Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepato-splenic scintigraphy with 99mTc-S-colloid was performed in twelve patients with bacterial endocarditis. These images showed that the size of the liver varied from normal to a severe hepatomegaly, depending on the presence of congestive heart failure. Intrahepatic distribution of the radiocolloid was slighty irregular in all cases. The spleen was conspicuously enlarged, and showed irregular distribution of the radiopharmaceutical. In some cases intrasplenic concentration defects caused by infarcts, abscesses or cysts, were observed. The relative uptake of radiocolloid by the spleen, varied from hypo- to hyperconcentration according to the degree of lymphoid hyperplasia caused by the infection. In two cases, both with congestive heart failure, concentration of the radiocolloid was evident in the bone marrow. The scintigraphic pattern observed in these patients with bacterial endocarditis can be easily differentiated from that caused by only congestive heart failure, which is similar to the observed in patients with cirrhosis of the liver and/or portal hypertension.
Arch Inst Cardiol Mex
PMID:[Hepato-splenic scintigraphy in finding indications of bacterial endocarditis. Preliminary report]. 719 44

The efficacy and side effects of the combination therapy of thiazide and furosemide administered to patients with refractory heart failure, for a prolonged period of time, were assessed. Thirty-two patients were hospitalized during the years 1985-1991. Left heart failure (left ventricular ejection fraction (LVEF = 22.4% +/- 6.6%) was present in 26 patients, right heart failure in 3 patients, chronic renal failure, cirrhosis and bilateral pleural effusion were present each in one patient. Chlorothiazide 0.5 g daily was added to conventional therapy. Patients were monitored closely during hospitalization and later as outpatients. During hospitalization, addition of chlorothiazide caused a reduction of 4.8 +/- 4.0 kg in patients' weight, serum potassium decreased from 4.4 +/- 0.6 to 4.0 +/- 0.5 mmol/l (P < 0.005) and serum sodium from 139.0 +/- 4.7 to 136.8 +/- 5.5 mmol/l (P < 0.05). The duration of the combined therapy was 17.2 +/- 19.1 months. Thirteen patients had short treatment (1.6 +/- 0.8 months) and 19 patients had prolonged treatment (26.5 +/- 19.0 months). No specific characteristics distinguished patients in both groups. Thiazides were discontinued in 19 patients, 10 of which had side effects. In only 5 of the 19 patients treated for the prolonged period had thiazides to be discontinued because of side effects. Addition of thiazides to furosemide is efficacious in severe heart failure. The combination should be started during hospitalization. Many patients can be maintained on this combination for a prolonged period of time on an ambulatory basis.
Int J Cardiol 1995 Jun 30
PMID:Prolonged therapy by the combination of furosemide and thiazides in refractory heart failure and other fluid retaining conditions. 759 35

Diuretic drugs have historically been developed for the treatment of sodium and water retention in edematous disorders. The latter have traditionally been an amalgam of congestive heart failure, nephrotic syndrome, cirrhosis and chronic renal failure. With a > 50-year tradition of this approach to development, diuretic drugs have not been evaluated specifically for their safety and efficacy profile in patients with congestive heart failure. Yet, they are the most frequently prescribed drug class for this disorder. Furthermore, they remain the only drug class in congestive heart failure not subjected to large scale clinical trials. Sodium and water retention within this group of patients is related primarily to functional rather than to structural renal abnormalities. The reduction of glomerular filtration rate, increase in aldosterone secretion and abnormal profile of atrial natriuretic factor, all produce sodium retention and can be related to the severity of heart failure. Diuretic drugs have not been scrutinized in a manner similar to that of other drugs for the management of heart failure. Controversy persists regarding direct vascular effects, objective end points of assessment and the magnitude of adverse effects such as activation of neurohormonal pathways. These issues may be addressed by the establishment of reasonable objective end points, better stratification of patients in clinical trials and prospective trials in large clinical series. Even mortality studies should be considered.
J Am Coll Cardiol 1993 Oct
PMID:Clinical trials of diuretic therapy in heart failure: research directions and clinical considerations. 810 3

A 62-year-old man with liver cirrhosis and hypoxemia was admitted to evaluate the etiology of hypoxemia. The patient had noticed exertional dyspnea for three years. Physical examination, laboratory tests, ultrasonography and liver scintigraphy revealed liver cirrhosis. The arterial blood gas test showed hypoxemia (PO2 46.3 mmHg). Chest roentgenogram showed old pulmonary tuberculosis and the pulmonary function test demonstrated decreased FEV 1.0% and %DLco, which did not account for the marked hypoxemia. Contrast echocardiography was performed by injecting hand-agitated saline into the antecubital vein. Three seconds after the right ventricle was opacified, the contrast echoes appeared in the left atrium and then the left ventricle. Pulmonary arteriography revealed no pulmonary arteriovenous fistula. Hemodynamic data showed low pulmonary vascular resistance. Contrast echocardiography by injecting hand-agitated saline from the catheter tip was performed at both pulmonary arteries and the left atrium was opacified by each injection. The hypoxemia was mainly attributed to a intrapulmonary arteriovenous shunt. Although the etiology of hypoxemia in liver cirrhosis seems to be multifactorial, the intrapulmonary arteriovenous shunt is the most important factor. Contrast echocardiography was useful for detecting this shunt.
J Cardiol
PMID:[Contrast echocardiographic detection of pulmonary arteriovenous shunt in a hypoxemic patient with liver cirrhosis]. 816 48

