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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcoholic cirrhosis represents the terminal stage of alcoholic liver disease (ALD) and one of the main causes of death among alcohol abusers. The aim of this review was to provide an update on alcoholic cirrhosis, with an emphasis on recent findings. Increased alcohol consumption in developing countries is expected to increase cirrhosis mortality. There is a need, therefore, to develop new approaches to the prevention of ALD, including more attention to co-factors that may increase risk of ALD (i.e., obesity and diabetes, chronic HCV infection, and smoking). Furthermore, a better understanding of the pathological mechanisms on the basis of alcohol cirrhosis represents a cornerstone in order to develop new pharmacological treatments. Inflammatory and immune responses along with oxidative stress and alterations in adipokine secretion might contribute in different ways to the evolution of alcohol-induced fibrosis/cirrhosis. As of this date, patients with severe alcoholic hepatitis with a Maddrey Discriminant Factor (MDF) 32 should be offered pentoxifylline and/or corticosteroids unless contraindications exist. For ambulatory patients, S-adenosylmethionine (SAMe) may be considered in a motivated patient with nutritional support. Current studies do not support use of anti-tumor necrosis factor (TNF)-alpha antibody. Finally, achieving total alcohol abstinence should represent the main aim in the management of patients affected by any stage of cirrhosis. In the last decades, several drugs able to increase abstinence and prevent alcohol relapse have been evaluated and some of them have obtained approval for alcohol dependence. Patients with alcoholic cirrhosis; however, are usually excluded from such treatments. A recent study demonstrated the efficacy and safety of baclofen in inducing and maintaining alcohol abstinence in cirrhotic alcohol-dependent patients with cirrhosis. All together the information available suggests the need of a multimodal approach in the clinical management of these patients.
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PMID:Understanding and treating patients with alcoholic cirrhosis: an update. 1938 82

It is well known that insulin resistance affects osteodystrophy, and there is an important relationship between insulin resistance and hepato-biliary disease. It is also well known that hepato-biliary and pancreatic disease is associated with osteodystrophy. In the present review, we describe the mechanism of diabetes and osteodystrophy due to hepato-biliary and pancreatic disease. Hepatic osteodystrophy is associated with malabsorption, abnormalities of vitamin D metabolism, inflammatory cytokines, receptor activator of NF-kappaB ligand, and insulin-like growth factor-1. In particular, tumor necrosis factor-alpha and malabsorption are important factors for viral and alcoholic hepatitis, respectively. Malabsorption due to steatorrhea is important for cholestatic disease and chronic pancreatitis. A greater focus on non-alcoholic steatohepatitis (NASH) and further investigations to clarify the relationship between osteodystrophy and NASH are needed.
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PMID:[Hepato-biliary and pancreatic disease and osteodystrophy]. 1972 Nov 98

Inflammation can be either beneficial or detrimental to the liver, depending on multiple factors. Mild (i.e., limited in intensity and destined to resolve) inflammatory responses have indeed been shown to exert consistent hepatoprotective effects, contributing to tissue repair and promoting the re-establishment of homeostasis. Conversely, excessive (i.e., disproportionate in intensity and permanent) inflammation may induce a massive loss of hepatocytes and hence exacerbate the severity of various hepatic conditions, including ischemia-reperfusion injury, systemic metabolic alterations (e.g., obesity, diabetes, non-alcoholic fatty liver disorders), alcoholic hepatitis, intoxication by xenobiotics and infection, de facto being associated with irreversible liver damage, fibrosis, and carcinogenesis. Both liver-resident cells (e.g., Kupffer cells, hepatic stellate cells, sinusoidal endothelial cells) and cells that are recruited in response to injury (e.g., monocytes, macrophages, dendritic cells, natural killer cells) emit pro-inflammatory signals including - but not limited to - cytokines, chemokines, lipid messengers, and reactive oxygen species that contribute to the apoptotic or necrotic demise of hepatocytes. In turn, dying hepatocytes release damage-associated molecular patterns that-upon binding to evolutionary conserved pattern recognition receptors-activate cells of the innate immune system to further stimulate inflammatory responses, hence establishing a highly hepatotoxic feedforward cycle of inflammation and cell death. In this review, we discuss the cellular and molecular mechanisms that account for the most deleterious effect of hepatic inflammation at the cellular level, that is, the initiation of a massive cell death response among hepatocytes.
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PMID:Decoding cell death signals in liver inflammation. 2356 86

