Medical aspects of liver disease. The role of liver biopsy.
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Acute Disease↗
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Vascular liver diseases.
This article reviews the primary circulatory liver diseases, which include Budd-Chiari syndrome, obstruction of the hepatic portion of the inferior vena cava, portal vein thrombosis, sinusoidal obstruction syndrome (veno-occlusive disease), nodular regenerative hyperplasia, and peliosis hepatis. In addition, two systemic cardiovascular diseases that impair hepatic circulation, ischemic hepatitis and congestive hepatopathy, are briefly discussed. A characteristic of the primary circulatory liver diseases is that portal hypertension usually precedes liver dysfunction; however, this is not the case with the primary parenchymal liver diseases, in which liver dysfunction always progresses before portal hypertension is manifested. Significant overlap exists among the diseases and risk factors that predispose patients to the primary circulatory liver diseases, though the pathogenesis of individual diseases varies.
Budd-Chiari Syndrome↗
Liver disease in the geriatric patient.
Normal functioning of the liver does not seem to change significantly in dogs and cats as a result of age. Despite this, older dogs and cats are at greater risk for the development of liver disease. The diagnosis of liver disease is initiated by the veterinarian's suspicion that liver disease might be present, followed by the case history and a physical examination. The initial workup for the older dog or cat with suspected liver disease should begin with a CBC, serum chemistry profile, and urinalysis. This may be followed by a liver function test, radiographic or ultrasonographic imaging studies, hepatic fine-needle aspiration, and, ultimately, liver biopsy.
Aging↗
High prevalence of viral infection in adults with homozygous and heterozygous alpha 1-antitrypsin deficiency and chronic liver disease.
OBJECTIVE: To determine the prevalence of chronic liver disease in adults with homozygous (Pi ZZ) and heterozygous (Pi Z) alpha 1-antitrypsin deficiency and to assess the presence of other possible risk factors for the development of chronic active hepatitis and cirrhosis of the liver in these patients. DESIGN: Cross-sectional study. SETTING: A referral-based university hospital. PATIENTS: Consecutive patients (164) with the Pi ZZ and Pi Z phenotype with and without chronic liver disease. MEASUREMENTS: The presence of antibody to hepatitis C virus (anti-HCV) was determined using an assay incorporating synthetic peptide antigen from capsid protein (United Biomedical [UBI] assay) and a second-generation enzyme immunoassay (Abbott test); the presence of antibody to hepatitis B virus (anti-HBV) was determined using radioimmunoassays incorporating hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg); assays for antinuclear antibody and antimitochondrial antibody (M2 subtype) were also done, and alcohol abuse was assessed by history. RESULTS: Among patients with cirrhosis (32%), 62% were anti-HCV positive by the Abbott test (P = 0.006), and 41% were anti-HCV positive by the UBI assay (P = 0.007). Thirty-three percent of patients with cirrhosis had hepatitis B virus (HBV) infection (P = 0.01); 41% had a history of alcoholism; and 12% had features of autoimmune liver disease. Only five patients (9%) with cirrhosis had no other risk factor for chronic liver disease. Among patients with chronic active hepatitis (7%), 80% were anti-HCV positive by the Abbott test (P = 0.002), and 75% were anti-HCV positive by the UBI assay (P less than 0.001). Thirty percent of patients with chronic active hepatitis had HBV infection (P = 0.023); 18% had autoimmune hepatitis; and 8% abused alcohol. Only two patients (17%) had no additional risk factor for the development of chronic active hepatitis. Among patients with steatosis of the liver (48%), 5% were anti-HCV positive by the Abbott test, and none were anti-HCV positive by the UBI assay; 18% had serologic evidence of past HBV infection, and 28% abused alcohol. Among patients without chronic liver disease (13%), no viral infection could be found; 9% were alcoholics. CONCLUSIONS: Chronic liver disease in patients with alpha 1-antitrypsin deficiency is associated with a high prevalence of viral infection; this infection, rather than alpha 1-antitrypsin deficiency alone, may be the cause of the liver disease in such patients.
Adolescent↗
Bone disorders in cholestatic liver diseases.
