspecific. Definitive or specific antitussive therapy depends on determining the aetiology or operant pathophysiological mechanism, and then initiating specific treatment. Since the cause of chronic cough can almost always be determined, it is possible to prescribe specific therapy that can be almost uniformly successful. Non-specific antitussive therapy is directed at the symptom; it is indicated when definitive therapy cannot be given. Practically speaking, the efficacy of nonspecific therapy must be evaluated in double-blind, placebo-controlled, randomised studies of pathological cough in humans. Such studies have demonstrated the efficacy of dextromethorphan, codeine and ipratropium bromide aerosol in patients with chronic bronchitis. While the preferred treatment for patients with cough due to angiotensin converting enzyme (ACE) inhibitor therapy is withdrawal of the offending drugs, it may be possible to ameliorate the cough by adding nifedipine, sulindac or indomethacin to the treatment regimen. The efficacy of protussive therapy has not been well documented. Although hypertonic saline aerosol and erdosteine in patients with bronchitis, and amiloride aerosol in patients with cystic fibrosis have been shown to improve mucus clearance, their clinical utility has not been adequately studied.
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PMID:Appropriate use of antitussives and protussives. A practical review. 769 10

Chronic cough is a common symptom presenting to all clinicians. Every effort should be made to determine the cause(s) of cough because specific therapy has a higher likelihood of success than empiric therapy. Evaluation begins with a complete history, physical examination, routine health screen laboratory testing, chest film, and pulmonary function testing. Further investigation should be guided by the response to treatment of the most likely diagnostic possibilities: postnasal drip, cough-variant asthma, gastroesophageal reflux, chronic bronchitis, bronchiectasis, and ACE inhibitor induced. The majority of each patient's workup can be performed and ordered by the primary care physician.
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PMID:Chronic cough. 787 96

Postinfectious cough has been drawing attention as a factor involved in the etiology of chronic cough in the United States. In Japan, clinical features of postinfectious chronic cough (PICC) have not been described in detail. We investigated 22 patients with PICC diagnosed by the established criteria (Jpn. J. Allergol. 1995; 44: 1418). All patients were nonsmokers and none received ACE inhibitors. None had a history of atopy or sinus diseases. There were four men and 18 women with a median age of 65 years. These 22 patients underwent clinical examinations including chest roentgenograms, respiratory function tests, eosinophil counts in venous blood, serum IgE titers, antibody titers to Mycoplasma pneumoniae, sputum cytologic findings taken from ten patients, and histological features of bronchial biopsy specimens obtained from two patients; all findings were within normal limits. Clinical course of cough in 20 of the patients with PICC was evaluated using a cough diary. One patient did not keep a cough diary. Ten patients improved with dextromethorphan hydrobromide (D) and oxatomide (O). Three of the remaining 9 patients improved with Bakumondo-to (B) only, 4 with D+O+B, and 2 with D+O+B+ozagrel hydrochloride. The duration of cough before treatment showed a significant correlation with the time from the start of treatment to recovery (r = 0.47, p < 0.05). These results indicate that PICC tends to occur in elderly women and to improve with treatment combining with D, O, and B. We hope to establish a standard therapy for postinfectious chronic cough.
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PMID:[Clinical features of postinfectious chronic cough]. 923 11