Hepatocellular carcinoma (HCC) accounts for 85-90% of liver cancers and is one of the most frequent carcinomas in the world. HCCs classically develop against the background of chronic liver diseases. Common causes of such liver diseases are viral hepatitis, alcoholic hepatitis, or immune-related diseases; however, 15-50% of patients with HCCs have none of these classic antecedents, especially in developed countries. In this context, obesity and diabetes mellitus have been found to exhibit an increased risk of HCC. Both conditions are associated with insulin resistance. The tumorigenic effects of insulin resistance and complementary hyperinsulinemia could be mediated directly by insulin signaling, or indirectly related to changes in endogeneous hormone metabolism, particularly insulin-like growth factor I. Conversely, insulin resistance may be a consequence of obesity and hepatic inflammation, both of which can themselves promote tumorigenesis, mainly through cytokine production and/or generation of oxidative stress. Because the prevalence of obesity is now increasing throughout the world, insulin resistance is sure to be emphasized as a major factor in hepatocarcinogenesis in the foreseeable future.
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PMID:Insulin resistance and hepatocarcinogenesis. 2619 Apr 83

Rapid excessive alcohol drinking frequently causes disturbance of consciousness due to head trauma, brain edema, hypoglycemia, hyponatremia, hepatic coma and so on, provoked by acute alcohol intoxication. Rapid differential diagnosis and management are extremely important to save a life. On the other hands, the chronic users of alcohol so called alcoholism has many kinds of physical diseases such as liver diseases (i.e., fatty liver, alcoholic hepatitis, alcoholic liver cirrhosis and miscellaneous liver disease), diabetes mellitus, injury to happen in drunkenness, pancreas disease (i.e., acute and chronic pancreatitis and deterioration of chronic pancreatitis), gastrontestinal diseases (i.e., gastroduodenal ulcer), and so on. Enough attention should be paid to above mentioned diseases, otherwise they would turn worse more with continuation and increase in quantity of the alcohol. It should be born in its mind that the excessive drinking becomes the weapon threatening life.
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PMID:[Physical diseases in alcoholism]. 2639 19

Nonalcoholic fatty liver disease (NAFLD) is the liver disease associated with obesity, diabetes, and the metabolic syndrome. Although steatosis is a key histologic feature, liver biopsies of patients with NAFLD can show a wide range of findings. Nonalcoholic steatohepatitis (NASH) is a progressive subtype of NAFLD first defined by analogy to alcoholic hepatitis. Young children may have an alternate pattern of progressive NAFLD characterized by a zone 1 distribution of steatosis, inflammation, and fibrosis. Several grading and staging systems exist, but all require adequate biopsies. Although NASH generally shows fibrosis progression over time, some patients show regression of disease.
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PMID:Histology of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis in Adults and Children. 2706 70

In 1980, Ludwig et al. first reported patients of steatohepatitis who lacked a history of excessive alcohol consumption but showed liver histology resembling alcoholic hepatitis and progression to cirrhosis of the liver accompanied by inflammation and fibrosis. The development of nonalcoholic steatohepatitis (NASH) is associated with obesity, diabetes mellitus, insulin resistance, and hyperlipidemia. However, the pathogenesis of NASH remains incomplete. A "multiple-hit" hypothesis for the pathogenesis of NASH based on an animal model has been proposed and remains a foundation for research in this field. We review the important dietary and genetic animal models and discuss the pathogenesis of NASH.
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PMID:Murine Models of Nonalcoholic Fatty Liver Disease and Steatohepatitis. 2733 18

