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

The intracellular sodium, potassium, and water content of isolated leucocytes was estimated in 47 patients with cirrhosis. The values for sodium showed a wide scatter. In patients without ascites the mean value was significantly increased but in those accumulating ascites it was normal, although often reduced in individual subjects. Reduced values were found in patients with hyponatraemia associated with end-stage cirrhosis and diuretic treatment. Changes in leucocyte water content closely followed those in sodium content. Leucocyte potassium content was normal except in patients accumulating ascites in whom it was significantly reduced, indicating whole body depletion, and this could be corrected by administration of spironolactone.
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PMID:Changes in the electrolyte content of leucocytes at different clinical stages of cirrhosis. 68 May 96

The question is still open, whether a pathologic formation of fibrinogen or an insufficient stabilized fibrin are causative factors within the complex disorders in hemostasis in patients with liver cirrhosis. Thus, 45 patients with liver cirrhosis, which was proven by liver biopsy, were investigated by means of sodium-dodecyl-sulfate (SDS) polyacrylamidgel-electrophoresis in order to evaluate, whether the liver produces a pathological fibrinogen or whether the formation of fibrin from fibrinogen is defect. The fibrin stabilizing factor (factor XIII) was measured by immunological methods. In order to have a mean of the stage of the disease, 37 patients were subdivided by the extend or their porto-caval collateral circulation and further 8 patients were investigated having bleeding from esophageal varices. By the results evidence accrued that in advanced stages of liver cirrhosis and a marked porto-caval collateral circulation polymerization of fibrinogen was insufficiently, especially, the formation of alpha-chains was altered, whereas the formation of gamma-dimers, the separation of fibrinopeptides from fibrinogen, and the aggregation of fibrinmonomers were normal. This defect in fibrin structure was positive correlated with the stage of liver cirrhosis, which correlated negative with the plasma activity of factor XIII. In vitro, the defect in fibrin formation, from fibrinogen was abolished by adding factor XIII to the assay. Thus, in liver cirrhosis fibrin formation is altered because of factor XIII deficiency, but a normal fibrinogen is synthesized by the liver. In consequence, the administration of factor XIII preparations is suggested as one clinical action among others to benefit the hemostatic disorders, especially in patients with bleeding from esophageal varices.
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PMID:[Fibrinogen and fibrin structure in patients with cirrhosis of the liver (author's transl)]. 70 17

In the present study, we undertook to examine the relationship between urinary sodium retention and systemic hemodynamics in dogs with experimental portal cirrhosis induced by the sporadic feeding of dimethylnitrosamine. Sodium handling was studied by blanace techniques; plasma volume was measured serially with Evan's blue; and CO, blood pressure, CVP, and PVR were monitored through indwelling catheters. Six dogs were studied while standing quietly in a Pavlov sling, in a serial fashion starting 4 weeks after drug administration and continuing for some 3 months thereafter, until all dogs developed cirrhosis and ascites. Urinary sodium retention commenced generally between the ninth to twelfth week following the initation of treatment, but renal perfusion remained normal. Plasma volume expansion was noted within 1 week following the onset of sodium retention. Ascites was generally detected about 2 weeks following the initiation of sodium retention. No alteration in CO or PVR could be detected until ascites was present in significant amount. At that time, CO rose and PVR fell by about 20%. ABP tended to fall during the period of observation, but this was not significant. The initiation of sodium retention in this canine model does not depend on antecedent changes in CO or PVR.
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PMID:Temporal relationships between urinary salt retention and altered systemic hemodynamics in dogs with experimental cirrhosis. 71 96

Renal prostaglandins have several potential functions in renal physiology. Perhaps their best documented role is the maintenance of renal blood flow during renal ischemia, although they are apparently not essential to blood flow autoregulation in the absence of ischemia. Alterations in sodium excretion parallel the hemodynamic changes induced by prostaglandin infusions and prostaglandin inhibition with indomethacin. A direct action on sodium balance is unproven. Numerous studies, in vivo and in vitro, have convincingly demonstrated that prostaglandins or their precursors stimulate renin release and prostaglandin inhibition blunts renin release independent of hemodynamic and electrolyte balance. These functions of prostaglandins have implicated them in the manifestations of Bartter's syndrome, the nephropathy of liver cirrhosis, renovascular hypertension, and other nephropathies.
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PMID:Prostaglandins: renin release and renal function. 72 86

In an attempt to evaluate the role of renin-angiotensin system in the contols of blood pressure and aldosterone secretion in the patients with cirrhosis and asictes, 7 patients were infused of an antagonist of angiotensin II, Sar-1 Ile-8 angiotensin II, intravenously to inhibit the action of renin-angiotensin system and to observe changes in arterial pressure and plasma aldosterone. In 1 patient with recent onset of severe ascites and high plasma renin activity, blood pressure and plasma aldosterone decreased during the infusion. In contrast, mild rise in blood pressure and various changes in plasma aldosterone were observed in the other 6 patients with normal plasma renin activity. These results suggest variable angiotensin dependency in the controls of blood pressure and plasma aldosterone in the patients with cirrhosis and ascites according to the stage of the disease, the states of sodium and water balance and/or palasma renin activity.
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PMID:Role of renin-angiotensin system in the controls of blood pressure and aldosterone in patients with cirrhosis and ascites. 73 36

