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)

The problem of sudden cardiac death (SCD) in the aged impends on 14% of the adult population in the Slovak Republic and it often involves people who are still effectively active. It is now generally known that a person ill with his heart is never too old to benefit from the stratification of his/her cardiovascular risk. In clinical practice it is possible to suggest to use the combination of non-invasive methods as the first step in basic stratification of risk in the aged (Holter ECG monitoring, echocardiographically assessed ejection fraction of the left ventricle, ergometric test). Regarding the prevention of SCD it is necessary to teach the patients at risk to distinguish the symptoms of the impending collapse/SCD. After myocardial infarction, also in the aged, the therapy by acetylosalicylic acid, Beta-blockers and ACE inhibitors is indicated. There are fewer contraindications to this therapy than it has been presented until now. Antiarrhythmic drugs class I are not to be used. Also in the aged, regarding the prevention of tachycardiac SCD, the most prospective antiarrhythmic drugs are amiodaron and sotalol. The attention should be paid also to other factors in coincidence with sudden cardiac death that can be influenced by therapy (consequential antiischaemic therapy, homeostasis of the internal environment, early cardiostimulatory therapy of bradycardiac disturbances of rhythm, optimal timing of surgical therapy of valvular defects if indicated, prevention of pulmonary embolism, etc.). In the aged it is necessary to create a wider space in the field of invasive cardiological therapy. In general it is possible to state that the knowledge on etiopathogenetic stratification and specific characteristics of prevention and therapy of SCD in the aged are limited. This fact only emphasizes the inevitability to concentrate on the research in this area.
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PMID:[Sudden cardiac death in the aged]. 947 34

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

The circulating levels of angiotensin I-converting enzyme (ACE) are linked with a 287-base pair insertion/deletion (I/D) polymorphism at intron 16 of the ACE gene. Thus, the homozygous deletion (D/D genotype) could cause chronic vasoconstriction, arterial hypertension and, possibly, coronary artery disease. Also, the increase in plasminogen activator inhibitor-1 level and impaired fibrinolysis were related with the D/D genotype. The D allele has been recently associated with venous thrombosis among African-American men as well as among patients that underwent elective total hip replacement. We assess the risk of venous thromboembolism (VTE) linked with each genotype of the I/D ACE gene polymorphism in a Caucasian population by means of a case-control study. We genotyped the ACE gene in a series of 148 patients aged 45.0 +/- 16.0 years (range, 11-80 years), objectively diagnosed in our centre of deep-vein thrombosis or pulmonary embolism, and in 240 thrombosis-free subjects (25-75 years) from the same geographic area. The observed difference in D allele frequencies between patients (0.56) and controls (0.62) was nonsignificant overall; however, statistical significance (P = 0.05) was found by considering the recessive hypothesis (D/D versus I/ D + I/I) [odds ratio (OR) = 0.64, 95% confidence interval (CI95) = 0.42-0.99]. The OR was 0.88 (CI95 = 0.51-1.53; P = 0.65) for the dominant hypothesis (D/D + I/D versus I/I genotypes). The relative risk for the D allele was close to 1 for the dominant hypothesis, both considering gender and recurrent tendency; however, it was protective in men regarding the recessive hypothesis (OR = 0.53, CI95 = 0.29-0.97, P = 0.04). The I/D ACE allele distribution was similar among the 46 thrombophilic patients (antithrombin, protein C or protein S deficiencies, factor V R506Q, factor II G20210A or lupus anticoagulant). In conclusion, among (Spanish) Caucasians, this study does not support the hypothesis that the deletion allele (D) of the ACE gene could be a significant risk factor for VTE, being protective in men.
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PMID:Risk of venous thromboembolism associated with the insertion/deletion polymorphism in the angiotensin-converting enzyme gene. 1093 9

