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PubMed1994

Amount and duration of alcohol intake in patients with chronic liver disease: an Italian multicentre study. AISF Group for the Study of Alcohol and Liver Disease.

We report the results of an Italian multicenter study aimed at measuring retrospectively the lifetime amount and duration of alcohol consumption in non-selected consecutive patients with chronic liver disease. We used a standardized, reproducible questionnaire for measuring the lifetime daily alcohol intake (globally and separately for wine, beer and spirits), total alcohol intake and duration of alcohol consumption in 1,258 patients recruited from 17 medical centers. Wine intake contributed to the total alcohol intake in a proportion ranging from 44% to 85% throughout the centers. Spirits and beer intake contributed in smaller proportions (15% to 56%; and 3% to 27%, respectively). Males showed higher alcohol intake: those from northern-central Italy showed significantly higher intake than their southern-insular counterparts; of these, younger patients also showed a higher alcohol intake, due to a higher beer and spirit intake. Older patients showed higher intakes in southern-insular Italy, whereas the opposite was found in northern-central Italy. In this area, a longer duration of alcohol consumption was found, reflecting an earlier start in the use of alcohol. In conclusion, we believe that measuring alcohol intake on a wide series of patients in a multicenter study is feasible. This should stimulate gastroenterologists to approach the relationship between alcohol and liver disease using standardized and epidemiologically correct methods, and form the basis for well-designed case-control studies on a large scale, aimed at clarifying the risk of both hepatic and extrahepatic diseases associated with alcohol intake.

Alcohol Drinking↗
PubMed2000

Molecular pathogenesis of liver disease: an approach to hepatic inflammation, cirrhosis and liver transplant tolerance.

The hallmarks of chronic liver diseases are chronic inflammation, cellular damage, regeneration and fibrosis. An appreciation of intrahepatic molecular expression patterns in normal and diseased liver provides clues for understanding pathogenic pathways whilst studies of the structure and function of molecules implicated in liver disease provide insights into their potential as therapeutic targets. We have examined the expression, function, molecular structure and structure-function relationships of type IV dipeptidyl aminopeptidases. In particular, the roles of CD26/DPPIV in T-cell proliferation and chemotaxis and of fibroblast activation protein in human cirrhosis are discussed. We have investigated the pathogenesis of liver disease by characterising patterns of cytokine and growth factor expression in experimental and human cirrhosis. We have quite recently expanded this approach to use differential gene expression analyses to elucidate overall pathways of gene activation and suppression in human cirrhosis. In addition, our detailed molecular and cellular studies of the mechanisms of spontaneous liver transplant tolerance have generated novel insights into this process. This review touches on these diverse aspects of liver function and disease.

Adenosine Deaminase↗
PubMed1992

Peritoneal dialysis in end-stage renal disease patients with preexisting chronic liver disease and ascites.

PURPOSE: Hemodialysis in patients with chronic liver disease and ascites may be complicated by intradialytic hypotension, limiting the amount of ultrafiltration and resulting in massive ascites. Successful maintenance peritoneal dialysis (PD) has not been previously reported as an alternative to hemodialysis in this population. PATIENTS AND METHODS: Nine patients with chronic renal failure, chronic liver disease, and tense ascites prior to beginning PD are described. All chronic PD catheters were placed percutaneously by the nephrology staff. Seven patients were maintained primarily on continuous ambulatory peritoneal dialysis, whereas two were on intermittent peritoneal dialysis. RESULTS: PD catheters were placed without serious hemorrhage or bowel injury. PD provided adequate clearance and volume maintenance for each patient. Fifteen episodes of peritonitis occurred in 18 patient-years of PD. All episodes of peritonitis were successfully treated with intraperitoneal antibiotics without catheter removal. Only one patient had a decline in the serum albumin level of 0.5 g/dL or more during the course of chronic PD. Three of the nine patients are still alive and on PD for durations of 18 to 24 months. One patient insidiously developed sclerosing peritonitis after 8 years on PD and is now on hemodialysis, and another patient switched to hemodialysis because she was no longer able to care for herself or to manage her PD. Four patients died while maintained on PD; three deaths were due to complications of liver failure within the first 4 months of PD and the fourth was due to empyema after 4 years of PD. CONCLUSION: PD can be used successfully to treat chronic renal failure in patients with chronic liver disease and ascites when the liver disease itself is not rapidly fatal. PD may be better tolerated than hemodialysis and perhaps should be the renal replacement treatment of choice in these patients.

