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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the major component of renal cortical membranes as well as membrane fluidity and Na+, K+, ATPase activity have been studied in membranes from the renal cortex of rats with experimental liver cirrhosis, which show renal sodium and water retention, and in normal animals. Rats with cirrhosis of the liver show a decrease in cholesterol, phospholipid and protein content, without changes in cholesterol/phospholipid molar ratio. In addition there is a small decrease in 14:0 and 18:2 and an increase in 20:4 content, without differences in unsaturation degree. Membrane fluidity was decreased in renal membranes from cirrhotic rats when compared with normal ones. Na+, K+, ATPase activity was higher in cirrhotic than in normal renal membranes could be related with the changes in renal water and electrolyte changes shown by cirrhotic rats.
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PMID:Alterations in the physicochemical properties of renal cortical membranes in rats with experimental cirrhosis of the liver. 170 76

Torasemide (torsemide) is a high-ceiling loop diuretic which acts on the thick ascending limb of the loop of Henle to promote rapid and marked excretion of water, sodium and chloride. Like furosemide (frusemide), its major site of action is from the luminal side of the cell. Torasemide is at least twice as potent as furosemide on a weight-for-weight basis, produces equivalent diuresis and natriuresis at lower urinary concentrations and has a longer duration of action, allowing once-daily administration without the paradoxical antidiuresis seen with furosemide. Torasemide also appears to promote excretion of potassium and calcium to a lesser extent than furosemide. In trials of up to 48 weeks' duration in patients with mild to moderate essential hypertension, torasemide, administered as a single daily dose, has been shown to achieve adequate blood pressure control reaching steady-state within 8 to 12 weeks. Those patients not responding initially have generally responded to a doubling of the dose. Comparative trials of up to 6 months show torasemide is as effective as indapamide, hydrochlorothiazide or a combination of triamterene/hydrochlorothiazide in maintaining control of blood pressure. Torasemide has also been used successfully to treat oedematous states associated with chronic congestive heart failure, renal disease and hepatic cirrhosis. In short term trials control of blood pressure, bodyweight and residual oedema has been sustained. Torasemide appears to be a useful alternative to furosemide in these patients, providing potent and long-lasting diuresis while being relatively potassium and calcium sparing. In clinical trials to date torasemide has been well tolerated with adverse effects of a mild, transient nature reported by only small numbers of patients. Changes in biochemical parameters have been common, including decreases in plasma sodium and potassium levels and increases in plasma creatinine and uric acid levels. These changes are typical of loop diuretics. No changes were clinically significant nor were clinically relevant changes noted in glucose metabolism, cholesterol or triglyceride levels or in haematological values. Thus, torasemide is an interesting new loop diuretic with potential use in the treatment of mild to moderate essential hypertension and of oedematous states in which diuretic therapy is warranted. Preliminary studies suggest it to be as efficacious as other diuretics in common use and to have some advantage over furosemide in duration of action and in effects on potassium and calcium. However, further long term trials in larger groups of patients are needed to delineate the place of torasemide in therapy fully, both as a single agent and in combination with other currently accepted drug regimens.
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PMID:Torasemide. A review of its pharmacological properties and therapeutic potential. 170 90

Sclerotherapy of bleeding esophageal varices in liver cirrhotics is a common procedure, but little is known about the possible entry of sclerosants into the systemic circulation. We injected a mixture of thrombin, sodium tetradecyl, and cefazolin and studied the effect of this sclerosant on selected hemostasis parameters. Twenty-four patients with liver cirrhosis (Child's Classification C) were studied 29 times. Blood samples were drawn before and immediately after the injection of the sclerosant. In seven patients we collected a sample 30 minutes and 24 hours after treatment. Before injection, almost all patients had elevated D-dimer, t-PA and PAI-1 levels. Fibrinogen, antithrombin, alpha-2 antiplasmin, and protein C were decreased. Only thrombin/antithrombin III complex (TAT) levels were within normal ranges. Immediately after the injection, TAT, D-dimer, and t-PA levels rose significantly (P less than 0.001, P less than 0.01, P less than 0.001), PAI-1 and PC levels decreased (P less than 0.01), while antithrombin, alpha-2 antiplasmin, and fibrinogen concentrations were unchanged. TAT and D-dimer levels were still elevated after 24 hours (P less than 0.05). These data indicate that thrombin entered the systemic circulation (elevated TAT) and that the hemostasis system was briefly systemically activated (elevated D-dimer). In spite of these changes in the hemostasis system, clinically there were no detectable thrombotic or hemorrhagic complications.
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PMID:Hemostasis activation during esophageal variceal sclerotherapy with thrombin in cirrhotics. 171