Anthracyclines, found to be efficacious in the treatment of a broad spectrum of pediatric malignancies, are cardiotoxic and may lead to heart failure even a long time after successful treatment of cancer. It is thought that subtle abnormalities can progress to the more permanent myocardial disease, resulting in cardiomyopathy which may progress to congestive heart failure. There are some precipitating factors leading to the sudden onset of cardiac symptoms such as increase in afterload or preload. We describe a young patient with congestive heart failure treated with doxorubicin (cumulative mean dose 420 mg/m2) in infancy because of pelvic sarcoma in whom the appearance of symptoms was related to pulmonary embolism. Four years before hospital admission, the patient presented echocardiographic abnormalities such as left ventricular fractional shortening and thickness reduction and he was treated with ACE-inhibitors. The myocardial ischemia, which is present in pulmonary embolism, probably worsened the left ventricular systolic function and caused congestive heart failure.
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PMID:[Biventricular heart failure in patient treated with anthracycline in childhood: myocardial dysfunction is not always the cause]. 1518 68

Anthracyclines, found to be efficacious in the treatment of a broad spectrum of pediatric malignancies, are cardiotoxic and may lead to heart failure even a long time after successful treatment of cancer. It is thought that subtle abnormalities can progress to the more permanent myocardial disease, resulting in cardiomyopathy which may progress to congestive heart failure. There are some precipitating factors leading to the sudden onset of cardiac symptoms such as increase in afterload or preload. We describe a young patient with congestive heart failure treated with doxorubicin (cumulative mean dose 420 mg/m2) in infancy because of pelvic sarcoma in whom the appearance of symptoms was related to pulmonary embolism. Four years before hospital admission, the patient presented echocardiographic abnormalities such as left ventricular fractional shortening and thickness reduction and he was treated with ACE-inhibitors. The myocardial ischemia, which is present in pulmonary embolism, probably worsened the left ventricular systolic function and caused congestive heart failure.
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PMID:[Heart failure in a subject treated with anthracyclines in childhood: myocardial dysfunction is not always the only reason of it]. 1534 97

We conducted a systematic and comprehensive meta-analysis on all candidate genes to assess their genetic contribution to the aetiology of venous thromboembolism (VTE) (pulmonary embolism and deep venous thrombosis) in all ethnic groups. Electronic databases were searched until and including January 2008 for any candidate gene investigated in VTE. Odds ratios (OR) and 95% confidence intervals (CI) were determined for each gene disease association using fixed and random effect models. Our meta-analyses included approximately 126,525 cases and 184,068 controls derived from 173 case-control studies, which included 21 genes (28 polymorphisms). Statistically significant associations with VTE were identified for factor V G1691A (OR 9.45; 95% CI 6.72-13.30, p < 0.0001), factor V A4070G (OR 1.24; 95% CI 1.02-1.52, p = 0.03), prothrombin G20210A, (OR 3.17; 95% CI 2.19-3.46, p < 0.00001), prothrombin G11991A, (OR 1.17; 95% CI 1.07-1.27, p = 0.0007), PAI-1 4G/5G, (OR 1.62; 95% CI 1.22-2.16, p = 0.0008), alpha-fibrinogen Thr312Ala (OR 1.37; 95% CI 1.14-1.64, p = 0.0008), all in Caucasian populations. MTHFR/ C677T in Chinese/Thai populations (OR 1.57; 95% CI 1.23-2.00, p = 0.0003), and ACE I/D in African American populations (OR 1.5; 95% CI 1.03-2.18, p = 0.03) were found to be significantly associated with VTE. Factor XIII Val34Leu (OR 0.80; 95% CI 0.68-0.94, p = 0.007) and beta-fibrinogen 455 G/A (OR 0.84; 95% CI 0.72-0.97, p = 0.02) both showed significantly protective effects. Our work supports a genetic aetiology to VTE disease and provides reliable risk estimates.
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PMID:The genetics of venous thromboembolism. A meta-analysis involving approximately 120,000 cases and 180,000 controls. 1965 65

