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PubMedDate not supplied

Polycystic ovary syndrome and severe nonalcoholic steatohepatitis: beneficial effect of modest weight loss and exercise on liver biopsy findings.

OBJECTIVE: To report a case of biopsy-documented nonalcoholic steatohepatitis (NASH), which improved appreciably through moderate exercise and weight loss in a young woman with polycystic ovary syndrome (PCOS) and insulin resistance. METHODS: We present a detailed case report, including laboratory and pathologic findings. In addition, we review the recent literature regarding the association of insulin resistance with NASH and PCOS. RESULTS: A 24-year-old woman was referred to the Duke Gastroenterology Clinic for evaluation of long-term high serum aminotransferase levels. She also reported a history of chronically irregular menses, infertility, and hirsutism and was diagnosed with PCOS. Subsequent glucose tolerance testing suggested the presence of insulin resistance. Liver biopsy findings were consistent with severe nonalcoholic steatohepatitis. Under the supervision of her physician and an exercise physiologist, the patient initiated a diet and exercise program that resulted in an 11.5% weight loss during approximately 8 months and yielded normalization of her aminotransferase levels. A repeat liver biopsy done 13 months after the initial biopsy revealed a substantial decrease in steatosis and a reduction in inflammation. CONCLUSION: Women with PCOS and insulin resistance have an increased risk of developing many of the consequences of the dysmetabolic syndrome, including type 2 diabetes, hypertension, and hyperlipidemia. This case report suggests that fatty liver and NASH may be other important diseases to identify in such women. It also demonstrates the improvement in this condition with moderate exercise and weight loss.

Adult↗

PubMedDate not supplied

Acanthosis nigricans in patients with nonalcoholic steatohepatitis: an uncommon finding.

OBJECTIVE: To determine the prevalence and the metabolic characteristics of acanthosis nigricans (AN) in a group of 28 study subjects with biopsy-proven nonalcoholic steatohepatitis (NASH). METHODS: The study participants (15 female and 13 male patients, 20 of whom were white subjects; mean body mass index, 32.7 +/- 5.7 kg/m2; mean age, 45.7 +/- 11.3 years) underwent an oral glucose tolerance test (OGTT), frequently sampled intravenous glucose tolerance test (FSIGT), and fasting metabolic panels. AN status was clinically determined, and fat mass was measured by dual-energy x-ray absorptiometry. RESULTS: All study subjects had insulin resistance (IR), and 15 (54%) had the metabolic syndrome (by Adult Treatment Panel III criteria). Of the 28 patients, 4 (14%) had AN (AN+) and 24 did not (AN-). AN+ subjects had a higher body mass index (37.7 +/- 5.6 versus 31.5 +/- 4.3 kg/m2), fat mass (38.9 +/- 4.0 versus 29.2 +/- 2.3 kg), and leptin levels (17.2 +/- 3.9 versus 9.3 +/- 1.6 ng/mL) (P<0.05). They also had significantly higher indices of insulin secretion: fasting and stimulated insulin and C-peptide levels from OGTT and FSIGT. Metabolic syndrome prevalence was 40% in AN- versus 75% in AN+ subjects (not significantly different). Although the AN+ group had significantly lower fasting and OGTT-derived indices of insulin sensitivity in comparison with the AN- group, their FSIGT indices were similar. Waist circumference (a surrogate of visceral adiposity) and cytokine profiles were similar in the AN+ and AN- groups. CONCLUSION: AN was not highly prevalent in our study cohort with NASH, despite the high prevalence of IR. Hyperinsulinemia and total adiposity, rather than visceral adiposity and IR, were the indices most predictive of AN. The use of AN as an index of IR in patients with NASH appears to have limited diagnostic value.

Acanthosis Nigricans↗

PubMed2005

[Nonalcoholic steatohepatitis, the enigma of bad progression].

Still, very little is known about the precise pathogenetic mechanisms, the triggering events and in particular, the evolution and treatment of nonalcoholic steatohepatitis (NASH). It is part of the broad spectrum of nonalcoholic fatty liver diseases (NAFLDs). Mainly, it has been reported as a benign disease, associated with metabolic disorders commonly occurrence en the general population. Nevertheless, the syndrome can lead to cirrhosis, liver failure or hepatocellular carcinoma, requiring liver transplantation. We present one patient with diagnosis of NASH, who was treated initially for overweight, HTA and hyperlipaemia with incompleted response and who showed a quickly progress to cirrhosis but no cause of liver decompensated disease could be identified. Currently she is at end-stage waiting a liver transplantation. Controlled and multicentric studies with the same definition of NASH and the study end-points are needed, and will provide information about diagnosis features and novel therapies to early management of the disease.

