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

In 34 out-patients with essential hypertension, the antihypertensive effect and the trough-to-peak ratios of once-daily enalapril or lisinopril were compared by ambulatory blood pressure monitoring (ABPM) according to a crossover design. The drug dose was titrated and a thiazide diuretic was added if necessary to attain a target office BP of less than 140/90 mm Hg. Both drugs significantly lowered BP but the effect of lisinopril was greater (P < 0.009): day- and night-time mean BP fell from 152/98 and 135/84 mm Hg, respectively to 133/85 and 118/74 mm Hg with enalapril and to 129/83 and 116/70 mm Hg with lisinopril. BP goal was reached with an average dose of 18 mg enalapril with 8 mg hydrochlorothiazide and with 17 mg lisinopril combined with 6 mg diuretic. Trough:peak ratio values, which were calculated after Fourier analysis of ABPM data in individual patients, were independent of drug dose. The combination with the diuretic resulted in slightly higher trough:peak ratios than with ACE inhibitor monotherapy, but the difference was not significant. The median trough:peak ratio in patients when using enalapril-based therapy was 0.48 and, when taking lisinopril-based treatment, it was 0.65 (n = 28, P < 0.005). A significant correlation was found between trough:peak ratio and changes in daytime mean arterial pressure (MAP; Spearman r= 0.43) and night-time MAP (r= 0.66). When 24-h ABPM was performed starting 24 h after last drug intake, both ACE inhibitors still had a significant antihypertensive effect (P < 0.001), which was similar for both drugs. Eleven patients reported minor side effects. Four patients stopped ACE-inhibitor treatment because of cough. The data show that lisinopril has a longer duration of action than enalapril.
 ...
PMID:Lisinopril versus enalapril: evaluation of trough:peak ratio by ambulatory blood pressure monitoring. 1040 91

In the paper available information concerning the influence of treatment with angiotensin converting enzyme inhibitors (ACE-I) on cough, bronchial hyperreactivity and bronchoconstriction are reviewed. Cough occurs in 0.7% to 19% of patients treated with angiotensin converting enzyme inhibitors according to various reports. In the mechanism of angiotensin converting enzyme inhibitor-induced cough accumulation of bradykinin and substance P due to decreased degradation of this mediators caused by ACE-I may be involved. Part of tussive effect may be mediated via prostaglandins and histamine. In a few studies symptoms of airway obstruction and asthma worsening in relation to treatment with this drugs was reported. However, majority of reports suggest safety in taking ACE-I by patients with asthma. The only effective method to relieve angiotensin converting enzyme-induced cough is a drug withdrawal. The change of drugs within the whole class of ACE-I does not bring effect.
 ...
PMID:[Cough, bronchoconstriction and bronchial hyperreactivity in relation to treatment with angiotensin-converting enzyme]. 1043 3

Valsartan is a specific angiotensin II receptor antagonist with high selectivity for the AT(1) receptor subtype. After oral administration of single or repeated once-daily doses, valsartan 40-80 mg inhibits the pressor response to angiotensin II for 24 hours. In patients with mild-to-moderate hypertension, efficacy of valsartan appears to be independent of age, sex, and race, and is at least equivalent to that of calcium antagonists, ACE inhibitors, or thiazide diuretics. Response rate to valsartan 160 mg o.d. is significantly greater than after receiving losartan 100 mg o.d. Valsartan has additive effects with other antihypertensive drugs and combination therapy is effective in severe hypertension and in hypertension with renal insufficiency, where renal function is well maintained. Valsartan has good tolerability with a side-effect profile indistinguishable from placebo and superior to that of comparable drugs. Valsartan does not cause cough or adverse metabolic effects; first dose hypotension and rebound hypertension on abrupt withdrawal have not been encountered. Valsartan has clear clinical advantage in the management of hypertension. Its impact on prognosis in patients with a high risk of cardiovascular morbidity and mortality is under evaluation.
 ...
PMID:Clinical advantage of valsartan. 1044 90

ACE inhibitors are well established in the treatment of arterial hypertension, heart failure and diabetic and/or hypertensive nephropathy with albuminuria. The important trials for the various indications are briefly discussed. In Switzerland 11 ACE inhibitors are available for clinical use, differing mainly in their pharmacokinetic and pharmacodynamic properties. The characteristics of practical relevance regarding oral bioavailability, elimination mechanisms and half-life, as well as the necessary dosage modifications in patients with renal, hepatic and cardiac failure, are presented. All ACE inhibitors except captopril and lisinopril are administered as prodrugs. The bioavailability among ACE inhibitors varies widely with a range from 11% (trandolapril) to more than 60% (captopril). The great majority of ACE inhibitors are eliminated predominantly through the kidneys. However, benazepril, fosinopril, ramipril, spirapril and trandolapril also have a hepatic (metabolic) route of elimination. Since half-life varies from 1 h (captopril) to 30 h (spirapril) we drew up, for simplicity, a table of 3 groups with short, medium and long t1/2. In renal insufficiency dose adjustment is required only below a creatinine-clearance level of 30 ml/min. These dosage reductions are not required in liver diseases, but renally excreted drugs such as lisinopril should be preferred. Treatment with ACE inhibitors in severe heart failure should be initiated carefully, with low doses and concomitant diuretic treatment added or maintained. Most common adverse effects of ACE inhibitors are hypotension, cough, hyperkalaemia and renal failure. Less frequent adverse effects are angioedema, bone marrow suppression and also foetal damage. Thus, ACE inhibitors are contraindicated in pregnancy.
 ...
PMID:[Comparative evaluation of ACE inhibitors: which differences are relevant?]. 1046 7

