Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to describe unexplained and explained natural deaths among decreased above 1 year of age in a series of medico-legal autopsies collected over a 20-year period (1972-1992). Unexplained natural deaths can be defined as those deaths where no cause-of-death is revealed after post-mortem and without circumstances indicating violent death. The death was considered to be natural in 491 cases above 1 year of age among a total of 2004 medico-legal autopsies. In 428 of these cases an explanation as to the cause-of-death was reached. The three most frequently encountered causes-of-death were complications to coronary atherosclerosis (62.6%), diseases of the lung (12.4%) and diseases in the central nervous system (9.8%). Among 59 cases with unexplained natural death, 50 had various chronic diseases or fatty liver. In 43 of these cases the deceased had epilepsy or chronic alcoholism. In nine cases (1.8% of the natural deaths) no explanation to the cause-of-death could be given.
 ...
PMID:Unexplained and explained natural deaths among persons above 1 year of age in a series of medico-legal autopsies. 971 61

The understanding of how alcohol damages the liver has expanded substantially over the last decade. In particular, the genetics of alcoholism, the genesis of fatty liver, the role of oxidant stress, interactions between endotoxin and the Kupffer cell, and the factors that control activation of the hepatic stellate cell (HSC) have been the focus of a great deal of research. Genetic mechanisms for increasing the risk of alcoholism include alterations in alcohol metabolizing enzymes as well as neurobiological differences between individuals. The development of fatty liver may involve both redox forces, oxidative stress, and alterations in peroxisome proliferator activated receptor function. Oxidative stress is now known to involve both microsomal and mitochondrial systems. Recent studies implicate stimulation of Kupffer cells by portal vein endotoxin as a cause of release of cytokines and chemokines, hepatocyte hyper-metabolism, and activation of HSC. These actions appear to be in part gender-dependent and may explain the susceptibility of women to alcoholic liver disease. Activation of HSC underlies liver fibrosis and cirrhosis of all types; control of this activation might permit control of the progression of fibrosis. These advances suggest a number of new approaches as therapy for alcoholic liver injury.
 ...
PMID:Pathogenesis of alcoholic liver disease: newer mechanisms of injury. 1063 42

Alcohol-induced diseases of the liver, such as fatty liver, hepatitis and cirrhosis with the potential development of hepato-cellular carcinoma can cause many effects on the skin. Even though they are not caused by excessive alcohol alone, but also by other diseases of the liver or other diseases of internal organs, an experienced person will be able to carry out specific diagnostic procedures. Skin symptoms due to liver diseases include 1. Vascular changes, such as spider nevi, teleangiectasias and palmar erythema. 2. Nail changes, particularly white nails. 3. Changes of the mucous membranes, i.e. glossy tongue. 4. Changes due to altered hormones, particularly gyneco-mastia, female distribution of hair and testicular atrophy and 5. Changes in the color of the skin like icterus and melanosis cutis. Rarely pruritus and other diseases of the skin are seen, such as porphyria cutanea tarda, which is often caused by an altered liver function. In the final stages of alcoholism, the neglect of personal hygiene particularly of the skin is evident (cutis vagantium). Since the exact mechanism of the skin symptoms remains obscure, it is difficult to evaluate the significance. Most often they do not correlate with the severity of the liver disease.
 ...
PMID:[Skin manifestations of alcoholic liver damage]. 1080 82