The hepatorenal syndrome is defined as the spontaneous onset of progressive renal failure in patients with far advanced hepatic disease, usually on the basis of cirrhosis. The clinical characteristics of the syndrome include azotemia, oliguria, hyponatremia, low urinary sodium excretion and the absence of abnormal findings in the urinary sediment. Although the results of a large number of studies suggest that abnormal histologic features in the kidneys are infrequent, changes such as glomerulosclerosis, degeneration of tubular cells and alterations in the basement membranes have been described. Theories on the pathophysiologic aspects of the syndrome, including reduced plasma volume, inferior vena cava hypertension and active renal vasoconstriction, are presented. The last of these is currently the most widely accepted theory in which there is a selective redistribution of blood flow away from the cortical nephrons to the medullary nephrons on the basis of selective cortical vasoconstriction. The role of the synpathetic nervous system, as well as that of plasma renins in the cause of this condition is explored. Therapy for the hepatorenal syndrome generally has failed to ameliorate extremely unfavorable mortality rates. Such factors as the effects of plasma volume expansion; various pharmacologic agents, including dopamine, Octopressin and metaraminol; portacaval shunt; transplantation of the liver, and steroids are discussed. Regardless of specific therapy, the few patients who do survive tend to demonstrate a significant reversible component with respect to hepatic disease.
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PMID:The hepatorenal syndrome. 78 80

Six patients with chronic uremia in whom ascites developed during maintenance hemodialysis are described. Their clinical and biochemical findings are reviewed and compared with data of 10 hemodialyzed patients without ascites. Liver cirrhosis was the origin of ascites in only one case. Hypoalbuminemia, liver cirrhosis, congestive heart failure, peritonitis, peritoneal tuberculosis and carcinomatosis were uniformly absent in the other patients. Long-term and marked overhydration seems to be at the origin of ascites. Lack of peripheral edema, probably due to ascites compartmentalization, was a constant finding in every noncirrhotic patient with ascites. When long-term overhydration was stopped after successful kidney transplantation or by means of diminished water and salt ingestion, reversal of the syndrome was attained. Nevertheless, ascites because of liver cirrhosis was not influenced by means of kidney transplantation. In three patients with ascites who did not receive a transplant, a significant reduction in water and salt ingestion was reached after intensive psychotherapy which led to reversal of the ascitic syndrome. In one anephric patient ascites did not develop despite water overloading. Survival has not been influenced by the formation of ascites. Further research is needed to determine the mechanism of sodium transfer across the peritoneal membrane. Influence of humoral factors can be considered, if an active transport mechanism could be demonstrated.
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PMID:Ascites in patients undergoing maintenance hemodialysis. Report of six cases and physiopathologic approach. 78 11

The surface features of single cells and of multicellular tissue units in cirrhotic rat livers have been studied by scanning electron microscopy (SEM). Cirrhosis of the liver was produced in rats by simultaneously treating them with carbon tetrachloride and sodium phenobarbital. Connective tissue septa consisted of a losse mesh-work of fibers in which fibroblasts were embedded. The arrangement and surface features of hepatocytes in cirrhotic nodules differed from those found in parenchyma of normal livers. Hepatocytes in cirrhotic nodules universally formed plates two cells thick. The portion of the hepatocyte surface covered by microvilli was greatly increased in cells from cirrhotic livers, and this was reflected in a corresponding reduction in the area occupied by the smooth-surfaced narrow intercellular space. Canaliculi between hepatocytes in cirrhotic livers were reduplicated and frequently branched. hepatocyte surfaces covered by microplicae and flattened microvilli, typical of connective tissue-facing surfaces in normal livers, were greatly increased in cirrhotic livers corresponding to the increase in connective tissue. Where hepatocytes directly contacted fibroblasts (and not fibers), their surfaces were entirely smooth. Sinusoidal endothelial cells in cirrhotic livers contained only isolated, relatively sparse pores, and they lacked both sieve plates (pore complexes) and large fenestrations.
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PMID:Surface features of cirrhotic liver. 82 92

Two patients with cirrhosis and ascites complicated by extensive unilateral pleural transudates refractory to therapy with dietary sodium restriction, diuretics, and repeated thoracentesis were successfully managed by tetracycline-induced pleural symphysis. The intrapleural instillation of this antibiotic prevented the recurrence of the effusion and substantially relieved the patients' symptoms with minimal undesirable side effects.
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PMID:Tetracycline-induced pleural symphysis for recurrent hydrothorax complicating cirrhosis. A new approach to treatment. 83 May 83

The object of this study was to localize increased sodium resorption in rats with chronic hepatic cirrhosis. Cirrhosis was induced by the administration of phenobarbital and carbon tetrachloride. The animals retained salt and water after loading and showed edema and ascites. Salt and water balance, clearance, and micropuncture tests were performed. Five or six weeks after the start of procedures to induce injury, the rats were unable to excrete salt and water loads promptly. Urine flow and sodium concentration were significantly less in cirrhotic rats with edema and ascites than in the normal controls. The glomerular filtration rate was slightly lower in the right, nonmicropunctured kidney but was the same in the left. The nephron glomerular filtration rates of surface nephrons were equal in both the experimental and control rats. The fractional proximal resorption rate was notably greater in cirrhotic rats, as was the total proximal nephron resorption rate. That increased proximal resorption alone might account for diminished sodium and water excretion cannot be demonstrated from this study, although we believe that major evidence is provided of the importance of proximal resorption in this phenomenon.
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PMID:A micropuncture study of salt and water retention in chronic experimental cirrhosis. 85 Nov 88


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