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PubMedDate not supplied

Tamoxifen-induced non-alcoholic steatohepatitis in patients with breast cancer: determination of a suitable biopsy site for diagnosis.

We have evaluated the distribution of fatty infiltration in the liver for determination of a suitable biopsy site for diagnosis of tamoxifen-induced non-alcoholic steatohepatitis (NASH) in patients with breast cancer. Thirty-eight consecutive breast cancer patients undergoing tamoxifen treatment were analyzed by CT to identify hepatic steatosis (HS) via calculation of the liver/spleen CT ratio in Couinaud's 8 areas. We defined hepatic fatty infiltration as a liver/spleen ratio of less than 0.9. The extent and distribution of the fatty infiltration was assessed using the liver/spleen ratio of the patients who had the lowest CT ratio below 0.9 in the 8 areas. Thirteen (34.2%) of the 38 patients had hepatic fatty infiltration. The liver/spleen ratios of each area differed significantly in all patients (p<0.0001). The CT ratio of these 13 patients was significantly lower in the right lobe than the left lobe (p<0.0001), although the ratios did not differ significantly among the 4 areas of the right lobe (p=0.52). Needle biopsy for diagnosis of NASH should be performed at the right lobe, which contains significantly more infiltrated fat than the left lobe in the liver.

Adult↗

PubMed2003

[Nonalcoholic steatohepatitis: a review].

The nonalcoholic steatohepatitis (NASH) is a liver disease of people who do not drink alcohol, with the histology of an alcoholic liver disease. It is the second or third most prevalent liver disease in western countries. The risk factors are the female gender, a middle age, a diabetes and a dyslipidemia. Some cases of NASH can reach the cirrhosis stage. The most common sign of the disease is an aminotransferase level elevation.

Fatty Liver↗

PubMed2003

[Systemic lupus erythematosus with steroid induced non-alcoholic steatohepatitis: a case report].

A 56-year old Japanese female was admitted to our hospital because of the increased levels of serum AST, ALT, and gamma-GTP. She was diagnosed with systemic lupus erythematosus in September, 1996 and had been on a regular glucocorticoid therapy since then. Abdominal ultrasonography showed the mild fatty liver, and hepatic histopathology revealed a typical and remarkable steatohepatitis, a remarkable neutrophil infiltration, and Mallory bodies. Because she had no history of alcohol-drinking, diagnosis of non-alcoholic steatohepatitis (NASH) was made. Treatment was started with a low-calorie diet, bed-rest, and an oral administration of alpha-tocopherol and bezafibrate with favorable effects on her serum levels of AST, ALT, gamma-GTP, and LDH. When a patient on a glucocorticoid therapy shows signs of fatty liver, diabetes mellitus, hyperlipidemia, an insulin resistance, NASH should be considered as one of the differential diagnosis. This is particularly important since proper therapy with a low-calorie diet and drugs with anti-oxidant activities improve this potentially progressive disease before resulting in liver cirrhosis and hepatic carcinoma.

Antioxidants↗

PubMedDate not supplied

[Nonalcoholic and alcoholic steatohepatitis].

NASH (Nonalcoholic Steatohepatitis) and ASH (Alcoholic Steatohepatitis) are both diseases with increase frequency which may complicate up to 50% of liver cirrhosis. They are considered as risk factors for liver carcinoma. In order to diminish the incidence of liver cancer, NASH and ASH need a close follow-up. These two entities need to be known not only by gastroenterologist, but also by general practitioners, endocrinologists, nutritionists and cardiologists.

Fatty Liver↗

PubMedDate not supplied

Nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease is a clinicopathologic syndrome that encompasses several clinical entities. The spectrum of conditions ranges from simple steatosis to steatohepatitis, fibrosis and end stage liver disease. The condition was originally described in obese, diabetic, middle-aged females without a history of significant alcohol use with liver histology consistent with alcoholic hepatitis. It is known that this entity occurs without any particular sex predilection, in lean individuals, as well as an increasing number of obese children. Other terms have been used to describe this clinical entity such as alcohol-like hepatitis, pseudo-alcoholic hepatitis, diabetic hepatitis and steatonecrosis. Ludwig and colleagues introduced the term nonalcoholic steatohepatitis (NASH) to describe patients fitting the picture of alcoholic hepatitis but without a history of significant alcohol abuse. The term nonalcoholic fatty liver disease (NAFLD) is used more frequently to include the spectrum of conditions that range from steatosis through steatohepatitis, fibrosis and cirrhosis. NASH is reserved for patients with steatohepatitis and fibrosis. NAFLD is now being recognized as the most common cause of elevated liver enzymes in the United States. Although the exact etiology of NAFLD is not known, it may be caused by insulin resistance coupled with increased oxidative stress to the hepatocytes. No specific therapy has been approved for this condition and the mainstay of management is weight loss.