Proposed reflex mechanisms for generalized neurohumoral activation in heart failure include decreased input from inhibitory baroreceptor afferent vessels and increased input from excitatory afferent vessels arising from arterial chemoreceptors, skeletal muscle metaboreceptors or the lungs. Not all subjects with left ventricular dysfunction have increased sympathetic nerve activity, but the magnitude of sympathoneural activation appears to independently predict survival. This association suggests both a causative mechanism linking sympathetic activation with adverse outcome and a therapeutic opportunity to improve the prognosis of such patients by inhibiting central sympathetic outflow. Generalized sympathetic activation is not unique to heart failure, and its functional consequences appear to be both organ- and condition-specific. Sympathetic activation is present in other disorders such as mild hypertension, cirrhosis and aging that do not share the dim prognosis of congestive heart failure. The adverse effects of adrenergic activation on the diseased myocardium may be a function of the magnitude and time course of increases in cardiac sympathetic nerve activity, the mechanical and electrophysiologic consequences of nonuniform abnormalities of sympathetic innervation in the failing heart and the absence of specific countervailing mechanisms present in other conditions also characterized by increased sympathetic traffic. The hypotheses that activation of adrenergic drive to the diseased myocardium is the causative mechanism linking sympathoexcitation to adverse outcome and that interventions that inhibit sympathetic outflow to the heart will improve the prognosis of patients with congestive heart failure have not been specifically tested. Greater understanding of the mechanisms responsible for the heterogeneity of sympathetic activation in response to ventricular dysfunction, for cardiac-specific and generalized activation of the sympathetic nervous system and for the stimulation or suppression of countervailing mechanisms capable of resisting its adverse effects is fundamental to the development of better therapies for congestive heart failure.
J Am Coll Cardiol 1993 Oct
PMID:Clinical aspects of sympathetic activation and parasympathetic withdrawal in heart failure. 837 99

Many epidemiological studies have shown that moderate alcohol intake, from 10 to 30 g of ethanol a day, decreases cardiovascular mortality from atherosclerotic ischaemic heart disease and ischaemic stroke as compared to non-drinkers. This beneficial effect outweighs the risks of alcohol consumption in subgroups of people with a higher risk of atherosclerosis: the elderly, people with coronary risk factors and patients with previous coronary events. It has not been demonstrated that alcohol intake, even in moderate amounts, is beneficial for the general population, in particular, men under the age of 40 and women under 50, because it raises mortality due to other causes, especially injury, cirrhosis of the liver and some types of cancer, thereby outweighing the benefits for coronary artery disease. Thus, alcohol consumption should not be recommended as a prophylaxis for the general population. Guidelines on alcohol drinking habits--whether to continue, to start, to modify or to stop--must be given on an individual basis, taking into account the relative risks and benefits for each patient. The benefits of moderate alcohol consumption on the cardiovascular system seem to be exerted fundamentally through its effects on plasma lipoproteins, principally by raising high density lipoprotein (HDL) cholesterol and to a lesser degree, by decreasing low density lipoprotein (LDL) cholesterol. It appears to exert additional beneficial effects on the heart by decreasing platelet aggregability and by bringing about changes in the clotting-fibrinolysis system. Although there has been some debate about the relative superiority of different types of alcoholic beverages (wine, beer or hard liquor), and to a greater extent, about different types of wine, there is no current evidence of any kind of beneficial effect from other components of the beverage besides ethanol. Thus, it does not seem appropriate to recommend any particular type of alcoholic drink, except for sociocultural reasons. The added benefits from some components of different types of wine with a high antioxidant activity on plasma lipoproteins remain only an interesting hypothesis. Meanwhile, encouraging a healthy diet, flavonoid rich and with a predominance of natural ingredients (fruit, legumes, cereals and seeds), in the general population should stop the current tendency of Southern European countries from abandoning the Mediterranean diet. Because of the multifactorial nature of coronary heart disease, it is necessary to remember that atherosclerotic risk reduction is achieved by behavior modification of multiple risk factors present in individual patients and in the general population. Therefore, guidelines regarding alcohol intake should always be linked to pertinent recommendations about other atherosclerotic risk factors.
Rev Esp Cardiol 1998 Jun
PMID:[Wine and heart]. 1021 74