Osteopenia is a recognised complication of cholestatic liver diseases (CLD), usually ascribed to metabolic bone diseases such as osteomalacia or osteoporosis, with a prevalence from 10 to 56%, depending on the nature of liver disease. Primary biliary cirrhosis (PBC) is the condition causing osteopenia more frequently, but other cholestatic liver diseases like primary sclerosing cholangitis (PSC), haemochromatosis and alcoholic liver disease are also frequently associated with this disorder. The pathogenesis of bone disease in both adults and children with chronic cholestasis is not completely understood. There has been considerable disagreement regarding the relative importance of osteomalacia versus osteoporosis as the factors leading to osteopenia of liver disease. Osteopenia predisposes to atraumatic fractures, particularly in PBC patients undergoing orthotopic liver transplantation and treated with high corticosteroid doses. Bone mineral density measurement is the best way to assess the presence and severity of osteopenia in CLD patients, while laboratory tests give important information about the metabolic status of the bone. In this review prevalence data, diagnostic tools, pathophysiology and treatment of osteopenia in CLD are discussed.
Adrenal Cortex Hormones↗
Liver disease in women. Alcohol, autoimmunity, and gallstones.
Some liver diseases, such as autoimmune liver disease, affect women far more often than men. Others, such as alcohol-related disease, progress more rapidly in women than in men. An increased index of suspicion will lead to improved diagnosis and earlier treatment of women with liver disease.
Adult↗
Liver transplantation for alcoholic liver disease: a consideration of reasons for and against.
Orthotopic liver transplantation is a clinical procedure that has been accepted widely as the treatment of choice for individuals with advanced chronic liver disease. As such, its application to the important clinical problem of alcoholic liver disease is inevitable. The arguments for and against liver transplantation for individuals with advanced alcoholic liver disease are presented.
Humans↗
Treatment of patients with non-alcoholic fatty liver disease: current views and perspectives.
Non-alcoholic fatty liver disease is considered a component of the metabolic syndrome associated with obesity. Problems still exist concerning non-alcoholic fatty liver disease patients in clinical practice, for example: (a) how to diagnose non-alcoholic fatty liver disease and its type; (b) how to select patients candidate to treatment; (c) how to treat selected patients. Non-alcoholic fatty liver disease includes steatosis and non-alcoholic steatohepatitis, but only non-alcoholic steatohepatitis evolves into cirrhosis and the absolute risk of mortality for non-alcoholic fatty liver disease is low. As yet, no tools, other than liver biopsy, are available to differentiate the various types of non-alcoholic fatty liver disease. Many drugs are, currently, under study to treat non-alcoholic fatty liver disease, even if well-performed trials are until necessary to define the best treatment. At the moment, the entity of the problem and the characteristics of patients frequently put the physician, in clinical practice, to choose the therapeutic approach arbitrarily which is considered more effective for each individual patient. Probably the future will consider the possibility of treating non-alcoholic fatty liver disease with more than one drug, by considering the various aspects and degree of this syndrome. Actually each physician should select the individual treatment on the basis of his/her knowledge and experience, by never forgetting the old saying 'primum non nocere'. However, the epidemiological entity of the problem, the characteristics of the patients, generally young, the frequent lack of clinical evidence of involvement of the liver, are all the factors that require vast well-performed clinical trials in order to define the best therapeutic approach for each individual patient.
Anti-Obesity Agents↗
Comparative allograft histology after liver transplantation for cryptogenic cirrhosis, alcohol, hepatitis C, and cholestatic liver diseases.
BACKGROUND: End-stage liver disease for which no cause can be identified, cryptogenic cirrhosis, is a common indication for liver transplantation. Allograft inflammation and fibrosis have been reported to recur with similar frequencies after liver transplantation for cryptogenic cirrhosis and hepatitis C (HCV). METHODS: We determined sequential posttransplant allograft histology in four groups of recipients: 31 transplanted for cryptogenic cirrhosis, 70 for cholestatic etiologies, 40 for alcoholic liver disease, and 56 for HCV. Modified hepatitis activity index (HAI) and fibrosis stage were determined at 4 months, 1 year, and at most recent biopsy posttransplantation. RESULTS: The prevalence of HAI > or = 2 among cryptogenic recipients was similar to that of cholestatic and alcoholic recipients at 4 months, 1 year, and at most recent evaluation (mean 45+/-17 months posttransplantation). For HCV-infected recipients, the frequency of HAI > or = 2 was more than for cryptogenic recipients at 1 year (52 vs. 29%, P=0.04) and at most recent evaluation (64 vs. 15%, P=0.003). Fibrosis scores for cryptogenic, cholestatic, and alcoholic recipients were similar at all timepoints. The proportion of HCV-infected recipients with fibrosis stage >2 was more than that of cryptogenic recipients at 4 months (29 vs. 12%, P=0.05), 1 years (46 vs. 7%, P=0.0002), and at most recent evaluation (42 vs. 15%, P=0.06). None of the cryptogenic recipients developed cirrhosis. RESULTS: The frequency of elevated HAI and fibrosis stage in recipients who undergo transplantation for cryptogenic cirrhosis is similar to that of recipients who undergo transplantation for cholestatic etiologies and significantly less than that of HCV-infected recipients. Fibrosis stage and HAI are generally stable after transplantation for cryptogenic cirrhosis. These data do not suggest a viral etiology of liver disease in the majority of patients with cryptogenic cirrhosis.
