Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty patients with alcoholic cirrhosis, ascitic during 13.6 +/- 13 months (mean +/- S.D.) were cured of ascites and followed up during 2 to 9 years (4.3 +/- 2.7 years). Twenty six were compared with a same number of cirrhotics, matched for age and sex, who died during the year after the first admission. Many biological data show statistical difference. Nevertheless no valuable prognosis can be predicted in an individual case. The clinical improvement is associated with major, sometimes total biological recovery. Other complications of cirrhosis (gastro-intestinal bleeding, hepatoma) may occur (7 cases with 5 deaths) or alcoholic hepatitis if alcohol withdrawal is stopped (3 cases, 2 deaths). Some associated diseases look unexpectedly frequent: diabetes (4 cases), obesity (9), nodular lipomatosis (14 cases) whose frequency looks higher than that can be calculated for a similar group of healthy subjects.
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PMID:[Recovery after treatment for cirrhotic ascites : a study of 90 cases. Frequency of arterial hypertension (author's transl)]. 49 44

Obesity is associated either with hepatic steatosis, a well known and innocuous entity or with non alcoholic steatohepatitis. This latter lesion has been recently individualized. It affects mainly middle-aged, obese women, with diabetes and/or hyperlipidaemia. It is morphologically very similar to alcoholic hepatitis. We review the literature considering 1) histologic hepatic lesions of the obese, 2) epidemiologic, clinical and biological characteristics of the non alcoholic steatohepatitis, 3) evolution and treatment of the non alcoholic steatohepatitis and 4) present physiopathological considerations. We conclude by considering the clinician's attitude in front of an obese potentially afflicted by a non alcoholic steatohepatitis.
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PMID:[Obesity: danger for the hepatocytes?]. 133 21

A 28-year-old woman with diabetes mellitus and alcoholic hepatitis presented a rare case of Buschke Lowenstein tumor, or giant condyloma of vulva. HPV DNA of this tumor was detected by in situ hybridization using tritium labeled HPV 6 b, 16 and 18 DNA. This tumor appeared to harbour HPV 6 b DNA, but other HPV DNAs were negative. The distribution of HPV 6 b DNA was detected in the nucleus of the squamous epithelium showing koilocytosis. Total vulvectomy and resection of the clitoris were done. The postoperative course was uneventful and there has been no recurrence of tumor so far.
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PMID:[A case report of Buschke-Lowenstein tumor (giant condyloma)]. 184 13

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.
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PMID:Alcoholic liver disease: pathologic, pathogenetic and clinical aspects. 205 45

Hepatocytes and bile duct epithelium express several types of cytokeratins, the characteristic intermediate-filament proteins of epithelial cells. The cytokeratin antigen expression was studied in normal and diseased livers, intrahepatic cholangiocarcinomas, and hepatocellular carcinomas by immunohistochemical methods using a panel of polyclonal and monoclonal antibodies to cytokeratins. Ten percent formaldehyde solution-fixed, paraffin-embedded sections obtained from ten patients without liver disease, 18 patients without liver disease, 18 patients with different stages of primary biliary cirrhosis, 14 patients with alcoholic hepatitis, ten patients with fatty liver hepatitis secondary to diabetes mellitus or morbid obesity, five patients with hepatocellular carcinomas, and five patients with cholangiocarcinomas were examined. The results suggested that hepatocytes and bile duct epithelium retain their distinct cytokeratin profiles in liver disease, including malignant transformation. Therefore, demonstration of cytokeratins in the liver is useful in establishing the cellular origin of neoplasms and understanding the pathogenesis of liver diseases.
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PMID:Expression of cytokeratins in normal and diseased livers and in primary liver carcinomas. 246 75

Liver biopsies from nine patients with maturity-onset diabetes and fatty liver hepatitis were semiquantitatively assessed, and the findings compared with those in alcoholic hepatitis. Overall appearances were similar, but the lesion in some diabetics was periportal rather than perivenular in location, and nuclear vacuolation of hepatocyte nuclei was always present. The inflammatory infiltrate often included neutrophil leucocytes, as in the alcoholic. In three patients with multiple biopsies, progression appeared to be slow, but one patient developed cirrhosis.
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PMID:The pathology of diabetic hepatitis. 263 85

About 90 per cent of morbidly obese patients show histological abnormalities of the liver. One third of patients have fatty change involving more than 50 per cent of hepatocytes. Fatty liver disease can be divided into four histological groups: Fatty liver, fatty hepatitis, fatty liver with portal fibrosis, and cirrhosis. Most patients show only fatty change. Alcohol, drugs, diabetes, poor nutrition, and weight-reducing surgery contribute to progressive liver damage, but morbid obesity alone may lead to severe disease showing all the features of alcoholic hepatitis and may end in cirrhosis and liver failure. The accumulation of fat alone is unlikely to be the stimulus to inflammation and fibrosis. Only one fifth of patients have complaints that arise from the liver. The development of severe fatty liver disease may also be asymptomatic and rarely shows the florid picture associated with alcoholic hepatitis. There is poor correlation of liver function test results with morphology in obesity. ALT levels exceeding twice the normal limit have some predictive value for histological grades of severity, but they are present in few patients. Pericentral and pericellular fibrosis in prebypass liver biopsies may be an important prognostic lesion for the development of fatty hepatitis and cirrhosis. In contrast with the frequent progression to massive fatty change, inflammation and fibrosis after bypass surgery, weight loss by low-calorie dieting, or starvation is accompanied by improvement in fatty change and return of liver function tests to normal.
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PMID:Fatty liver disease in morbid obesity. 331 4