A pressure-overload model in the rat by banding the pulmonary trunk (PT) was developed to investigate alterations in gene expression in left- and right-ventricular compartments during the transition from compensated right-ventricular (RV) hypertrophy to right heart failure. Right heart failure in rat is characterized by liver cirrhosis, hydrothorax and ascites. The diameter of constriction was found to determine the time course of heart failure development. Only the RV free wall and the right atrium increased in weight, without a difference between compensated and failing RV. An increase in circulating ANP revealed a hypertrophic response of the myocardium, while increased circulating ammonia levels discriminated between compensated hypertrophy and failure. As parameters for stress, fibrosis and Ca2+-handling, changes in the pattern and level of the mRNAs encoding atrial natriuretic peptide (ANP), collagenIIIalpha1, and sarcoplasmic endoplasmic reticular calcium ATPase 2 (SERCA2), phospholamban (PLB) and calsequestrin (CSQ) were studied by Northern blot and in situ hybridization analyses. Pulmonary trunk banding resulted in an induction of ANP mRNA, a moderate increase in collagenIII alpha1 mRNA and a decrease in SERCA2 and PLB mRNA levels in both the left and right ventricles, but changes were most pronounced in the myocardium surrounding the RV cavity. Increased ammonia blood levels are a promising prognostic marker to detect the development of right heart failure.
J Mol Cell Cardiol 1998 Sep
PMID:Changing patterns of gene expression in the pulmonary trunk-banded rat heart. 976 42

We report a case of a mitral endocarditis caused by Streptococcus pneumoniae in a 48 year old man diagnosed with moderate mitral stenosis and liver cirrhosis. The clinical features were fever with penicillin-sensitive pneumococcal bacteremia, meningitis and pneumonia. Only transesophageal echocardiography could confirm the presence of vegetations. In spite of vancomycin therapy, the patient required mitral valve replacement, with good results. Some clinical aspects of this uncommon cause of infective endocarditis are discussed.
Rev Esp Cardiol 1998 Dec
PMID:[Austrian's syndrome (endocarditis, meningitis and pneumonia caused by Streptococcus pneumoniae). Apropos of a rare case]. 992 54

In clinical trials, all lipid-lowering agents have been associated with mild, asymptomatic elevations of alanine aminotransferase (ALT) and asparate aminotransferase enzymes. This, along with the fact that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors are hepatotoxic in some animals, led the US Food and Drug Administration (FDA) to recommend monitoring of liver enzymes for all lipid-lowering agents, except the bile acid sequestrants. Because the drugs act by different mechanisms, ALT elevations may be a pharmacodynamic effect related to lipid lowering, rather than a direct effect of the drug. Animal studies support this assumption. ALT elevations of 3 times the upper limit of normal occur in <3% of patients in clinical trials of lipid-lowering drugs. The elevations are transient and often dose-related, and they usually revert to normal while continuing therapy and have never been associated with hepatotoxicity. Confounding factors include alcohol, acetaminophen, and pre-existing liver disease, such as chronic hepatitis C and type II diabetes with fatty liver, which are both associated with mild, intermittent elevations of ALT. The more important issue is whether or not lipid-lowering agents are hepatotoxic. There are case reports of hepatotoxicity (cholestasis, jaundice, hepatitis, chronic active hepatitis, fatty liver, cirrhosis and acute liver failure) with all of the drugs, except cholestyramine. To date there are just 5 cases of documented liver failure linked to lovastatin. There is no evidence that monitoring reduces the rate of hepatotoxicity. Mild elevations of ALT that occur with many drugs, including HMG-CoA reductase inhibitors, do not predict hepatotoxicity. Liver enzyme elevations appear to be a class characteristic of lipid-lowering agents. Hepatotoxicity is a rare idiosyncratic reaction, occurring only with sustained released nicotinic acid.
Am J Cardiol 2000 Jun 22
PMID:Defining patient risks from expanded preventive therapies. 1085 89

Cardiac troponin I levels are frequently above normal values in several disease states in which myocardial necrosis is not a prominent aspect, particularly in pulmonary embolism, heart failure, liver cirrhosis, septic shock, renal failure and arterial hypertension. Sub-clinical myocardial necrosis has been postulated to be the cause of the phenomenon. Studies performed so far have not included pathological data to confirm this hypothesis. Increased troponin I plasma levels may be the result of myocardial strain, especially the type of strain that accompanies some forms of cardiac dilatation or hypertrophy. Troponin I may act as a marker of myocardial strain, either acute (in pulmonary embolism, septic shock and acute heart failure) or chronic (in chronic cardiac, renal and hepatic failure, as well as in arterial hypertension). The apparent paradox of elevated levels of troponin I without elevated levels of creatine kinase in several disease states might be solved if troponin I could be released from myocardial cells without the disruption of myocardial cell plasma membranes. Precise pathological studies are needed to elucidate whether increased troponin I with normal CK is associated with myocyte death, and, if so, with necrosis or with apoptosis.
Rev Port Cardiol
PMID:Cardiac troponin I in systemic diseases. A possible role for myocardial strain. 1158 28


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