Biopsy↗
De Ritis ratio as diagnostic marker of alcoholic liver disease.
Patients suffering from Alcoholic Liver Diseases (ALD) are often diagnosed by spectrum of physical manifestations and laboratories abnormalities. Among biochemical abnormalities De Ritis Ratio (AST/ALT ratio) is more sensitive during any phase of the disease. This ratio is based on common tests of liver function test and can be investigated in any laboratory and is more relevant in countries like Nepal where alcohol abuse is a major cause of liver disease. Clinically diagnosed 103 ALD cases and 73 healthy controls were enrolled for the study. Selected parameters of liver function tests were analyzed by Vitalab Selectra-2 autoanalyser using Merck diagnostic kits and statistically analyzed by student "t" test. The De Ritis ratio was calculated from serum AST and ALT values and was found 2. 30:1 in patients compared to of 1.10:1 in control group. AST and ALT value showed mild to moderate elevation as it was 124.80 +/- 86.24 IU/L and 54.21 +/- 39.72 IU/L in patients compared to 35.00 +/- 23.49 IU/L and 31.48 +/- 17.79 IU/L in controls. The increase in AST and ALT level in patients was statistically significant (p < 0.001) and (p < 0.01) respectively. > or = - Glutamyl Transferase showed 425.26 +/- 36.40 IU in alcoholics compared to 70.55 +/- 27.35 IU/L in controls, a significant increase observed (p<0.001) However Alkaline Phosphatase activity was observed within normal limit. Serum Total Protein (TPR) and Albumin (ALB) showed 6.86 +/- 1.01 g/dl and 2.71 +/- 0.78 g/dl in patients with Albumin: Globulin ratio of 0.61:1 compared to 7.51 +/- 1.74 g/dl and 4.03 +/- 0.61 g/dl in controls with the ration of 1.15:1, a significant decrease in albumin (p < 0.001) without alteration of Total Protein in patients. Total and Direct bilirubin showed 2.32 +/- 1.10 mg/dl and 1.26 +/- 0.88 mg/dl in alcoholics higher than the control of 1.06 +/- 0.60 mg/dl 0.38 +/- 0.31 mg/dl (p<0.001). Diagnosis of ALD is straight forward with history-and compatible clinical features but alcoholic's denial and under estimation of alcohol abuse becomes an obstacle in confirmation. A mild to moderate disproportionate elevation of AST than ALT activity making De Ritis Ratio > 2:1, supported by reversal of Albumin/globulin ratio facilitates the diagnosis.
Adult↗
Pharmacologic management of nonalcoholic fatty liver disease.
Nonalcoholic fatty liver disease (NAFLD) is an emerging epidemic in Western societies, and therapeutic modalities to treat this condition are needed desperately. Most early treatment studies tended to focus on improvement in the serum aminotransferases. Presently, treatment of NAFLD is aimed at improving the underlying steatosis, necroinflammatory activity, and fibrosis because elevations of the aminotransferases may not accurately reflect these important histologic endpoints. Unfortunately, well-defined treatment options are few,which is largely due to limited experience reported in small, prospective pilot trials. This article focuses on the various therapeutic agents that have been evaluated in the treatment of NAFLD and their efficacy as well as their limitations.
Antihypertensive Agents↗
Bile acids in liver disease associated with inflammatory bowel disease.
To investigate the possibility that bowel-related liver disease is due to accumulation of abnormal bile acids in the enterohepatic circulation, bile acids have been measured in gall-bladder bile and portal blood of patients with chronic bowel disease, none of whom had liver disease. There was no difference in the composition and concentration of bile acids in bile and portal blood compared with control patients. In a second study, serum bile acid composition and concentrations were similar in two groups of patients with liver disease, whether they had bowel disease or not. In a further study, post-prandial serum bile acid concentrations were not elevated in a group of patients with chronic bowel disease, making it unlikely that subcliical liver disease was present. No evidence has been found to support the hypothesis that bowel-related liver disease in man results from the action of abnormal bile acids.