A computer model was developed with decision analysis software to explore the long-term clinical and economic outcomes of alcohol abstinence maintenance with either standard counselling therapy or standard therapy plus 48 weeks of adjuvant acamprosate in detoxified alcoholic patients. Important complications of alcoholism were modelled using Markov processes, and included relapse (return to drinking), alcohol-related hepatic disease, acute and chronic pancreatitis, acute and chronic gastritis, oropharyngeal carcinoma, oesophageal carcinoma, alcoholic cardiomyopathy, alcohol-related peripheral neuropathy, alcoholic psychosis, accidental death, and suicide. Probabilities of developing complications were dependent on whether the patients within the cohort remained abstinent or had relapsed. Relapse rates, probabilities, and costs for acamprosate therapy and treatment of complications were taken from published literature. The analysis was performed from the German health insurance perspective. Life expectancy and total lifetime costs (costs of initial abstinence maintenance therapy plus costs of complications) were calculated for a typical male cohort with average age of 41 years, 80% with fatty liver, 15% with cirrhosis, 22% with chronic pancreatitis, and 1% with alcoholic cardiomyopathy at baseline. Life expectancy with and without acamprosate therapy was 15.90 and 14.70 years respectively, and discounted (5% per annum) average total lifetime costs per patient were DEM 46 448 and DEM 49 549 respectively. We conclude that, despite the acquisition costs of DEM 2177, adjuvant acamprosate therapy was both clinically and economically attractive under conservative assumptions.
 ...
PMID:The long-term cost-effectiveness of improving alcohol abstinence with adjuvant acamprosate. 1102 23

Associated visceral organ involvement evidence by systemic fibrosis has not been explored in oral submucous fibrosis (OSF). The investigations in this aspect were limited to loco-regional sites of naso/oropharynx and oesophagus. The study of whether the oral fibrosis is part of a systemic spectrum of disease involving multiple organs is an interesting pursuit. With this intention the patients diagnosed on clinical and histological grounds for OSF were concurrently tested by biophysical means for the presence of endomyocardial fibrosis (EMF), pancreatic (PF) and retroperitoneal fibrosis (RPF), which are endemic to the area studied. Twenty-five (n = 25) cases of OSF who visited the Department of Oral pathology & Microbiology. Govt. Dental College, Trivandrum, India for symptomatic relief of their illness comprised the study group. Ten (n = 10) age and sex matched healthy volunteers comprised the control. All the subjects have had undergone cardiologic and gastrointestinal investigations to rule out the possibility of concurrent EMF and PF. The patients were all of Indian ethnic extraction and mostly (> 90%) were from low socio economic classes. The mean age of the patients was 54.16 +/- 14.6 years, including 18 females and 7 males (F:M = 2.57:1). The severity of fibrosis was unrelated to the age of patients (P > 0.05). All the patients were chewers of areca quid (12%)/tobacco (88%). In addition to quid chewing 3/25 (12%) patients smoked 'bidi' and 6/25 (24%) consumed home brewed liquor (arrack/toddy) which contain about 40-50% ethanol. Statistically no relationship was observed between the clinical stages of OSF and severity of epithelial dysplasia in this study (P > 0.05). Out of the 25 patients, 5 (20%) showed sclerotic aortic value which may be an age related finding. Also 7 (28%) patients were found to be hypertensive and interstitial lung disease was present in 2 (8%). The possibility of EMF in one female patient who showed thickened RV apical endocardium was ruled out by cardiac catheterisation. Thus none of the patients showed evidence of endomyocardial fibrosis. The pancreas was found to be hyperchoic in 8(32 1/4) by ultra sonography. Liver was found to be hyperchoic in 6 (24%). Fat stain in stool samples was found to be positive in 13(58%). The hyperchogenecity of pancreas may be due to alcoholism or an underlying endocrine pancreatic insufficiency like diabetes and not due to pancreatic fibrosis. The positivity of fat stain could be due to fatty liver/alcoholism. Thus the study fails to reveal any evidence of pancreatic fibrosis in the group. The lack of any evidence of an associated visceral organ fibrosis in OSF made it prudent to believe that this is a loco-regional disease, initiated by local factors and propagated under their influence without systemic involvement.
 ...
PMID:Visceral organ involvement is infrequent in oral submucous fibrosis (OSF). 1144 4