Fatty Liver↗

PubMedDate not supplied

Clinical spectrum and natural history of non-alcoholic steatohepatitis with normal alanine aminotransferase values.

Non-alcoholic fatty liver disease (NAFLD) including nonalcoholic steatohepatitis (NASH) is a well-established cause for chronic liver disease. In most studies on NASH, elevation in alanine aminotransferase (ALT) is taken as one of the diagnostic criteria. However, the clinical and histological spectrum and natural history of NAFLD with normal ALT are not well explored. This study was planned to define the clinical spectrum and natural history of patients with NAFLD with normal ALT, and to compare them with NAFLD with abnormal ALT. A prospective study including 81 consecutive patients with ahistological diagnosis ofNAFLD was planned during the period from 1999 to 2003. Consecutive (n=81) patients with the histological diagnosis of NAFLD were included in the study. In all the patients, clinical, anthropometric, laboratory, histological and imaging features were noted at the baseline. All these patients were followed up regularly at 6-month intervals. Of the 81 cases, 25 patients (including 60% cirrhotics) had persistently normal enzyme, whereas 56 (including 23% cirrhotics) had abnormal ALT. Both the groups were comparable with respect to distribution of age, gender, ethnicity, clinical features, imaging features, histological severity and laboratory features; except a higher incidence of diabetes and higher occurrence of advanced liver disease at baseline in NAFLD with normal ALT. Natural history of NAFLD was better in patients without cirrhosis irrespective of baseline ALT levels than in patients with cirrhosis; except for a higher incidence of decompensation in cirrhotics with normal ALT. The entire clinical and histological spectrum of NAFLD is seen in patients with normal ALT and is not different from patients with abnormal ALT. In patients with diabetes and hepatomegaly in the absence of other obvious liver diseases, even normal ALT may not rule out advanced liver disease, and liver biopsy may be necessary to identify the severity of liver disease.

Adult↗

PubMed2005

[Effect of Endotoxin on the expression of peroxisome proliferator-activated receptor alpha in the development of nonalcoholic steatohepatitis in rats].

OBJECTIVE: To study the effect of endotoxin on the expression of peroxisome proliferator-activated receptor alpha (PPARa) in the development of nonalcoholic steatohepatitis in rats. METHODS: A model of nonalcoholic steatohepatitis (NASH) was developed with Wistar rats fed a chow containing 20% maize oil for 14 weeks. The endotoxin group rats were intraperitoneally injected with lipopolysaccharide (LPS, 1 g/L, 3.0 ml/kg) once 4 hours before the end of the experiment. The concentrations of lipids, endotoxin, tumor necrosis factor-a, malondialdehyde, free fatty acid in plasma and hepatic tissues were determined and the degree of hepatocytic steatosis was studied. The expression of PPARa mRNA in hepatic tissues was measured using reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: The expression of PPARa mRNA in the hepatic tissue of the LPS group was downregulated markedly in comparison to that of the control group. The level of free fatty acid and endotoxin by secreting tumor necrosis factor-a increased and triglyceride accumulated in the liver caused malondialdehyde content to increase, then lipid peroxidation process enhanced and ALT activity increased. Thus, hepatic injury and inflammatory reaction could be accelerated. CONCLUSION: Endotoxemia can enhance hepatocellular steatosis and lead to NASH due to its downregulating the expression of PPARa mRNA.

Animals↗

PubMed2005

Etiological factor of hepatocellular carcinoma in Italy.