Pneumonia is a major direct cause of death in the elderly. Although aspiration based on a reduced cough reflex is one of the causes of pneumonia in the elderly, there are few studies of angiotensin-I converting enzyme inhibitors (ACE inhibitors), which are antihypertensive drugs that induce cough, as a factor influencing the incidence of pneumonia in institutionalized elderly subjects. To assess the effect of ACE inhibitors and dihydropiridine calcium-channel blockers on the incidence of pneumonia, we conducted a hospital-based case-control study. Cases were 55 pneumonia patients aged > or = 65 years during a 1-year period. The controls were elderly subjects, frequency matched to the cases by age and gender (n = 220). Data were collected on known risk factors and on medication for hypertension, consisting of ACE inhibitors, calcium-channel blockers, and nonantihypertensive medication. The significance of differences in risk factors was analyzed using univariate and multivariate comparisons of cases and controls. After adjustment for potential confounding factors, the relative risk estimates for pneumonia were 0.38 (95% confidence interval [CI], 0.15-0.97) and 1.84 (95% CI, 0.89-3.78) for ACE inhibitors and calcium-channel blockers, respectively, relative to nonantihypertensive medication. The preventive effect of ACE inhibitors on pneumonia was apparent in long-acting ACE inhibitor users (0.24; 95% CI, 0.07-0.88). We conclude that ACE inhibitor use is an independent factor reducing risk of pneumonia among elderly inpatients.
 ...
PMID:Reduction of risk of pneumonia associated with use of angiotensin I converting enzyme inhibitors in elderly inpatients. 1098 61

Bronchopulmonary infections caused by trichomonads have been reported mainly in patients with pre-existing pulmonary or debilitating disease (e.g. bronchial carcinoma, lung abscess, bronchiectasis). Pulmonary trichomoniasis is most often due to infection with Trichomonas tenax, usually regarded as a harmless commensal of the human mouth, and may rarely be caused by other trichomonas species. A 45 year old female presented with a dry cough, exertional dyspnoea and malaise. These symptoms persisted for 6 months regardless of anti-inflammatory and anti-obstructive inhalative therapy. Sarcoidosis of the lungs, diagnosed 20 years prior, had been asymptomatic since and there was no coexistent disease. Laboratory data revealed increased ACE-levels (90 IE/ml) and lung function showed bronchial hyperreactivity on histamine challenge. No other abnormalities were found (chest x-ray, bronchoscopy, lung function test, blood count and serum calcium). The diagnosis was based on the cytological identification of numerous trophozoites of T. tenax in the bronchoalveolar lavage. Therapy with oral metronidazol for 40 days led to complete recovery from symptoms and normalisation of ACE serum levels. The patient has remained well for 12 months since. The pathogenicity of oral trichomonads in the non-immunocompromised host remains uncertain. Our patient had no known medical risk factors by comparison with published cases. The case illustrates the clinical relevance of pulmonary trichomoniasis in an otherwise healthy person.
 ...
PMID:[Pulmonary trichomoniasis: diagnosis based on identification of irritation in bronchoalveolar lavage]. 1068 41

Information from clinical and pharmacokinetic studies of angiotensin-converting enzyme inhibitors (ACEIs) has come from subjects who are mostly male and Caucasian, but the use of ACEIs extends to populations worldwide. Significant differences between Chinese in general and male Caucasians have been demonstrated in the pharmacokinetics/dynamics of other drug classes that could have implications for the use of ACEIs in the Chinese population. These include: significant Chinese/Caucasian genetic variation in the renin-angiotensin system based on an insertion/deletion (O/D) polymorphism of the ACE gene; the genetic determination of plasma ACE activity in the Chinese population; and genetic factors involving the disease substrate which may also influence the response to treatment. Oral and IV pharmacokinetic data from various studies of Chinese and Caucasian subjects are available for cilazapril, fosinopril, and perindopril, and pharmacodynamic data are available for eight different ACEIs. Based on these data, there are few differences among the pharmacokinetics of ACEIs between Chinese and Caucasians. Most ACEIs showed good blood pressure lowering efficacy in Chinese (benazepril, enalapril, fosinopril and spirapril), with perhaps less blood pressure lowering with cilazapril or a relatively shorter-term effect with cilazapril or perindopril compared to Caucasions. Chinese experience more cough from ACEIs (captopril and enalapril) than Caucasians. Data suggest that fosinopril may not induce cough in as many subjects as other ACEIs, and this seems to be true of Chinese as well. The mechanism, currently unknown, could involve fosinopril's dual elimination pathway (hepatic and renal). Pharmacokinetic data also support the use of fosinopril in congestive heart failure where elimination pathways may be impaired. In conclusion, ethnic differences between Chinese and Caucasians with respect to ACE and AGT gene polymorphism, which might be expected to differentially affect the action of ACEIs in these two ethnic groups, do not, in fact, have such an effect. Rather, differences among the ACEIs appear to be more important. Journal of Human Hypertension (2000) 14, 163-170.
 ...
PMID:Does Chinese ethnicity affect the pharmacokinetics and pharmacodynamics of angiotensin-converting enzyme inhibitors? 1069 29