Adult↗
Predicting recidivism after orthotopic liver transplantation for alcoholic liver disease.
With appropriate selection criteria, patients with end-stage alcoholic liver disease who undergo orthotopic liver transplantation have similar graft and patient survivals as patients undergoing transplantation for other causes. However, because of the possibility of recidivism after orthotopic liver transplantation there is still reluctance to transplant alcoholic patients. This study examined the association between pretransplant psychosocial variables and the risk of recidivism after orthotopic liver transplantation. At our institution, 43 patients received orthotopic liver transplantation for the referral diagnosis of alcoholic liver disease from February 1, 1988 to May 1, 1991. This represented 17% of all first transplants (43 of 257) performed during this period. Patients were interviewed before orthotopic liver transplantation by a single psychiatrist and responses to a defined set of questions were entered into a clinical database. All 43 patients diagnosed with alcoholic liver disease and a comparison group of patients transplanted for diagnoses other than alcoholic liver disease received a postoperative questionnaire regarding past and present alcohol use. Patients enrolled in the study all had at least 7 mo of follow-up, with the median follow-up being 21 mo. Eighty-six percent of alcoholic liver disease patients (37 of 43) and 86% of patients in the comparison group (37 of 43) of ALD patients agreed to participate in the study. Nineteen percent of alcoholic liver disease patients (7 of 37) and 24% of patients in the comparison group (9 of 37) admitted to having used alcohol after orthotopic liver transplantation, wtih 8% (3 of 37) and 11% (4 of 37) currently using alcohol, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Assignment of steatotic livers by the Mayo model for end-stage liver disease.
Prognosis after liver transplantation depends on a combination of recipient and donor variables. The purpose of this study is to define an allocation system of steatotic donor livers relative to recipient model for end-stage liver disease (MELD) score. We reviewed 500 consecutive OLT, computing the MELD score for each recipient. Fatty infiltration in grafts was categorized in no steatosis, 10-30%, 30-60% and > or = 60% steatosis. MELD score did not affect preservation injury and graft dysfunction, which were increased with fat content. Recipient and graft survivals lowered when increasing MELD score. Outcome in low-risk recipients (MELD < or = 9) was not altered with steatosis, except those with > or = 60%. Survival functions in moderate-risk recipients (MELD 10-19) were moderately affected with 10-30% steatosis and severely with those with >30. Exactly 30-60% steatotic grafts work poorly in high-risk recipients (MELD > or = 20), and very poorly with > or = 60% steatosis. Prognosis of candidates is optimally influenced when divergence of recipient-donor risks is presented.
Adolescent↗
Improvement of alanine aminotransferase by administration of suplatast tosilate plus ursodeoxycholic acid in patients with resistance to ursodeoxycholic acid monotherapy on hepatitis C virus-related chronic liver disease.
OBJECTIVE: Inflammatory liver damage and viral persistence after hepatitis C virus (HCV) infection are known to be related in host immunity. Suplatast tosilate is an immunomodulator that selectively inhibits type 2 cytokine production by helper T cells. We investigated the efficacy and safety of the administration of suplatast tosilate for patients with HCV infection by examining the level of serum alanine aminotransferase (ALT) and viremia. PATIENTS AND METHODS: Thirty-eight patients who had shown resistance to ursodeoxycholic acid (UDCA) therapy (600 mg/day tid) over 6 months for HCV-related chronic liver disease were randomized into two groups and received UDCA alone (600 mg/day tid) or UDCA (600 mg/day tid) plus suplatast tosilate (300 mg/day tid) by means of sealed envelopes. RESULTS: After 24 weeks, serum ALT was decreased in the patients receiving UDCA plus suplatast tosilate, with the mean reduction being 40.2% (from 132 to 79 IU/l; p=0.001). In the patients receiving UDCA alone, ALT decreased by 8.3% (from 133 to 122 IU/l; ns). Multiple comparison of individual ALT changes showed that the UDCA plus suplatast tosilate achieved significantly greater improvement (p = 0.001). However, serum HCV RNA was unchanged in both groups. Two patients developed adverse reactions to suplatast tosilate, which resolved promptly after the discontinuation of the therapy. CONCLUSION: These findings suggest that suplatast tosilate promotes biochemical improvement in the patients with chronic hepatitis C.
