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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previously regarded as an obscure disorder, nonalcoholic steatohepatitis (NASH) has recently emerged as an important chronic liver disease. NASH is within a spectrum of disorders characterized by excessive accumulation of fat in the liver, including simple hepatic steatosis (fatty liver), inflammation and necrosis (steatohepatitis), and fibrosis. Collectively, the disorders are called nonalcoholic fatty liver disease (NAFLD). Estimates of the prevalence of these individual conditions are suspect because liver biopsy is required for definitive diagnosis and is not generally performed. Although these conditions have traditionally been thought of as diseases of obese women, and are frequently associated with diabetes mellitus and hypertriglyceridemia, they have also been identified in lean men. Insulin resistance appears to be a common factor. These conditions are difficult to distinguish from each other clinically, and no biochemical or radiological test reliably establishes the diagnosis. A ratio of serum aspartate to alanine aminotransferase levels of less than one can distinguish NAFLD from alcoholic liver disease, but this is a nonspecific finding. Fatty infiltration imparts a diffuse echogenicity to the liver at ultrasonography, but this test cannot easily distinguish fat from fibrous tissue or identify cases of NASH. Only histological examination can establish the diagnosis of NASH, grade its severity, determine the prognosis and guide treatment.
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PMID:Motion - all patients with NASH need to have a liver biopsy: arguments for the motion. 1242 34

Tuberculosis has a major adverse impact on solid organ transplant recipients; this article attempts to define this fact. The prevalence of posttransplant tuberculosis is increasing globally and currently is 13.7% at our center. The transplant surgery divides the continuum of pretransplant tuberculosis and posttransplant tuberculosis; immunosuppression accounts for a greater severity of the latter. Cyclosporin and tacrolimus are associated with an earlier onset of tuberculosis when compared with prednisolone and azathioprine immunosuppression. Disseminated disease is more common in nonrenal transplants. The risk for developing posttransplant tuberculosis in renal transplant recipients increased 2.25 times independently with cytomegalovirus (CMV) and twice with chronic liver disease; OKT3 treatment enhances the risk 1.8-fold. Tuberculosis occurring after 2 years of transplantation, diabetes mellitus, posttransplant diabetes mellitus, chronic liver disease, CMV, and deep mycoses each independently confer a risk, 1.5-times or higher, for death. Disseminated disease entails a 2-fold risk. Treatment with or without rifampicin is possible; the former is associated with a higher risk for allograft rejection. Isoniazid prophylaxis is recommended for high-risk patients with apparent clinical efficacy. However, in endemic areas, attendant liver disease makes it a difficult goal.
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PMID:Mycobacterial infections in organ transplant recipients. 1249 44

Steatohepatitis, of either alcoholic or nonalcoholic etiologies, is ultimately diagnosed by clinical-pathologic correlation and is characterized histologically by lesions that differ from the portal-based chronic inflammation and fibrosis of most other forms of chronic liver disease. With the increasing prevalence of steatohepatitis in our society, it is likely that some patients will have coexistent clinical and/or histopathologic findings of steatohepatitis concurrently with another form of liver disease. The aim of this study was to document clinical and histologic findings in biopsies in an academic referral center. Ninety-three non-allograft liver biopsies with lesions of both steatohepatitis and another liver disease were retrospectively identified in 85 patients. The finding of coexisting disease represented 5.5% of all hepatitis C biopsies and 4.0% of other forms of chronic liver disease in the 34 month time period. Clinical chart review of patients with concurrent disease showed the following: Group 1, patients with hepatitis C (n = 54); Group 2, patients with hepatitis C and prior or current history of more than 80 g/d alcohol consumption (n = 20); Group 3, patients with other forms of chronic liver disease (n = 11). Groups 1 and 3 had <10 g/d alcohol use. Obesity (body mass index >30) was noted in 75%, 60%, and 33% respectively, while 94%, 87% and 100% of patients were considered overweight (body mass index > or = 25). Diabetes was reported in 35%, 25%, and 9%. The concurrence of clinical and histologic features of steatohepatitis with another chronic liver disease may be a reflection of the frequency of steatohepatitis in the population at large.
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PMID:Concurrence of histologic features of steatohepatitis with other forms of chronic liver disease. 1252 13

