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PubMed1979

Glucocorticoid and mineralocorticoid hormones in chronic liver diseases.

In patients with chronic liver disease a dissociation of the two most important partial functions of the adrenal cortex may be observed. A widening of the zona glomerulosa is associated with an increased aldosterone secretion and an atrophy of the zona fasciculata with a decreased cortisol production rate. In acute alcoholic liver damage there are sometimes remarkable special features concerning the adrenal function. The pathogenesis of the altered C21-steroid hormone metabolism is nonuniform and depends upon the etiology of the liver disease. Following factors may play role: 1. Decreased activity of specific hepatic enzymes a)direct enzyme damage b)indirect enzyme activity decreasing processed by deficiency of hydrogen from NADPH 2. Decreased hepatic blood flow 3. Disturbance of intracellular transport of substrates (e.g. cholestasis 4. Changes of transport proteins. 5. Direct or reactive changes of other factors of hormonal feedback systems (hypothalamus-pituitary-adrenal or gonadal-system; renin-angiotensin-aldosterone-system).

Adrenal Cortex↗
PubMed1981

Ultrasonography of alcoholic liver disease with histological correlation.

In alcoholic liver disease (fatty infiltration, alcoholic cirrhosis), the liver is diffusely abnormal on ultrasound. Changes in size, dilatation of the hepatic veins, and ascites may also occur. The authors conducted a histological correlation of these abnormalities in 22 alcoholic patients and 16 controls, grading the changes on a scale of 0 to 4+ for fat, fibrosis, and necrosis and noting tumor whenever present. Ultrasound detected abnormality in 21 cases (sensitivity = 95%) and correctly identified 15 controls (specificity = 94%). Of the 5 tumors seen, 4 hepatomas were detected and biopsied and 1 metastatic squamous-cell carcinoma was missed. Applications of commercially available A-scan module are considered and its limitations discussed. With the exception of minimal change (1+ fat or fibrosis), ultrasound detected many of the pathological changes seen in alcoholic liver disease.

Adult↗
PubMed1989

Urinary hydroxyproline and hydroxylysine excretions in relation to hepatic hydroxyproline content in chronic liver disease.

In patients with or without various chronic liver diseases, the total urinary excretion of hydroxyproline and hydroxylysine and the hepatic content of hydroxyproline were examined. In 7 patients without liver disease, the urinary excretion of hydroxyproline and hydroxylysine were 10.3 +/- 1.5 and 1.31 +/- 0.21 mmol/mol creatinine, respectively, and the hepatic content of hydroxyproline was 4.9 +/- 0.6 mumol/g of wet liver. In 33 patients with liver disease, the urinary excretion of hydroxyproline and hydroxylysine and the hepatic content of hydroxyproline were increased in proportion to the severity of liver disease. The hepatic content of hydroxyproline showed a significant correlation with the urinary excretion of hydroxyproline and hydroxylysine (r = +0.406 and r = +0.531, respectively). These results suggest that the study of urinary hydroxyproline and hydroxylysine excretion may yield useful information on the metabolism of hepatic collagen in chronic liver disease. Moreover, urinary hydroxylysine excretion seemed to be a better index of hepatic collagen metabolism than urinary hydroxyproline excretion; perhaps urinary hydroxylysine excretion is not much affected by dietary collagen intake.

Adult↗
PubMed2003

[Alcoholic liver disease--established treatment and new therapeutic approaches].

Alcoholic liver disease is the most frequent organ damage encountered in chronic alcoholics and the annual death rate attributed to alcohol-induced end-stage liver disease exceeds that of car accidents. Alcoholic liver damage occurs mainly due to the toxicity of its first metabolite acetaldehyde, and due to interactions with numerous macro- and micronutrients. Established treatment options comprise psychotherapy aiming to achieve abstinence, nutritional therapy, management of hepatological complications, and liver transplantation in selected individuals. Since these therapeutic approaches are unsuccessful in many patients, pharmacological therapies of alcoholic liver disease are being investigated. Many drugs failed to be beneficial or have even shown toxicity. However, some agents are promising, such as S-adenosyl-L-methionine (SAMe), pentoxifylline, metadoxin, polyenylphosphatidylcholine or inhibitors of the cytochrome P450 2E1 isoenzyme. In severely ill patients with alcoholic hepatitis, drugs with anti-tumor necrosis factor alpha activity are currently investigated in clinical trials. If and how far corticosteroids are beneficial remains controversial and their use should be restricted to selected patients. Anabolic steroids used to enhance the nutritional status may lead to serious side effects while having a marginal benefit. Silymarin has not been proven efficacious in alcoholic cirrhosis and clinical trials are ongoing which aim to elucidate its therapeutic value in less advanced stages of liver disease.