Cirrhosis from any cause is present in the majority (93.1%) of hepatocellular carcinoma (HCC) cases in Italy, it seems to be the common pathway by which several risk factors extent their carcinogenic effect. The mortality rate of HCC in Italy has progressively increased during the period 1969-1994, reflecting the rising number of persons living with cirrhosis as consequence of the remarkable advances in medical management of such patients. Most HCC develops in cirrhosis caused by known and preventable risk factors (hepatitis B virus, HBV, hepatitis C virus, HCV, alcohol and possibly non-alcoholic steatohepatitis, NASH). Unlike alcohol and NASH, HBV and HCV chronic infections act as a risk factors for HCC both because they induce cirrhosis and because they increase the risk in patients with cirrhosis. Moreover, case-control and prospective studies have shown a synergistic effect on HCC risk, when both viral infections occur. Currently, HCV infection is detected in the majority (76.4%) of HCC cases in Italy, reflecting the large cohort of subjects infected with this virus via the iatrogenic route during the 1950s and 1960s. The low rate of HCV infection in the younger Italian generations may generate a downward trend in the HCC mortality rate in the years to come.

Age Factors↗

PubMed2005

[The roles of PPARs in digestive diseases].

Peroxisome proliferator-activated receptor gamma (PPARgamma), one of the nuclear receptors, is expressed at high levels in adipose tissue and is related to adipocyte differentiation and insulin sensitivity. PPARgamma is also expressed at high levels in digestive organs, especially in the colon epithelium. The physiological and pathological roles of PPARgamma in the gastrointestinal tract have been investigated and recognized as an endogenous regulator of innate immunity, inflammation, and cell proliferation. PPARgamma ligands have recently been reported to improve the condition of patients with non-alcoholic steatohepatitis (NASH). Thus, PPARgamma ligands are indeed potential benefit candidates for various digestive diseases. In this review, we will focus on the current knowledge and new insights of the roles of PPARgamma in digestive diseases, especially in (1) inflammatory bowel disease (IBD), (2) colon cancer, and (3) NASH.

Animals↗

PubMed2005

[Role of PPARs in the pathophysiology of nonalcoholoic fatty liver disease].

Pathogenic role of intrahepatic lipid accumulation in insulin resistance and metabolic syndrome has been well documented. Liver steatosis constitutes a risk factor for nonalcoholic steatohepatitis (NASH), one of the leading causes of obesity-related morbidity and mortality. Although pathophysiology of steatosis is multifactorial, a line of evidence from rodent studies suggests that PPARalpha and PPARgamma are involved. PPARalpha is highly expressed in liver and its activation by agonists leads to augmented fatty acid oxidation and protects against steatosis. PPARgamma, which is transcriptionally up-regulated in steatosis, activates lipogenic enzymes and exacerbates steatosis. However, recent human studies have suggested that PPARgamma agonists improve NASH possibly by its primary insulin-sensitizing effect on adipocytes. PPARs modulation is becoming a rational and effective therapeutic approach for the treatment of nonalcoholic fatty liver disease.

Fatty Liver↗

PubMedDate not supplied

Adipokines and liver fibrosis.

Liver fibrosis involves different cell types, and should be regarded as a "wound healing" response that occurres in conditions of chronic liver injury and is characterized by inflammation, activation of matrix-producing cells, matrix deposition and remodeling, and epithelial cell regeneration or an attempt thereof. Liver damage may be caused by several agents or conditions, resulting in different degrees and types of tissue inflammation and in activation of matrix-producing cells, such as the hepatic stellate cells (HSC). HSC undergo a phenotypic transition (known as "activation") to myofibroblast-like cells that synthesize different extracellular matrix components. Obesity is associated with the development of NASH, and has been indicated as an independent factor for the progression to fibrosis. In liver diseases, the biologic actions of the adipokines, such as leptin, adiponectin and resistin, released by adipocytes or locally produced by liver and/or inflammatory cells, may contribute to clarify the mechanisms of progression in NASH. The clinical and experimental findings accumulating on this class of molecules could represent the basis to devise a better management strategy for the patients with chronic liver disease.

Adipocytes↗

PubMedDate not supplied

Fatty liver and drugs.

Drug-induced liver diseases (DILD) are clinico-pathologic patterns of liver injury caused by drugs or other foreign compounds. Steatohepatitis is a rare form of DILD, and drugs account for fewer than 2% of non-alcoholic steatohepatitis (NASH). Drugs known to be capable of inducing steatosis and steatohepatitis can be divided into three broad groups: those that cause steatosis and steatohepatitis independently (e.g., amiodarone, perhexiline maleate); drugs which can precipitate latent NASH (e.g., tamoxifen); drugs whic duce sporadic events of steatosis/steatohepatitis (e.g., carbamazepine). Clinical DILD syndromes include acute viral hepatitis-like injury, acute liver failure, cholestatic hepatitis,liver disease with signs of hypersensitivity, autoimmune hepatitis-like injury, acute venous-Outflow obstruction, chronic cholestasis, ciirrhosis, steatosis and steatohepatitis. The clinical picture is by no means dependent on the mechanism of injury (direct hepatotoxicity, idiosyncratic reactions, hypersensitivity reactions). Reliable diagnosis of drug-induced liver disease requires demonstration of close correlation between the patient history and clinical, laboratory, and histological data.

