Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serum-ascites albumin difference is reported to be superior to ascitic total protein, ascitic-to-serum total protein ratio, lactic dehydrogenase, and ascitic-to-serum lactic dehydrogenase ratio in differentiating between ascites from liver disease and malignant ascites, S-A greater than 1.1 reflecting portal hypertension. We analyzed ascitic fluid from 46 consecutive patients with chronic liver disease, 28 patients with ascites associated with malignancy, 10 patients with right-sided heart failure, 4 patients with hypothyroidism, and 6 patients with miscellaneous causes of ascites to determine if this albumin difference is indeed a more valuable parameter. Analysis of our data confirms with a larger number of patients that the serum-ascites albumin difference is a more reliable indicator of transudative ascites, better termed portal hypertensive ascites. Malignant ascites without liver metastases had features of nonportal hypertensive ascites, and the serum-ascites albumin difference confirms this. The characteristics of malignant ascites associated with liver metastases, however, resemble those of the portal hypertensive ascites complicating liver disease. This new parameter is also helpful in distinguishing congestive heart failure with high protein ascites and portal hypertensive ascitic features from malignant ascites without liver metastases. Of particular note, myxedematous ascitic fluid, classically categorized as exudative, had an S-A greater than 1.1, indicating the possible role of portal hypertension in the development of ascites in these patients.
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PMID:Usefulness of serum-ascites albumin difference in separating transudative from exudative ascites. Another look. 316 91

The long-term follow-up of 80 heart transplant patients (70 men, 10 women) from January 1982 to July 1985 who had received cyclosporine (CsA) showed a high incidence of mild to severe liver dysfunction. Fifty patients (62.5%) had long-lasting postoperative biological disturbances (alanine amino transferase greater than 2N and/or alkaline phosphatase greater than 1.5N for 3 months or more). Most patients were asymptomatic; eight were icteric, and one had arthralgia. The most common biological feature consisted of isolated elevation of ALAT (27 cases). Assessment of causes led to a definite etiology in 42 patients: 7 cardiac failure, 13 HBsAg-positive liver disease (26%) (chronic persistent hepatitis 8, chronic active hepatitis 2, subacute necrosis 2). Fourteen patients (28%) sustained non-A, non-B (NANB) hepatitis (chronic persistent hepatitis 5, chronic active hepatitis 1, cirrhosis 1), and 7 (14%) sustained a drug-related hepatitis. Liver biopsy and complete virus screening was contributive to the diagnosis in nearly all patients. Additionally, prolonged impairment of liver function tests occurred in 62% of heart transplant recipients, mostly during the first 6 postoperative months. Hepatitis B virus (HBV) and NANB hepatitis accounted for 26% and 28% of the cases of liver dysfunction, respectively; drug-induced hepatitis may have been involved in 14% of the cases. Complete hepatitis virus screening should be performed before heart transplant and in any case of abnormal liver function posttransplantation. HBV vaccination prior to heart transplant is recommended in HBsAg- and HBcAb-negative candidates for heart replacement. Long-term follow-up of these patients is mandatory to assess the severity of these liver dysfunctions.
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PMID:Prevalence and causes of long-lasting hepatic dysfunction after heart transplantation: a series of 80 patients. 329 31

Host factors play an important role in the dosing requirements of theophylline. Theophylline metabolism and clearance depend principally on liver cell function rather than on hepatic flow. The effects of acute hypoxemia require more study; however, patients with chronic obstructive pulmonary disease who have chronic hypoxemia appear to have some impairment of clearance. Clearance is variably and sometimes drastically reduced in patients with liver disease and heart failure, and is reduced by some viral infections. It is not impaired by renal failure. Current split-virus vaccine mixtures do not appear to affect clearance. Clearance is increased in patients with cystic fibrosis and hyperthyroidism. The depressed clearance seen in the severely ill patients who require intensive care improves with improvement in the patient's condition, but the individual factors involved have not been identified. An area requiring more study is the effect of pH on the apparent distribution volume for theophylline. In the presence of liver disease, heart failure, or serious illness, caution must be applied in theophylline dosing, with frequent monitoring of serum levels. Stable patients also warrant an initially conservative dose until serum levels are obtained to guide further dose adjustments.
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PMID:Effect of disease states on theophylline elimination. 353 54