Clinical Trials as Topic↗
PubMed2000

Long-term follow-up after liver transplantation for alcoholic liver disease under tacrolimus.

BACKGROUND: Liver transplantation (LTx) for alcohol-related liver disease (ALD) is an accepted modality of treatment and is one of the most common indications for LTx in the United States. The present report examines the long-term patient survival, graft survival, rates of recidivism, and development of de novo cancers in this group, and compares these results with a contemporaneous group of patients who were transplanted for non-ALD indications. METHODS: Between August 1989 and December 1992, 185 adults received LTx for ALD (group I). During the same time interval, 649 adults received LTx for non-ALD (group II). The mean follow-up time was 94+/-10.7 months for group I vs. 92+/-11 months for group II. Kaplan-Meier survival estimates and the incidence of cancers using Surveillance Epidemiologic End Result data were compared in both groups. RESULTS: At 5 years after orthotopic LTx, the overall patient survival and graft survival for group I were 72.0% and 66.5% vs. 66.5% and 60.3% for group II, respectively. After 5 years, the patient survival and graft survival for the alcoholic group were significantly lower (P=0.001) compared to the non-alcoholic group. The rate of de novo oropharyngeal cancer and lung cancer was 25.5 times and 3.7 times higher, respectively, in ALD group compared with the general population matched for age, sex, and length of follow-up (P=0.001), whereas this was not higher in the non-ALD group. Prior pretransplant length of sobriety and alcohol rehabilitation was not associated with the rate of post-LTx rate of recidivism, which was 20%. Out of 79 deaths in group I, only 1 was attributed to recidivism and 3 to noncompliance with recidivism. The other deaths occurred from de novo cancer (n=13), posttransplant lymphoproliferative disorder (n=5), age-related complications (n=23), and other infection or miscellaneous causes (n=34). CONCLUSIONS: Patient and graft survival past 5 years after orthotopic LTx is significantly lower for ALD for a variety of reasons (P=0.001). The rate of upper airway malignances was significantly higher in ALD patients than for non-ALD post-LTx patients and the general public. Graft loss/death related to recidivism or chronic rejection was extremely low. More attention is needed for early diagnosis of de novo cancer and prevention of cardiorespiratory and cerebrovascular complications.

Adult↗
PubMed1999

[Incidence of TT virus infection in patients with non-A to G liver disease].

The sera of patients with liver disease associated with non-A to G hepatitis were examined for the presence of TTV DNA. These patients included 18 cases with AH, 8 cases with CH, 6 cases with LC, 4 cases with HCC, and 36 cases with blood donors. The detection of TTV DNA was performed as described by Nishizawa et al. TTV DNA was detected in 60.0%, 62.5%, 66%, 50%, 28% of the patients with AH, CH, LC and HCC, respectively. Among the patients with AH, the aminotransferases and total bilirubin values were lower in the TTV DNA-positive than -negative patients. Among the patients with chronic liver disease, however, there were no differences in the blood chemistry results between the TTV DNA-positive and -negative patients. The histological study of the liver tissues from a TTV positive patient with CH showed no evidence of necro-inflammatory reaction, although there was evidence of irregular regeneration in the TTV DNA-positive a patient. These results suggest that TTV infection may modify the pathological condition of the liver disease.

Adult↗
PubMed2001

Association between duplex Doppler sonographic flow pattern in right hepatic vein and various liver diseases.