Amiodarone↗

PubMed2002

The pathology of nonalcoholic steatohepatitis.

Nonalcoholic fatty liver disease (NAFLD) is an increasingly recognized form of chronic liver injury. Nonalcoholic steatohepatitis (NASH) is the term applied to the microscopically-defined subset of NAFLD with known progression to cirrhosis and the complications that may be associated, including metabolic imbalances, liver failure and hepatocellular carcinoma. NASH is also being considered as a significant precursor of end-stage liver disease, ''cryptogenic cirrhosis'', in which the histologic features of the initial liver disease can no longer be appreciated. Because of the increasing prevalence and the known significance of this form of liver disease, current investigations are focused on discerning the clinical features of susceptible patients, the histopathologic findings that characterize the entity and serve as markers of progression, pathogenetic mechanisms that result in triglyceride accumulation, liver injury and fibrosis, and ultimately, treatment options.

Journal Article↗

PubMed2006

Non-alcoholic fatty liver disease and hepatitis C infection.

Non-alcoholic fatty liver disease (NAFLD) is now recognized as one of the most important causes of chronic liver disease in Western Countries, and is the hepatic manifestation of metabolic syndrome. The prevalence of NAFLD has increased with the global epidemic of obesity and type 2 diabetes mellitus. The pathophysiological hallmark of NAFLD is insulin resistance, associated with mediators of oxidative stress and inflammatory cytokines. Although simple steatosis by itself is generally benign, patients with histologically proven non-alcoholic steatohepatitis (NASH) can progress to cirrhosis. Hepatitis C (HCV) is another common cause of liver disease with some potential for progression to cirrhosis. Steatosis is present in almost 50% of patients infected by HCV. Hepatic steatosis in the setting of another liver disease (such as HCV) is associated liver disease progression. In particular, significant fibrosis is observed in patients with HCV whose liver biopsies show significant steatosis or superimposed NASH. This article reviews the host and viral factors potentially involved in the interaction between NAFLD and HCV. These factors include mediators of metabolic syndrome such as adipokines, inflammatory cytokines, factors associated with oxidative stress, lipid peroxidation products, as well as apoptosis and hepatic stellate cell activation with the resultant deposition of extracellular matrix. In addition to the mediators of metabolic syndrome (host factors), hepatic steatosis can be influenced by viral factors. The most important viral factor is HCV genotype 3, which has been independently associated with hepatic steatosis. Finally, superimposed NAFLD and visceral fat are associated with lower response rates to antiviral therapy in non-genotype 3 patients. Furthermore, viral clearance is associated with the resolution of hepatic steatosis in HCV genotype 3 but not other HCV genotypes. In these genotypes, hepatic steatosis and its impact on response to therapy are related to metabolic syndrome. Thus, the management of obesity and metabolic syndrome in patients with chronic hepatitis C may be important for reducing the risk of progression as well as improving the efficacy of antiviral therapy.

Fatty Liver↗

PubMed2006

Anterior instrumentation for correction of adolescent thoracic idiopathic scoliosis: historic prospective study.

