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)

Elevated circulating CEA levels occur in patients with benign gastrointestinal and hepatic disorders. These are usually less than 10 ng/ml. Of clinical importance is the influence of liver disease on the interpretation of CEA. At least 50% of patients with severe benign hepatic disease have elevated CEA levels, most often active alcoholic cirrhosis, and also chronic active and viral hepatitis, and cryptogenic and biliary cirrhosis. Patients with benign extrahepatic biliary obstruction may have increased plasma CEA, the highest in patients with co-existent cholangitis and especially liver abscess. The liver appears to be essential for the metabolism and/or excretion of CEA. Hence, liver work-up is needed to assess any patient with an elevated CEA. A damaged liver may further augment elevated CEA levels due to cancer. The increased circulating CEA observed in some patients with active ulcerative colitis tends to correlate with severity and extent of disease and usually returns to normal with remission. CEA levels also may be mildly elevated in patients with pancreatitis and in adults with colonic polyps. Smoking may contribute to the increased CEA levels seen in patients with alcoholic liver disease and pancreatitis. Therefore, in interpreting mildy elevated circulating CEA levels in patients with GI tract diseases, one must consider benign as well as malignant etiologies.
Cancer 1978 Sep
PMID:Carcinoembryonic antigen (CEA) levels in benign gastrointestinal disease states. 36 Dec

Xipamide (4-chloro-5-sulphamyl-salicylic acid 2', 6'-dimethylanilide) is a diuretic and antihypertensive agent. A clinical trial of the drug was performed in 11 patients, 8 with nephrotic syndrome, 1 with oedema and ascites due to hepatic cirrhosis, and 2 with congestive cardiac failure due to idiopathic cardiomyopathy. The drug proved to be potent, safe and efficacious. Side-effects were similar to those encountered with other thiazide-derived diuretics, but were not of a severe nature. Wider clinical usage of xipamide would appear to be warranted.
S Afr Med J 1978 Sep 30
PMID:Xipamide in the management of renal, hepatic and cardiac oedema. 36 81

As part of a double-blind, randomized, controlled trial to evaluate the effect of colchicine on liver cirrhosis, 43 cirrhotic patients were assigned to either a placebo (20 patients) or a colchicine (23 patients) treatment group. Colchicine 1 mg and an indistinguishable placebo were administered orally on a daily dose 5 days a week. In the colchicine group, 12 were males and 11 females, while in the control group 13 were males and 7 females. The time elapsed between diagnosis and inclusion in the study was 14.1 mo for the controls and 14.5 mo for the patients on colchicine. Mortality related to the liver disease occurred in 4 patients on colchicine and 8 patients on placebo. Although the probability of surviving in the colchicine group was greater than that of the placebo, the difference did not reach statistically significant levels. Of the colchicine-treated patients, in three a remarkable decrease in liver fibrosis was observed in serial biopsies. In two other patients, carcinoma of the liver developed. Six of the survivors on colchicine have improved clinically, noticing disappearance of ascites and edema, as well as a decrease in the size of the spleen. All the survivors on placebo continue to show clinical deterioration. In contrast to the usual drop of serum albumin seen in the cirrhotic patients, those receiving colchicine increased and maintained their serum albumin levels throughout the study. Serum proline values were elevated only in the alcohol cirrhotic patients. Serum alkaline phosphatase increased only in those patients receiving colchicine. The results indicate that in some cases, liver fibrosis could be modified by treatment with antifibrotic drugs. The use of colchicine at present should remain within controlled studies.
Gastroenterology 1979 Sep
PMID:Treatment of cirrhosis with colchicine. A double-blind randomized trial. 37 54