PURPOSE: The aim of this study was to evaluate the association between the Doppler sonographic waveforms in the right hepatic vein and various liver diseases. METHODS: We performed Doppler sonography of the right hepatic vein in 225 individuals (189 patients with liver disease and 36 control subjects). Patients were categorized on the basis of their histologic diagnosis: cirrhosis (n = 122), fibrosis (n = 23), fatty liver disease (n = 11), metastatic liver disease (n = 8), and noncirrhotic liver disease with neither fatty infiltration nor metastases (n = 25). The waveforms of the hepatic veins were categorized as type 1, triphasic; type 2, biphasic; or type 3, flat. RESULTS: Type 1 waveforms were found in 100% of the control subjects and in patients with each of the various liver diseases, including 40% of those with cirrhosis. Type 2 waveforms were not found in control subjects or in patients with either fatty infiltration or metastatic liver disease. Type 2 waveforms were, however, found in 16% of patients with cirrhosis, 13% of patients with fibrosis, and 4% of patients with other noncirrhotic liver diseases. Type 3 waveforms were found in 43% of patients with liver cirrhosis, 13% of patients with liver fibrosis, 27% of patients with fatty liver disease, and 50% of patients with metastatic liver disease. In contrast, type 3 waveforms were not found in any control subjects or in patients with other noncirrhotic liver diseases without fatty liver or metastases. CONCLUSIONS: Type 3 waveforms in the right hepatic vein are suggestive of liver cirrhosis, although they may also occur in patients with fibrosis, fatty liver disease, or metastatic liver disease.

Adult↗
PubMed2004

[Serum interleukin-6 concentrations in patients with alcoholic liver disease].

Serum interleukin-6 concentrations in patients with alcoholic liver disease Pathogenesis of alcoholic liver disease (ALD) is not well defined, but immune mediated hepatic injury is thought to be important. The main aim of this study was estimation of serum concentrations of IL-6 in patients with chronic alcoholic liver disease and determination of correlations between IL-6 serum concentration and occurrence of clinical manifestations, biochemical parameters and a stage of ALD. 85 patients with the diagnosis of chronic ALD and 35 healthy subjects (mached for age and sex) were enrolled into the study. Serum concentration of IL-6 was measured with ELISA. Serum IL-6 concentrations were markedly elevated in the all analyzed groups of patients with ALD when compared with healthy controls. When compared in groups, patients with alcoholic cirrhosis and chronic alcoholic hepatitis had the highest and patients with fatty liver had the lowest serum IL-6 concentrations. In addition, IL-6 concentrations were higher in patients with hepatic encephalopathy than in those without liver failure. Furthermore, we found statistically significant correlation between serum IL-6 and albumin concentrations. High IL-6 concentrations were associated with high mortality in patients with ALD. These findings suggest that IL-6 is an important immunological factor associated with alcoholic liver disease.

Adult↗
PubMed1982

Complement activation in chronic liver disease.

Patients with HBsAg positive chronic active liver disease (CALD) and primary biliary cirrhosis (PBC) exhibit increased C3d concentrations and changes in the serum concentrations of the complement components consistent with activation of the classical and alternative pathways. In these patients the concentrations of the regulatory proteins, C3b inactivator (C3bINA) and beta IH globulin, are normal. Patients with HBsAg negative CALD and alcohol induced liver disease (ALD) exhibit no evidence of an increased level of complement system activation. In these patients diminished serum concentrations of complement components appear to be related to diminished hepatic synthetic function. C4 synthesis may be specifically reduced in autoimmune chronic active liver disease.

Complement Activation↗
PubMed1993

Prevalence and characterization of neutrophil cytoplasmic antibodies in autoimmune liver diseases.

