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At least 19 recordsLinked to original sources
PubMed2001

Hepatopulmonary syndrome in poorly compensated postnecrotic liver cirrhosis by hepatitis B virus in Korea.

BACKGROUND: Hepatopulmonary syndrome (HPS) refers to the association of hypoxemia, intrapulmonary shunting and chronic liver disease. But there is no clear data about the prevalence of HPS in postnecrotic liver cirrhosis by hepatitis B virus (HBV), the most common cause of liver disease in Korea. The aim of this study was to investigate the prevalence of HPS in poorly compensated postnecrotic liver cirrhosis by HBV, and the correlation of the hepatopulmonary syndrome with clinical aspects of postnecrotic liver cirrhosis by HBV. METHODS: Thirty-five patients underwent pulmonary function test, arterial blood gas analysis and contrast-enhanced echocardiography. All patients were diagnosed as HBV-induced Child class C liver cirrhosis and had no evidence of intrinsic cardiopulmonary disease. RESULTS: Intrapulmonary shunt was detected in 6/35 (17.1%) by contrast-enhanced echocardiography. Two of six patients with intrahepatic shunts had significant hypoxemia (PaO2 < 70 mmHg) and four showed increased alveolar-arterial oxygen gradient over 20 mmHg. Only cyanosis could reliably distinguish between shunt positive and negative patients. CONCLUSIONS: The prevalence of intrapulmonary shunt in poorly compensated postnecrotic liver cirrhosis by HBV was 17.1% and the frequency of hepatopulmonary syndrome was relatively low (5.7%). 'Subclinical' hepatopulmonary syndrome (echocardiographically positive intrapulmonary shunt but without profound hypoxemia) exists in 11.4% of cases with poorly compensated postnecrotic liver cirrhosis by HBV. Cyanosis is the only reliable clinical indicator of HPS of HBV-induced poorly compensated liver cirrhosis. Further studies are required to determine if the prevalence and clinical manifestations of HPS varies with etiology or with geographical and racial differences.

Adult↗
PubMed1974

A study of carbohydrate metabolism in postnecrotic cirrhosis liver.

Intravenous glucose tolerance, insulin tolerance, tolbutamide, and glucagon tests were carried out in 21 patients with postnecrotic cirrhosis. Based arbitrarily on the bromsulphthalein retention they were divided into group A, nine patients with less impaired liver function, and group B, 12 patients with greater impairment of liver function. Intravenous glucose and insulin tolerances were reduced in both groups. The hypoglycaemic effect of tolbutamide was similar in the controls and in both groups of cirrhotic patients but this was achieved at higher plasma insulin levels in group B indicating resistance of the liver to the effect of endogenous insulin. The blood glucose response to glucagon was markedly impaired in group B patients which is consistent with this hypothesis. In contrast to the insulin response to glucose and tolbutamide, the insulin response to glucagon was reduced in the cirrhotic patients. Fasting human growth hormone and free fatty acid levels were elevated in both groups but they were not considered to be important factors in the production of insulin resistance.

Adult↗
PubMed1982

Down-regulation of insulin receptors in postnecrotic cirrhosis of liver.

Eighteen patients with postnecrotic cirrhosis of liver, including three patients who had had a portosystemic shunt operation, and 19 normal controls were studied. The tests performed included monocyte insulin receptor assay, iv glucose tolerance test, glucagon test, and insulin tolerance test. Insulin resistance was documented by the presence of fasting hyperglycemia and glucose intolerance together with hyperinsulinemia as well as resistance to exogenous insulin. The binding of [125I]insulin to monocyte insulin receptors was significantly decreased in cirrhotic patients compared with that in controls (P less than 0.02), and this was due to a significant decrease in the high affinity association constant (P less than 0.005). There was a significant negative correlation between the fasting insulin level and maximum [125I]insulin binding in cirrhotic patients (r = -0.8; P less than 0.02). Cirrhotics that had had a shunt operation showed a higher fasting insulin level, a greater insulin resistance, and a smaller maximum [125I]insulin binding to insulin receptors than those without shunt. All of these findings suggested a down-regulatory effect of hyperinsulinemia on the monocyte insulin receptors. An impaired glycemic response to glucagon was also found in cirrhotics, the exact mechanism of which remains to be elucidated. However, as the increases in plasma cAMP after glucagon were similar in cirrhotics and controls, the fault apparently did not lie in the glucagon receptor.