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.
 ...
PMID:[Proposals for a rationale and for rational diagnosis of coughs]. 1078 50

Patients aged 60 years and older with essential hypertension were treated with an angiotensin-converting enzyme inhibitor (ACE-I), delapril (Adecut) or a long-acting calcium (Ca)-antagonist, manidipine (Calslot) for 3 years. The incidences of cardiovascular events as well as drug-related side effects were compared between the two groups to investigate whether both classes of antihypertensive drugs are beneficial in elderly hypertensive patients. There were no significant differences in characteristics of patients between the two intervention groups, except for slightly lower blood pressure (P = .08) in the Ca-antagonist group at the initiation of the study. There were no significant differences in total death between the two groups. Cardiovascular events (both fatal and nonfatal) were noted in 34 of 699 patients (22.5/1000 patient-years) in the ACE-I group and 50 of 1049 patients (19.7/1000 patient-years) in the Ca-antagonist group, with no significant difference found between the two groups. The correlation between cardiovascular incidence and the blood pressure attained during treatment showed a J-shaped phenomenon and suggests that an excessive reduction less than 120 mm Hg in systolic blood pressure (SBP) is unnecessary and may be harmful in certain cases. Side effects were more frequent in the ACE-I group than in the Ca-antagonist group (P = .01). Cough was the major adverse event, occurring in 5.0% of patients in the ACE-I group. In conclusion, the study indicates that both ACE-I (delapril) and Ca-antagonist (manidipine) were equally beneficial for reducing cardiovascular morbidity and mortality in elderly hypertensive patients. However, tolerability of ACE-I was lower due to the adverse event of coughing.
 ...
PMID:Practitioner's Trial on the Efficacy of Antihypertensive Treatment in the Elderly Hypertension (The PATE-Hypertension Study) in Japan. 1082 95

The effective treatment of hypertension is an extremely important consideration in patients with end-stage renal disease (ESRD). Virtually any drug class--with the possible exception of diuretics--can be used to treat hypertension in the patient with ESRD. Despite there being such a wide range of treatment options, drugs which interrupt the renin-angiotensin axis are generally suggested as agents of choice in this population, even though the evidence in support of their preferential use is quite scanty. ACE inhibitors, and more recently angiotensin antagonists, are the 2 drug classes most commonly employed to alter renin-angiotensin axis activity and therefore produce blood pressure control. ACE inhibitor use in patients with ESRD can sometimes prove an exacting proposition. ACE inhibitors are variably dialysed, with compounds such as catopril, enalapril, lisinopril and perindopril undergoing substantial cross-dialyser clearance during a standard dialysis session. This phenomenon makes the selection of a dose and the timing of administration for an ACE inhibitor a complex issue in patients with ESRD. Furthermore, ACE inhibitors are recognised as having a range of nonpressor effects that are pertinent to patients with ESRD. Such effects include their ability to decrease thirst drive and to decrease erythropoiesis. In addition, ACE inhibitors have a unique adverse effect profile. As is the case with their use in patients without renal failure, use of ACE inhibitors in patients with ESRD can be accompanied by cough and less frequently by angioneurotic oedema. In the ESRD population, ACE inhibitor use is also accompanied by so-called anaphylactoid dialyser reactions. Angiotensin antagonists are similar to ACE inhibitors in their mechanism of blood pressure lowering. Angiotensin antagonists are not dialysable and therefore can be distinguished from a number of the ACE inhibitors. In addition, the adverse effect profile for angiotensin antagonists is remarkably bland, with cough and angioneurotic oedema rarely, if ever, occurring. In patients with ESRD, angiotensin antagonists are also not associated with the anaphylactoid dialyser reactions which occur with ACE inhibitors. The nonpressor effects of angiotensin antagonists--such as an influence on thirst drive and erythropoiesis--have not been explored in nearly the depth, as they have been with ACE inhibitors. Although ACE inhibitors have not been compared directly to angiotensin antagonists in patients with ESRD, angiotensin antagonists possess a number of pharmacokinetic and adverse effect characteristics, which would favour their use in this population.
 ...
PMID:Risk-benefit ratio of angiotensin antagonists versus ACE inhibitors in end-stage renal disease. 1083 Feb 52


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>