The AA., after the literature revision concerning the autoantibodies in the autoimmune diseases, have examined the cases of acute and chronic hepatitis happened in the period 1972-1976. After a short observation of used methodologies the AA. have connected the presence of autoantibodies (FN, SM, AM) with the rate of immunoglobulins in single groups of liver diseases, divided in acute hepatitis, chronic persistent hepatitis, chronic active hepatitis, liver cirrhosis (cryptogenetic and alcoholic). The results are that while the immunoglobulins fractions increase, although in different manner, in every pattern of liver disease studied, instead, there are no typical changes of single immunoglobulins rate in the groups with autoantibodies. Statistically it is not possible to assert that single antibodies belong to immunoglobulins determinate class. Finally it had been impossible to demonstrate sex and age influence on the immunoglobulins increase in the groups of liver disease with autoantibodies.
Quad Sclavo Diagn 1978 Sep
PMID:[Quantitative alterations of the immunoglobuline classes and the presence of autoantibodies in liver diseases (author's transl)]. 37 4

To clarify further the etiology of the carbohydrate intolerance in idiopathic hemochromatosis, we investigated the glucose, insulin, C-peptide, and glucagon responses to arginine (0.5 g/kg) infused during 30 min in lean normal subjects; in insulin-requiring subjects with hemochromatosis, genetic diabetes, and total pancreatectomy; and in nondiabetic cirrhotic subjects without portosystemic shunting. Serum insulin, C-peptide, and glucagon responses (30K antibody) were determined by RIA, and glucose level was determined by a glucose oxidase technique. Hemochromatotic and genetic diabetic subjects had similar basal glucose (157 +/- 25 vs. 168 +/- 40 mg/dl) and C-peptide (0.73 +/- 0.42 vs. 0.65 +/- 0.22 ng/ml) values, with subnormal C-peptide peak responses to stimulation (1.05 +/- 0.38 and 1.40 +/- 0.83 vs. 3.95 +/- 0.4 ng/ml in normals; P less than 0.05). No glucagon or C-peptide response to arginine was seen in any pancreatectomized subject. Similar but excessive glucagon levels were present in hemochromatosis, diabetes, and cirrhosis under basal conditions (166 +/- 24, 232 +/- 111, and 263 +/- 116 vs. 76 +/- 15 pg/ml; P less than 0.05) and after arginine stimulation (782 +/- 80, 834 +/- 123, and 902 +/- 275 vs. 489 +/- 81 pg/ml; P less than 0.05) when compared with normals. The excessive glucagon levels found in hemochromatosis, diabetes mellitus, and cirrhosis contrast to the absent response in pancreatectomized subjects and indicate that generalized islet cell destruction is not the major factor in diabetic hemochromatotic subjects.
J Clin Endocrinol Metab 1979 Sep
PMID:Pancreatic alpha-cell function in diabetic hemochromatotic subjects. 38 22

The uptake of (125)I albumin microaggregates (U-(125)I-AMA) from portal blood, during a single passage through the hepatic reticuloendothelial system, has been found to be generally decreased in cirrhosis. To investigate if a similar phenomenon occurs for the colloid flowing through the hepatic artery, the U-(125)I-AMA was first calculated in normal dogs after injection of a mixture of (51)Cr red blood cells ((51)Cr-RBC) and (125)I-AMA into the hepatic artery by comparing hepatic indicator dilution curves (IDC) obtained with both indicators. In nine dogs, the U-(125)I-AMA from hepatic artery blood was generally over 90%, as previously reported for the same colloid flowing through the portal vein in another group of normal dogs. This approach was then applied in nine patients with alcoholic cirrhosis who underwent combined umbilicoportal vein, hepatic vein, and hepatic artery catheterisation because of severe portal hypertension. Hepatic indicator dilution curves were obtained in the nine patients after injection of a mixture of (51)Cr-RBC and (125)I-AMA into the portal vein and the hepatic artery. The U-(125)I-AMA from portal and hepatic artery blood was measured by comparing (51)Cr-RBC and (125)I-AMA hepatic IDC. U-(125)I-AMA varied between 5.2 and 90.5% after portal vein injection and between 13.7 and 90.1% after hepatic artery injection; not difference was found between paired values. In all patients the extraction of indocyanine green (E-ICG) was calculated during a continuous infusion and significant correlations were found between E-ICG and U-(125)I-AMA from portal blood (r=0.931; p <0.001) or from hepatic artery blood (r=0.861; p <0.005). The decreased uptakes can be related to intrahepatic shunts or sinusoidal changes responsible for ineffective phagocytosis and restricted access of dye to parenchymal cells. These data indicate that in cirrhosis the hepatic artery and portal vein blood is cleared of colloid and ICG in a similar fashion and suggest nearly identical blood supply to the regenerative nodules by the hepatic artery and portal vein. Thus U-(125)I-AMA from hepatic artery or portal vein blood, as well as the E-ICG, may be used to estimate the functional hepatic blood supply in cirrhosis; this may prove to be useful in the prognosis of patients before portacaval shunts.
Gut 1979 Sep
PMID:Arterial and portal blood supply in cirrhosis: a functional evaluation. 38 41