Adult↗
PubMed1992

Anamnestic response to hepatitis B vaccine in nonalcoholic liver cirrhosis patients with and without HBV-DNA.

Two methods were used to unveil a possible previous hepatitis B virus (HBV) infection in patients with postnecrotic liver cirrhosis. The anamnestic response to a booster injection of HB vaccine was assessed, and the polymerase chain reaction (PCR) technique for the detection of HBV-DNA in serum and liver tissue, using primers to span the precore and core regions, was employed. Seventeen patients with postnecrotic liver cirrhosis were selected from a population with a high prevalence of HBV infection and were compared with 11 liver cirrhosis patients who were positive for antibodies to surface antigen (anti-HBs) IgG antibodies. All patients were given one dose of HB vaccine into the deltoid muscle, and anti-HBs titers were measured 1 and 4 wk after injection. Three of 17 patients, initially negative for anti-HBs, showed a primary response, with titers of anti-HBs rising from 0 to a maximum of 85 mIU/ml after 4 wk; the rest had no response. Of the 11 patients positive for anti-HBs, of whom nine were also IgG anti-HBs positive, only four had an intense anamnestic response, with anti-HBs titers rising to more than 10 times the initial values (up to 10,800 mIU/ml). Serum HBV-DNA was detected in eight patients in the antibody-negative group and in only one patient in the antibody-positive group (p less than 0.02). None of the four patients with positive anamnestic response had HBV-DNA in the serum. The prevalence of HBV-DNA in the liver was similar in both groups. Absence of HBV-DNA in serum of most patients positive for anti-HBs supports the hypothesis that HBV particles released from the liver may be captured by antibodies in the serum. We conclude that assessment of the anamnestic response to HB vaccine has no diagnostic advantage, compared with direct measurement of conventional HBV serological markers in patients with liver cirrhosis. Moreover, we suggest that this type of immunologic response may not occur when virion-associated HBV-DNA is present in the serum.

Biomarkers↗
PubMedDate not supplied

Prevalence of anti-HCV among Chinese patients with acute and chronic liver disease.

To assess whether the hepatitis C virus plays an important role in Chinese patients with acute and chronic liver disease, antibodies to HCV (anti-HCV) were measured by enzyme immunoassay in 67 patients with type A and B acute viral hepatitis, 165 patients with non-A, non-B (NANB) hepatitis, 438 patients with chronic hepatitis, 200 patients with postnecrotic liver cirrhosis, 72 patients with alcoholic liver disease, 55 patients with non-alcoholic fatty liver, 24 patients with toxic and drug-induced hepatitis, and 20 patients with other chronic liver diseases. Anti-HCV was not detected in sera from patients with type A and B acute viral hepatitis, toxic and drug-induced hepatitis, primary biliary cirrhosis, Wilson's disease, or lupoid hepatitis. The anti-HCV prevalence was found to be highest in patients with NANB hepatitis (59% in sporadic and 73.2% in transfusion-associated), 16.4% in non-alcoholic fatty liver, 5.6% in alcoholic liver disease, 6.8% in chronic hepatitis, and 16% in postnecrotic liver cirrhosis. In patients with chronic hepatitis, the anti-HCV prevalence was significantly higher in HBsAg-negative (15/34, 44.1%) than in HBsAg-positive cases (15/404, 3.7%; P less than 0.0001). The results indicate that HCV is a major agent of NANB hepatitis and plays an important role in HBsAg-negative chronic liver disease in Taiwan.

Acute Disease↗
PubMed1999

A pilot study on the hemodynamic effect of short-term ursodeoxycholic acid therapy in patients with stable liver cirrhosis.

