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PubMed1987

[Diagnostic potentials of computed tomography in focal liver diseases].

98 patients with focal liver diseases were examined by computer tomography: 29 patients with primary liver cancer, 44 patients with liver metastases, 16 patients with liver cysts, 4 patients with hemangioma and 5 patients with liver abscess. In 92.9% of the patients examined the computer tomographic examination gave accurate information about the focal liver disease. Only in 7 patients (7.1%) the examination failed. The characteristics of the liver changes found by computer tomography in primary liver cancer, liver metastases, cysts, hemangioma and liver abscess are discussed as well as the factors for the failure of the examination.

Carcinoma↗
PubMed2006

Molecular diagnosis of chronic liver disease and hepatocellular carcinoma: the potential of gene expression profiling.

Gene expression profile analysis through DNA microarrays and other high-throughput technologies permit simultaneous investigation of all genes within a biologic sample, providing a snapshot of the transcriptional state of healthy or diseased tissue. Although most of the current applications are still geared toward research (study of disease mechanisms/signaling pathways involved, identification of novel oncogenes/tumor suppressor genes), clinical diagnostic applications of this approach are beginning to enter more routine molecular usage. There are clear examples where a group of genes, or "signature," can provide clinically useful information (e.g., cancer prognosis and response to treatment). Importantly, the identification of genes that are up-regulated during tumorigenesis is heralding a new era of targeted molecular therapies in oncology. In addition, the high capacity of the technologies available allow for the identification of new biomarkers for early diagnosis. In the future, gene expression profiling ("disease fingerprinting") is likely to complement liver biopsy in the molecular differential diagnosis of chronic liver diseases and hepatocellular carcinoma (HCC). There has already been some success in the identification of subtypes of HCC based on derived sets of signature gene clusters. Data recently reported have been able to provide the first molecular classification of HCC, although more comprehensive studies are required to confirm these results and translate them into the clinical practice. In fact, variations in gene expression in normal and diseased livers, as well technical factors, are obstacles to the routine use of microarray-based methods in the liver clinic. Continued progress is anticipated in the practical application of gene array methods to refine diagnosis and therapy of HCC.

Carcinoma, Hepatocellular↗
PubMed1983

Contrasting relations between suppressor-cell function and suppressor-cell number in chronic liver disease.

75 patients with various chronic liver diseases were investigated by simultaneous assay of suppressor-cell function and enumeration of suppressor T cells by monoclonal antibody. In chronic active hepatitis and primary biliary cirrhosis, substantial defects in suppressor-cell function were associated with negligible alterations in the proportions of suppressor cells. Defective suppressor-cell function was also evident in most patients with HBsAg-positive liver disease and in some with alcoholic liver disease. While the expected relations between suppressor-cell function and the proportions of helper or suppressor cells and the helper/suppressor ratio were apparent in alcoholic liver disease, the results in the HBsAg-positive, HBeAg-positive patients were in direct contrast. This apparent anomaly may reflect functional heterogeneity of the lymphocyte population detected by the monoclonal antibody OKT8, which identifies suppressor and cytotoxic cells. This study demonstrates that in the absence of simultaneous measurement of function, enumeration of T-cell subsets with monoclonal antibodies is an inadequate assessment of immunoregulatory balance.

Autoantibodies↗
PubMed1993

Biotinidase activity in patients with liver disease.

To investigate whether biotinidase deficiency may occur in liver disease, we determined biotinidase activity, biotin levels, and organic acids in patients with liver disease. Serum biotinidase activity in patients with liver disease (2.63 +/- 1.40 nmol/min/ml) was significantly lower than in the control group (5.43 +/- 1.06 nmol/min/ml). Serum biotinidase activity in decompensated liver cirrhosis (LC) and hepatoma was significantly lower than in acute viral hepatitis (AVH), chronic viral hepatitis (CVH), and compensated LC. The mean serum level of biotin in decompensated LC (1.8 +/- 0.6 microgram/ml) and hepatoma (1.7 +/- 0.8 microgram/ml) was significantly lower than in the control group (2.5 +/- 1.0 microgram/ml), and urinary excretion of biotin was increased in patients with liver disease, particularly in decompensated LC. Biotinidase activity correlated positively with serum biotin level and correlated negatively with urinary biotin level. Moreover, in four of five patients with severe liver disease the excretion of propionate, lactate, and 3-hydroxybutyrate decreased after biotin supplementation. The data for patients with severe liver disease so resembled those for late-onset multiple carboxylase deficiency that biotinidase deficiency is likely in patients with severe liver disease.