H1 antihistamines have been shown to have antitussive effects in patients with asthma and postnasal drip. In Japan, no study has been performed to determine whether orally administered oxatomide, H1 antihistamine, can reduce the chronic cough seen in patients with post-upper-airway infection (postinfection). Patients who had chronic cough of more than three weeks' duration and a history of post-upper-airway infection took part in the study. None had any history of nasal disease, gastroesophageal reflux, bronchial asthma, or other chronic pulmonary disease. All patients were non-smokers, and none used ACE inhibitors. They had normal CRP concentrations, peripheral white blood cell and eosinophil counts, serum IgE concentrations, titers of cold agglutinins and antibodies to Mycoplasma pneumoniae, chest roentgenograms, and respiratory function tests. A prospective randomized, open design was used. The effect of one week of treatment with dextromethorphan (D) or with D plus oxatomide (D + O) on the severity of cough, as estimated by cough diary, were examined. Twenty-two patients entered the study, and 20 were eligible for efficacy and side-effect analyses. Nine patients receiving D and 11 receiving D + O completed the protocol. Patients' characteristics before the start of the study, such as severity and duration of cough, and laboratory data, were not significantly different between the two groups. From trial day 5 to 7, improved rates of cough were significantly higher with D + O than with D alone (p < 0.05). Combination therapy with oxatomide and dextromethorphan reduces subjective perception of cough as estimated by cough diary. These results suggest that oxatomide, H1 antihistamine may improve chronic cough in patients with post-upper-airway infection.
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PMID:[Effects of oxatomide, H1-antagonist, on postinfectious chronic cough; a comparison of oxatomide combined with dextromethorphan versus dextromethorphan alone]. 952 65

Cough becomes chronic after three weeks of evolution. Chronic cough is due to four syndromes in 90% of cases: postnasal drip syndrome, asthma, gastroesophageal reflux and chronic bronchitis. Each syndrome needs a specific therapeutic approach. Antitussive drugs like dextromethorphan are prescribed in cases of complicated cough. Cough secondary to angiotensin converting enzyme inhibitors must not be neglected. In case of failure of initial check up or lack of response to specific therapy, a more thorough examination must be conducted in a specialized centre.
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PMID:[Chronic cough]. 1052 11

Cough is probably the most frequent symptom in chest diseases. Hence, a rational and economical diagnostic procedure is essential to prevent unnecessary costs to the health services, i.e. acute bronchitis, a self-limiting disease, which is the most frequent cause for cough should not involve extensive per case costs. History, physical examination, chest X-ray and lung function testing--which constitute both the first and second, i.e. the basic level of a stepwise approach--allows to diagnose causes in most patients with cough. Without evidence of the cause after completing this basic diagnostic procedure patients with acute cough may require blood gases analysis, electrocardiography, echocardiography, lung perfusion study, spiral CT angiography, bronchoscopy or laboratory examinations for diagnosis of pulmonary embolism, aspiration or (seldom) pleuritis sicca. Chronic persistent cough (CPC) is diagnosed if the basic standard approach to chronic cough fails to lead to final diagnosis. Patients will then need further subtle diagnostic management, i.e. bronchial provocation testing, 24 hour pH probe, ENT- or neurological examination, high resolution CT of the thorax and bronchoscopy. We present two algorithms for the rational diagnostic approach to acute (figure 1) and chronic (figure 2) cough. Each algorithm considers spectrum and frequency of causes on the one hand, the positive predictive value, costs and patient discomfort due to the examination on the other. Nonetheless, despite extensive examination up to 20% of patients suffering from CPC the cause remains unclear [11]. Frequently, the capsaicin cough challenge test can reveal an idiopathic upregulation of the cough reflex as the hypothesised underlying condition. Psychogenic cough however, a rare condition in adults should not coincide with hypersensitivity of the cough reflex. Inconsistency and low reproducibility of results of the capsaicin challenge in patients with psychogenic cough preclude his routine clinical use. In conclusion, the very common acute bronchitis and the ACE inhibitor-induced cough do not require any other diagnostic procedure except patient history and physical examination. A simple basic diagnostic approach will usually allow to evaluate acute and chronic cough. In the remaining cases the proposed algorithm should be used for best results and to prevent excessive costs.
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PMID:[Proposals for a rationale and for rational diagnosis of coughs]. 1078 50

