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)

The activity of ethanol metabolising enzymes was assessed in 51 patients with alcoholic and non-alcoholic liver disease using tracer doses of [1-14C]ethanol and measuring 14CO2 excretion in the breath. Alcoholic patients with only fatty infiltration of the liver showed significantly increased activity compared with controls. Comparing alcoholic patients with cirrhosis and a serum albumin greater than 28 g/l, activity in those with a recent history of continued heavy drinking was significantly greater than in patients who had abstained from alcohol. In addition, both groups of alcoholic cirrhosis showed significantly more activity than patients with non-alcoholic cirrhosis. The activities of patients with acute alcoholic or viral hepatitis were normal when their prothrombin times were less than 7 sec prolonged, but were reduced when prolongation exceeded 7 sec. These results demonstrate that in chronic alcoholic liver disease, even with cirrhosis, alcohol can still increase the activity of ethanol oxidising enzymes provided hepatic function remains adequate. However, this response is lost in acute liver damage and in chronic alcoholic disease with severe hepatic dysfunction.
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PMID:[1-14C]Ethanol breath test in alcoholic liver disease. 65 31

Thirteen family members of a patient with chronic active hepatitis type B were investigated. The family included both parents, 6 sons, and 5 daughters. The parents were second cousins. HBsAg, liver tests, immunological evaluation, and HLA typing were performed on all subjects. Percutaneous liver biopsies were done on the mother and 5 of the 6 sons. The mother and all 6 sons had HBs antigenemia. The mother was free from any evidence of liver disease whereas all 6 sons had abnormal liver and immunological tests. The liver biopsies of 5 sons showed chronic active hepatitis with variable degrees of progression toward cirrhosis. The 6th son could not be biopsied in view of his prolonged prothrombin time. The father and the 5 daughters were HBsAg negative and had no evidence of liver disease. Immunological abnormalities were present in all of the effected children and in the mother and 3 daughters. This is the second report in the English literature on the familial occurrence of chronic active hepatitis type B. It emphasizes the predominance of this entity in the male offspring and confirms the presence of immunological abnormalities in the relatives of such patients. There was no evidence to link the inheritance of an immunological abnormality to clear the HBsAg to the histocompatibility complex.
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PMID:Genetic and immunological aspects of familial chronic active hepatitis (type B). 66 17

Antipyrine half-life (AP t1/2) was measured in 62 patients with, and 10 control patients without, liver disease to ascertain possible factors which may be useful in identifying patients with abnormal drug metabolism. Antipyrine metabolism was normal or marginally impaired in patients with compensated cirrhosis or acute hepatitis, whereas it was frequently abnormal in those with chronic active hepatitis or advanced alcoholic liver disease. A high degree of correlation was found among AP t1/2 and prothrombin time, hepatic encephalopathy, and ascites. Of patients with severely impaired drug metabolism, 80% had one or more of these features. The severity of histological changes in liver biopsies was of additional help in predicting impaired drug metabolism. Concurrent drug ingestion enhanced antipyrine metabolism in most patients with liver disease as well as in control patients. Inadequate diet was associated with prolongation of AP t1/2, but other environmental factors such as alcohol ingestion, cigarette smoking, and coffee consumption did not affect rates of drug metabolism in patients with liver disease. Consideration of all of the above factors allows qualitative predictions of the rate of hepatic drug metabolism in patients with liver disease, as assessed by the AP t1/2.
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PMID:Drug metabolism in liver disease. Identification of patients with impaired hepatic drug metabolism. 71 Aug 27

