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

Regencrative nodular hyperplasia (RHN) is a rare condition, the diagnosis of which is based upon histological findings. It is seen in Felty's syndrome with portal hypertension (PHT), as was the case in the patient reported here. This was a 72-year-old man, with long standing rheumatoid arthritis, hepatosplenomegaly, a neutrophil leucopaenia and oesophageal varices responsible for recurrent haematemeses. Despite a portocaval anastomosis, the patient died from postoperative acute hepatic failure. Histological study revealed changes in the hepatocytes and the reticulin system typical of RNH without cirrhosis. The relationship between Felty's syndrome and RHN, as well as the mechanism of the hypertension, are discussed in the light of cases from the literature.
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PMID:[Anatomo-clinical study of a case of regenerative nodular hyperplasia of the liver with Felty's syndrome and portal hypertension]. 54 55

Hyperkinetic portal hypertension is caused by pathological arterioportal shunts. Clinical differentiation is necessary between extrahepatic fistulas, splenoportal hypertension (arteriovenous anastomoses at the level of the pre-penicilary arteries) and intrahepatic fistulas in "active" cirrhosis and malignant tumors. This paper reports the clinical and angiographic features of eight patients with this type of fistula. A review of the literature is also presented (144 cases). Because of the severity of this disease, surgical intervention is necessary. The surgical technique depends on the organ-related necessity of vascular preservation.
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PMID:[Hyperkinetic portal hypertension. Arterioportal fistula: problems--case reports--review of the literature]. 64 68

A study was done on the action of splenohepatoplasty upon intrahepatic and prehepatic portal hypertension. Portal hypertension was induced Wistar rats following the establishment of cirrhotic conditions. Hepatic cirrhosis was obtained in these rats by an oral, daily dose of tioacetamide during a four and five month period. Prehepatic hypertension was produced in dogs by the installation of a rubber cylinder, completely covered by cellophane paper, around the trunk of the vena porta. This procedure brought about a progressive compression of the vena porta. The application of splenoheptoplasty is a highly valuable treatment for portal hypertension as a derivative system and for intrahepatic portal hypertension as a derivative regenerative system.
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PMID:Simultaneous treatment of portal hypertension and hepatic cirrhosis by splenohepatoplasty. 68 92

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

The plasma proteins are constantly shuttling between intravascular and extravascular mass of a specific plasma protein is determined by its individual rate of synthesis and the mean total time it spends in plasma. The ratio of intravascular to total mass (distribution ratio) is determined by the relative rate, at which it passes from plasma to interstitial spaces (transcapillary escape rate: TER) and the relative return rate via lymph. TER in a specific organ depends on the local leakiness of the microvasculature. The overall value in normal man varies with the molecular weight of the protein being about 5%/h of the intravascular albumin mass, 3%/h for IgG and less than 1%/h for IgM. The higher the TER, the lower is the intravascular fraction. Hypertension, diabetes mellitus, burns, myxedema and certain types of liver cirrhosis will increase TER. In hypertension and diabetes this may be compensated for by an increased lymphatic return rate. Hypoproteinemia due to malnutrition or urinary or gastrointestinal loss is accompanied by a shift from the extravascular to the intravascular space.
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PMID:Intra- and extravascular distribution of albumin and immunoglobulin in man. 73 85

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

The degree of arteriosclerosis in 176 autopsies of liver cirrhosis (patients in the age range of 51 to 70 years) was compared with that of controls (without liver disease). It was found that the "protective influence" of liver cirrhosis of the process of arteriosclerosis is only true for normotonic. Associated with arterial hypertension severe arteriosclerosis is predominant in liver cirrhosis. There is even some evidence that arteriosclerosis in hypertonics with liver cirrhosis is more increased than in controls without liver diseases. The factors influencing arteriosclerosis in liver cirrhosis are discussed.
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PMID:[Arteriosclerosis and liver cirrhosis (author's transl)]. 91 28

A 55-year-old woman developed symptoms suggestive of hepatitis 12 weeks after first receiving methyldopa for hypertension. Liver biopsy showed chronic aggressive hepatitis with subacute hepatic necrosis. Methyldopa was discontinued, but after exhibiting transient clinical improvement, the patient's condition progressively deteriorated until she died of hepatic failure, in spite of therapy with massive doses of corticosteroids and other nonspecific measures. During the terminal stage, a considerable decrease in the size of the liver was observed. At autopsy, the liver was found to be small, shrunken, and scarred; histological sections demonstrated postnecrotic cirrhosis. Such a rapid and relentless progression of methyldopa-induced liver injury is undoubtedly rare, but it may be prevented by careful supervision of patients who exhibit liver function abnormalities early in the course of therapy.
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PMID:Methyldopa-induced liver injury. Rapid progression to fatal postnecrotic cirrhosis. 94

We have documented a highly significant increment in hepatic arterial flow following a portacaval shunt in patients with cirrhosis of the liver and portal hypertension. In contrast with other hemodynamic variables, the increment in arterial flow was directly related to morbidity, hospital mortality, and long term survival. Patients with increments smaller than 100 ml/min had the worst clinical results. They accounted for all of the hospital mortality, the largest incidence of encephalopathy, and the worst long term cumulative survival rates. The extent of the increment was not related directly to the type of shunt but, rather, to some intrinsic capability of the cirrhotic liver to increase its arterial flow in response to the relief of sinusoidal hypertension produced by the shunt. This capablilty appears related to the degree of entrapment of the hepatic arterioles by the fibrous tissues of cirrhosis. This encasement of arterioles should change the elastic properties of the hepatic arterial bed and we propose to measure these properties by determining the characteristic input impedance of the arterial bed.
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PMID:Hepatic artery flow improvement after portacaval shunt: a single hemodynamic clinical correlate. 96 97

1. Male death rates from hypertension and stroke in England and Wales in 1949-53 were highest in those socio-economic and occupational groups with the highest death rates for cirrhosis of the liver (and presumably with highest alcohol intake. 2. In prevalence data from the Busselton population in Western Australia in 1969, there was a significant association between hypertension and a history of heavy drinking. 3. Together with other data, these observations suggest that up to 30% of hypertension in affluent countries may prove to be attributable to the use of alcohol.
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PMID:Alcohol use, hypertension and coronary heart disease. 107 3


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