Obesity is associated with a number of metabolic and haemodynamic risk factors for cardiovascular disease and type 2 diabetes mellitus. This risk depends on a complex of metabolic and haemodynamic consequences of (visceral) fat accumulation, which probably results from the continuous delivery of fatty acids to the liver via the portal vein. Hypertriglyceridaemia, hyperinsulinaemia, hypertension, insulin resistance and increased hepatic glucose production are all independent risk factors for atherosclerosis. Their combination increases the risk of cardiovascular disease considerably. Triglyceride storage in hepatocytes is another consequence of increased fatty acid supply to the liver. Until recently, hepatic steatosis was considered a harmless condition secondary to obesity or alcoholism. However, it may lead to non-alcoholic hepatic steatosis, which predisposes to liver fibrosis and even cirrhosis.
 ...
PMID:[Abdominal obesity: metabolic complications and consequences for the liver]. 1160 19

Healthy subjects 40 years old were used as controls in a study of stellate cells (S-100 protein-containing cells, or S-100 cells) in subjects with chronic alcoholism and fatty liver or fatty cirrhosis. S-100 cells were sparsely found in the adenohypophysis of control subjects, and these cells sometimes formed small clusters. However, in chronic alcoholics with fatty liver or fatty cirrhosis, the number of stellate cells in the anterior pituitary tended to be 17 times higher than it was in the control group. No increase in the number of S-100 positive cells that constitute the large and small follicles in the intermediate pituitary. The physiological function of the S-100 protein has not yet been identified. The fact that an increase in prolactin-secreting and growth hormone-secreting cells, as well as a decrease in gonadotrophs were observed in the hypophysis of alcoholics suggests that the function of stellate cells may be closely related to these phenomena. Our results also imply that the stellate cells found in the anterior and intermediate pituitary differ in function although they both produce S-100 proteins.
 ...
PMID:Increase of S-100 protein-positive stellate cells in the anterior pituitary of chronic alcoholic patients with fatty liver or fatty cirrhosis. 1286 44

Previous studies suggest that hepatic cytochrome P450 2E1 (CYP2E1) activity is increased in individuals with chronic alcoholism, nonalcoholic steatohepatitis (NASH), and morbid obesity, and may contribute to liver disease. We studied 16 morbidly obese subjects with varying degrees of hepatic steatosis and 16 normal-weight controls. Obese subjects were evaluated at baseline, 6 weeks, and 1 year after gastroplasty, a procedure that leads to weight loss. Hepatic CYP2E1 activity was assessed by determination of the clearance of chlorzoxazone (CLZ), an in vivo CYP2E1-selective probe. Liver biopsy tissue was obtained during surgery for histopathology. Both the total and unbound oral CLZ clearance (Cl(u)/F) was elevated approximately threefold in morbidly obese subjects compared with controls (P <.001). The Cl(u)/F was significantly higher among subjects with steatosis involving >50% of hepatocytes, compared with those with steatosis in < or =50% of hepatocytes (P =.02). At postoperative week 6 and year 1, the median body mass index (BMI) of subjects who underwent gastroplasty decreased by 11% and 33%, total oral CLZ clearance declined by 16% (P <.01) and 46% (P <.05), and Cl(u)/F decreased by 18% (P <.05) and 35% (P =.16), respectively. Moreover, those subjects with a year 1 BMI <30 kg/m(2) exhibited a median Cl(u)/F that was 63% lower (P =.02) than the respective clearance for all other subjects. In conclusion, hepatic CYP2E1 activity is up-regulated in morbidly obese subjects. A positive association between the degree of steatosis and CYP2E1 activity preoperatively and between the extent of obesity and CYP2E1 activity postoperatively, suggests that CYP2E1 induction is related to or caused by hepatic pathology that results from morbid obesity.
 ...
PMID:CYP2E1 activity before and after weight loss in morbidly obese subjects with nonalcoholic fatty liver disease. 1288 87