The effect of propylthiouracil (PTU; 300 mg/day) on alcoholic liver disease was evaluated in 133 patients in a short-term randomized double-blind trial. Severity of the disease was assessed by a composite clinical and laboratory index (CCLI). A normalization rate (NR) representing the rate of improvement in CCLI was calculated. Patients with alcoholic hepatitis, with and without cirrhosis, showed a significantly higher NR on PTU (43.6 +/- 4.6) than on placebo (19.8 +/- 3.3; P less than 0.001). A similar effect was observed in patients with abnormal prothrombin (no biopsy): NR was 32.9 +/- 6.9 on PTU and 2.6 +/- 3.7 on placebo (P less than 0.005). The effect of PTU on each clinical and laboratory component of the CCLI was also compared in these two groups. In 38 patients with alcoholic hepatitis and in 25 with abnormal prothrombin, those on PTU showed a greater improvement in 15 of 15 items (P less than 0.001) and 14 of 15 (P less than 0.01), respectively. When patients were divided according to the severity of the disease into those in the lower and upper halves of the CCLI range (81 and 52 patients, respectively), PTU was shown to have a significant effect only in the latter: The NR was 41.4 +/- 3.8 on PTU and 22.5 +/- 4.2 on placebo (P less than 0.005). PTU was ineffective in patients with inactive cirrhosis.
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PMID:Effect of short-term therapy with propylthiouracil in patients with alcoholic liver disease. 75 31

Furosemide is frequently used for ascites and causes adverse reactions (AR). In an intensive prospective drug monitoring study of 1,920 patients, 172 (8.9%) had cirrhosis of the liver and received furosemide. Mean age was 53 years, and 66.3% were male; and 87% had alcoholic cirrhosis. Eighty-eight (51.2%) had 221 events that by consensus of the monitoring team and attending physicians were either definitely of probably related to furosemide. No AR was fatal but 24% of patients had severe reactions. Almost all reactions were dose-related (96%). The most common were electrolyte disturbances (23.3% of patients) and volume depletion (14%). Furosemide-induced coma occurred in 20 (11.6%) patients and was more frequent in patients with prior hepatic encephalopathy (p less than 0.0005). Higher total doses (p less than 0.001), hyerbilirubinemia (p less than 0.05), prolonged prothrombin time (p less than 0.02), and longer hospital stay (p less than 0.001) were associated with higher frequencies of AR to furosemide. The frequency of hypokalemia did not decrease when potassium chloride or potassium-sparing diuretics were added to furosemide therapy. Frequdncy of AR did not correlate with age, sex, renal impairment, serum albumin, transaminase, or alkaline phosphatase.
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PMID:Furosemide-induced adverse reactions in cirrhosis of the liver. 75 67

Among 134 patients with chronic active liver disease, selected by identical clinical, biochemical and morphologic criteria, assigned to standard treatment programs and followed at regular intervals, 21 of 105 failed treatment with standard regimens containing steroids. Treatment failure was more common in patients whose serum contained hepatitis B surface antigen, those with more severe liver disease as judged by liver function tests (prothrombin time) and hepatic morphology (subacute hepatitis or cirrhosis). Early diagnosis of treatment failure, based on changes in liver function tests rather than on clinical features of deterioration, coupled with the immediate administration of higher doses of prednisone with or without higher doses of azathioprine, resulted in disappearance of clinical and biochemical features of disease activity in the majority of patients. These results were greatly superior to those earlier reported by us from patients chosen by identical criteria but treated by conventional measures. However, when endogenous encephalopathy developed the outlook was grave, regardless of previous or subsequent therapy. We recommend that patients at risk for failing conventional treatment be identified early, followed carefully with serial liver function tests, and be treated promptly with higher doses of medication when deterioration occurs.
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PMID:Failure of customary treatment in chronic active liver disease: causes and management. 79 99

Serial measurements of complement components were performed in fifty-nine patients with acute, uncomplicated hepatitis and twelve with alcoholic cirrhosis. Thirty-one of the former group had detectable hepatitis B antigen. Abnormal complement profiles were observed in nine patients with hepatitis B and seven with antigen-negative hepatitis. Low levels of C4, C3 and factor B were common in the subjects with cirrhosis and confined to those cases with severe reduction in serum albumin and/or prothrombin index. By contrast, the complement changes in the patients with hepatitis occurred without significant alteration in these parameters; certain subjects also had reduction in C1q and C5 and a significant number had C3d detectable in fresh plasma. The pattern of abnormality suggests predominant involvement of the classical pathway and it is concluded that this results, at least in part, from an immune process evident only in the early clinical phase of hepatitis. Such gross changes in complement are likely to reflect immune-complex activity and it is proposed that these complexes may be important in the clearance of virus material. The data supports a previous suggestion that recovery from acute hepatitis is primarily dependent on host immune competence rather than viral cytotoxicity or generation of immune complexes.
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PMID:Acute hepatitis: significance of changes in complement components. 89 Oct 25