3-Hydroxybutyric Acid↗
PubMed2005

Symptoms of obstructive sleep apnea in patients with nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is a term often used to describe two related conditions: a relatively benign, nonalcoholic fatty liver (NAFL) and potentially aggressive, nonalcoholic steatohepatitis (NASH). Both conditions (NAFL and NASH) occur in the setting of peripheral insulin resistance. Recently, obstructive sleep apnea (OSA) has been proposed as an independent risk factor for insulin resistance. To date, few studies have documented the prevalence of OSA or symptoms of OSA (SOSA) in NAFLD patients. The objectives of this study were (1) to document the prevalence of SOSA in patients with NAFLD and (2) to determine whether prevalence rates for SOSA differ in NAFL versus NASH patients. One hundred ninety biochemically defined NAFLD patients (116 NAFL and 74 NASH), of whom 50 (18 NAFL and 32 NASH) had undergone liver biopsy, completed a Modified Berlin Sleep Apnea Questionnaire for SOSA. Risk factors for NAFLD were also documented in NAFL and NASH patients. Eighty-seven of the 190 (46%) NAFLD patients met questionnaire criteria for SOSA. The prevalence of SOSA was similar in both biochemically (45% versus 49%, respectively; P = 0.66) and histologically (39% versus 63%, respectively; P = 0.11) defined NAFL and NASH patients. Other risk factors for NAFLD such as body mass index, plasma cholesterol and triglyceride levels, and prevalence of diabetes were also similar in the two groups. Approximately one-half of NAFLD patients, whether NAFL or NASH, have SOSA. Further studies are required to determine whether a causal link exists between NAFLD and OSA.

Adult↗
PubMed2005

Contribution of adipose tissue and de novo lipogenesis to nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is a component of the metabolic syndrome, with a clinical spectrum ranging from simple fatty liver to steatohepatitis, cirrhosis, and hepatocellular carcinoma. The primary event of NAFLD is the accumulation of triacylglycerols (TAGs) in hepatocytes. In this issue of the JCI, Donnelly et al. report on their use of stable isotope methodology to show that fatty acids stored in adipose tissue and fatty acids newly made within the liver through de novo lipogenesis are the major sources of TAGs in the liver and are secreted as lipoproteins in NAFLD.

Adipose Tissue↗
PubMed2005

The reverse target sign in liver disease: a potential ultrasound feature in cirrhotic liver nodules characterization.

In patients with suspected liver disease, ultrasound is the most commonly performed initial imaging modality. We report a patient who had previously undiagnosed liver cirrhosis with target-shaped lesions interspersed throughout the liver parenchyma on ultrasound seen as multiple uniform round shaped lesions with varying isoechoic to hyperechoic centres surrounded by a hyperechoic rim. We have termed this the "reverse" target sign as there is inversion of the typical echoic pattern that is normally seen in metastatic liver disease. We suggest this ultrasound sign may represent a method for differentiating cirrhotic liver nodules from other nodular liver lesions.

Diagnosis, Differential↗
PubMed1990

Acute phase proteins in endemic chronic liver diseases.

Forty patients with chronic liver disease and ten normal controls were investigated for acute phase proteins. Mixed schistosomal cases with chronic hepatitis or cirrhosis showed more marked changes, while pure schistosomal group showed serum levels closer to normal values. This could be a differentiating point between the two categories. Also the more significant changes in the mixed groups indicate more involvement of the immune system in the pathogenesis of those groups.

Acute-Phase Proteins↗
PubMed1981

Medical evaluation of the patient with liver disease prior to surgery.