Ascites↗
PubMed1991

[Positive rate of serum anti-HCV in various liver diseases and the clinico-pathological study of chronic liver disease in alcoholics].

The aim of this study was to elucidate the positive rate of serum anti-HCV in alcoholic (with negative HBsAg and without blood transfusion history) and non-alcoholic (type-B and type-NANB) patients with chronic liver diseases. The clinico-pathological difference between anti-HCV positive and negative alcoholic patients was also investigated. Anti-HCV (Chiron C-100-3) was assayed with Ortho EIA kit in 196 patients. Liver function tests and the histological findings were evaluated in 111 cases of chronic hepatitis (CH) and 39 of liver cirrhosis (LC). Following results were obtained. [1] Positive rate of serum anti-HCV in alcoholic patients was 40% in CH, 36% in LC and 100% in hepatocellular carcinoma. In non-alcoholic type-NANB group, it was 75%, 68% and 69%, respectively. [2] Serum GGT/ALT ratio was higher in anti-HCV negative patients than positive patients both in CH and LC alcoholics. In non-alcoholic group, it was higher in type-NANB patients than type-B patients. [3] Among the histological findings in CH alcoholics, lymph follicles in the portal area were characteristic in anti-HCV positive patients, while these were not seen in negative patients. [4] In LC alcoholics, regenerative nodules were irregular in size in anti-HCV positive patients, while these were even and small in negative patients. [5] Serum HCV-RNA was detected in two out of 14 anti-HCV negative patients. [6] A female alcoholic patient who showed positive serum anti-HCV and negative HCV-RNA was presented. [7] For the evaluation of the influence of HCV in alcoholics, further studies have to be continued with more sensitive HCV markers.

Adult↗
PubMed1995

The frequency of 4977 base pair deletion of mitochondrial DNA in various types of liver disease and in normal liver.

Using a polymerase chain reaction (PCR) method, we tested for the hepatic mitochondrial DNA (mtDNA) deletion in 40 hepatic tumors (28 hepatocellular carcinomas [HCCs], 9 other malignant tumors, and 3 benign tumors) and in the livers of 71 patients, including 16 pediatric patients with end-stage liver disease who underwent living related donor liver transplantation and 16 liver donors. A 4977 base pair (bp) deletion of mtDNA was detected in 36 of 55 specimens of non-tumor portions of adult liver (65.5%). However, none of the specimens obtained from cirrhotic livers of the 16 pediatric patients younger than 13 years of age had the 4977 bp deletion. The frequency of mtDNA deletion was significantly decreased compared with normal liver in HCCs (7 of 28) and other malignant liver tumors (2 of 9). The frequency of this deletion was unrelated to the presence of liver cirrhosis, patient's gender, hepatitis B virus surface antigen status, and hepatitis C virus antibody status.

Adolescent↗
PubMed2004

Liver disease in pregnancy.

Liver dysfunction during pregnancy can be caused by conditions that are specific to pregnancy or by liver diseases that are not related to pregnancy itself. This review attempts to summarize the epidemiology, pathophysiology, and management of the different pregnancy-related liver diseases, and to review different liver diseases not related to pregnancy and how they may affect or be effected by pregnancy. Some of the liver diseases specific to pregnancy can cause significant morbidity and mortality both to the mother and to the fetus, while most of the liver diseases not specific to pregnancy do not have a deleterious effect on the pregnancy itself.

Female↗
PubMed1976

Alpha 1-antitrypsin deficiency and infantile liver disease.

Infantile liver disease with deficiency of serum alpha1-antitrypsin is illustrated by a description of the clinical, biochemical, and pathological findings in two affected families. The simplicity of the diagnostic tests is emphasized. Review of 61 biopsies of liver from children and adolescents provided a further 3 cases. It is prudent to exclude this metabolic defect in children with a history of "neonatal hepatitis".

Child↗
PubMed2000

Isolated liver transplant and sequential small bowel transplantation for intestinal failure and related liver disease in children.