A high prevalence of type 2 diabetes mellitus in patients with hepatitis C virus (HCV)-related chronic liver diseases has been reported in numerous studies. Other studies failed to confirm this observation. We have studied the relative prevalence of type 2 diabetes mellitus in two groups of patients respectively presenting with HCV-related chronic liver disease (224 patients) and chronic liver diseases of other etiologies (30 hepatitis B virus-HBV-related chronic liver disease, 22 alcoholic liver cirrhosis), in order to confront them. Our study revealed a higher prevalence of diabetes mellitus in the group of patients with HCV-related chronic liver disease in comparison with the group of patients with chronic liver disease of other etiologies (32.5 vs 15.3%; p = 0.03). Patients with HBV-related liver disease had diabetes in 6.6% of cases, and the difference with patients with HCV-related disease was significant (p = 0.007). Our study confirms a higher prevalence of type 2 diabetes mellitus in patients with HCV-related chronic liver disease. It could be suggested that type 2 diabetes mellitus in patients with HCV-related chronic liver disease could be facilitated by hepatic iron overload and mitochondrial damage.
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PMID:[Prevalence and significance of type-2 diabetes mellitus in chronic liver disease, correlated with hepatitis C virus]. 1273 22

Diabetes mellitus is a common endocrine disorder that is becoming a major public health problem. Viral hepatitis infection is one of the most common causes of chronic liver disease. Several reports from different parts of the world found an association between these two common disorders. In this review we highlight some of the epidemiological aspects of these two disorders, discussed some of the possible mechanisms and questions to be answered to understand this link and be able to solve this mystery.
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PMID:Diabetes mellitus and viral hepatitis: the unsolved mystery. 1286 4

This study examines the association between education and mortality from specific causes of death based on mortality records for 1996 and 1997, and 1996 population census data from the Region of Madrid (Spain). Poisson regression models were used to estimate the percentage increase in mortality associated with 1 year less education. The percentage increases in mortality from stomach cancer, lung, bladder and liver cancers, for aids, chronic obstructive pulmonary disease, pneumonia and influenza, and chronic liver disease and cirrhosis were higher in men than in women, whereas the percentage increases in mortality from colon cancer, diabetes mellitus, ischemic heart disease and nephritis, nephrosis and nephrotic syndrome were higher in women. The results found for some causes of death--lung cancer, ischemic heart disease, diabetes mellitus and chronic obstructive pulmonary disease--reflect the variations by educational level in the prevalence of lifestyle-related risk factors in men and women. Various hypotheses have been suggested for other causes of death, but it is not known why the magnitude of the association between education and mortality from some causes of death differs between men and women. Future studies of this subject may provide some clues as to the underlying mechanisms of this association.
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PMID:The size of educational differences in mortality from specific causes of death in men and women. 1288 84

Nonalcoholic fatty liver disease (NAFLD) is a well recognised form of chronic liver disease that has recently gained greater recognition. Originally described in the late 1950s, NAFLD is currently considered the leading cause of abnormal liver enzyme levels in the US, closely paralleling the increase in obesity and diabetes mellitus. NAFLD has a worldwide distribution, affecting both adults and children, and typically is seen in association with obesity, diabetes, hypertension and hypertriglyceridaemia. Most patients are asymptomatic and usually present with mild elevations in aminotransferases. The natural history of NAFLD is not clearly defined but progression to cirrhosis and end-stage liver disease is well recognised in some patients. The accumulation of hepatic steatosis is thought to occur initially, primarily through hepatic and peripheral insulin resistance, which leads to altered glucose and free fatty acid metabolism. The progression from simple fatty liver to more severe forms of NAFLD (nonalcoholic steatohepatitis and cirrhosis) is much less clear but evidence suggests that oxidative stress may preferentially enhance proinflammatory cytokines, which leads to cellular adaptations and dysfunction followed by development of inflammation, necrosis and fibrosis. Therapeutic modalities remain limited and are largely focused on correcting the underlying insulin resistance or reducing oxidative stress. However, at the present time, there are several limitations to the current potential therapies, mainly because of the lack of large-scale, prospective, randomised studies, as well as clearly defined histological endpoints. Ultimately, the future for potential therapeutic modalities to treat this disease are quite promising, but further research is needed to clearly demonstrate which therapy or therapies will be effective at eliminating fatty liver disease and its potential complications.
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PMID:Advances in the understanding and treatment of nonalcoholic fatty liver disease. 1460 46

