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

The earliest and most reproduceable lesion associated with chronic alcohol abuse is fatty liver. In some alcoholics this may be superseded by alcoholic hepatitis, which may represent the link between the early lesion and cirrhosis. Alcoholic cirrhosis usually begins as a regular, monolobular variety, but is eventually transformed into an irregular, multilobular type. All stages of alcoholic liver injury have now been produced in the baboon, despite high protein and vitamin supplemented diets. Alcohol may therefore now be regarded as a direct hepatotoxin. Epidemiological studies have indicated that alcoholic liver injury begins with an intake of more than 80 g ethanol a day, and that cirrhosis is generally not seen with an intake of less than 160 g per day. The development of cirrhosis correlates with the total duration and amount of alcohol ingested. Complications of alcoholic cirrhosis include iron overload and primary hepatic carcinoma.
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PMID:Relation of alcoholic liver injury to cirrhosis. 4 93

Monooxygenase enzymes are involved in the biotransformation of drugs and of environmental carcinogens. The activity of 7-ethoxycoumarin 0-deethylase and associated NADPH-cytochrome c reductase was determined in 9000 g supernatant from bioptically obtained liver specimens from patients with various liver diseases in order to study in vitro drug metabolising capacity. Monooxygenase and reductase activity was significantly higher in the livers of 21 patients with alcoholic liver disease (fatty liver, alcoholic hepatitis, cirrhosis of the liver) than in 22 normal controls or in six patients with chronic active hepatitis. The raised activity of drug-metabolising enzymes obtained from alcoholics with liver damage differs from normal values found in five alcoholics without liver disease. Both groups were comparable in respect to the amount of alcohol consumed and duration of abuse. A strikingly low monooxygenase activity was observed in eight patients with cirrhosis of the liver and ascites, with, however, no apparent effect on reductase activity. The results show that alcoholic liver disease is associated with enhanced monooxygenase and reductase activity, but alcoholism, per se, is not. This rise of drug-metabolising enzyme activity could lead to selectively increased rates of biotransformation in patients with alcoholic liver damage.
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PMID:Monooxygenase enzyme activity in alcoholics with varying degrees of liver damage. 11 58

Chronic alcoholism is a frequently unrecognized cause of ketoacidosis in nondiabetic patients. Seven episodes of alcoholic ketoacidosis were observed in three patients. No consciousness disturbances were present. Semi-quantitative tests for ketones were strongly positive in urine, weakly positive in serum. The anion gap was between 25 and 41 mEq/l; serum lactate was between 0.9 and 9.0 mEq/l, and, in all cases, below the anion excess. Blood glucose ammonia was increased. Massive fatty liver was documented in all patients. All ketosis episodes followed an increase of alcohol ingestion associated with one to four week-starvation and vomiting; however, at the time of admission, alcohol was weakly increased in blood. In the four episodes where diagnosis was correct, ketoacidosis was rapidly corrected without insulin administration. In conclusion, in some nondiabetic subjects, the occurence of alcohol prolongated ingestion together with starvation and vomiting is responsible for ketoacidosis; because alcoholic ketoacidosis has often a mild clinical expression, its true prevalence is underestimated; insulin administration is not required.
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PMID:[Alcoholic ketoacidosis (author's transl)]. 53 15

It has been postulated in recent years that idiopathic necrosis of the head of the femur may possibly be caused by arteriolar obstruction by fat emboli emanating from a fatty liver, which would act as a reservoir, due to various causes such as alcoholism and prolonged steroid therapy. A similar situation has been found in human pathology in post traumatic fat embolism. The writers have reviewed forty five cases of post traumatic fat embolism which had passed the pulmonary filter. All the cases were reviewed after a minimum of two years, since this is considered the minimum time within which necrosis can manifest itself radiologically. In none of these cases was there any evidence of necrosis of the head of the femur. These findings, supported by other critical considerations. do not lend support to the theory of fat embolism as a case of idiopathic bone necrosis.
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PMID:Fat embolism as a cause of idiopathic necrosis of the head of the femur. Review of forty five cases of post traumatic fat embolism. 55 16

Among 2 952 non-selected liver biopsies of adults in the 5-years-period 1970-1974 506 cases (17%) of clinically proved chronic alcoholics were found. Most of the patients are males, and even young men at an age of less than twenty years are taken with. The number of 31 professional drivers within this group is remarkable and alarming, too. The histomorphological picture may be divided into liver changes without any abnormal state (39%), fatty liver (40%), alcoholic hepatitis (18%) and cirrhosis (3%). Chronic alcoholism can be considered as one of the most important causes of the fatty liver. Clinical and pathological aspects of alcoholic liver changes are discussed.
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PMID:[Liver biopsy changes in chronic alcoholism]. 64 47