Cs pharmacokinetic profiles using HPLC have aided in predicting necessary dosage alterations for specific groups of transplant patients. Additional information has been gained by HPLC profiles in nontransplant subjects who are healthy or have a stable disease state. The clinician now knows that liver disease not only impairs Cs elimination but may also have a pronounced effect upon drug absorption. While the cardiac failure patient may have reversible inhibition of Cs clearance, other factors may affect the distribution of the drug to lower dosage requirements. Impaired renal function is not an impediment to Cs elimination, but malabsorption similar to that observed in liver and bone marrow transplant patients may still occasionally complicate therapy. Pharmacokinetic information on Cs must be integrated into the complex care plan of a transplant patient to optimally utilize and monitor this pharmacologic agent.
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PMID:Cyclosporine pharmacokinetic profiles in liver, heart, and kidney transplant patients as determined by high-performance liquid chromatography. 353 65

The most frequently used calcium antagonists verapamil, diltiazem and nifedipine have common pharmacokinetic properties. Renal excretion of the drugs is minimal because of their lipophilicity, and the drugs are mainly metabolized by the liver. The rate of elimination depends not only on hepatic function but also on hepatic blood flow. Following oral administration only a fraction of the dose reaches the systemic circulation because of extensive first-pass metabolism. Elderly patients, patients with liver disease and patients in cardiac failure accompanied by decreased hepatic blood flow may experience untoward side effects that usually can be predicted by the known pharmacologic properties of the drugs, such as excessive vasodilatation following nifedipine and bradycardia and av-block following verapamil. Clinically important interactions with other drugs may result from inhibition of the metabolism of certain drugs (carbamazepine, cyclosporine, quinidine) by verapamil and/or diltiazem, inhibition of renal excretion (digoxin) by verapamil and diltiazem, and synergistic effects of beta blockers and verapamil.
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PMID:[Clinical pharmacology of calcium antagonists]. 357 61

Two adolescent patients referred for evaluation of severe "hepatitis" were found to have clinically unsuspected cardiac failure. Clinical profiles were characterized by anorexia, malaise, right upper quadrant pain, mild jaundice, initially predominantly indirect hyperbilirubinemia, profound elevations of transaminases, and prolonged prothrombin time. Left ventricular failure and low cardiac output were documented by clinical examination, echocardiography, and measurements of pulmonary capillary wedge pressure and cardiac index. Acute and chronic intrinsic liver disease was ruled out by appropriate tests. At autopsy, pathologic lesions of centrilobular necrosis characteristic of hepatic hypoxia were noted, and there was evidence of marked myocardial degeneration. These two cases emphasize the need for careful cardiac examination when evaluating acute hepatitis.
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PMID:Severe cardiomyopathy simulating hepatitis in adolescence. 369 46

Piretanide is a potent 'loop' diuretic whose principal site of action is in the thick ascending limb of the loop of Henle. When administered orally or intravenously to healthy volunteers it rapidly increases diuresis and electrolyte excretion, and the effects are short-lived. In comparative studies, piretanide has generally been found to be 5 to 7 times more potent than frusemide (furosemide) but only one-tenth as potent as bumetanide, on a weight-for-weight basis. Piretanide 6 to 12 mg/day, in conventional or sustained release formulations, has been shown to significantly lower elevated blood pressure in a large proportion of patients with mild to moderate hypertension. Comparative trials of up to 3 months duration indicate that at this dosage piretanide is of comparable antihypertensive efficacy as hydrochlorothiazide 50 to 100 mg/day, but has significantly less effect on serum potassium levels. Short term studies in patients with oedema caused by renal, hepatic or cardiac failure demonstrated that piretanide 6 to 9 mg is of similar diuretic potency as frusemide 40 mg and bumetanide 1 mg. In medium term trials in patients with congestive heart failure piretanide 6 mg/day produced equivalent symptomatic improvement as frusemide 40 mg/day. When used to treat oedema caused by liver disease, piretanide 12 to 24 mg/day was successful in only about 50% of patients, but spironolactone added to the treatment regimen greatly increased the response rate. Generally, piretanide has been well-tolerated in clinical trials, although the conventional tablet formulation has caused a relatively high incidence of acute adverse effects--these were greatly reduced with the introduction of the sustained release formulation. Serum concentrations of most electrolytes have not shown any consistent adverse trends and hyperuricaemia and hypokalaemia have been encountered infrequently. Thus, piretanide appears to offer an effective alternative to other 'loop' diuretics for the treatment of oedematous diseases and to hydrochlorothiazide for the management of mild to moderate hypertension. However, its relative place in therapy remains to be clarified with wider clinical experience.
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PMID:Piretanide. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy. 389 5