Adult↗

PubMed2000

Non-alcoholic steatohepatitis: association with obesity and insulin resistance, and influence of weight loss.

Non-alcoholic steatohepatitis (NASH) is a disease of emerging identity and importance, and is now considered as one of the commonest liver diseases in western countries. It is frequently associated with severe obesity, especially abdominal adiposity, and is intimately related to various clinical and biological markers of the insulin resistance syndrome. Especially, both the prevalence and the severity of liver steatosis are related to male sex, body mass index, waist circumference, hyperinsulinaemia, hypertriglyceridaemia and impaired glucose tolerance or type 2 diabetes. A substantial weight loss following gastroplasty is accompanied by a marked reduction in the prevalence and the severity of the various biological abnormalities of the metabolic syndrome and, concomitantly, by an important regression of liver steatosis in most obese patients. However, in some patients, this rapid and drastic weight loss may result in a mild increase in inflammatory lesions (hepatitis), despite the regression of steatosis, which might result from the rapid mobilization of fatty acids or cytokines from adipose tissue, especially visceral fat. The intimate relationship between NASH and obesity leads to the concept that NASH may be considered as another disease of affluence, as is the insulin resistance syndrome and perhaps being part of it.

Diabetes Mellitus, Type 2↗

PubMed2000

[Non-alcoholic steato-hepatitis].

The term Non-Alcoholic Steatohepatitis (NASH) was introduced to describe a group of patients in whom liver biopsy shows the typical morphology of Alcoholic Steatohepatitis, without the presence of any significant alcohol consumption. The presence of steatosis and inflammatory infiltrate in liver biopsy is essential for the diagnosis of NASH. Other chronic liver diseases--such as Hepatitis B and C as well as Autoimmunohepatitis--which can cause similar morphologies have to be excluded. The pathophysiology of NASH is essentially still unclear. On the one hand toxic effects of oxidated fatty acids are suspected, on the other hand it is postulated that the fatty liver is very vulnerable and that actual hepatitis is triggered by an additional stressor. The disease has a benign clinical course and the typical patient is asymptomatic with elevated liver enzymes. Despite the paucity of symptoms the risk of cirrhosis is approximately 8-17%. No established treatment exists. Preliminary reports suggest a positive effect of gradual weight loss and ursodeoxycholic-acid but further studies are needed to confirm this observation.

Adolescent↗

PubMed2000

Nonalcoholic steatohepatitis: clinicopathological profile.

AIMS: To evaluate clinicopathological spectrum of nonalcoholic steatohepatitis (NASH) METHODOLOGY: Total 210 patients with chronic liver disease were evaluated. Detailed history has taken with clinical examination, laboratory investigations, radiological findings and liver biopsy whenever possible. RESULTS: From 210 patients of chronic liver disease, 13 (6.19%) were diagnosed to have NASH (M:F = 9:4, age range 37-72 years, mean age 55.4 +/- 9 years). Of 13 patients, four were referred for asymptomatic enzyme elevation, nine had right hypochondriac pain. Risk factors were diabetes in four cases, obesity four, steroid treatment two and hyperlipidemia in three cases. Laboratory investigations showed abnormal liver enzymes in all the cases. Ultrasonography and CT scan was helpful in predicting fatty liver. Liver biopsy showed steatosis with inflammation in all, fibrosis in two and cirrhosis in one patient. CONCLUSION: NASH is an important form of chronic liver disease, and is characterised by hepatomegaly, elevated liver enzymes. It is essential to diagnose this condition due to its progression to liver fibrosis and cirrhosis in some patients.

Adult↗

PubMed2001

The role of Kupffer cells in non-alcoholic steatohepatitis of rats chronically fed with high-fat diet.

OBJECTIVE: To explore the role of Kupffer cells in non-alcoholic steatohepatitis (NASH) by means of rat model. METHODS: Nineteen male SD rats were randomized into model group (n=10) and normal group (n=9), with a high-fat diet and standard diet for 12 weeks, respectively. Routine histologic features of hepatic section were observed by HE staining. The number and shape of Kupffer cells in the liver were detected by immunohistochemistry and penetrated electron microscope, respectively. RESULTS: All rats of model group developed NASH, which was characterized by obesity and hyperlipidemia. Histopathological examination showed hepatocellular macrovesicular steatosis, lobular inflammatory cell infiltration and necrosis. Compared with normal group, the count of Kupffer cells in the liver was largely increased, and the Kupffer cells in the model group were activated to some extent. Furthermore, these changes of Kupffer cells were in accordance with the degree of steatosis, inflammation and necrosis in the liver of the model group. CONCLUSION: The number and activity of Kupffer cells are increased significantly in NASH induced by high-fat diet, and Kupffer cells might be involved in the pathogenesis of steatohepatitis.