Patients with liver disease have increased morbidity and mortality following general anesthesia and surgery when compared with the general population. The increase in mortality appears to be directly related to the severity of hepatic parenchymal cell failure and to the magnitude and duration of the surgical procedure. The importance of preoperative detection of subclinical liver disease by use of a variety of blood tests has been emphasized. However, with the exception of hepatitis B and non-A non-B hepatitis, a precise diagnosis of the exact cause of liver disease is usually less important to the anesthesiologist than is a full characterization of the severity of hepatic dysfunction. Recognition and understanding of the central metabolic role played by the liver in maintaining carbohydrate, fat, and protein homeostasis can help in predicting and managing abnormalities which may complicate the preoperative, interoperative, and postoperative periods. Liver failure after anesthesia and surgery is treated by the same management principles used for liver failure with acute hepatitis. The incidence of postoperative renal failure may be increased in patients who have severe hyperbilirubinemia and its occurrence should be differentiated from the hepatorenal syndrome. It should be understood that complications of portal hypertension may develop in the absence of overt hepatic parenchymal cell failure and that liver failure may occur without gross evidence of portal hypertension. Either situation must be recognized and treated as far in advance of surgery as possible. In general, elective surgery in the patient with liver disease should be delayed until consequences of hepatic parenchymal cell dysfunction and portal hypertension are optimally corrected.

Bile↗
PubMed2003

Treatment of Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is very common in the United States, and in some patients it may lead to cirrhosis, liver failure, and liver cancer. NAFLD encompasses a spectrum of liver injury, ranging from steatosis to steatohepatitis, advanced fibrosis, and cirrhosis. Nonalcoholic steatohepatitis (NASH), an advanced form of NAFLD, histologically comprises steatosis, balloon degeneration, inflammation, and fibrosis in varying degrees. It is generally believed that simple steatosis is benign with minimal risk of progression, whereas NASH is progressive and can lead to cirrhosis. The commonly associated risk factors for NAFLD include obesity, hyperlipidemia, and diabetes mellitus. The pathogenesis of NAFLD and NASH is not fully known; however, current evidence suggests that insulin resistance and lipid peroxidation play a role in the pathogenesis of this condition. Currently, there are no proven effective therapies available for the treatment of NASH. Although there are numerous studies that have explored various treatments for NASH, these generally consist of small numbers of patients with suboptimal endpoints. Treatment strategies for NAFLD and NASH can be broadly divided into 1) treatment or control of underlying risk factors such as hyperlipidemia, diabetes mellitus, and obesity; and 2) specific pharmacologic therapy such as insulin sensitizers, antioxidants, or cytoprotective agents. Newer thiazolidinediones, such as rosiglitazone and pioglitazone, have shown promise in the treatment of NASH in pilot studies. However, these agents should not be used in clinical practice until their efficacy and safety are firmly established in larger studies. Despite encouraging initial studies, the recently completed multicenter, randomized, controlled trial failed to show any efficacy for ursodeoxycholic acid in the treatment of NASH. Other agents, such as vitamin E, betaine, probucol, and atorvastatin, have been explored as therapeutic agents for NASH. However, none of these studies have shown convincingly their utility in the treatment of NASH. Attempts to identify optimal therapy for patients with NASH are being vigorously pursued by the research community and important advances are expected within next several years. Until then, subjects should be advised to avoid alcohol, lose weight, and exercise regularly, and meticulous attention should be paid to the control of their risk factors such as diabetes and hyperlipidemia.

Journal Article↗
PubMed2005

Steatosis: co-factor in other liver diseases.

