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)

Patients with a metabolic block in the conversion of THCA into cholic acid develop cirrhosis and hemolysis, and die of hepatic failure. In these patients, THCA is largely conjugated to taurine (tauro-THCA) and excreted instead of being converted into cholic acid. In the present study, the effects of tauro-THCA on hemolysis, bile flow, and hepatic morphology were evaluated in bile fistula rats. All rats infused with tauro-THCA at rates of 0.25, 0.50 or 0.75 micronmol/min developed hemolysis with hemoglobinuria. A direct toxic effect of tauro-THCA on washed human red blood cell membranes was demonstrated at a concentration of 8 X 10(-4) M. Liver biopsy sections from rats infused for a 2 hr period with tauro-THCA were examined by electron microscopy and showed dilation of the rough endoplasmic reticulum and distortion of mitochondrial membranes. Cholestasis was not induced, since tauro-THCA actually caused a greater choleretic response for a given rate of bile salt excretion than did taurocholate. This study raises the possibility that the clinical liver disease seen in patients with a metabolic block in the conversion of THCA into cholic acid may be caused by tauro-THCA.
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PMID:Hepatic lesions and hemolysis following administration of 3alpha, 7alpha, 12alpha-trihydroxy-5beta-cholestan-26-oyl taurine to rats. 89 5

1) Fluid retention and ascites are rarely seen in patients with primary biliary cirrhosis (PBC). In an attempt to clarify this clinical observation, renal handling of sodium, water and divalent ions was studied during extracellular volume expansion (ECVE) and maximal suppression of antidiuretic hormone (ADH) secretion in 5 patients with PBC and 9 normal subjects. 2) Mean fractional excretion of sodium, water, phosphate and calculated fractional distal delivery of sodium were significantly greater in patients with PBC as compared with normal controls. Fractional CH20 for given fractional urine flow was similar in patients with PBC and normals. 3) The data suggest that patients with PBC have a greater diminution of proximal tubular reabsorption of sodium in response to ECVE than controls. This augmented elimination of salt during ECVE in patients with PBC may explain the rarity of ascites and edema in this type of cirrhosis.
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PMID:Renal handling of sodium, water and divalent ions in patients with primary biliary cirrhosis. 89 21

1-Sar-8-ala angiotensin II (saralasin) was infused intravenously in graded doses of from 0.1 to 10 mug/kg/min to five patients with cirrhosis and ascites after three days of restricted sodium intake. In each patient blockade of AII by saralasin produced a marked fall in blood pressure, a rise in plasma renin activity (PRA) and plasma renin concentration (PRC) and, in four of the five, a fall in plasma aldosterone (PA). The rise in PRA and PRC correlated poorly with changes in blood pressure. The effects of saralasin rapidly reversed after cessation of the infusion. Plasma volume was normal or high in each case. Three patients were mildly hypotensive in the control state, and all five were resistant to the pressor effect of infused AII. After three days of salt loading, the above effects of saralasin were diminished but not abolished. In four normal subjects, after salt depletion, saralasin infusion induced qualitatively similar but much smaller changes in blood pressure, PRA and PRC. In two cirrhotic patients without ascites, after salt depletion, saralasin infusion caused a rise in blood pressure with no significant changes in PRA, PRC or PA. These results provide evidence that in patients with cirrhosis and ascites circulating AII is active in support of blood pressure, in direct suppression of renal renin release, and in stimulation of aldosterone release.
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PMID:Effect of blockade of angiotensin II on blood pressure, renin and aldosterone in cirrhosis. 94 Feb 84

Thanks to diuretics, adequate diet, and other measures, the treatment of cirrhotic ascites in recent years has brought better results. Nonetheless, a certain number of patients do not respond to the above mentioned treatment. Such patients are afflicted with so called Refractory Ascites on which diuretics have no effect. In recent years the concentrated continuous reinjection methods has been accepted. During a nine month period, we have treated and analyzed thirty patients with severe Hepatic Ascitogenic Cirrhosis. The results have shown: 8 patients with satisfactory improvement with one reinjection, in 2 patients Ascites did not reoccur; 6 patients died; 6 patients failed to return for a control reexamination; in 2 patients, ascites persisted even after repeated reinjections. The patients were given diuretics the third week following the reinjection, and were put on a low salt diet. Ascites reoccurred, and to a greater degree during the second third, and fourth month. A reduced sodium level was corrected by the reinjection and by the administration of NaCl during the reinjection. K and Cl levels did not change significantly. Urea levels, which were elevated in many cases were normalized. Ammoniums and Phenols also tended to normalize following reinjection. Bilirubin values were highly variable especially in two patients. One of whom had a severely damaged liver (direct bilirubin), the other of whom had bleeding varicoses of the esophagus (indirect bilirubin). Both of these patients died. In such cases reinjection should not be performed until the bilirubin values fall below 5 mgr %. Of the six patients who died, four died of unforeseen esophageal hemorrhaging. A larger number of patients grew more tolerant of diuretics. Preparation for a Portocaval Shunt with the reinjection method is of a special advantage because of an overall improvement in condition, making surgery possible. Complications resulting from reinjection were insignificant and transitory. As a whole, our results (sixteen patients in satisfactory condition), showed that Continuous Venous Reinjection of peritoneal fluid, even though a palliative method, represents a significant step forward in the treatment of Ascites in the severely ill.
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PMID:[Treatment of cirrhotic ascites by means of venous concentrated reinjected of the peritoneal fluid]. 99 28