Fat-storing (Ito) cells are perisinusoidal liver cells thought to play a central role in vitamin A metabolism and fibrongenesis. Glucocorticoids have been shown to be beneficial in the treatment of certain types of liver diseases by delaying the development of cirrhosis. To study the regulatory effects of dexamethasone on Ito cell gene expression, Ito cells were isolated from normal rat liver and primary cultures were established. The effect of dexamethasone on the synthesis of alpha 2-macroglobulin, apolipoprotein E, fibronectin and actin was examined. Protein synthesis was studied both at the protein level and at the RNA level by means of biosynthetic labeling, immunoprecipitation followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and by Northern blot analysis of total RNA. After exposure to dexamethasone for 20 hr, alpha 2-macroglobulin protein synthesis was increased threefold, whereas apolipoprotein E expression was decreased 80%. Biosynthesis of fibronectin remained unaffected by hormone treatment. The dexamethasone effect became detectable 5 hr after beginning the exposure. Deinduction kinetic experiments showed that the glucocorticoid effect was detectable more than 12 hr after the replacement of the dexamethasone-containing culture medium by medium without the hormone. Corresponding to the data obtained at the protein level, dexamethasone increased the steady-state levels of alpha 2-macroglobulin-specific messenger RNA and reduced apolipoprotein E-specific transcripts, whereas fibronectin and actin messenger mRNA remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dexamethasone modulates alpha 2-macroglobulin and apolipoprotein E gene expression in cultured rat liver fat-storing (Ito) cells. 171 36

In this study the risk of thrombosis in the portal venous system was assessed in patients with chronic variceal bleeding undergoing sclerotherapy. Twenty-two patients with cirrhosis were prospectively studied with angiography before initiation of sclerotherapy and at mean (+/- SD) 26 +/- 17-month (range, 8-63 months) follow-up. Sclerotherapy consisted of flexible endoscopy, intravariceal and paravariceal, using sodium morrhuate (1.5%-2%) and sodium tetradecyl sulfate (0.5%-1.5%), to obliteration. The mean number of sessions was 6.5 +/- 2.2 (range, 3-11), with a mean total amount of sclerosant of 62 +/- 25 mL (range, 25-112 mL). No patient developed splenic or portal vein thrombosis as shown by arteriography. The flow patterns of portal perfusion, vessel size, and coronary vein visualization showed no significant change. Only one patient had spontaneous reversal of portal flow. Splenic vein histology, examined in five patients in whom sclerotherapy failed and who required shunt surgery, was not significantly different from that in eight patients who had no prior sclerotherapy. It is concluded that under the conditions of the current study, chronic sclerotherapy did not increase the risk of thrombosis in the portal venous system and did not significantly alter the histology of the portal hypertensive splenic vein.
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PMID:Endoscopic variceal sclerosis does not increase the risk of portal venous thrombosis. 172 55

Nitric oxide is a vasodilator tonically secreted by endothelial cells that is involved in the regulation of arteriolar tone. This study, which includes two protocols, was performed to investigate whether nitric oxide plays a role in the pathogenesis of arterial hypotension in cirrhosis with ascites. In protocol 1, the administration of increasing doses (25, 50, 250, 500 and 1,000 micrograms.kg-1.min-1) of the nitric oxide biosynthesis inhibitor N omega-nitro-L-arginine to 18 conscious rats with cirrhosis and ascites produced, at each dose tested, a significantly greater increase in arterial pressure than in 17 conscious control rats. At the lowest dose of N omega-nitro-L-arginine, arterial pressure significantly rose in cirrhotic rats but not in controls. In protocol 2, arterial pressure, estimated renal plasma flow, glomerular filtration rate and sodium excretion were measured in 12 cirrhotic rats with ascites and 10 control rats before and during the sequential infusion of previously selected doses of N omega-nitro-L-arginine (25, 50 and 250 micrograms.kg-1.min-1). Changes in arterial pressure reproduced those observed in protocol 1. In control rats, N omega-nitro-L-arginine caused a decrease in estimated renal plasma flow without affecting glomerular filtration rate or sodium excretion. In contrast, N omega-nitro-L-arginine administration to cirrhotic animals did not produce any appreciable renal vasoconstrictor effect, and it increased glomerular filtration rate and sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenesis of arterial hypotension in cirrhotic rats with ascites: role of endogenous nitric oxide. 173 39