The hypothesis that mictochondrial damage is a significant factor in the pathogenesis of alcoholic liver disease (ALD) was investigated by enzymic analysis of mitochondrial fractions isolated from needle biopsy specimens from control patients, patients with fatty liver due to chronic alcoholism, and from patients with other forms of liver disease. Enzymes associated with the inner and outer mitochondrial membranes showed normal levels in ALD. Enzymes associated with the mitochondrial matrix, glutamate dehydrogenase, malate dehydrogenase and aspartate aminotransferase showed significantly raised levels in ALD, but the levels in patients with non-alcoholic liver disease was normal. In addition, analysis of the mitochondria by sucrose density gradient centrifugation revealed no differences between control tissue and liver from patients with alcoholic liver disease. These results do not indicate that there is significant mitochondrial damage in ALD. The raised mitochondrial matrix enzymes may represent an adaptive response to the ethanol load.
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PMID:Mitochondrial enzyme activities in liver biopsies from patients with alcoholic liver disease. 65 61

Consecutive liver biopsies from alcoholic, diabetic and overweight patients are compared morphologically and in addition a comparison is made between groups with a combination of two or three of the above conditions. Both fatty change and morphological activity are greater in the groups with alcoholism, and this gives good reason to believe that the activity in the form of alcoholic hepatitis is the cause for the more common development of cirrhosis in alcoholic fatty liver than in fatty liver with other aetiology.
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PMID:Morphological features in non-cirrhotic livers from patients with chronic alcoholism, diabetes mellitus or adipositas. A comparative study. 71 11

A distict alcoholic withdrawal syndrome in chronic alcoholics cannot only be induced upon withdrawal of alcohol or dose reduction but also occurs upon continuous and long lasting consumption of larger quantities of alcohol. In the latter case we deal with an alcoholic predelirium which is characterized by simultaneous occurence of neurologic, vegetative and gastrointestinal disturbances as well as mental symptoms like anxiety, increased irritability and disturbance of sleep. In parallel to this alcoholic withdrawal syndrome from internal medical view a characteristic symptomatology can be observed in patients with chronic alcohol abuse. In most cases younger patients are concerned who, concomitantly with predelirant symptoms frequently display a labile hyperlipidemia and additional obesity, fatty liver, hyperlipidemia and often also hyperuricemia. Based on ten typical cases the combination of symptoms as described above is introduced. This combination can according to Feuerlein be defined as "alcohol-syndrome". The difficulties of diagnosis are shown because in many cases not the alcohol abuse but primarily vegetative and other functional disturbances dominate the clinical appearance. Additionally the pathogenetic connection between the described symptoms and alcohol abuse are discussed.
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PMID:[The "alcohol-syndrome" from internal medical view (author's transl)]. 86 89

Acute alcoholic hepatitis is an anatomical (fatty liver with sclerosing hyaline necrosis) and a clinical (hepatomegaly with a variety of symptoms of hepatic failure) entity arising out of chronic alcoholism, and of a typically 'pre-cirrhotic' state. Although fatal in 25% of acute cases due to failure of homeostasis, it often leaves a centrilobular scarring necrosis which in more than 60% of cases progresses to nodular cirrhosis. Continued alcoholism worsens the prognosis. Alcoholic hepatitis may be confused with acute abdominal catastrophes or with a hepatoma. The characteristic Mallory bodies found on liver biopsy are found rarely in non-alcoholic hepatitis. There is no effective treatment for this disease except reduction of alcohol intake; indeed, the disease may become self-perpetuating.
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PMID:[Acute alcoholic hepatitis]. 92 58

"Cures" embrace by definition a broad spectrum starting from taking waters in health resorts to hospital treatment in modern rehabilitation centers. The effectiveness of traditional cure procedures is discussed. Effectiveness of drinking cures, baths and mud packs in liver disease has not yet been proven. Controlled trials are necessary. Clinical treatment is indicated in alcoholic liver damage, viral hepatitis with a protracted course, chronic aggressive hepatitis and compensated cirrhosis of the liver; such treatment, however, is questionable in fatty liver and in chronic persistent hepatitis. Data concerning the effectiveness of treatment of chronic liver diseases are given. The following conclusions are drawn: patients with liver disease ought to be hospitalized when undergoing cures, indications have to be precised, collaboration of patients has to be stimulated, hospital discipline has to be tight, therapy of alcoholism has to include several psychosocial aspects, treatment after leaving hospital has to be improved.
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PMID:[Is there a therapeutic effect of cures undergone by patients with chronic liver disease? (authors transl)]. 92 80


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