Animals↗

PubMed2000

Thiazolidinedione hepatotoxicity: a class effect?

Type 2 diabetes mellitus, which affects approximately 7% of the population, is a disease of relative insulin insufficiency manifested by insulin resistance in skeletal muscle, liver and adipose tissue. This results in increased hepatic glucose production with compensatory hyperinsulinaemia. The secondary hyperinsulinaemia is associated with an increased incidence of hepatocellular carcinoma and non-alcoholic steatohepatitis (NASH). It is estimated that insulin resistance is present in 50-70% of patients with NASH and that the incidence of NASH in type 2 diabetes is 60-80%. The prevalence of cirrhosis in established type 2 diabetes is as high as 10% and the prevalence of hepatitis C is 3-11%. It was in this setting that the insulin sensitisers were developed. The thiazolidinediones represent a significant and unique pharmacological breakthrough for the management of type 2 diabetes mellitus. The first of the drugs, troglitazone, proved to be hepatotoxic and has been withdrawn from the market. Two cases of hepatotoxicity of rosiglitazone have been reported. It remains unclear whether or not hepatotoxicity is a class effect or is related to the unique tocopherol side chain of troglitazone. However, it appears that the incidence of hepatotoxicity of rosiglitazone is much lower than that of troglitazone. It is not yet known if any hepatotoxicity occurs with pioglitazone.

Chemical and Drug Induced Liver Injury↗

PubMed2003

[Nonalcoholic steatohepatitis. Three case reports].

Non-alcoholic steatohepatitis (NASH) may develop in a subset of patients with non-alcoholic fatty liver disease (NAFLD). NASH is strongly associated to the metabolic syndrome with insulin resistance and obesity. NASH can progress to liver fibrosis, cirrhosis and chronic hepatic failure and eventual need for a liver transplantation. Three case stories are presented with characteristic clinical and histopathological changes.

Adult↗

PubMedDate not supplied

[Non-alcoholic fatty liver].

Non alcoholic fatty liver disease (NAFLD) and its more agressive form, non alcoholic steatohepatitis (NASH) are entities that are becoming subject of interest of the medical community in general, especially because of the increased prevalence of diabetes and obesity in the world population. There is solid evidence linking NAFLD with the so called metabolic syndrome or syndrome X, to the point of accepting hepatic steatosis and its spectrum as one more element of the latter, along with diabetes, hipertension, hypertriglyceridemia and obesity. Insulin resistance seems to be the common link between these entities. Clinical evaluation of every patient with abnormal aminotransferase levels should take into account non alcoholic fatty liver and its spectrum, especially if the subject is obese or diabetic. Despite the important developments in the field of imaging, currenty the only way to differentiate NASH from simple NAFLD is by performing a liver biopsy, which should be discussed extensively with the patient. The prognosis of simple NAFLD is generally benign, but if there is fibrosis, ballooning of the hepatocytes, inflammation and Mallory bodies there is risk to progression to cirrhosis. Liver histology in NAFLD is indistinguishable from alcoholic hepatitis, although the clinical course is generally more benign. Despite this long and protracted clinical course, an important number of subjects have complications of cirrhosis including hepatocellular carcinoma, and many patients require a liver transplantation. There is no specific treatment for this condition, although every therapeutic regimen should include a gradual and supervised weight reduction, a balanced diet and exercise, as well as correction of precipitant factors. There is currently no specific pharmacologic treatment for NASH or NAFLD. Current body of evidence and some pilot studies suggest that the future might be concentrated in agents improving insulin resistance. Meanwhile, we should do our best to study the prevalence of NAFLD in our country and, when clinically pertinent, study histologically those patients with high risk of fibrosis.

Disease Progression↗

PubMedDate not supplied

Prevalence of obesity, diabetes mellitus and hyperlipidaemia in patients with cryptogenic liver cirrhosis.