A unique hepatic adenoma developed in a 26-year-old woman who had used oral contraceptives for 10 years and Tolinase (tolazamide sulfonylurea) for adult-onset diabetes mellitus for five years. Clinically, radiographically, and grossly, the neoplasm showed the usual features of a hepatic adenoma, but microscopically it strongly resembled alcoholic hepatitis with steatonecrosis and Mallory bodies. The surrounding hepatic parenchyma was entirely normal. On transmission electron microscopy these Mallory bodies appeared to be tangles of intermediate filaments. They stained readily with antibodies to cytokeratin but not with antibodies to epidermal keratin or vimentin, just as in "alcoholic" hyalin.
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PMID:"Alcoholic hepatitis" in a hepatic adenoma. 359 92

Two groups, 16 nonalcoholic steatohepatitis patients (group I) and 22 alcoholic hepatitis patients (group II) classified according to the presence or absence of drinking and their histological characteristics, were compared on the basis of clinical, biochemical, and liver biopsy findings. The frequencies of female patients (p less than 0.01), obesity (p less than 0.001), and maturity-onset diabetes (p less than 0.005) were significantly greater in group I than in group II. The serum glutamic pyruvic transminase (p less than 0.05) and gamma-glutamyltranspeptidase (p less than 0.05) contents were significantly greater in group II than in group I. The cholinesterase content (p less than 0.05) was significantly less in group II. Significant differences were found in the grades of nuclear vacuolation (p less than 0.001, Fisher's exact probability test), periportal pericellular fibrosis, proliferation of bile ductules, and changes in the shape of the portal tracts (p less than 0.001, Wilcoxon's rank-sum test). Zonal necrosis in group I was seen in only severe steatohepatitis. These clinical and biochemical findings were found to be useful in differentiating nonalcoholic steatohepatitis from alcoholic hepatitis. Liver biopsy was of limited value at best in separating the two conditions.
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PMID:Comparison between nonalcoholic steatohepatitis and alcoholic hepatitis. 360 26

A 68-year-old male patient without any previous thyroidal disease developed three times of transient primary hypothyroidism associated with protein-calorie malnutrition (PCM). Because of his diabetes mellitus, alcoholic hepatitis, chronic pancreatitis and blind loop syndrome, his nutritional balance was easily disturbed leading to PCM. Although he recurrently developed primary hypothyroidism associated with PCM, this condition was completely restored by protein-calorie repletion. The possibility of dietary iodine deficiency was negated by the observation that his daily urinary iodine secretion was more than 4 mg/day. Plasma amino acid analysis revealed severe depletion of phenylalanine, tyrosine and other essential amino acids and raised the possibility that this hypothyroidism was caused by amino acid deficiency. In order to clarify the mechanisms of this primary hypothyroidism, we have investigated the change of thyroid functions during protein-calorie repletion by total parenteral nutrition (TPN). We then removed iodine from the nutrients for TPN to ascertain that iodine deficiency was not the cause of the primary hypothyroidism in the present case. In spite of the removal of iodine, serum T4 and T3 suddenly increased from 1.1 micrograms/dl and less than 25 ng/dl to 3.5 micrograms/dl and 59 ng/dl, respectively, in a few days after the beginning of TPN. They continued to increase thereafter and reached 6.3 micrograms/dl and 115 ng/dl in 6 weeks. Serum free T4 also showed a sudden increase from 0.56 ng/dl to 1.7 ng/dl after TPN and remained above 1.3 ng/dl thereafter. Serum reverse T3 showed a rapid increase after TPN, but, 4 weeks later, returned to the previous level before TPN. Serum TSH decreased from 120 microU/ml to 17 microU/ml in a few days after TPN and reached a level within normal range in 4 weeks. Serum TBG gradually increased from 10.7 micrograms/ml to 29.2 micrograms/ml in 6 weeks. These results show that the T4 synthesis was extremely impaired by PCM in spite of the strong stimulation by TSH and that this suppression of T4 synthesis by PCM led the patient recurrently to the primary hypothyroidism. We have next investigated the possibility whether the deficiency of phenylalanine and tyrosine could cause a suppression of T4 synthesis because tyrosine is an important substrate of T4. For this purpose we removed phenylalanine and tyrosine from TPN and added iodine to prevent iodine deficiency due to prolonged iodine-depleted nutrition. Reduction of phenylalanine and tyrosine resulted in a marked decrease in serum T4, T3 and TBG in 7 weeks, but gave no change to free T4. Serum TSH remained within normal range.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Contribution of amino acid deficiency to primary hypothyroidism associated with protein-calorie malnutrition]. 393 44


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