To evaluate the diagnostic significance of neutrophil cytoplasmic antibodies in chronic liver diseases, we assessed the prevalence of neutrophil cytoplasmic antibodies in autoimmune liver diseases, in particular in primary sclerosing cholangitis, autoimmune chronic active hepatitis and primary biliary cirrhosis, and we also determined the specificity of perinuclear-pattern neutrophil cytoplasmic antibodies for these autoimmune liver diseases by testing sera from patients with nonautoimmune chronic liver diseases. Neutrophil cytoplasmic antibodies were detected in 79% of sera from patients with primary sclerosing cholangitis (n = 24), in 88% of sera from patients with autoimmune chronic active hepatitis (n = 24) and in 28% of sera from patients with primary biliary cirrhosis (n = 25). The presence of neutrophil cytoplasmic antibodies in these diseases correlated significantly (p < 0.008) with the presence of cirrhosis. Neutrophil cytoplasmic antibodies were not detected in nonautoimmune liver diseases. All neutrophil cytoplasmic antibody-positive sera produced a perinuclear fluorescence pattern on ethanol-fixed granulocytes. On neutrophils fixed with paraformaldehyde, a granular cytoplasmic immunofluorescence pattern was observed, demonstrating the cytoplasmic nature of the antigen or antigens involved. Further characterization studies showed that neutrophil cytoplasmic antibodies in autoimmune liver diseases are not directed against myeloperoxidase, proteinase 3 or elastase, the neutrophil cytoplasmic antibody specificities associated with necrotizing vasculitis, glomerulonephritis or both. On Western blots neutrophil cytoplasmic antibodies in autoimmune liver diseases showed reactivity with either lactoferrin, a 67/66-kD protein combination or a 40-kD polypeptide. Reactivity with either of these proteins was observed in sera from patients with primary sclerosing cholangitis (38%), autoimmune chronic active hepatitis (17%) and primary biliary cirrhosis (20%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2005

Long-term management of alcoholic liver disease.

Despite the epidemics of viral hepatitis C and nonalcoholic fatty liver disease, alcohol remains one of the major causes of liver disease. Commonly, hepatitis C and other liver diseases are found in association with alcohol consumption. This association in many instances is noted to accelerate the progression of liver disease. In many respects, the long-term management of alcoholic liver disease is not dissimilar from the long-term management of patients with cirrhosis from other etiologies. One major element is the abstinence of alcohol use. The ability to maintain sobriety has a major impact on the outcome of patients with alcoholic cirrhosis because maintaining abstinence can lead to significant regression of fibrosis and possibly early cirrhosis. Similarities in managing patients with cirrhosis due to alcohol or cirrhosis from other causes include vaccination to prevent superimposed viral hepatitis and screening for esophageal varices and hepatocellular carcinoma with subsequent appropriate therapy.

Adrenal Cortex Hormones↗
PubMed1995

Combined liver and kidney transplantation in patients with chronic nephritis associated with end-stage liver disease.

A variety of renal diseases can be associated with end-stage liver diseases requiring orthotopic liver transplantation (OLT), including cirrhosis-associated glomerulonephritis (GN), and nephropathy unrelated to the liver disease. A retrospective survey showed that nine patients undergoing liver transplantation in our centre had histologically proven GN or interstitial nephritis with renal failure and/or nephrotic-range proteinuria, and experienced severe complications post-OLT since nephrotoxic immunosuppressive drugs (CsA and FK506) could not be adequately given. Four of the nine patients died. Therefore, combined liver-kidney transplantation has been suggested as first choice treatment in such patients. From January 1990 to February 1994, in patients with end-stage liver disease referred for OLT, and who presented with unexplained renal function impairment and/or significant proteinuria, severe nephropathy was confirmed by renal biopsy in nine: four mesangiocapillary GN with immune deposits, one membranous nephropathy, two diabetic glomerulosclerosis and two interstitial nephritis. All underwent liver transplantation immediately followed by kidney transplantation. The postoperative period was uneventful, and neither death nor renal failure were recorded. Combined transplantation resulted in all patients in the normalization of renal function, and in the disappearance of proteinuria within the first postoperative month. From 6 months to 4 years post-transplant, the renal function remained within normal ranges in all patients. Routine renal transplant biopsy was performed in two patients with pre-transplant cirrhosis-associated GN, and showed no evidence of recurrence of the original nephropathy. We conclude that combined liver-kidney transplantation is an adequate therapeutic option in patients with end-stage liver disease associated with advanced kidney disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1981

Platelet lipid composition and platelet aggregation in human liver disease.