Seven hundred and sixty cardiorespiratory studies, from 151 critically ill or high-risk general surgical patients with extrapulmonary (S) or pulmonary (P) sepsis, cirrhotic liver disease (L), or cardiac failure (C), were analyzed to assess the determinants of a simple, easily obtained measure of respiratory oxygen exchange, the respiratory index (RI). The pattern of cardiorespiratory abnormalities was studied and correlated with the change in RI. The most important relations were with shunt (QS/QT), mixed venous O2 (PvO2), VD, and VE. Higher F1O2 and positive end-expiratory pressure (PEEP) were needed as the RI rose, indicating a greater severity of illness. Regression analysis of all types of critically ill patients and surgical controls showed that QS/QT, PvO2, and F1O2 interacted together to explain most of the variability of the RI. The regressions in each homogeneous patient disease category were all highly significant (p less than .0001) but had somewhat similar coefficients and explained the variability in RI to different degrees. The data suggest that patients with extrapulmonary sepsis or cirrhotic liver disease have an increase in RI (over that in controls) primarily due to a large increase in CI at the high QS/QT caused by the ventilation/perfusion (VA/QT) maldistribution characteristic of these diseases. However, patients with P or C have a disproportionate rise in RI at any given QS/QT compared to that in high-flow states alone, suggesting in P a direct alveolar limitation of oxygen exchange over and above any level of VA/QT mismatching, and suggesting in C a disproportionate decrease in PvO2 that magnifies the QS/QT effect even though VA/QT is more uniform.
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PMID:The physiologic meaning of the respiratory index in various types of critical illness. 407 5

During the active phase of viral hepatitis urinary folate loss was found to be 8.0 to 48.3 (mean 31.1) mug./day, compared with a normal urinary folate excretion of 0.1 to 18.0 (mean 9.5) mug./day. In cirrhosis and cardiac failure with congestive hepatomegaly the corresponding values were 25.8 to 55.0 (mean 35.7) mug./day and 2.5 to 61.6 (mean 26.9) mug./day, respectively. Urinary folate loss may be a significant factor in the aetiology of folate deficiency of chronic liver disease, particularly when dietary intake is poor.After prolonged dialysis in Visking casing urinary folate was almost totally dialysable, but an appreciable fraction of serum folate was not, even after 72 hours. The dialysable (free) folate fraction of serum and urine disappeared maximally during the first six hours' dialysis, and was virtually cleared after 24 hours' dialysis; clearance curves in normal individuals and in liver disease were comparable. The non-dialysable serum folate fraction was of similar magnitude in all subjects studied, in spite of marked variation in total folate, and probably represented protein-bound folate.
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PMID:Serum and urinary folate in liver disease. 578 81

The concentration of antithrombin III (AT) was determined with a chromogenic method in plasma samples from 1,302 patients referred for evaluation of the haemostatic system. A clearly subnormal AT level (below 60%) was found in 129 patients. In ten cases, this was explained by known (8 cases) or suspected (2 newborns) hereditary deficiency. Only in 5% of the 600 cases referred with definite or suspected thrombosis, AT was below 60%. These cases had a lethality of about 20%. In about 30% of the cases with liver disease, AT was below 60%. In a group of 72 patients with either severe infection, cardiac insufficiency, malignancy or suspected DIC for other reasons, AT was below 60%. Also in this group lethality was about 50% despite lack of a clear DIC blood profile in 67 of the 72 patients. The results indicate that an AT value below 60% of normal, unexplained by hereditary deficiency, carries a grave prognosis.
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PMID:On the clinical significance of acquired antithrombin deficiency. 608 56


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