AIM: To compare the results of anterior instrumentation and standard posterior procedure for correction of adolescent thoracic idiopathic scoliosis. METHODS: The study included 50 patients with adolescent thoracic idiopathic scoliosis who underwent corrective spinal surgery. Anterior spinal fusion by use of modified Zielke ventral derotation system (anterior approach to spine through thorax) was performed in 25 patients, whereas posterior approach was used in 25 patients. The average preoperative thoracic curve in coronal plane was 66.7 +/- 9.9 degrees and 65.0 +/- 11.7 degrees in the anterior and posterior correction groups, respectively. The median age of patients before surgery was 14 years (range, 12-18) in the anterior and 16 years (range, 13-18) in the posterior correction group. Women-to-men ratio was 22 to 3 in each group. Coronal and sagittal correction, apical vertebral body rotation, rib hump, and rib depression correction were measured before surgery and at the first (30 days after surgery) and at the second follow-up visit (at least 2 years after surgery). Posteroanterior and laterolateral radiographs of the erect spine were used (according to the method of Cobb and Nash-Moe) to assess coronal, sagittal, and horizontal plane corrections. Rib hump and rib depression were measured with Thulbourne-Gillespie measuring device. The differences in scoliosis correction parameters in the two groups were tested with Student two-tailed t test. RESULTS: In the coronal plane, the thoracic curve of 66.7 +/- 9.9 degrees before surgery in the anterior correction group was reduced to 14.8 +/- 8.7 degrees after surgery (78.1 +/- 12.4% relative correction), and the curve of 65.0 +/- 11.7 degrees in the posterior correction group was corrected to 29.2 +/- 7.8 degrees after surgery (55.1 +/- 8.6% relative correction) (P<0.001). Apical vertebral body rotation correction according to the Nash-Moe classification from 2.0 +/- 0.4 degrees to 0.8 +/- 0.6 degrees was achieved in the anterior correction group (62.0 +/- 26.6% relative correction) and from 1.7 +/- 0.5 degrees to 1.4 +/- 0.5 degrees in the posterior correction group (12.0 +/- 21.8% relative correction) (P<0.001). Rib hump correction from 22.4 +/- 15.5 mm to 5.4 +/- 5.2 mm was found in the anterior correction group (70.9 +/- 26.0% relative correction) and from 25.3 +/- 7.0 mm to 13.6 +/- 6.8 mm (48.4 +/- 16.5% relative correction) in the posterior correction group (P = 0.084). CONCLUSION: Compared with the standard posterior approach, the anterior approach resulted in better three-dimensional correction of idiopathic thoracic scoliosis.

Adolescent↗

PubMed2006

Serum leptin concentrations in chronic hepatitis.

The objectives of this research were to investigate the leptin levels among Chronic Hepatitis B Virus (HBV), Chronic Hepatitis C Virus (HCV) and non-alcoholic steatosis hepatitis (NASH) diseases of Thai patients compared with controls. Twenty of each HBV, HCV and NASH patients compared with sixty people as the control group from the Outpatient Department at the Hospital for Tropical Diseases, Bangkok, Thailand were investigated. Fasting blood samples were collected for investigation of leptin concentration, liver enzyme function tests and hematological variables. The serum leptin concentration of liver patients was significantly higher than that of control subjects. It might be due to the accumulations of fat cells in liver disease patients. However, there is no relationship between leptin level and other parameters such as BMI, ALT, AST, ALP and hematological variables. Liver enzyme functions levels are much higher in patients groups. White blood cells counts, platelets and hematocrit values are slightly lower in liver disease patients. Therefore, it is concluded that physiological regulation of leptin maintains in relation to body fat, even in chronic viral liver diseases. This finding and the apparent stage suggest the possibility that in the course of chronic viral diseases, serum leptin levels may reflect the extent of liver dysfunction.

Adult↗

PubMed2006

[Insulin resistance].

Insulin resistance is closely associated with fat accumulation in liver. Thus, it has been suggested that insulin resistance is one of the important factor in development of non-alcoholic steatohepatitis(NASH). For example, insulin resistance in adipocyte results in increased lipolysis and delivery of free fatty acids(FFAs) to the liver, which induce fatty liver. If there is insulin resistance in skeletal muscle, hyperinsulinemia and/or hyperglycemia might increase fat accumulation in liver, through, at least in part, increased sterol-regulatory element binding protein-1c(SREBP-1c) activation. However, hepatic insulin resistance might prevent fat accumulation in liver, because insulin strongly induces lipogenesis. Thus, the tissue specific insulin resistance should be considered in the pathogenesis of NASH.

Adipocytes↗

PubMed2006

[Mutation of mitochondrial DNA in patients with non-alcoholic steatohepatitis].

When the numbers of mutations per 1,000 bases of mitochondrial DNA were compared among three groups of Al-Hep, NASH and FL, there were significantly more mutations in ND1 and COII of Al-Hep and NASH than in FL. When details of the base mutation were investigated by group, the transition type of mutation between T:A and C:G occurred in control and coding regions. In FLS and FLS-ob mice, mutations in the D-loop and coding regions of mitochondrial DNA were investigated by sequencing analysis. The average number of mutations per clone in each region was more than 5-fold higher in FLS-ob than in FLS. In addition, the mutations were mostly transition-type mutations. These data indicate that nitric oxide plays an important role in mitochondrial DNA mutations.

Animals↗