Abnormal plasma lipoproteins in patients with liver disease are associated with an increase in erythrocyte cholesterol concentration and a raised erythrocyte cholesterol/phospholipid molar ratio. We hypothesized that their platelets would also have an increased cholesterol/phospholipid ratio and that this might affect aggregation in vitro. Platelet aggregates by adrenaline and ADP was measured in 34 patients with a variety of liver diseases and in 20 normal subjects and the values were related to platelet lipid composition. The platelet cholesterol/phospholipid ratio was 13% higher in the patients and correlated closely with erythrocyte cholesterol/phospholipid ratio. Platelet aggregation was reduced in most of the patients and inversely correlated with the cholesterol/phospholipid ratio. Cross-incubation and hemostasis studies indicated that there were no inhibitory factors present in the plasma; the defect was in the platelets. In contrast, other workers have shown that cholesterol-rich platelets, either from patients with Type IIa hyperlipoproteinemia or prepared in vitro, aggregate more readily than normal platelets. However, the phospholipid and fatty acid compositions of our patient platelets were also abnormal: the lecithin/sphingomyelin ratio was increased and was inversely correlated with aggregation; the proportion of arachidonic acid was decreased and positively correlated with the aggregation. In our patients with liver diseases the effects of the altered phospholipid and fatty acid composition presumably overrode those of the increased cholesterol content so that instead of enhanced aggregation, only reduced or normal aggregation was seen. We conclude that the reduced platelet aggregation seen in liver disease may reflect a decrease in arachidonic acid availability for prostaglandin and/or thromboxane production.

Blood Platelets↗
PubMed1982

Clinical aspects of bile acid metabolism in liver diseases.

For a long time, it has been assumed that the liver plays an important role in the formation and excretion of bile acids and that the metabolism of bile acids, therefore, can be disturbed to some extent in liver diseases. Pathophysiological aspects of the disturbed metabolism of bile acids remained obscure at the time when procedures of qualitative and quantitative analyses, identification and estimation of bile acids began to be utilized in practice 20 years ago. Since then, the metabolism of bile acids has been clarified in individuals under normal as well as pathological circumstances. Because of a functionally and morphological close relation between hepatic epithelial cells and the metabolism of bile acids, the pathophysiological aspects of the disturbed metabolism of bile acids in parenchymatous inflammatory diseases of the liver, fatty liver, cholestasis and primary hepatocellular carcinoma are attracting considerable attention. First applied to the measurement of human bile acids in blood plasma in 1965, gas-liquid chromatography has been utilized as a standard method in medical practice. Recently, radioimmunoassay and enzyme linked radioimmunoassay have been utilized. This progress in the estimation of bile acids has awoken our interest in the pathophysiological significance of bile acids in liver diseases. The author reviewed the information on bile acid metabolism in liver diseases which has been reported up to the present.

Bile Acids and Salts↗
PubMed2003

Alcohol in alcoholic liver disease is a causative factor for development of allergic skin manifestations.

BACKGROUND: We frequently observed allergic skin reactions in patients with documented history of alcoholic liver disease (ALD). To assess the potential association between alcohol-induced liver damage and urticaria a prospective randomized trial investigating immunologic parameters in various stages of alcoholic liver disease was designed. Fifty patients were available for analysis. METHODS: By means of a multivariate discriminant analysis seven out of a number of laboratory and clinical parameters (level of serum proteins, serum globulins, gamma globulins, albumin/globulin ratio, and immunoglobulins A, E, and G) have been found important for analysis. They were compared with age, general clinical status, degree of progression of alcoholic liver disease, and frequency of appearance of type I skin reactions. Results were further processed by means of logistic general linear models, Chi-square test, and summarized in a structural equation model. RESULTS: Alcoholic liver disease does not influence IgA, IgG, and A/G Index directly, but it increases levels of IgE. About 13% of variance of IgA, IgG, and A/G Index are affected by group membership only in non-alcoholic liver disease, and 27% of variance of IgE can be explained by alcoholic liver disease. There were striking differences in IgE content between alcoholic liver disease and control groups. Degree of liver disease had a negative impact on A/G Index, and on IgA, and a positive on IgG. About 16% of variance can be explained by degree of liver disease. IgE is not degree related. Alcoholic liver disease as a disease was found as the most important predictor of skin reactivity (p = 0.0046). Of all immunologic parameters investigated IgE followed by A/G Index was found as the most significant predictor of allergic skin reactions. The extent of alcoholic liver disease plays not a role in allergic skin manifestations. Alcoholic nature of liver disease itself is a significant factor causing allergic skin reactions (p = 0.0002), but alcoholism itself as an independent factor contributes to increased incidence of skin allergies. CONCLUSIONS: Alcoholic liver disease plays an important role in development of type I allergic skin manifestations. This effect has a direct mechanism through alcohol itself, and an indirect through elevation of IgE. Alcohol in liver disease and not liver disease causes immunologic abnormalities and accounts significantly for increased appearance of allergic skin reactions regardless of the extent of underlying liver disease.

