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)

We report a successful practical protocol for readministration of spironolactone in a patient with cirrhosis and severe ascites whose initial exposure to spironolactone resulted in erythema multiforme. Because salt and water restriction and other diuretics were ineffective, readministration of spironolactone was considered appropriate. In the absence of in vitro or in vivo diagnostic tests for drug allergy to spironolactone, serial increasing doses from 1 mg to 400 mg were administered over a 14 day period and tolerated uneventfully. A mild maculopapular rash appeared a month later but resolved despite continuation of spironolactone. The patient has now received spironolactone successfully for a total of 20 months without evidence of subsequent drug hypersensitivity. Although proven drug hypersensitivity attributable to spironolactone is very rare, when allergic manifestations have occurred in a patient who may require readministration of spironolactone, we believe that the suggested protocol for test-dosing be considered.
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PMID:Readministration of spironolactone in the spironolactone-intolerant patient. 347 49

Non-steroidal anti-inflammatory drugs (NSAIDs) may produce acute renal failure, papillary necrosis and interstitial nephritis. These adverse drug reactions are rare but have been reported in patients with congestive heart failure, cirrhosis, renal parenchymal disease, lupus nephritis and hypertension. All these conditions may be associated with hypovolaemia and an activated renin-angiotensin system, when renal blood flow and glomerular filtration depend on local renal prostaglandin biosynthesis. A severe impairment of renal function may occur when this synthesis is inhibited by NSAID treatment. It is possible that 1 in 100 of elderly patients have renal parenchymal disease, 1 in 100 arteriolar nephrosclerosis, 1 in 200 unilateral or bilateral renal artery stenosis and an unknown number suffer from atheroembolic renal disease. Fortunately, only a small proportion of 'at risk' patients given NSAIDs appear to develop renal failure. Perhaps bilateral renal disease or salt depletion are necessary factors? Whatever the explanation, NSAIDs should be used with caution in the elderly.
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PMID:Pharmaco-epidemiological considerations in patients with arthritis and vascular disease of the kidney. 349 36

In a series of studies, peritoneovenous shunting (PVS) has been used to dissect out some of the many factors involved in salt and water retention associated with hepatic ascites. Careful metabolic studies showed that, immediately following PVS, diuresis and natriuresis were associated with a marked rise in cardiac output, renal plasma flow and creatinine clearance, and a significant fall in the elevated serum aldosterone and plasma renin activity to within the normal range. Despite these changes, sodium excretion in these patients remained abnormal when challenged with a high salt diet. In contrast, an immediate increase in water excretion was not associated with a reduction in the elevated antidiuretic hormone (ADH) levels which do, however, decrease to some extent after 2 weeks. Thus, in the long term, these cirrhosis patients will have improved systemic and renal hemodynamics and function and normalization of the renin-aldosterone axis and ADH, yet will still have a "sodium-retaining lesion," the nature of which still needs to be elucidated.
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PMID:The use of peritoneovenous shunting in unravelling the pathogenesis of ascites in cirrhosis. 351 75

We discuss current perspectives in ascites, focusing on newer developments of interest to clinicians and stressing the value and limitations of therapeutic paracentesis. Because there is considerable evidence to support both the "underfilled" and "overflow" hypotheses for the development of ascites, current concepts concentrate on integration of these two theories. In the management of ascites the rate of ascites mobilization is more important than the method by which excess peritoneal fluid is removed; thus salt restriction may not have to be rigid if diuretics are used judiciously. An approach to intractable ascites emphasizes the difference between unresponsive and refractory ascites, but in both situations a conservative philosophy is recommended. Nonhepatic causes of ascites are briefly reviewed since their management may require principles different from those used in cirrhosis.
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PMID:A clinical view of recent advances in ascites. 351 34

A patient with cirrhosis and coexistent hyporeninemic hypoaldosteronism secondary to diabetic nephropathy rapidly formed ascites despite marked reductions in plasma aldosterone concentration and urinary aldosterone excretion. To my knowledge, this association has not been previously reported. This case supports the concept that hyperaldosteronism is not a necessary component of the salt retention of advanced liver disease. Furthermore, it suggests that certain renal disorders should be considered in cases of cirrhosis and ascites with decreased plasma renin activity.
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PMID:Hyporeninemic hypoaldosteronism in a patient with cirrhosis and ascites. 353 21

Cirrhotic dogs without intrahepatic hypertension (IHH) never retain sodium or expand plasma volume. To test the hypothesis that IHH may cause urinary sodium retention early in cirrhosis, we prepared cirrhotic dogs (chronic biliary obstruction) who underwent simultaneous hepatic denervation with end-side portacaval anastomoses. Such animals, along with appropriate controls and unanesthetized were studied by balance techniques. In the experimental group, plasma volume never increased, and sodium retention did not occur until 2 days prior to the appearance of detectable ascites. In a sham-denervated group, plasma volume increased by 10% and sodium retention occurred on the average 8.4 days prior to ascites. When the portal veins were left intact, the sham-denervated group showed the usual magnitude of plasma volume expansion observed in cirrhotic dogs (18.3%) with a 7-day delay between sodium retention and ascites appearance. Those dogs with hepatic denervation demonstrated a 9.2-day delay with 12.6% expansion of plasma volume. When ascites was mobilized with a peritoneovenous valve, and dogs were subjected to a high salt diet (130 meq/day), denervated dogs excreted the load normally, whereas sham-denervated dogs retained sodium and developed anasarca. We conclude that in cirrhotic dogs with IHH, liver denervation prevents early non-volume-related sodium retention.
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PMID:Hepatic denervation alters first-phase urinary sodium excretion in dogs with cirrhosis. 366 18