Alcoholic liver disease (ALD) presents considerable challenges to clinicians. Screening for alcohol abuse and alcoholism should be routine and repeated annually with close attention to signs and symptoms of liver disease. In patients with evidence of liver dysfunction or injury, consideration should be given to performance of liver biopsy for diagnosis and prognosis and prior to initiation of medication with the potential for significant side effects. Therapy depends on the spectrum of pathological liver injury: alcoholic fatty liver, alcoholic hepatitis, and cirrhosis. Abstention is the foundation of therapy for an alcohol problem. Alcoholic fatty liver should improve with abstention, but the similarity to the pathogenesis of nonalcoholic fatty liver and potential for progressive injury merits consideration of lipotropic agents. The continuing mortality, poor acceptance of corticosteroids, and identification of tumor necrosis factor-alpha (TNF-alpha) as an integral component has led to studies of pentoxifylline and, recently, anti-TNF antibody to neutralize cytokines in the therapy of severe alcoholic hepatitis. Antioxidant therapy of alcoholic cirrhosis has significant promise but will require large clinical trials.
 ...
PMID:Diagnosis and therapy of alcoholic liver disease. 1534 2

Alcoholic liver disease is a major cause of illness and death in the United States. In the initial stages of the disease, fat accumulation in hepatocytes leads to the development of fatty liver (steatosis), which is a reversible condition. If alcohol consumption is continued, steatosis may progress to hepatitis and fibrosis, which may lead to liver cirrhosis. Alcoholic fatty liver has long been considered benign; however, increasing evidence supports the idea that it is a pathologic condition. Blunting of the accumulation of fat within the liver during alcohol consumption may block or delay the progression of fatty liver to hepatitis and fibrosis. To achieve this goal, it is important to understand the underlying biochemical and molecular mechanisms by which chronic alcohol consumption leads to fat accumulation in the liver and fatty liver progresses to hepatitis and fibrosis. In addition to alcohol consumption, dietary fatty acids and obesity have been shown to affect the degree of fat accumulation within the liver. Again, it is important to know how these factors modulate the progression of alcoholic liver disease. The National Institute on Alcohol Abuse and Alcoholism and the Office of Dietary Supplements, National Institutes of Health, sponsored a symposium on "Role of Fatty Liver, Dietary Fatty Acid Supplements, and Obesity in the Progression of Alcoholic Liver Disease" in Bethesda, Maryland, USA, October 2003. The following is a summary of the symposium. Alcoholic fatty liver is a pathologic condition that may predispose the liver to further injury (hepatitis and fibrosis) by cytochrome P450 2E1 induction, free radical generation, lipid peroxidation, nuclear factor-kappa B activation, and increased transcription of proinflammatory mediators, including tumor necrosis factor-alpha. Increased acetaldehyde production and lipopolysaccharide-induced Kupffer cell activation may further exacerbate liver injury. Acetaldehyde may promote hepatic fat accumulation by impairing the ability of peroxisome proliferator-activated receptor alpha to bind DNA, and by increasing the synthesis of sterol regulatory binding protein-1. Unsaturated fatty acids (corn oil, fish oil) exacerbate alcoholic liver injury by accentuating oxidative stress, whereas saturated fatty acids are protective. Polyenylphosphatidylcholine may prevent liver injury by down-regulating cytochrome P450 2E1 activity, attenuating oxidative stress, reducing the number of activated hepatic stellate cells, and up-regulating collagenase activity. Nonalcoholic steatohepatitis may develop through several mechanisms, such as oxidative stress, mitochondrial dysfunction and associated impaired fat metabolism, dysregulated cytokine metabolism, insulin resistance, and altered methionine/S-adenosylmethionine/homocysteine metabolism. Obesity (adipose tissue) may contribute to the development of alcoholic liver disease by generating free radicals, increasing tumor necrosis factor-alpha production, inducing insulin resistance, and producing fibrogenic agents, such as angiotensin II, norepinephrine, neuropeptide Y, and leptin. Finally, alcoholic fatty liver transplant failure may be linked to oxidative stress. In vitro treatment of fatty livers with interleukin-6 may render allografts safer for clinical transplantation.
 ...
PMID:Role of fatty liver, dietary fatty acid supplements, and obesity in the progression of alcoholic liver disease: introduction and summary of the symposium. 1567 Jun 59


<< Previous 1 2 3 4 5 6 7 8 9 Next >>