Non-alcoholic steatohepatitis (NASH) is emerging as an important cause of cryptogenic cirrhosis. Obesity, diabetes mellitus and hyperlipidaemia are important risk factors for NASH. The presence of these risk factors in patients with cryptogenic cirrhosis may suggest NASH as an aetiology of cirrhosis in them. Twenty-five patients of cryptogenic cirrhosis were compared with 18 patients of hepatitis B virus and hepatitis C virus related cirrhosis and primary biliary cirrhosis for the presence of obesity, diabetes mellitus and hyperlipidaemia. Patients with cryptogenic cirrhosis were found to have a significantly higher body - mass index increased prevalence of diabetes mellitus and lower high-density lipoprotein compared to the controls. Increased body weight and diabetes mellitus may play a role in the causation of cirrhosis in patients with cryptogenic cirrhosis.

Body Mass Index↗

PubMedDate not supplied

[The metabolic syndrome: a concept in evolution].

The concept metabolic syndrome intends to incorporate in a single disorder all biologic consequences of insulin resistance and associated conditions. The objective of this paper was to discuss strengths and limitations of current definitions of the metabolic syndrome, its epidemiology, and its association with non-alcoholic steatohepatitis (NASH). Definitions proposed by the World Health Organization (WHO) and the National Cholesterol Education Program (NCEP) are specific but possess low sensitivity for detecting insulin resistance. Cut-off points used in these definitions should be "but are not" adjusted for ethnicity; as a result, in non-Caucasian subjects there is lack of agreement among these. For example, in a Mexican population-based survey prevalence was 13.61% using the WHO definition and 26.6% employing NCEP-III criteria. Cases identified with WHO criteria have a more severe form of the disease. NASH is the most common cause of abnormal levels of serum aminotransferases. It shares some aspects of its pathophysiology with the metabolic syndrome and its prevalence is higher among cases with metabolic syndrome compared to with general population. NASH appears to be the hepatic manifestation of the metabolic syndrome.

Fatty Liver↗

PubMedDate not supplied

[Prevalence of non-alcoholic esteatohepatitis in adults with metabolic syndrome in Oaxaca].

Nonalcoholic steatohepatitis (NASH) is a chronic liver disease that occurs in patients with no significant alcohol consumption, characterized for macrovesicular steatosis, hepatocellular necrosis, mixed inflammatory infiltrate and various grades of fibrosis and, in some cases, Mallory bodies. The prevalence of this disease is unknown; recent studies indicate that in the general population, incidence is about 3%, although the rates are higher in some subpopulations as are obesity and diabetes mellitus. The goal of this work was to determine the prevalence of non-alcoholic steatohepatitis in one sample of patients with the metabolic syndrome, patients at "Presidente Juárez" Regional Hospital. It was a cross-sectional and descriptive study in which, by means of random selection a sample of 110 patients with type 2 diabetes mellitus, arterial hypertension, obesity and dyslipidemia, alone or in combination was chosen. We carried out a clinical and laboratory evaluation, selecting those patients with persistent elevation of aminotransferases for whom additional studies were made, in order to exclude other causes of enzyme abnormality. Five patients were selected for percutaneous liver biopsy, all they had NASH. The prevalence of NASH was 4.54%. The clinical and laboratory characteristics of these patients will be discussed in the article.

Adult↗

PubMed2005

[Some parameters of carbohydrate and lipid metabolism in patients with non-alcoholic steatohepatitis].

The pathogenesis of non-alcoholic steatohepatitis (NASH) has not been fully studied yet. At the same time, some key points of its forming are already clear. In this regard, the authors studied disturbances of carbohydrate and lipid metabolism in patients with NASH. This included evaluation of fatty acid (FA) and lipoprotein (LP) spectrum, as well as measurement of triglyceride (TG), malonic aldehyde and glucose blood concentrations. The study found that an important role in the pathogenesis of NASH is played by carbohydrate and lipid dysmetabolism, manifested by hyperglycemia, glucose tolerance disorder, and type II diabetes. Other manifestations include hyperlipoperoxidcholia, high concentrations of chylomicrons, low density lipoproteins, and triglycerides, as well as low concentration of high-density lipoproteins. The spectrum of higher fatty acids is characterized by high concentration of saturated fatty acids and deficit of polyunsaturated fatty acids.

Adult↗

PubMed2004

The prevalence of nonalcoholic steatohepatitis in Thai patients with non-HBV, non-HCV chronic hepatitis.