Recipients of hematopoietic cell transplantation may be at risk for developing acute kidney injury (AKI), and this risk may be increased in patients who undergo transplantation for severe systemic sclerosis (SSc) due to underlying scleroderma renal disease. AKI after transplantation can increase treatment-related mortality. To better define these risks, we analyzed 91 patients with SSc who were enrolled in 3 clinical trials in the United States of autologous or allogeneic hematopoietic cell transplantation (HCT). Eleven (12%) of the 91 patients with SSc in these studies (8 undergoing autologous HCT, 1 undergoing allogeneic HCT, 1 pretransplantation, 1 given i.v. cyclophosphamide on a transplantation trial) experienced AKI, of whom 8 required dialysis and/or therapeutic plasma exchange. AKI injury in the 9 HCT recipients developed a median of 35 days (range, 0-90 days) after transplantation. Ten of 11 patients with AKI received angiotensin-converting enzyme inhibitor (ACE-I) therapy. The etiology of AKI was attributed to scleroderma renal crisis in 6 patients (including 2 with normotensive renal crisis), to AKI of uncertain etiology in 2 patients, and to AKI superimposed on scleroderma kidney disease in 3 patients. Eight of the 11 patients died, one each because of progression of SSc, multiorgan failure, gastrointestinal and pulmonary bleeding, pericardial tamponade and pulmonary complications, diffuse alveolar hemorrhage, pulmonary embolism, graft-versus-host disease, and malignancy. Limiting nephrotoxins, cautious use of corticosteroids, renal shielding during total body irradiation, strict control of blood pressure, and aggressive use of ACE-Is may be of importance in preventing renal complications after HCT for SSc.
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PMID:Acute kidney injury in patients with systemic sclerosis participating in hematopoietic cell transplantation trials in the United States. 2070 86

Post-transplant erythrocytosis is defined as an increase in hematocrit above 55%. It occurs in 10%-15% of renal transplant recipients, most commonly from 8 to 24 months after transplantation. Twenty-five percent of patients experience spontaneous remission within 2 years, while 75% develop symptoms and signs of hyperviscosity (headache, hypertension, plethora). The etiology is multifactorial and includes erythropoietin, renin-angiotensin system (RAS) and IGF-1 as the main factors. RAS inhibition with either ACE inhibitors or angiotensin receptor blockers is efficient therapy which decreases hematocrit in 90% of patients within 2 to 6 weeks, thus decreasing the incidence of fatal complications (like pulmonary embolism and stroke).
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PMID:[Post-transplant erythrocytosis]. 2235 5

In 2011 several articles seemed significant for the practice of general medicine. Diagnosis of hypertension needs several measurements and may need 24-hour ambulatory blood pressure monitoring. Glycosylated hemoglobin is a reliable tool to diagnose diabetes mellitus. The ABCD2 score with neurological imaging help the triage of transient ischemic attacks. Pulmonary embolism can be treated as outpatient for low risk patients. Gluten-free diet may be tried in irritable bowel syndrome. Nitrofurantoin is a reasonable alternative for simple urinary tract infection in women, but antibiotics are not needed after drainage of an uncomplicated skin abscess. Subclinical thyroid dysfunction is a risk factor of osteoporosis in older men. Sequential use of MMSE and ACE scores is a promising approach to assess medical decision-making capacity.
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PMID:[2011 findings from literature on general internal ambulatory medicine]. 2236 76

Sarcoidosis can manifest with clinical signs suggestive of pulmonary embolism (PE). A 36-year-old male patient presented with a 2-day history of left-sided pleuritic chest pain and dyspnoea. He was hypoxicand tachypnoeic, and initial blood tests showed a positive plasma D-dimer. Subsequent arterial blood gas showed respiratory alkalosis with type 1 respiratory failure. He was suspected to have a PE, and CT pulmonary angiogram (CTPA) was urgently arranged. This latter investigation did not show any impairment in pulmonary arterial blood flow but revealed bilateral hilar and mediastinal lymphadenopathy suggesting sarcoidosis. Serum calcium and ACE were also elevated. The patient was treated conservatively and discharged after 2 days with out-patient endobronchial ultrasound and clinic follow-up arranged.
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PMID:Sarcoidosis: clinical mimicry of pulmonary embolism. 2433 73


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