The clinical course of patients with cirrhosis of the liver is frequently complicated by progressive impairment of renal sodium handling leading to the formation of ascites. The occurrence of ascites is generally accompanied by the activation of several hormones and intrarenal autacoids and a complex derangement of systemic, portal and renal hemodynamics. The earliest "underfilling" theory of sodium retention proposes that ascites formation leads to hypovolemia and secondary sodium retention. According to the "overflow" theory, ascites formation is a secondary event with respect to sodium retention, which occurs as a primary phenomenon in the absence of hypovolemia. A third recently developed theory suggests that peripheral arteriolar vasodilation is the primary event of intravascular underfilling. The major documented site involved in arteriolar vasodilation is the splanchnic circulation. Occurrence of underfilling is not related to a reduction of plasma volume but to the enlargement of the vascular compartment. Vascular underfilling triggers a series of hemodynamic and hormonal compensatory events such as an increase in cardiac output and plasma volume, activation of the renin-angiotensin-aldosterone and sympathetic nervous system and non-osmotic hypersecretion of antidiuretic hormone and sodium retention, all of which aim at refilling the vascular compartment. In patients with compensated cirrhosis, i.e. without ascites, compensatory events maintain blood volume despite vascular underfilling, and so these patients do not develop ascites. In patients with decompensated cirrhosis, vascular underfilling due to arterial vasodilation, together with a reduced oncotic pressure and a severe degree of portal hypertension, favours the development of ascites. Underfilling of the arterial circulation is at its maximum in functional renal failure and the hepatorenal syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ascites in liver diseases. 174 50

Current concepts of the pathophysiology of ascites formation in cirrhosis of the liver have become more complex. Traditionally, the initiating event of renal sodium and water retention in cirrhosis was considered to be ascites formation ("underfilling" hypothesis) or primary renal dysfunction ("overflow" hypothesis). Changes in systemic, splanchnic and renal hemodynamics, as well as of volume regulating hormones observed in cirrhosis are compatible with a decrease in effective blood volume as suggested by the "underfilling" hypothesis. These changes, however, have been shown to precede ascites formation. This observation, together with the demonstration of an increase in total blood volume in cirrhosis prompted the "overflow" hypothesis. However, many studies are incompatible with this concept and, in addition, the agent causing primary renal sodium retention in cirrhosis still remains to be defined. The recently proposed "vasodilation" hypothesis reconciles the most salient features of both theories, proposing peripheral arterial vasodilation as the initiating event of decreased effective blood volume and renal sodium retention. Further studies are needed to elucidate the temporal relationship and more precisely define the character of hemodynamic, humoral and renal changes in cirrhosis of the liver.
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PMID:Pathophysiology of ascites formation in cirrhosis of the liver. 176 51

We describe the successful use of combined ascitic-fluid and furosemide infusion as a therapeutic option in the management of massive diuretic-resistant ascites and severe oliguria of hepatic cirrhosis in a 30-year-old Nigerian male farmer. It is simple, safe, convenient and effective treatment modality. The mechanics of this procedure seen against the backgroup of the pathogenesis of sodium retention and renal dysfunction in hepatic cirrhosis is discussed.
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PMID:Combined ascitic--fluid and furosemide infusion: a therapeutic option for massive diuretic-resistant ascites and severe oliguria of hepatic cirrhosis. 180 97

Microbial culture of lung specimens from 569 autopsied cases from 1986 to 1989 revealed methicillin-resistant Staphylococcus aureus (MRSA) in 28 cases, which were subsequently analyzed clinicopathologically. The number of MRSA positive cases has markedly increased in recent years (2 cases in 1986, 2 in 1987, 6 in 1988, 18 in 1989). The most frequent underlying disease was neoplasm, which was seen in 17 cases. Of non-neoplastic diseases, liver cirrhosis and diffuse panbronchiolitis were prevalent. Twenty-four cases had received a course of antibiotic therapy. Antibiotics frequently administered were third-generation Cephem and Imipenem/cilastatin sodium (used in 20 cases). Antibiotics o which MRSA was sensitive were administered in only one case (minocycline). Sputum culture was performed in only 10 cases, 5 of which were MRSA positive. MRSA had acquired resistance to fosfomycin and ofloxacin. Histological examination revealed complication by pneumonia in 19 cases. In 7 of these 19 cases, MRSA was the only pathogen detected. Pulmonary MRSA infection detected at autopsy is frequently seen in patients with terminal stage cancer, but it is frequently not diagnosed and is undertreated. This may be a factor responsible for the recent marked increase in the proportion of MRSA in pathogens causing infection within medical institutions.
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PMID:[Clinicopathological study of methicillin-resistant Staphylococcus aureus detected by pulmonary microbial culture in autopsied cases]. 180 80


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