In non-smokers the underlying causes for chronic persistent cough (CPC) e.g. chronic cough without diagnostic chest X-ray or pulmonary function test--are usually as follows: several common upper airways diseases, bronchial (cough type) asthma, gastrooesophageal reflux or treatment with an ACE (angiotensin converting enzyme)--inhibitor. In 10% of CPC however the cause remains uncertain. We report a 30 year old non-smoker with severe coughing and repeated vomiting for two months. No laboratory or technical data could be collected suggestive of a common cause of CPC: Upper airways disease, bronchial flow limitation or hyperresponsiveness, ACE inhibitor medication, B. pertussis infection, gastrooesophageal reflux disease (by 24 hours pH-probe) were ruled out. Fiberbronchoscopic findings remained unremarkable, except for the bronchial biopsy specimen, which showed moderate eosinophilic inflammation of the mucosa and marked thickening of the subepithelial layer. Since the cough was non-productive, sputum induction with 3 ml nebulised 3% NaCl solution was performed. 28% of the granulocytes were eosinophil stained. A low quality morning sputum (< 1 ml) showed 21% eosinophilia. Thus, the diagnosis of eosinophilic bronchitis was established. 400 micrograms budesonide dry powder inhalations b.i.d. for one week resolved the cough, treatment was stopped after three weeks. No recurrence was seen two months later. Both the cough type asthma and the eosinophilic bronchitis could represent a form fruste of classical bronchial asthma beyond wheezing or dyspnoea, but with the common main symptom: cough. Since hyperresponsiveness and cough are phenotypic hallmarks of cough variant asthma, in eosinophilic bronchitis--beside cough--another two features of asthma are present: eosinophilic inflammation of the mucosa along with sputum eosinophilia and subepithelial layer thickening. Not surprisingly, eosinophilic bronchial inflammation could be shown in patients with cough variant asthma as well, who--up to 56% during a four year-period--develop classic asthma. The long-term outcome of eosinophilic bronchitis is not known, however. Thus, asthma, cough variant asthma and cough due to eosinophilic bronchitis can mirror different phenotypes or phases of the same entity. CPC due to either the cough type asthma or the eosinophilic bronchitis is like asthma fast responding to inhalative steroids. (Induced) sputum staining should be added to the diagnostic armamentarium of CPC.
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PMID:[Eosinophilic bronchitis without asthma--an additional rare cause for chronic persistent cough (CPC)? A 30-year old patient with severe CPC due to eosinophilic bronchitis without asthma or hyperreactivity]. 1144 11

Arterial hypertension is a major risk factor for microangiopathic diabetic complications and associated with an increased cardiovascular morbidity and mortality. An intensified antihypertensive treatment reduces microangiopathic complications and cardiovascular morbidity and mortality in diabetic patients. Even in normotensive type 1 and type 2 diabetic patients, the treatment with ACE inhibitors may prevent the later development of diabetic nephropathy. Treatment with ACE inhibitors increases the concentrations of bradykinin, which is responsible for the side effects such as cough and urticaria in some patients. On the other hand, bradykinin may have beneficial intrarenal effects decreasing the intraglomerular pressure. The novel angiotensin II receptor type 1 antagonists do not influence the bradykinin concentrations and seem to be tolerated by patients suffering from chronic cough with ACE inhibitor therapy. It is still unclear whether the different intrarenal effects are of clinical relevance in the long-term treatment of diabetic patients. In studies with diabetic animals the nephroprotective effects of ACE inhibitors and angiotensin II type 1 receptor antagonists are comparable. It was shown that glucose and lipid metabolism is not influenced by treatment with angiotensin II type 1 receptor antagonists. Further compared to Felodipine the reduction of urinary albumin excretion rate (UAER) was more pronounced by Losartane in Chinese type 2 diabetic patients. Short-term studies directly comparing the renal effects of ACE inhibitors with AT II type 1 receptor antagonists revealed similar reduction of blood pressure and albumin excretion rate in patients with diabetic nephropathy, so a combination of both substances might be useful. Data from ongoing long-term trials are still missing. Further, it is unknown whether different phenotypes of the ACE gene (DD, II polymorphism) require different therapeutic options. In conclusion, treatment with angiotensin II receptor antagonists is well-tolerated and has no adverse effects on metabolic control in diabetic patients. The beneficial effect on microangiopathic complications however has to be proven in randomized long-term studies in direct comparison with ACE inhibitors, which were clearly shown to delay the development and progression of diabetic nephropathy.
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PMID:[Angiotensin II type-1 receptor antagonists and diabetes mellitus]. 1145 Jan 65


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