The aim of this paper is to evaluate the relationships among the increase of serum bile acids (SBA) and other common liver function tests in subjects with liver cirrhosis. Our results show that SBA levels are well-correlated with the seriousness of the disease (classified according to Child's criteria), and with the presence of ascites, of oesophageal varices, of hepatic encephalopathy and with the gamma-globulin level. SBA also appear to be well-correlated with total bilirubinemia, and, at a lower extent, with cholesterolemia and albuminemia; no significant linear correlation was found among SBA and cholestasis (alkaline phosphatase, gamma-glutamyl-transpeptidase) or cytolysis (transaminases) indexes. In conclusion, the SBA increase in liver cirrhosis without evidence of cholestasis (as in our patients) seems to be related to liver cell reuptake disturbances and to the presence of porto-systemic shunts, with consequent alterations in entero-hepatic bile salt recirculation.
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PMID:[Serum bile acids in cirrhosis: correlation with liver function parameters and with the severity of the disease]. 367 66

Basal sympathetic nervous system activity was assessed in 8 unmedicated patients with alcoholic cirrhosis using a previously developed radiotracer method for measuring total and renal noradrenaline release to, and clearance from, plasma. Compared to the control group total noradrenaline clearance was significantly increased in the patients with advanced alcoholic cirrhosis (Pugh grade C) [1.89 +/- 0.13 vs 1.51 +/- 0.11 l/min, P less than 0.05) indicating that endogenous plasma noradrenaline levels underestimate total sympathetic nervous system activity in these patients. Renal noradrenaline clearance was similar to controls independent of the severity of the liver disease. Both total and renal noradrenaline release were significantly increased in the patients with cirrhosis. The ratio of renal to total noradrenaline release was similar in cirrhotic (26 +/- 7%) and control (23 +/- 5%) groups. Increased arterial plasma adrenaline levels, indicative of adrenal medullary stimulation, were also evident in the patients with cirrhosis and correlated significantly with total noradrenaline spillover (r = 0.732, P less than 0.05). These results strongly suggest that in patients with cirrhosis, rather than a preferential increase in renal sympathetic tone, the increase is part of a pattern of generalized sympathoadrenomedullary activation. Although renal renin secretion was significantly increased in the cirrhotic group no correlation with renal noradrenaline release was seen (r = 0.199), raising the possibility that in cirrhosis renal sympathetic tone is not a major determinant of renal renin secretion. Finally, renal noradrenaline release did not correlate with renal blood or plasma flow but an influence of the sympathetic nervous system on renal function was suggested by the correlation observed between total noradrenaline spillover and impaired salt (r = -0.683, P less than 0.05) and water excretion (r = -0.702, P less than 0.05) demonstrated in the cirrhotic patients.
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PMID:Total and renal sympathetic nervous system activity in alcoholic cirrhosis. 390 56

Sensitive tritiated radioimmunoassay was developed for conjugated chenodeoxycholic acid, using immunogen prepared by the mixed anhydride method. The obtained molar bile salt-BSA ratio in the immunogen was 19:1. The distinguishing features of the immunization procedure were a preliminary vaccination of the animal with antitubercular vaccine (VDS), and the administration of very small doses of immunogen (50 micrograms). Assay sensitivity for this bile salt fell in the picomole range with the standard curve extending from 1.5 to 150 pmol. Specificity of the antiserum was compared with that of the commercially available "Glycochenodeoxycholic acid RIA kit" (Nordiclab Oy, Oulu, Finland), and proved to be satisfactory. Fasting serum conjugated chenodeoxycholic acid concentration in 25 healthy subjects and 15 patients with cirrhosis was 0.63 mumol/l and 43.05 mumol/l, respectively. The assay was performed on unextracted sera.
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PMID:Production and properties of antiserum for radioimmunoassay of serum conjugated chenodeoxycholic acid and its preliminary application. 403 40

Secretion of bile salts into the duodenum was studied in eight normal subjects, in 10 patients with cirrhosis, and in two cholecystectomized subjects. Duodenal juice was aspirated continuously through a double-lumen tube during an unstimulated period, after an intravenous injection of pancreozymin/cholecystokinin, and during a continuous intravenous infusion of secretin given at a rate of 3 units per kilogram body weight per hour. Precautions were taken to try to ensure quantitative recovery during the studies, and recovery of an infused nonabsorbable marker was greater than 80% in all subjects. Secretin induced a flow of a greater volume of juice in the cirrhotic patients than in the normal group (49 to 57 ml per 10 minutes compared with 28 to 49 ml per 10 minutes). This change may have resulted from a higher effective dose of secretin if it is assumed that the cirrhotic liver fails to catabolize secretin. The bile acid response to pancreozymin/cholecystokinin followed by secretin in the cirrhotic subjects resembled that seen in patients after cholecystectomy in whom pancreozymin/cholecystokinin induces only a slight increase in bile salt output but in whom the output of bile salts during rest and secretin stimulation is markedly greater than normal. This response in cirrhosis is probably best interpreted as due to impaired function of the gallbladder. The total amount of bile salt liberated over the two hours of the test in the cirrhotic patients was similar to normal The concentration of bile salt after pancreozymin/cholecystokinin was less than in normal subjects, but similar to that in cholecystectomized patients. It is unlikely therefore that deficient output or concentration of bile salt can be held responsible for steatorrhea in cirrhosis. THERE WAS A MARKED DECREASE IN THE DEOXYCHOLATE CONJUGATES AND A REDUCTION IN THE GLYCINE: taurine ratio in the bile of cirrhotic patients. The former change may reflect a change in bacterial flora and the latter a defect in hepatic conjugating mechanisms.
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PMID:Bile salt secretion in cirrhosis of the liver. 544 81


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