Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome. Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug-induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice-like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease. The clinical syndrome of alcoholic liver disease is the result of three factors--parenchymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension. Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol- or acetaldehyde-altered proteins, and questionably enhanced by viral hepatitis. Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug-induced injuries, jejunoileal bypass, and related "shortcircuiting" of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminophen is the prime example.
 ...
PMID:Alcoholic liver disease: pathologic, pathogenetic and clinical aspects. 205 45

Alcohol-like liver disease may be observed in patients with obesity or non insulin-dependent diabetes, or after treatment with such antianginal drugs as amiodarone and perhexiline maleate. In such cases cirrhosis is associated, at histology, with foci of acidophilic necroris, Mallory's bodies and inflammatory neutrophilic infiltrates. Alcohol-like liver disease is rare. It affects mostly women in their fifties and usually is clinically latent. Abnormalities of liver function tests mainly consist of increased serum aminotransferase levels. Complications of portal hypertension are uncommon. The pathogenesis of the disease remains purely hypothetical. In practice, in the absence of antianginal therapy the finding of cirrhosis in an obese and/or diabetic patient should prompt a search for excessive alcohol consumption before ascribing the cirrhosis to obesity and/or diabetes.
 ...
PMID:[Pseudo-alcoholic cirrhosis]. 206 19

Malnutrition is a common problem of patients undergoing liver transplantation. To treat malnutrition, it must first be identified through a nutritional assessment. Because many objective nutritional assessment parameters have limitations in end-stage liver disease, subjective nutritional indicators may be used as an alternative. Nutritional needs following transplantation are categorized as short and long term. The short-term nutritional goal, anabolism, can be complicated by the nutritional status of the patient, surgical procedures, and necessary medications. The increased nutrient needs during the early posttransplant phase require particular nutritional support. Nutrition-related problems following transplantation may include obesity, hyperlipidemia, hypertension, diabetes mellitus, hyperkalemia, edema, or osteoporosis. Dietetic advice relative to the nutritional needs of the liver transplant recipient can improve both the short- and long-term outcomes.
 ...
PMID:Nutritional implications of liver transplantation. 208 51

Insulin resistance is a cause for morning hyperglycemia seen in diabetic patients. Other reasons for morning hyperglycemia should be eliminated by performing an insulin response test. Once insulin resistance has been established as the cause of hyperglycemia, a step-by-step process should be used to establish the cause of the insulin resistance. Common causes of insulin resistance include hyperadrenocorticism, acromegaly, hyperthyroidism, and obesity. Hepatic disease, renal insufficiency, and sepsis are other causes of insulin resistance in practice. Less common causes include insulin antibodies, pregnancy, neoplasia, hyperandrogenism, and pheochromocytoma. If the underlying cause cannot be found or resolved, then increased doses of insulin are required to manage the hyperglycemia.
 ...
PMID:Problems in diabetes mellitus management. Insulin resistance. 213 77

Forty-two patients with nonalcoholic steatohepatitis were followed for a median of 4.5 yr (range = 1.5 to 21.5 yr). Except for two patients with lipodystrophy, all were obese; 35 of 42 were women, 26 of 32 were hyperlipidemic and 15 were hyperglycemic. Upper abdominal pain was the most common reason for presentation. Initial liver biopsy specimens showed the presence of macrovesicular fatty infiltration, lobular (acinar) inflammation, apoptosis, Mallory bodies (in four cases) and fibrosis (in 18 cases). Cirrhosis was present at initial diagnosis in one subject and in another two subjects liver biopsy showed marked fibrosis with disturbed architecture. Serial liver biopsy specimens revealed minimal or no apparent progression of the disorder in most of the patients, in keeping with their benign clinical course. However, one patient showed progression from fibrosis to cirrhosis during the 5-yr observation period, and in the patients with extensive fibrosis the liver disease evolved from one of active inflammation to one of inactive cirrhosis without fat or inflammation. The patient with cirrhosis later died of hepatocellular carcinoma. The severity or type of hepatic change did not correlate with the degree of obesity, hyperlipidemia or hyperglycemia. However, in individual patients, poorly controlled diabetes and rapid weight loss preceded the onset of steatohepatitis. We conclude that nonalcoholic steatohepatitis is a cause of hepatic inflammation histologically resembling that of alcohol-induced liver disease but usually slowly progressive and of low-grade severity. However, the disorder may ultimately result in cirrhosis. Nonalcoholic steatohepatitis should be distinguished from alcoholic steatohepatitis and recognized as a further cause of "cryptogenic cirrhosis."
 ...
PMID:The natural history of nonalcoholic steatohepatitis: a follow-up study of forty-two patients for up to 21 years. 1503 Sep 72