The prevalence of fatty liver is rising in association with the global increase in obesity and type 2 diabetes. In the past, simple steatosis was regarded as benign, but the presence of another liver disease may provide a synergistic combination of steatosis, cellular adaptation, and oxidative damage that aggravates liver injury. In this review, a major focus is on the role of steatosis as a co-factor in chronic hepatitis C (HCV), where the mechanisms promoting fibrosis and the effect of weight reduction in minimizing liver injury have been most widely studied. Steatosis, obesity, and associated metabolic factors may also modulate the response to alcohol- and drug-induced liver disease and may be risk factors for the development of hepatocellular cancer. The pathogenesis of injury in obesity-related fatty liver disease involves a number of pathways, which are currently under investigation. Enhanced oxidative stress, increased susceptibility to apoptosis, and a dysregulated response to cellular injury have been implicated, and other components of the metabolic syndrome such as hyperinsulinemia and hyperglycemia are likely to have a role. Fibrosis also may be increased as a by-product of altered hepatocyte regeneration and activation of bipotential hepatic progenitor cells. In conclusion, active management of obesity and a reduction in steatosis may improve liver injury and decrease the progression of fibrosis.

Apoptosis↗
PubMed2000

Pregnancy-Related Liver Diseases.

There are four unique liver diseases that occur only during pregnancy and resolve after delivery. Several liver diseases occur more commonly during pregnancy. These must be distinguished form acute or chronic liver diseases that coincidentally occur during pregnancy.

Journal Article↗
PubMed1986

Pathological spectrum of liver diseases in sickle cell disease.

Most pathologic studies of liver disease in sickle cell anemia and its variants were performed retrospectively on autopsy specimens, and, because of the prominent histologic features of intrasinusoidal sickling and Kupffer cell erythrophagocytosis, hepatic dysfunction was attributed to the intrahepatic sickling of erythrocytes in this hemoglobinopathy. We compared the liver histology from 19 patients who had liver biopsies to the autopsy specimens from 32 patients who succumbed to the complications of the hemoglobinopathy. In the former, nine patients had histological evidence of viral hepatitis. Four of these patients had both serological and immunohistochemical evidence of hepatitis B surface antigen. The features of biliary tree obstruction were found in two cases and alcoholic cirrhosis and sarcoid granuloma in one case each. Only one patient, who had recovered from septic shock, showed ischemic necrosis. In five patients incidentally biopsied during cholecystectomy, no significant lesions were found. Fourteen of the autopsy specimens showed ischemic necrosis, a result which was significantly different from the biopsy group. Ten cases had no significant morphologic changes other than heavy iron deposits. There were two cases with chronic active hepatitis, two with diffuse fibrosis, and one case each of cirrhosis, acute viral hepatitis, cholestasis, and giant cell hepatitis. Intrahepatic sickling and erythrophagocytosis were seen in almost all specimens and did not correlate with liver disease or transaminase elevation. Other than the patient with septic shock, ischemic necrosis was found only in postmortem material. These histological features may represent red cell destruction rather than the etiology of liver disease in these patients.

Adolescent↗
PubMed1978

Increased serum thyroid hormone binding and decreased free hormone in chronic active liver disease.

To determine whether chronic inflammatory disease of the liver increases serum thyroid hormone binding, we measured tri-iodothyronine resin binding ratios in nine patient with primary biliary cirrhosis and in nine with chronic active hepatitis. In each group, the average binding ratio was about 50 per cent higher than in control subjects. Thyroxinebinding globulin, measured by immunoassay in three patients, was elevated. Although average total thyroxine and tri-iodothyronine were increased slightly, the corresponding free hormone concentrations were lower than controls, probably because of decreased thyroid function associated with the high incidence of autoimmune thyroiditis in nonalcoholic (autoimmune) liver disease. Thyroid autoantibodies were found in 13 patients. Impaired hepatic thyroxine-to -tri-iodothyronine conversion may have contributed to the low free tri-iodothyronine. Thyrotropin was elevated in four patients. Because of increased serum thyroid hormone binding in these patients total thyroxine and tri-iodothyronine concentration can be normal despite hypothyroidism.

Autoantibodies↗
PubMedDate not supplied

A fish hook and liver disease: revisiting an old enemy.

Vibrio vulnificus is an uncommon but potentially devastating pathogen. Early recognition with prompt antimicrobial therapy and surgical treatment are key factors for a favorable outcome. Patients with diseases of the liver represent the group at highest risk of infection. However, clinicians are often unaware of underlying liver disease in these patients at the time of presentation. We present a case of fulminant V. vulnificus infection in a patient with previously undiagnosed liver disease.