In cirrhotic patients, the authors studied the modification of the pharmacokinetics of ampicillin in the plasma and in the ascitic fluid, as well as its concentration in the urine. The influence of the jaundice, the ascites and diuretics were studied. In cirrhosis, dilution and elimination of the antibiotic are modified, as is shown by the increase in T 1/2 alpha and T 1/2 beta. These anomalies seem to be due essentially to modifications in the distribution volume; the degree of hepatocellular insufficiency does not appear to be of importance. The ascites acts as an independent compartment, into which the antibiotic's passage in slight. The practical consequences are the following: less frequent injections, increasing of the fractionated doses, in situ injections of ampicillin in cases of infection of the ascitic liquid.
Pathol Biol (Paris) 1979 Sep
PMID:[Metabolism and kinetics of ampicillin elimination in cirrhosis. Therapeutical consequences. (author's transl)]. 38 20

Ninety patients with chronic diffuse liver disease were evaluated with free hepatic venography, wedge hepatic venography, hepatic vein pressure measurements, and liver biopsy. Free hepatic venograms were normal and minimally pruned in patients with hepatic sarcoidosis and fatty liver due to alcohol, and their biopsies showed little or no fibrosis. Pruning of hepatic vein branches on free hepatic venography correlated well with the corrected wedged hepatic vein pressure and with the degree of fibrosis in patients with alcoholic hepatitis, alcoholic cirrhosis, and postnecrotic cirrhosis. Free hepatic venography correlated better with hemodynamic measurements and fibrosis than did wedge hepatic venography. Free hepatic venography is a reliable predictor of the presence and degree of hepatic fibrosis and may be a useful alternative to liver biopsy in patients with clotting disorders.
AJR Am J Roentgenol 1977 Sep
PMID:Hepatic venography and wedge hepatic vein pressure measurements in diffuse liver disease. 40 97

Basal plasma growth hormone (GH) and GH responses after the administration of thyrotropin releasing hormone (TRH) were studied in 9 male alcoholic patients with cirrhosis. Basal GH was significantly higher in cirrhotic patients than in normal men. Intravenous injection of synthetic TRH (400 microgram) caused a significant increase in plasma GH in 7 out of the 9 cirrhotic patients examined, while it did not increase GH levels in normal subjects.
J Clin Endocrinol Metab 1977 Sep
PMID:Elevated basal growth hormone levels and growth hormone response to TRH in alcoholic patients with cirrhosis. 40 28

Serum immunoglobulins were determined in 39 healthy subjects and 55 patients with a variety of acute and chronic liver diseases. Elevation of IgG and IgA was frequently observed in healthy subjects and patients with acute viral hepatitis, liver cancer and miscellaneous liver disorders. IgG and IgM were elevated in cirrhosis of the liver.
J Pak Med Assoc 1977 Sep
PMID:Immunoglobulins in liver disease. 41 44


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