The significance of hepatic changes in methotrexate-treated RA patients is unclear at this time. In our group of RA patients, there was a slight increase in the incidence of triaditis and fat during methotrexate therapy. Disease duration greater than or equal to 10 years was associated with increased hepatic triaditis before treatment. Age greater than 50 years was associated with increased hepatic fat before and after treatment. It appears that patients' ages and duration of underlying RA account for some changes, independent of methotrexate therapy. Several of our patients changed from higher to lower histologic grade or had an apparent decrease in fibrosis, fat, or triaditis on the pathologists' reports and the blind readings of the repeat biopsies. This may be explained by sampling error. More importantly, some of these changes may not be of clinical significance. One report of methotrexate-induced cirrhosis in patients with psoriasis demonstrated that in all but one of 14 patients who continued receiving methotrexate the cirrhosis decrease or did not progress. This may also be true of the hepatic fibrosis seen in RA after methotrexate treatment. In this study, there did not appear to be changes seen on pretreatment liver biopsy that were predictive of subsequent fibrosis or cirrhosis. Our data indicate that pretreatment biopsy is unwarranted in a population similar to ours. However, our practice has been to try to avoid methotrexate in patients with diabetes, prior liver disease, alcoholism, or obesity because of previous reports suggesting that these patients are at increased risk for the development of cirrhosis. Only the above-mentioned patient, eventually diagnosed as having cirrhosis, might have been handled differently. Including the study, none of the approximately 700 RA patients in the literature having liver biopsies after methotrexate therapy have developed cirrhosis consequent to its use. Most of these had received a total dose of approximately 1,500 mg in small weekly doses, and alcohol was prohibited. Below this cumulative dose the risk of clinically significant liver damage in carefully selected patients is very low. In view of this experience, the recommendation that RA patients have liver biopsies after 1,500 mg of methotrexate (a holdover from the psoriasis literature) may be too conservative in low-risk RA patients, provided methotrexate is administered weekly and alcohol is prohibited. Recognizing that the absolute need for biopsy is unproven, a more realistic milestone for those choosing biopsy might be after each 2,000 to 2,500 mg.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Prospective analysis of liver biopsies before and after methotrexate therapy in rheumatoid patients. 277 58

Two patients who presented with steatohepatitis had acquired partial lipodystrophy. This association has not previously been well documented. A common pathophysiological mechanism in lipodystrophy, obesity-associated nonalcoholic steatohepatitis, and alcoholic liver disease is possible.
 ...
PMID:Steatohepatitis associated with limb lipodystrophy. 277 26

A 54-year-old woman with obesity, type II diabetes mellitus, hyperlipidemia, and massive hepatomegaly was found to have severe steatosis and cirrhosis on liver biopsy. Complete evaluation led to the diagnosis of fatty cirrhosis associated with obesity and diabetic mellitus. She underwent four months of fasting with a protein-carbohydrate and vitamin-mineral liquid supplement to control her weight and metabolic abnormalities and to evaluate the effect of this diet on her liver disease. She lost 40 pounds to ideal body weight, normalized her serum glucose and lipids, and decreased total liver height by one third. Liver biopsy at the completion of her diet showed inactive cirrhosis and complete resolution of steatosis. Supplemented fasting with only modest weight loss can safely resolve fatty liver in obese diabetics with nonalcoholic steatosis and cirrhosis. Aggressive dietary approaches to achieve long-term weight loss deserve study in this subgroup of diabetics with unexplained chronic liver disease.
 ...
PMID:Steatosis and cirrhosis in an obese diabetic. Resolution of fatty liver by fasting. 382 84

Modern contraceptive methods are discussed, with special emphasis on oral contraceptives, which are regarded as the most effective. They are also regarded as generally safe, although there are contraindications and the drugs should only be prescribed after careful examination. The need for selecting the drug most suitable for the individual patients, mainly on the basis of the characteristics of the menstrual cycle (suggesting a predominance of estrogen or progestin, within safety limits, such as 50 mcg of estrogen), is emphasized. The examinations required include a general clinical, gynecological, and breast examination, cytology tests, evaluation of the menstrual flow pattern, measurements of arterial pressure, weight, glucose, cholesterol and triglyceride levels, and urine tests. They should be repeated at 6-month intervals, or 3-month intervals in the case of high-risk patients (varicose veins, obesity, heavy smokers, high cholesterol and triglyceride levels, history of jaundice, slight heart condition, clinical or potential diabetes, porphyria or predisposition to uterine myoma). Oral contraceptives are contraindicated in cases presenting a history of thromboembolism, phlebitis, cerebral apoplexy; sickle cell anemia, which indicates a predisposition to thromboembolic accidents; serious liver disease or recent hepatitis; serious heart disease; hormone-dependent neoplasia (breast cancer); predisposition to uterine cancer; erythematous lupus; metorrhagia of unknown origin; psychic disorders, especially of a depressive type. They should also be avoided for 3-4 years after puberty, in order to avoid interfering with the development of the hypothalamus and with growth. A carcinogenic effect of the pill and an increase in the risk of giving birth to abnormal children can be ruled out, although the incidence of abortions due to chromosome anomalies after suspending treatment is rather high (due to the previous inhibition of ovulation, a situation similar to repeated pregnancies at short intervals, which involve the same risk).
 ...
PMID:[Current clinical problems of contraception]. 502 53

In order to assess insulin sensitivity for glucose utilization in the other type of diabetes, insulin sensitivity tests were performed in subjects with pancreatitis, liver disease, steroid treatment and hyperthyroidism. Insulin sensitivity for glucose utilization decreased in subjects with liver disease, steroid treatment and hyperthyroidism irrespective of the presence or absence of glucose intolerance. Hyperinsulinism was associated in most of the subjects with liver disease and steroid treatment, but even in normo-insulinemic subjects, insulin insensitivity was observed. Obesity was associated with only 2 cases in both pancreatitis and liver diseases and therefore was excluded as a major cause for insulin insensitivity in subjects studied. In subjects with pancreatitis, insulin sensitivity was not significantly decreased. It is to be noted that 4 out of 5 subjects with diabetic OGTT (oral glucose tolerance test) exhibited normal insulin sensitivity. The results indicate that in pancreatitis, tissue insulin sensitivity for glucose metabolism is not altered and therefore can be used as a marker to differentiate the other type of diabetes due to pancreatitis from type 1 or 2 diabetes. Although hyperinsulinemia may be attributable to insulin insensitivity in subjects studied at least in part, steroid and thyroid hormone are thought to act directly antagonistically with insulin for glucose metabolism.
 ...
PMID:Insulin sensitivity in pancreatitis, liver diseases, steroid treatment and hyperthyroidism assessed by glucose, insulin and somatostatin infusion. 614 89


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>