Leptin is involved in the regulation of food intake and is mainly secreted by adipocytes. Major secretagogues are cytokines such as TNF-alpha or IL-1. Leptin in turn upregulates inflammatory immune responses. Elevated leptin serum levels have been detected in patients with liver cirrhosis, a disease frequently associated with elevated levels of circulating cytokines as well as hypermetabolism and altered body weight. Recently, leptin has been detected in activated hepatic stellate cells in vitro and an involvement of leptin in liver fibrogenisis has been suggested. The current study was designed to further clarify the role of leptin in liver disease by characterizing leptin and leptin receptor expression in the development and onset of experimental liver fibrosis. Liver fibrosis and cirrhosis was induced in rats by use of phenobarbitone and increasing doses of CCl (4). Leptin and leptin receptor mRNA expression was determined by semiquantitative RT-PCR, protein expression by Western blot analysis and localization of leptin and its receptor by immunohistochemistry. Normal liver tissue does not express leptin, but leptin receptor mRNA. Increasing levels of leptin mRNA were detected in fibrotic and cirrhotic livers correlated to the degree of fibrosis. Leptin receptor mRNA expression was not significantly altered in damaged livers. Increasing levels of leptin were detected in fibrotic and cirrhotic livers, whereas protein expression of the receptor remained unchanged. Throughout different stages of liver fibrosis, leptin immunoreactivity was localized in activated hepatic stellate cells only, whereas immunoreactivity for the receptor was mainly seen on hepatocytes. In conclusion, leptin is expressed at increasing levels in activated hepatic stellate cells in vivo, which may therefore be a source of increased leptin tissue and serum levels contributing to the pathophysiology and morphological changes of chronic liver disease.
Exp Clin Endocrinol Diabetes 2004 Jan
PMID:Expression of leptin and leptin receptor during the development of liver fibrosis and cirrhosis. 1475 66

Ten percent of patients who undergo resection for hepatocellular carcinoma (HCC) associated with chronic liver disease have no detectable cause for this underlying liver disease. Recent studies have shown that patients with cryptogenic chronic liver disease frequently have risk factors for nonalcoholic fatty liver disease (NAFLD). This study examines the incidence of risk factors for NAFLD in patients with chronic liver disease who underwent resection for HCC. Among 210 patients with chronic liver disease who underwent resection for HCC, 18 (8.6%) had no identifiable cause for the underlying liver disease. These patients were assessed for obesity, diabetes mellitus, and histological features of the tumor and the adjacent liver parenchyma. Comparisons were made with matched patients with alcohol- and chronic-viral-hepatitis-related HCC. The prevalence of obesity (50% vs. 17% vs. 14%), diabetes (56% vs. 17% vs. 11%), aspartate aminotransferase/alanine aminotransferase ratio<1 (50% vs. 19% vs. 17%), and steatosis>20% (61% vs. 17% vs. 19%) was significantly higher in patients with cryptogenic liver disease than in patients with alcohol abuse and chronic viral hepatitis (P<0.0001 for each). Well-differentiated tumors were significantly more common in patients with cryptogenic liver disease (89% vs. 64% in patients with alcohol-related HCC vs. 55% in patients with chronic viral hepatitis-related HCC, P<0.0001). In conclusion, the hypothesis that obesity and diabetes mellitus may be important risk factors for cryptogenic chronic liver disease in patients with HCC is supported by the analysis of surgically treated patients. Whether HCC is primarily related to obesity and diabetes mellitus or secondarily to a NAFLD-like parenchymal lesions remains to be clarified.
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PMID:Obesity and diabetes as a risk factor for hepatocellular carcinoma. 1476 43

In this 11th article in a series, reference values of serum levels alpha(2)-macroglobulin alpha(2)M) are examined. The study is based on a cohort of 40,420 Caucasian individuals from northern New England that were tested in our laboratory between 1994 and 2000. Measurements were standardized against Certified Reference Material (CRM 470)/Reference Preparation for Proteins in Human Serum (RPPHS) and the results analyzed using a previously described statistical approach. Individuals with unequivocal laboratory evidence of inflammation (C-reactive protein >10 mg/L) were excluded in one leg of the study and included in the other, confirming that alpha(2)M does not respond to acute phase drive in man. Nephrotic syndrome, diabetes mellitus, and chronic liver disease have significant effect on levels of alpha(2)M. Dramatic changes occur during life with males higher from birth to age 12, females thereafter have higher values until the ninth decade. When values were expressed as multiples of the age- and gender-specific median levels, the resulting distributions fitted a log-Gaussian distribution well over a broad range. When patient data are normalized in this manner, the distribution parameters can be used to assign a centile corresponding to an individual's measurement thus simplifying interpretation.
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PMID:Reference distributions for alpha2-macroglobulin: a practical, simple and clinically relevant approach in a large cohort. 1506 15


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