Adult↗
PubMed1992

Genotype analysis for delta F508, G551D and R553X mutations in children and young adults with cystic fibrosis with and without chronic liver disease.

Genetic factors have been implicated in the pathogenesis of liver disease in cystic fibrosis. To investigate whether liver disease is associated with particular mutations of the defective gene in cystic fibrosis, we have determined the frequencies of three mutations--delta F508, G551D and R553X--in 111 children and young adults with cystic fibrosis by analysis of genomic DNA segments amplified by the polymerase chain reaction. Twenty-nine patients had severe liver disease with portal hypertension, 19 had clinical and/or biochemical evidence of liver disease but no associated portal hypertension and 63 had no evidence of liver disease. No significant differences in the frequencies of the delta F508, G551D or R553X mutations in the three clinical subgroups were found, and we conclude that the development of liver disease in cystic fibrosis is unlikely to be associated with a specific mutation in the gene. However, because 27% of cystic fibrosis chromosomes do not have a defined mutation, this possibility cannot be ruled out. A familial concordance for clinical liver disease of 20% in this study, compared with a reported prevalence of 4.7%, suggests that genes outside the cystic fibrosis locus and/or environmental factors are involved in the pathogenesis of liver disease in cystic fibrosis.

Adolescent↗
PubMed2005

Nonalcoholic fatty liver disease in the pediatric population: a review.

PURPOSE OF REVIEW: Nonalcoholic fatty liver disease is a common condition that may progress to end stage liver disease. It is closely associated with obesity and insulin resistance, two conditions whose prevalence is increasing dramatically in children. This could potentially make nonalcoholic fatty liver disease the most common liver disease in the pediatric population. This review will focus on the current knowledge regarding the epidemiology, clinical presentation, diagnosis, pathogenesis, and management of nonalcoholic fatty liver disease in children. RECENT FINDINGS: Recent studies suggest that nonalcoholic fatty liver disease is an increasingly recognized condition during childhood, especially in overweight and obese children. Although limited information is currently available on the natural history of the disease in the pediatric population, few cross-sectional studies and a single longitudinal cohort study with follow up data up to 16 years, showed that as in adults, nonalcoholic fatty liver disease in children may have a progressive clinical course with the development of cirrhosis. Emerging data from small pilot studies suggest weight loss through lifestyle modifications as well as insulin sensitizing and antioxidant medications may be of benefit. Moreover, recent advances in the understanding of nonalcoholic fatty liver disease pathogenesis may result in novel therapeutic targets to treat this disease. SUMMARY: Nonalcoholic fatty liver disease is probably the most common form of chronic liver disease in children and may continue to rise with the increasing prevalence of childhood obesity and metabolic syndrome. Recent studies have provided new insights regarding this condition in children. There is still much progress to be made in terms of the description of pediatric nonalcoholic fatty liver disease, its demographics, pathogenesis, and treatment as well as natural history and long-term prognosis.

Adolescent↗
PubMed1993

Investigation of alcoholic liver disease.

In heavy drinkers with clinical evidence of liver disease, routine investigations should exclude the possibility of other chronic liver diseases of non-alcoholic aetiology requiring specific therapy--these include chronic viral hepatitis, autoimmune diseases of the liver, Wilson's disease and genetic haemochromatosis. If abnormalities in liver biochemistry persist despite abstinence, or if the diagnosis of alcoholic liver disease is in doubt, a liver biopsy should be carried out. Studies evaluating the role of liver biopsy in alcoholic liver disease suggest that without histological confirmation the diagnosis will be inaccurate in 10-20% of patients. Serum biochemistry and the currently available imaging modalities have severe limitations in determining the relative contributions of fatty liver, alcoholic hepatitis and cirrhosis to the overall picture in alcoholic liver disease. Histological examination is therefore of additional value in determining the prognosis, which is worst in patients with a combination of alcoholic hepatitis and cirrhosis. There are a number of indices available, based on clinical and laboratory information, for evaluating the short-term prognosis, but these can only be used with accuracy if the histological pattern of damage has initially been evaluated.

Biopsy↗