Adjuvants, Immunologic↗
Clinical model for distinguishing nonalcoholic steatohepatitis from simple steatosis in patients with nonalcoholic fatty liver disease.
Nonalcoholic fatty liver disease (NAFLD) encompasses both simple steatosis and nonalcoholic steatohepatitis (NASH). Differentiation of these two entities requires histopathologic evaluation. The aim of this study was to establish a reliable diagnostic model for differentiating steatosis from steatohepatitis utilizing both clinical characteristics and a panel of biochemical markers of lipid peroxidation and fibrosis. Eighty subjects with biopsy proven NAFLD were enrolled, 39 with simple steatosis and 41 with histopathologic evidence of NASH. Demographic and laboratory data to include serologic testing for 8-epi-PGF(2alpha), transforming growth factor-beta (TGF-beta), adiponectin, and hyaluronic acid (HA) were obtained and compared between the two groups. There were significant differences between the two groups with respect to age (P=0.004), female gender (P=0.024), aspartate aminotransferase (AST) (P=0.028), body mass index (BMI) (P=0.003), fasting insulin (0.018), AST/alanine aminotransferase (ALT) ratio (AAR) (P=0.017), quantitative insulin sensitivity check index (QUICKI) (P=0.002), and HA (P=0.029). A composite index for distinguishing steatosis from NASH was calculated by summing the risk factors of age >or=50 years, female gender, AST>or=45 IU/l, BMI >or=30 mg/kg2, AAR>or=0.80, and HA>or=55 microg/l, and its accuracy was determined by receiver operating characteristic (ROC) analysis to be 0.763 (95% CI: 0.650-0.876). The presence of three or more risk factors had a sensitivity, specificity, PPV, and NPV of 73.7%, 65.7%, 68.2%, and 71.4%, respectively. In addition, HA at a cutoff of 45.3 microg/l was a good predictor of advanced fibrosis. In conclusion, we propose a noninvasive screening model for distinguishing simple steatosis from NASH. Identifying patients at risk for NASH will allow clinicians to more accurately determine who may benefit from liver biopsy.
Biomarkers↗
Alcoholic liver disease. An update.
The prevalence and incidence of alcoholic liver disease are constantly evolving. Alcoholic liver disease has a wide clinical spectrum. It may progress to cirrhosis and to end-stage liver disease requiring liver transplantation. The histological manifestations range from steatosis without inflammation to liver cell injury and ultimately to fibrosis and cirrhosis. In some cases, the histological manifestation is steatohepatitis, morphologically characterized by inflammation and necrosis. Currently, although there are no specific tests to establish a diagnosis of steatohepatitis, some serological, radiological, or laboratory tests may be useful. Liver biopsy is useful in confirming a suspected diagnosis and in assessing the extent of parenchymal damage. This review synthesizes the main aspects of the epidemiology, pathogenesis, morphological characteristics, diagnosis, treatment, and prognosis of alcoholic liver disease.
Humans↗
Increased risk of renal dysfunction due to interaction of liver disease and aminoglycosides.
To determine if aminoglycoside use and liver disease interact to cause an increased risk for renal dysfunction, data from 179 hospitalized patients who had been enrolled in a prospective, randomized trial of nafcillin/tobramycin versus cefotaxime were analyzed. The cefotaxime-treated patients served as a control group not receiving an aminoglycoside. Renal dysfunction occurred in seven of 88 (8 percent) given cefotaxime and 37 of 91 (41 percent) given tobramycin (p less than 0.001), in 11 of 29 (38 percent) with liver disease and 33 of 150 (22 percent) without liver disease (p less than 0.08), and occurred in 11 of 15 (73 percent) with both liver disease and tobramycin use and in 0 of 14 (0 percent) with liver disease and cefotaxime use (p less than 0.001). By logistic regression analysis, the relative odds of renal dysfunction developing during tobramycin treatment in a patient were 6.0 (95 percent confidence interval: 3.8 to 9.5). The relative odds of renal dysfunction developing in a patient receiving tobramycin and having liver disease were 31.8 (95 percent confidence interval: 19.7 to 51.4). This analysis demonstrates an interaction between tobramycin use and liver disease for increasing the risk of renal dysfunction.
Aminoglycosides↗