The aim of the present nationwide population-based cohort study was to explore the prevalence, risk factors, and survival outcome of new-onset diabetes (NOD) in recipients after liver transplantation.The National Health Insurance Research Database of Taiwan was searched for ICD-9-codes, 2248 patients who had received liver transplant without pretransplant diabetes from July 1, 1998 to December 31, 2012 were included in the study. The preoperative risks factors were considered and analyzed using logistic regression analysis, following adjustments for age and sex. All patients were followed up until the end of the study or death.The final dataset included 189 patients with NOD and 2059 without diabetes after liver transplantation. The prevalence of NOD was 8.4% and in 64% NOD appeared in the first year after liver transplantation. Preoperative clinical events, alcoholic liver cirrhosis, and hepatic encephalopathy were the most important risk factors for NOD after liver transplantation. The mortality rate was lower in NOD recipients than in non-NOD recipients within 5 years.In this study, we provide evidence that NOD recipients had better 5-year survival outcomes in this clinical population. The most important identifiable predictive factors for NOD after liver transplantation were alcoholic hepatitis, ascites, hepatic coma, and esophageal varices.
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PMID:Prevalence, predictive factors, and survival outcome of new-onset diabetes after liver transplantation: A population-based cohort study. 2733 69

Although liver transplantation has become accepted as a life-saving treatment of last resort for most life-threatening liver disorders, the use of liver transplantation to rescue patients with severe alcoholic hepatitis unresponsive to medical therapy remains controversial. I propose the concepts that alcohol use disorder is an illness, that on occasion results in alcoholic liver disease and that treatment of alcoholic liver disease, including treatment of patients with severe alcoholic hepatitis, combines treatment of the alcohol use disorder and of alcoholic liver disease. From this I derive the following principal to govern selection of patients for liver transplantation of patients with alcohol use disorder: that alcohol use disorder should impact suitability for liver transplantation as a co-morbid disorder, in the same way as other common co-morbid disorders such as diabetes mellitus or systemic hypertension, are factored in the selection process. We should relate the risk of drinking relapse to the prognosis of the patient after transplantation, rather than in a binary construct of likelihood of maintaining abstinence vs drinking.
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PMID:Liver transplantation for severe alcoholic hepatitis- The PRO view. 2824 Aug 37

This nationwide, population-based study aimed to clarify the effects of immunosuppressive regimens on new-onset diabetes after liver transplantation (NODALT). The National Health Insurance database of Taiwan was explored for patients who received liver transplantation without pre-transplant diabetes from 1998 to 2012. Information regarding clinical conditions and immunosuppressant utilization among these patients was analyzed statistically. Of the 2,140 patients included in our study, 189 (8.8%) developed NODALT. The pre-transplant risk factors for NODALT were identified as old age, male sex, hepatitis C, alcoholic hepatitis, and immunosuppressant use of tacrolimus (TAC). All patients used corticosteroids as a baseline immunosuppressant. The immunosuppressant regimen of cyclosporine (CsA)+TAC+mycophenolate mofetil (MMF) contributed most to NODALT (adjusted hazard ratio 7.596) in comparison with the regimens of TAC+MMF and CsA+MMF; this regimen also contributed significantly to higher post-transplant bacteremia, urinary tract infection, pneumonia, renal failure, and mortality rate. In conclusion, our analysis confirmed TAC-based immunosuppression contributes to higher NODALT incidence than CsA-based regimen, and TAC-CsA conversion due to any causes might lead to worse clinical outcomes. Clinicians should make better risk stratifications before prescribing immunosuppressants for liver transplant recipients.
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PMID:Impact of immunosuppressant therapy on new-onset diabetes in liver transplant recipients. 2886 Jul 88


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