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 SGOT/SGPT ratio is significantly elevated in patients with alcoholic hepatitis and cirrhosis (2.85 +/- 0.2) compared with patients with postnecrotic cirrhosis (1.74 +/- 0.2), chronic hepatitis (1.3 +/- 0.17), obstructive jaundice (0.81 +/- 0.06) and viral hepatitis (0.74 +/- 0.07). An SGOT/SGPT ratio greater than 2 is highly suggestive of alcoholic hepatitis and cirrhosis. It occurs in 70% of these patients compared with 26% of patients with postnecrotic cirrhosis, 8% with chronic hepatitis, 4% with viral hepatitis and none with obstructive jaundice.
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PMID:The SGOT/SGPT ratio--an indicator of alcoholic liver disease. 52 Jan 2

The effect of alcoholic patient sera on in vitro lymphocyte transformation was studied using mitogen-induced uptake of (3)H-thymidine to measure blastogenesis. With pokeweed mitogen as the stimulus, transformation of normal lymphocytes in sera of alcoholics with either normal or fatty livers was not significantly different from that obtained in pooled human serum (PHS). However, in sera of patients with either alcoholic hepatitis or inactive cirrhosis mean transformation was significantly reduced (P <0.001, <0.02 respectively). With phytohaemagglutinin-P or concanavalin A as mitogens, suppression of transformation was not as marked but followed the same pattern. A significant negative correlation was observed between the magnitude of transformation and serum bilirubin and aspartate aminotransferase levels. An intra-patient comparison of the effects on transformation of normal lymphocytes by simultaneously collected peripheral and portal venous sera, and of peripheral sera obtained before and after portasystemic shunt surgery, indicated that the factor(s) responsible did not originate in the splanchnic circulation nor did it accumulate in the serum because of failed hepatic clearance. By performing transformation experiments in the presence of inhibitory patient sera diluted with PHS it was possible to show that these sera caused true inhibition of transformation rather than suppression due to failure to sustain cell culture because of nutritional deficiencies. Inhibitory sera did not contain high levels of the enzyme thymidine phosphorylase and did not significantly inhibit binding of (125)I-labelled mitogens to the lymphocyte surface. These findings indicate that the inhibitory effect of sera from alcoholics is of potential in vivo importance, that the effect increases with the degree of heptocyte damage, and that it is unrelated to the nonhepatic metabolic affects of chronic alcoholism.
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PMID:Suppressive effect of alcoholic liver disease sera on lymphocyte transformation. 53 94

The m-GOT were studied in 57 patients with liver diseases, diagnosed by peritoneoscopy and biopsy. In acute hepatitis, the m-GOT rose to 100 units or there-about. But in chronic hepatitis, even in hepatitis B with sublobular necrosis, the m-GOT were low and 20--30 units. On the other hand, in alcoholic hepatitis, the m-GOT were 50--60 units which may be considered to be higher than expected for comparable their histological necrotic findings. These values were higher than OCT, which were measured at the same time. This results showed that there might be m-GOT induction by alcohol. In liver cirrhosis lower values were obtained. Generally m-GOT was liable to be lower as the lobular distortion was getting severer.
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PMID:Mitochondrial glutamic oxaloacetic transaminase and its clinical significance. 53 8

Serum somatomedin (SM) activity, measured as sulphation factor on chick embryo cartilage, and growth hormone (GH) levels were measured in peripheral, hepatic and renal veins of 23 patients with a alcoholic cirrhosis. SM activity (mean +/- SEM) was 0.65 +/- 0.05 U/ml in peripheral vein, 0.59 +/- 0.04 U/ml in hepatic vein, and 0.74 +/- 0.07 U/ml in renal vein. Mean GH levels were respectively 2.8, 2.5 and 3.1 ng/ml. Compared to peripheral vein, SM increase in renal vein was 19% (P less than 0.05). Serum SM activity was significantly lower in 13 patients with alcoholic hepatitis associated with cirrhosis than in other 10 patients (P less than 0.02 in hepatic blood and P less than 0.05 in peripheral blood). The decrease of SM activity seems related to cytolysis and hepato-cellular insufficiency. At last, in patients with alcoholic hepatitis, SM activity was lower in the hepatic vein than in the peripheral vein (P less than 0.05). The cause of this difference remains under discussion, no SM inhibitors being found in the serum samples used in this study.
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PMID:Serum somatomedin activity measured as sulphation factor in peripheral, hepatic and renal veins of patients with alcoholic cirrhosis. 58 Nov 14