Liver dysfunction is a well-recognized complication of intestinal failure in children. Advances in total parenteral nutrition (TPN) have allowed these children to survive while their intestinal tract gradually adapts. Unfortunately TPN may lead to cholestatic liver disease particularly in the young children. Progression of liver disease is associated with a poor prognosis and is an indication for small bowel transplantation. We report our experience of orthotopic liver transplantation in four children with short gut and sequential liver and small bowel transplantation in one child. All children had TPN-related liver failure. Causes of intestinal failure included necrotising enterocolitis (n=2), gastroschisis (n=1), intestinal atresia (n=1), and megacystic, microcolon syndrome (n=1). At the time of liver transplantation the children's mean age was 10.9 months (2.5-24) and weight 6.7 kg (4.8-10.1). The mean serum bilirubin was 522 micromol/liter (299-823), aspartate transaminase 423 IU/liter (49-1024) and international normalized ratio 2.8 (2-3.9). There were two deaths both from respiratory failure secondary to adenovirus pneumonia including the child who received a sequential small bowel transplant. Three children with isolated liver grafts are alive and off TPN at 20 months (mean) follow up (range 6-35). Isolated orthotopic liver transplantation has a role in selected children with intestinal failure, particularly those with short but normally functioning gut and progressing with satisfactory intestinal adaptation but developing liver disease. Those children with TPN-related liver disease and unadapted gut or irreversible intestinal disease need combined liver and small bowel transplantation. Sequential small bowel transplantation is feasible after orthotopic liver transplantation and may provide an option for the child with terminal liver and small bowel failure.

Adolescent↗
PubMedDate not supplied

Tolerance of chronically-diseased liver to prolonged hemihepatic ischemia during hepatectomy.

Seventeen patients with chronic liver disease underwent prolonged warm ischemia of hemi-lobe during liver resection. Those included 15 cirrhotic patients and two with chronic hepatitis. The hemi-hepatic ischemia was carried out with a liver clamp. The normothermic liver ischemia time of 40 to 70 minutes (53.8 +/- 10.4 minutes, mean +/- SD) were tolerated well with an acceptable postoperative course and no mortality. The liver with cirrhosis or chronic hepatitis can tolerate a hemi-hepatic ischemia of up to 70 minutes for patients with no high-risk factors.

Aged↗
PubMed1999

[Biochemical markers of fibrogenesis in liver diseases].

Chronic liver disease evaluation is a very complicated process requiring complex assessment of numerous liver functions. In addition to standard methods of investigation we perform biotransformation liver tests for evaluation of microsome enzyme system. Markers of fibrogenesis represent modern noninvasive tests for fibrotic liver process detection in different diseases. The key role in the process of fibrogenesis have the adipose liver cells (ITO cells) producing collagen I, III, IV and lamilin. These cells may be transformed into myofibroblasts-like cells under specific conditions. Kupffer cells and monocytes produce substances stimulating the proliferation and transformation of liver ITO cells as also proteoglycans and hyaluronic acid synthesis. Mediators of this fibrogenetic activity are platelet derived growth factor (PDGF), transforming growth factors alpha and beta, lymphokines and monokines released by T-lymphocytes and macrophages, interleukin 1-alpha and interferon-tau. Acetaldehyde and its metabolites are important stimulators of collagen production by liver fibroblasts. The most often used markers of hepatic fibrogenesis are the following: procollagen III peptide, procollagen IV. type (one of its end carboxypeptide chains is determined-either with 7s collagen or NC1), hyaluronic acid, fibronectin, tenascine and unduline. As the most sensitive markers of fibrinogenesis are considered: hyaluronic acid, laminine, procollagen IV. type. Less often used are enzymes participating in collagen synthesis: prolyl-4-hydroxylase,lysyl-hydroxylase, galactosyl-hydroxylysyl-glucosyl-transferase, monoaminooxidase and N-acetyl-beta-D-glucoseaminidase. Breakdown of collagen is a multienzymatic process, catalysed by collagenases and other proteolytic enzymes. Decreased activity of collagenase is a supporting factor of cirrhosis development. Cirrhosis may be connected also with the levels of inhibitors such as e.g. serum/tissue? inhibitor of metalloproteinase. Biochemical markers of fibrogenesis are useful in regular monitoring of disease development and treatment effectivness and should be an inseparable part of progression assessment in all chronic hepatopathies. (Fig. 3, Ref. 49.)

Chronic Disease↗
PubMedDate not supplied

Chronic liver diseases for the risk of hepatocellular carcinoma: a case-control study in Japan. Etiologic association of alcohol consumption, cigarette smoking and the development of chronic liver diseases.