UNLABELLED: This study aimed to determine the prevalence of nonalcoholic steatohepatitis in Thai patients with non-HBV, non-HCVchronic hepatitis. The clinical and laboratory findings associated with non alcoholic steatohepatitis were discussed. Forty-six patients with negative markers for viral hepatitis B and viral hepatitis C and no history of alcohol consumption or consumption less than 20 grams of ethanol per day were recruited. The informed consent for liver biopsy and blood collecting to identify the etiology of chronic hepatitis was performed. Most patients (76.1%) exhibited fatty metamorphosis of the liver which included steatosis (21.8%) as well as steatohepatitis (54.3%). Eleven of 46 patients (23.9%) were classified as cryptogenic chronic hepatitis. There were statistically significant differences between the fatty metamorphosis group and the cryptogenic chronic hepatitis group with regard to the fasting blood sugar, serum alkaline phosphatase, serum ferritin and histologically necroinflammatory grading score (p < 0.05). Between the steatosis group and the steatohe-patitis group, body mass index (BMI) was the only factor showing statistically significant difference (p = 0.02). Eight from 25 NASH-patients had diabetes mellitus (32.0%) and the AST to ALT ratio in this group was 0.6. The histopathological assessment for inflammation and fibrosis by using Knodell score, the fibrosis score which equal or higher than 3 was found in 20.0% of NASH-patients. CONCLUSION: The prevalence of NASH-patients in Thai patients, with non HBV, non HCV chronic hepatitis was 76.1%, while the liver biopsy can add the diagnostic yield especially in the group of unexplained chronic hepatitis with obesity, diabetes mellitus and dyslipidemia.

Adult↗

PubMedDate not supplied

The treatment of NAFLD.

Nonalcoholic fatty liver disease (NAFLD) is becoming an increasing cause of chronic liver damage. The decision of start a medical treatment is based on the documented risk of progression to cirrhosis and liver cancer, when steatohepatitis (NASH) occurs. The therapy of this syndrome requires, as obviously, some considerations on the natural history of the condition, on the efficacy and safety of various therapeutic options, as well as on the costs. Treatment of patients with NAFLD has typically been focused on the management of associated conditions such as obesity, diabetes mellitus and hyperlipemia. Weight loss improves insulin sensitivity, and NASH may resolve with weight reduction. Insulin resistance seems to be the common denominator in many cases of NAFLD. Two classes of drugs have been shown to correct insulin resistance: biguanides (e.g., metformin) and thiazolidinediones (e.g., rosiglitazone and pioglitazone). The last two decades have witnessed a considerable progress in the understanding of the mechanisms respon-sible for the fibrogenic progression of chronic liver diseases. Several drugs believed to be hepatoprotective or antifibrotic agent as UDCA, betaine, vitamin E, lecithin, beta-carotene and selenium have been used in patients with NASH. Silybin is the main component of silymarin that is absorbed when linked whith a phytosome. This substance reduces in rats the lipid-peroxidation and the activaction of hepatic stellate cells. In humans, some non controlled data show that silybin is able to reduce insulin resistance, liver steatosis and plasma markers of liver fibrosis.

Anti-Obesity Agents↗

PubMed2006

[Oxidative stress in metabolic syndrome and nonalcoholic steatohepatitis. Is it possible a role for vitamins in clinical practice?].

Metabolic syndrome (MS) is a worldwide medical problem characterized by a cluster of cardiovascular risk factors and metabolic modifications involving peripheral insulin resistance. Nonalcoholic steatohepatitis (NASH) represents the liver expression of this pathological condition. Both MS and NASH are characterized by proinflammatory status and increased oxidative stress. According this, we aimed to review the literature for considering a possible role for vitamins as therapeutical support in MS and NASH.

Adult↗

PubMed2006

[Non-alcoholic steatohepatitis : pathology and pathogenesis].

Nonalcoholic steatohepatitis (NASH) has become to be widely recognized as a significant cause of chronic liver injuries. Evidences suggest that development of NASH requires a double "hit". The "first hit" involves the accumulation of fat in the liver, and the "second hit" includes oxidative stress, cytokines, stellate cell activation, and fibrogenesis. Microscopically, some alcoholic hepatitis-like findings, hepatocellular steatosis, ballooning degeneration, Mallory body, acute and chronic lobular inflammation, and zone 3 perisinusoidal fibrosis are noted. Because ballooning degeneration and Mallory body denote progressive NASH, we should identify clearly these findings. The diagnosis of nonalcoholic steatohepatitis requires histopathologic evaluation, because the lesions of parenchymal injury and fibrosis cannot be detected by imaging studies or laboratory tests.

Adaptor Proteins, Signal Transducing↗