The role of liver size in drug metabolism was investigated in 34 chronic alcoholics and 28 controls by comparing antipyrine half-life with biopsy content and total amount of hepatic cytochrome P-450 (P-450) and liver weight. Liver size was significantly greater in alcoholics than in controls. Total P-450 was increased and antipyrine metabolism was enhanced in alcoholics with normal histology of the liver. In subjects with alcoholic hepatitis or cirrhosis, the antipyrine half-life was prolonged and P-450 was decreased. Alcoholics with fatty liver had a reduced P-450 content, but the total amount of P-450 and the antipyrine half-life were normal. The results demonstrate in alcoholics that an enlarged liver of normal histological appearance is associated with enhanced drug metabolism. In subjects with fatty liver the drug metabolizing capacity per unit weight of liver is often impaired, but the increase in liver size leads to undisturbed total oxidizing capacity and normal in vivo metabolism. In alcoholic hepatitis drug metabolism is impaired in spite of hepatomegaly. In cirrhosis the enlargement of the liver appears to compensate for the decreased P-450 content resulting in only slightly decreased total P-450, and the severly impaired in vivo drug metabolism may be due to derangement of blood flow.
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PMID:Liver size and indices of drug metabolism in alcoholics. 63 35

Among 2 952 non-selected liver biopsies of adults in the 5-years-period 1970-1974 506 cases (17%) of clinically proved chronic alcoholics were found. Most of the patients are males, and even young men at an age of less than twenty years are taken with. The number of 31 professional drivers within this group is remarkable and alarming, too. The histomorphological picture may be divided into liver changes without any abnormal state (39%), fatty liver (40%), alcoholic hepatitis (18%) and cirrhosis (3%). Chronic alcoholism can be considered as one of the most important causes of the fatty liver. Clinical and pathological aspects of alcoholic liver changes are discussed.
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PMID:[Liver biopsy changes in chronic alcoholism]. 64 47

Two studies investigating the association of liver disease with acute and chronic pancreatitis in alcoholics are presented. In a retrospective study of 50 patients, no clinical liver disease was found in 9 patients with acute pancreatitis, while 23 (56%) of 41 patients with chronic pancreatitis had liver disease by clinical criteria. Of this latter group, 8 were confirmed histologically; thus 19% of patients with chronic pancreatitis had biopsy-proven cirrhosis. Fifty alcoholic patients with pancreatitis were prospectively evaluated. All who had clinical evidence of liver disease were biopsied. No cases of liver disease were encountered in the 4 patients with acute pancreatitis. Although 28 (60%) cases of clinically diagnosed liver disease were present in 46 patients with chronic pancreatitis, only 20 of these seemed significant (cirrhosis, alcoholic hepatitis, severe fatty liver), for an incidence of 43%. Thus, clinically significant alcoholic liver disease occurs quite frequently in association with alcoholic pancreatitis. This association is meaningful in more effective management of these patients in general and in preoperative assessment of the risk of surgery in particular.
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PMID:Associated liver disease in alcoholic pancreatitis. 68 26

Chronic liver disease is not often reported in patients with haemophilia. Although a high incidence of abnormal liver function tests has been reported, the clinical significance of these findings and their relation to chronic liver disease cannot be established without a liver biopsy. The results of this procedure, carried out in 11 patients with severe haemophilia A and B, in whom SGOT had been persistently raised for three years, are reported. Five patients had chronic active hepatitis, four had chronic persistent hepatitis, one had cirrhosis, and one alcoholic hepatitis. No haemorrhagic complication followed the biopsy procedure, which was carried out in patients given prophylactic clotting factor concentrates. These results suggest that duration of abnormal liver function tests is likely to represent liver disease in haemophiliacs, and that biopsy should be considered to establish the diagnosis and plan a suitable therapeutic programme.
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PMID:A clinicopathological study of liver disease in haemophiliacs. 69 Feb 43

Consecutive liver biopsies from alcoholic, diabetic and overweight patients are compared morphologically and in addition a comparison is made between groups with a combination of two or three of the above conditions. Both fatty change and morphological activity are greater in the groups with alcoholism, and this gives good reason to believe that the activity in the form of alcoholic hepatitis is the cause for the more common development of cirrhosis in alcoholic fatty liver than in fatty liver with other aetiology.
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PMID:Morphological features in non-cirrhotic livers from patients with chronic alcoholism, diabetes mellitus or adipositas. A comparative study. 71 11

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


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