Adult↗
PubMed2002

Increased rate of bone loss at the femoral neck in patients with chronic liver disease.

OBJECTIVE: Patients with chronic liver disease (CLD) have an increased prevalence of osteoporosis. The aim of this study was to evaluate prospectively the rate of bone loss and potential predictors of increased bone loss in a cohort of patients with CLD. DESIGN: Bone mineral density (BMD) was measured at baseline and at follow-up by dual-energy X-ray absorptiometry at the lumbar spine and the femoral neck. RESULTS: Forty-three patients (31 female, 12 male) were available for a second measurement of BMD, with a median of 25 months (range 18-41) between the measurements. Mean annual bone loss at the lumbar spine and the femoral neck, respectively, was 0.6 +/- 2.0% and 1.5 +/- 2.4% in females and 0.8 +/- 1.9% and 2.9 +/- 2.0% in males. The BMD Z score decreased significantly over time at the femoral neck (P = 0.005 and P = 0.02 for females and males, respectively). Bone loss was increased significantly at the lumbar spine in patients classified as Child-Pugh B + C compared with those classified as Child-Pugh A (P = 0.04). Serum levels of bilirubin correlated independently and positively, and 25-hydroxy vitamin D3 levels negatively, with bone loss at the femoral neck. CONCLUSIONS: Patients with CLD have increased bone loss at the femoral neck. Advanced liver disease is associated with increased bone loss, and hyperbilirubinaemia and low levels of vitamin D3 are predictors of increased bone loss.

Adult↗
PubMed1992

Pathogenesis of pancreatic perilobular necrosis in patients with liver disease.

We often see perilobular necrosis of the pancreas in patients with liver disease at autopsy. This study was undertaken to determine the frequency and the mechanism of development of pancreatic perilobular necrosis in patients with liver disease. Pancreatic perilobular necrosis was seen in 21 per cent of 261 autopsied patients: in 41 per cent of 73 autopsied patients with liver disease and in 13 per cent of 188 autopsied patients without liver disease. Moreover, splanchnic congestion was present in 90 per cent of 30 pancreatic perilobular necrosis patients with liver disease. These data indicate that patients with liver disease develop perilobular necrosis of the pancreas more often than patients without liver disease, and that the high frequency may be a sequela of splanchnic congestion; that is, congestion of the pancreas and endotoxaemia due to congestion of the gut.

Adolescent↗
PubMed1982

Diagnostic and prognostic value of laboratory tests assessed in a follow-up study of 200 patients with liver disease.

Two hundred patients with liver disease were re-studied after six to eight years. The initial routine diagnosis (mainly based on morphological criteria) was confirmed in almost 80% of cases of chronic liver disease. In chronic active hepatitis, agreement was found in 86%. An alternative classification based on cluster analysis of clinical chemical results from the first admission was also to a great extent confirmed by the follow-up study. Discriminant analysis of clinical chemical data correctly allocated 94% of patients with alcoholic cirrhosis (who had low haptoglobin and albumin) into groups with different prognosis. Clinical chemical results differed between verified and non-verified cases of primary biliary cirrhosis. By retrospective examination , we found that 15 of 16 patients with this disease or chronic active hepatitis who were initially misclassified by biopsy findings could be correctly diagnosed by discriminant analysis of clinical chemical results.

Biopsy↗