BACKGROUND/AIMS: A great number of hepatocellular carcinoma (HCC) develop from chronic liver disease. Among a total of 23,000 deaths of HCC in 1988 in Japan, 82% had positive antibodies against HBV and/or HCV. In the present study we investigated the etiological factors involved in this process, employing patients with chronic hepatitis as controls. METHODOLOGY: In this study, alcohol consumption and cigarette smoking were investigated in 104 male patients with HCC which developed from chronic liver disease and 104 male controls with chronic liver disease without HCC (one for each case) matched for age. RESULTS: When compared with non-drinkers and non-smokers, the relative risk (RR) for developing HCC rose to 17.9 among those with both drinking and smoking habits. The risk was greater than for those in whom either habit existed alone. The RR decreased among ex-smokers who were non-drinkers or ex-drinkers, but it was still as high as 9.4. For current smokers, even if they were non- or ex-drinkers, the RR was 15.4. CONCLUSIONS: Drinking and the cigarette smoking were both risk factors, but the existence of synergism between them was also suggested. Therefore, patients with chronic liver disease should be thoroughly counseled to refrain from both drinking and smoking.

Alcohol Drinking↗
PubMed1999

[Pediatric liver diseases].

Pediatric liver diseases usually manifest as jaundice, hepatomegaly, ascites or edema and can reflect a metabolic or nonmetabolic condition. In unconjugated hyperbilirubinemia, hemolysis can be distinguished from transient or inherited glucuronidation deficiencies. Jaundice with conjugated hyperbilirubinemia should suggest extrahepatic bile duct obstruction (requiring immediate surgery) or intrahepatic mechanical or metabolic cholestasis. Hepatomegaly or hepatocellular necrosis suggests diseases characterized by hepatocyte damage or overload. Appropriate investigations and a painstaking physical examination are essential to establish the diagnosis and to identify the cause, since immediate treatment is needed in some cases.

Cholestasis↗
PubMed2005

Dysregulated cytokine metabolism, altered hepatic methionine metabolism and proteasome dysfunction in alcoholic liver disease.

Alcoholic liver disease (ALD) remains an important complication and cause of morbidity and mortality from alcohol abuse. Major developments in our understanding of the mechanisms of ALD over the past decade are now being translated into new forms of therapy for this disease process which currently has no FDA approved treatment. Cytokines are low molecular weight mediators of cellular communication, and the pro-inflammatory cytokine tumor necrosis factor (TNF) has been shown to play a pivotal role in the development of experimental ALD. Similarly, TNF levels are elevated in the serum of alcoholic hepatitis patients. Abnormal methionine metabolism is well documented in patients with ALD, with patients having elevated serum methionine levels, but low S-adenosylmethionine levels in the liver. On the other hand, S-adenosylhomocysteine and homocysteine levels are elevated in ALD. Recent studies have documented potential interactions between homocysteine and S-adenosylhomocysteine with TNF in the development of ALD. Altered proteasome function also is now well documented in ALD, and decreased proteasome function can cause hepatocyte apoptosis. Recently it has been shown that decreased proteasome function can also act synergistically to enhance TNF hepatotoxicity. Hepatocytes dying of proteasome dysfunction release pro-inflammatory cytokines such as Interleukin-8 to cause sustained inflammation. This article reviews the interactions of cytokines, altered methionine metabolism, and proteasome dysfunction in the development of ALD.

Cytokines↗
PubMed1990

Fibrinolysis and fibrinogenolysis in liver disease.

Patients with liver disease frequently have hemostatic abnormalities which include accelerated fibrinolysis. In order to assess the fibrinolytic state in liver disease, plasma levels of fibrinogenolysis products (FgDP), fibrinolysis products (FbDP), and fibrinogenolysis plus fibrinolysis products (TDP) were measured with newly developed enzyme-linked immunosorbent assays based on monoclonal antibodies in 36 patients with liver disease (six patients with acute hepatitis, seven with chronic hepatitis, ten with liver cirrhosis, 11 with hepatocellular carcinoma, and two with intrahepatic cholestasis). As compared with healthy subjects, mean plasma levels of FbDP (1,083 +/- SD 1,254 vs. 236 +/- 100 ng/ml, P = 0.005) and TDP (1,773 +/- 1,814 vs. 669 +/- 212 ng/ml, P = 0.001) were significantly elevated in patients with liver disease, whereas FgDP was normal (389 +/- 202 vs. 396 +/- 132 ng/ml, P = 0.87). Plasma FbDP correlated very well with TDP (r = 0.986, P less than 0.00001) in liver disease. In addition, FbDP and TDP but not FgDP correlated with plasma concentrations of thrombin-antithrombin III complex. When plotted by the disease categories, the magnitude of elevations of FbDP and TDP was the most prominent in acute hepatitis followed by hepatocellular carcinoma. These findings indicate that activation of fibrinolysis occurs following thrombin generation, but increased primary fibrinogenolysis is rare in liver disease.

Antithrombin III↗