OBJECTIVE: Total serum bile acid concentrations are elevated in individuals with liver disease. Ursodeoxycholic acid (UDCA) therapy in such patients results in a further significant rise in plasma levels to the extent that it becomes the major circulating bile acid. In laboratory animals, bile acids, such as taurocholic acid, have also been shown to possess a diuretic-like action, as they can promote diuresis, natriuresis, and kaliuresis by inhibiting tubular sodium reabsorption. The aim of the present study was to assess the effect of 1 month's UDCA therapy on cardiovascular function in cirrhotic patients. METHODS: Two groups of patients with cirrhosis were studied, six with primary biliary cirrhosis (PBC) and six with postnecrotic liver cirrhosis (PNC). Cardiovascular function was assessed by determination of blood pressure, heart rate, and by two-dimensional and pulsed Doppler echocardiography. RESULTS: In PBC patients, 1 month's treatment with UDCA significantly reduced diastolic volume without changing systolic, diastolic, and mean blood pressures, heart rate, systolic and stroke volumes, ejection fraction, cardiac output, and systemic vascular resistance. In PNC patients, UDCA significantly reduced cardiac output, with a tendency to reduce left ventricular volumes, without any changes in systolic, diastolic, and mean blood pressures. CONCLUSIONS: UDCA caused reductions in diastolic volume in the PBC patients and cardiac output in the PNC patients. Such reductions are not unlike that seen in individuals treated with diuretics. This diuretic-like action deserves further study, particularly in cirrhotic patients who are also being treated with diuretics or show evidence of cardiac myopathy.

Adult↗
PubMed1997

Growth hormone-stimulated insulin-like growth factor (IGF) I and IGF-binding protein-3 in liver cirrhosis.

BACKGROUND/AIMS: The aim of this study was to evaluate the liver's potential to generate insulin-like growth factor (IGF) I and IGF-binding protein-3 (IGFBP-3), following stimulation by human recombinant growth hormone, as a possible marker for liver functional reserve in patients with liver cirrhosis. METHODS: In a pilot study, 15 patients (mean age 56 years) with postnecrotic liver cirrhosis were divided into two groups according to disease severity (Child-Pugh score): Group 1 (n=8) with scores of 5-8 and Group 2 (n=7) with scores of 9-12. Five age-matched healthy subjects served as controls. Human recombinant growth hormone (0.06 mg/kg) was administered subcutaneously on 2 consecutive days. Serum levels of IGF-I and IGFBP-3 were measured before and up to 48 h after human recombinant growth hormone injection. Nutritional status was assessed by the creatinine-height index and was compared to lymphocyte count, body mass index, and muscle arm circumference. RESULTS: Baseline IGF-I levels were significantly lower in patients with cirrhosis than in controls, while no differences were noted between the two patient groups. IGF-I levels increased significantly after rhGH administration to the healthy controls, to a lower degree in Group 1, while no change occurred in Group 2. IGF-I levels at 24 h and beyond correlated significantly with the nutritional status, the Child-Pugh score, and the basal levels of GH-binding protein and IGFBP-3. IGFBP-3 serum levels did not change after rhGH stimulation. CONCLUSIONS: IGF-I generation after GH stimulation may provide a new dimension in the assessment of liver function and nutritional status in patients with liver cirrhosis.

Adult↗
PubMed2001

Erythrocyte creatine as a marker of excessive erythrocyte destruction due to hypersplenism in patients with liver cirrhosis.

OBJECTIVE: Erythrocyte creatine is a sensitive marker of erythrocyte age, and can be used to detect slight and continuous hemolysis. Excessive blood cell destruction caused by increased spleen function is important evidence of hypersplenism. This study evaluates the usefulness of erythrocyte creatine as a sensitive marker of excessive erythrocyte destruction due to hypersplenism in patients with liver cirrhosis. DESIGN AND METHOD: Erythrocyte creatine was determined by an enzymatic method in 50 patients with postnecrotic liver cirrhosis and 50 healthy controls. The spleen size was measured by ultrasonography and expressed as a spleen index. RESULTS: The patients with splenomegaly showed significantly higher erythrocyte creatine than those without splenomegaly (p < 0.005) and healthy controls (p < 0.001), but there was no significant difference in erythrocyte creatine between healthy controls and those without splenomegaly. Fourteen (93%) of the 15 patients with abnormally high erythrocyte creatine (> 1.8 micromol/g hemoglobin) had splenomegaly. There were no significant differences in reticulocyte count between healthy controls and the patients with and without splenomegaly. Erythrocyte creatine showed good correlations with spleen index (r = 0.67; p < 0.001) and reticulocytes (r = 0.63; p < 0.001). CONCLUSIONS: Erythrocyte creatine can be used for predicting erythropoietic status and estimating hypersplenism in patients with liver cirrhosis.

Aged↗