The plasma elimination curves of diazepam following intravenous administration of 10 mg were studied in nine patients with cirrhosis of the liver and four patients without liver disease. The data were analyzed according to a two compartment model. The mean biological half-life (T/2) of diazepam was increased five-fold in patients with cirrhosis compared to the controls (164 hours vs. 32.1 hours). The plasma clearance of diazepam could be correlated neither with a quantitative measure of liver function, as estimated by galactose elimination capacity, nor to semiquantitative measures of liver function, such as serum albumin and prothrombin. It is suggested that the plasma clearance of diazepam is an inaccurate index of its rate of hepatic metabolism due to the complex kinetics of the drug.
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PMID:Pharmacokinetics of diazepam in disordered liver function. 96 87

The intrasplenic injection of 99mTc-labeled albumin microspheres, followed 30 sec later by an injection of 99mTc-labeled red blood cells with recording of the progression of the two tracers, were performed in 110 patients. This also enabled the plotting of activity versus time curves on splenic, hepatic, cardiac, and pulmonary areas of interest, there by giving access to several hemodynamic variables. Scintillation image demonstrated splenoportal obstruction in 8 cases. Intrahepatic obstruction with reflux via collaterals were observed in 53 cases, 14 with umbilical reflux. In 13 cases, the patency of surgical portacaval anastomoses were verified. The splenoportal blood flow velocity was not significantly different in patients with cirrhosis (V = 10.1 cm per sec +/- 3.0 SD) and in normal subjects (V = 13.2 cm per sec +/- 5.8 SD). The fraction of shunted splenic flow in the case of cirrhosis varied from 0 to 100%; there was no relationship between this percentage and the seriousness of the clinical status. In 3 cases, the presence of intrahepatic shunts was detected. There was a very significant difference between mean transit time (MTT) of red blood cells in patients with cirrhosis (t = 12.2 sec +/- 4.4 SD) and those without cirrhosis (t = 19.9 sec +/- 3.7 SD). Among patients with cirrhosis, those with a history of jaundice had a shorter MTT than those without such a history. On the other hand, the MTT was not significantly different whether the patients with cirrhosis had or did not have hemorrhage, ascites or encephalopathy. There was a positive correlation (P less than 0.01) between MTT and plasma albumin concentration,and between MTT and prothrombin (P less than 0.01). Finally, there was a high negative correlation (P less than 0.001) between MTT and total serum bilirubin. Scintillation splenoportography is a useful technique for assessing hepatic hemodynamics and for demonstrating abnormalities of the intrahepatic circulation.
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PMID:Scintillation splenoportography: hemodynamic and morphological study of the portal circulation. 98 35

The high incidence of consumption coagulopathy in active liver cirrhosis prompted us to introduce low-dosage heparin therapy (LDHT) in the management of this condition. An investigation was carried out on 109 patients with clinical and biochemical evidence of progressive liver cirrhosis, which was designed to evaluate whether in addition to basic LDHT, the administration of either vitamin K1, human fibrinogen or partial prothrombin complex (Prothromplex 500) enhanced the results obtained with LDHT alone. The normotest, PTT, thrombin coagulase activity, fibrinogen and platelet count were determined at regular intervals. A significant increase in fibrinogen and platelet count was obtained within 14 days of LDHT in about 75% of the patients and the consumption coagulopathy was halted. Additional treatment with vitamin K1 did not bring about any further increase in the prothrombin complex. Substitution therapy with factors II, IX, X and fibrinogen combined with LDHT brought the expected results. The results reported in the literature and the aims of, and indications for LDHT are discussed.
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PMID:[The therapeutic management of consumption coagulopathy in progressive liver cirrhosis: low-dosage heparin therapy (author's transl)]. 99 29


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