Cell and humoral immunological tests were used in clinical examination of 47 patients suffering from cirrhosis of the liver; a mixed character of autoallergy was revealed in this form of pathology. Reproduction of passive anaphylaxis on guinea pigs with the aid of the sera and leukocytes of these patients pointed to the prevalence of cell allergy. Passive transmission of increased sensitivity to human hepatocytes from guinea pigs, preliminarily sensitized with salt extracts from human hepatocytes, to intact animals was realized. Active sensitization was accompanied by the formation of mixed allergy to the antigen obtained from the liver of a person who died accidentally, with the prevalence of the immediate type of reaction.
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PMID:[Study of the mechanisms of autoallergic reactions in cirrhosis of the liver]. 108 96

After a diffuse introductory discussion on S-adenosylmethionine methyltransferase activity, the results of an experimental trial carried out on 70 hospitalized patients with chronic hepatitis either persistent or aggressive, and with hepatic cirrhosis at various degrees, are reported. A first group of patients was treated with SAMe (S-adenosylmethionine) intravenously administered for 20 days at two daily doses of 15 mg. The second group was instead-receiving, still by i.v. route, 20 mg of fructose-1-6-diphosphage sodium salt, as a drug for comparison given twice a day at the doses of 2.5 over a 20 days' period. The protidemia picture and in particular the albuminic fraction, generally altered in all the cases under study, have been rapidly and significantly restored only in the group of patients treated with SAMe this indicating the efficacy of this molecule on the liver function.
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PMID:[Relations between protidopoiesis and biological transmethylations: action of S-adenosylmethionine on protein crasis in chronic hepatopathies]. 109 63

The factors involved in renin release have been extensively evaluated. The primary determinants are the transmural pressure at the afferent arteriole, sodium delivery to the macula densa, and the activity of the adrenergic nervous system. Other possible factors include circulating catecholamines, the serum and cerebrospinal fluid sodium concentration, serum potassium concentration, angiotensin II concentration, and antidiuretic hormone release. There is no convincing evidence that the renin-angiotensin system mediates renal autoregulation. Plasma renin activity is altered in a number of clinical settings. This parameter is elevated in most patients with cirrhosis and the nephrotic syndrome as well as in individuals with severe congestive heart failure. Despite inappropriately large weight gains, plasma renin suppresses normally with increased salt intake in edematous patients who have a normal glomerular filtration rate. The mechanisms of the alteration in the renin-angiotensin system in Bartter's syndrome is still not clear.
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PMID:Renin and the kidney. 110 Oct 89

Renal excretion of bile salts was studied in 17 patients with cirrhosis of the liver. The average quantity of bile salts in urine was 10.2 plus or minus 8.3 mg per 24 hr, 56% of which were sulfated. Of the individual urinary bile salts, 24% oithocholate were sulfated. In contrast, neither sulfated nor nonsulfated bile salts could be detected in urine from 2 normal subjects. Kinetics of bile salt metabolism was measured in 2 of the cirrhotic patients after oral administration of [14C] cholate and [3H] chenodeoxycholate. Approximately 3 to 12% of bile salts synthesized in liver were excreted in urine. Most urinary bile salts (76 to 80%) were sulfated, whereas only 4 to 5% of serum bile salts and 7 to 10% of biliary bile salts were sulfated. Renal clearance of cholate was more than 3 times greater than the clearance of chenodeosycholate or deoxycholate. Renal clearance of sulfated bile salts was 20 to 200 times greaterthan the clearance of the corresponding nonsulfated bile salts.
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PMID:Sulfation and renal excretion of bile salts in patients with cirrhosis of the liver. 111 55

Percutaneous liver biopsies obtained from patients with a history of chronic alcoholism and normal liver, fatty liver, alcoholic hepatitis, or active cirrhosis were incubated with tritiated proline to determine the pattern of collagen biosynthesis in these conditions. Incorporation of labeled proline and hydroxyproline into salt-soluble and insoluble fractions of collagen was evaluated by radiochemical analysis and tissue localization documented by autoradiography. Biopsy specimens of alcoholic hepatitis and cirrhosis exhibit a significant increase in the amount of radioactive proline and hydroxyproline in salt-soluble and insoluble collagen. Marked accumulation of radioactivity occurred over bile ducts, fibroblasts, and collagen fibers in the portal area and over hepatocytes, fibroblasts, and collagen fibers in the centrilobular area. Fatty liver is associated with an increase in uptake of proline and hydroxyproline in the salt-soluble fraction of collagem; silver grains appear in the periphery of fat-laden cells and in areas of focal inflammation. Digestion by collagenase indicates that labeling over fibroblasts and collagen reflects active synthesis, whereas, entry of proline into the cell protein pool is responsible for accumulation of radioactivity in other sites. In vitro ethanol causes a significant increase in the incorporation of proline and hydroxyproline into collagen in biopsy specimens of alcoholic hepatitis or active cirrhosis, but has no effect on collagen synthesis by normal or fatty liver.
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PMID:Collagen biosynthesis in liver disease of the alcoholic. 117 Feb 67

1. Dogs with bile-duct ligation retain salt and water and form ascites. The present study was under-taken to examine the role of haemodynamic factors in the aetiology of this sodium retention. 2. Haemodynamic studies were performed in five dogs before and 5 weeks after bile-duct ligation. 3. After the operation there was an insignificant fall in mean arterial pressure, a significant rise in mean cardiac index and significant fall in mean total peripheral resistance. 4. It is concluded that heart failure is not a factor in renal sodium retention of the dog with bile-duct ligation, since the central venous pressure was not elevated. 5. The haemodynamic pattern and the tendency to salt retention in the dog with chronic bile-duct ligation closely resemble findings reported in patients with cirrhosis of the liver, and it is suggested that oedema formation in patients with cirrhosis of the liver and dogs with chronic bile-duct ligation shares a common aetiology.
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PMID:Haemodynamic studies in dogs with chronic bile-duct ligation. 127 59


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