Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study conducted on 228 diabetic patients has shown a significant positive association between serum gamma-glutamyl transpeptidase (GGT) and triglyceride levels. Both fall with treatment, the most marked reduction occurring in patients on insulin. We suggest that the association between serum GGT and triglyceride levels and also the higher incidence of raised GGT and triglyceride levels in new diabetics may reflect hepatic microsomal enzyme induction of the rate-limiting enzymes of triglyceride synthesis. Serum GGT does not seem to correlate with hepatomegaly in diabetes mellitus.
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PMID:The association between serum triglycerides and gamma glutamyl transpeptidase activity in diabetes mellitus. 0 20

The levels of serum gamma-glutamyl transpeptidase (GGT) and, when appropriate, alkaline phosphatase (AP) and 5'-nucleotidase (NTD) have been measured as a routine in 276 patients with malignant haematological diseases during a 26-month trial period. GGT levels add no prognostic information to the routine haematological surveillance of leukaemia. Polychemotherapy does not appear to be an inducer of liver drug-metabolising microsomal enzymes. Polycythaemia rubra vera, myelofibrosis and chronic lymphocytic leukaemia may cause little change in GGT, AP and NTD levels despite marked hepatomegaly. A raised GGT in Hodgkin's disease and non-Hodgkin lymphoma is generally associated with active and widespread disease, but not necessarily a sign of malignant tissue in the liver. The elevations of GGT in myeloma may be secondary to liver infiltration though this group merits further detailed study.
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PMID:Evaluation of the usefulness of serum gamma-glutamyl transpeptidase levels in the management of haematological neoplasia. 2 19

Intensive care patients receiving prolonged total parenteral nutrition (TPN) developed alterations of liver function tests, seen in the activity of certain serum enzymes. Hepatomegaly and jaundice sometimes appeared. The changes in chemical pathology were in serum transaminases activity (GOT, GPT, GDH); alkaline phosphatase and gamma-glutamyltranspeptidase as indices of cholestasis; lactate dehydrogenase, hydroxybutyrate dehydrogenase and creatine phosphokinase, as enzymes related to energy metabolism; pseudocholinesterase, as a protein metabolism-related enzyme. The possible causes of these alterations in critically ill patients undergoing TPN are considered and a functional final metabolic interpretation is proposed.
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PMID:Metabolic changes during prolonged total parenteral nutrition in intensive care. 3 24

2-Deoxy-D-galactose, in a dose of 3 mmol/kg, was administered intraperitoneally twice daily to young rats for periods up to 12 weeks. This dosage schedule resulted in recurrent phosphate trapping predominantly in liver. UTP deficiency was excluded by simultaneous uridine injections. Phosphate trapping was caused by the rapid accumulation of 2-deoxy-D-galactose 1-phosphate and was most pronounced in liver but also demonstrated in small intestine, brain, spleen, and thymus. The marked, although transient, drop in the hepatic content of inorganic phosphate triggered the catabolism of adenine nucleotides and a loss of ATP. Other metabolic pathways affected by phosphate deficiency include glycogenolysis and glycolysis. Increasing with time, repeated doses of the galactose analog led to retardation and arrest of growth, hepatomegaly, and splenomegaly. The average relative liver and spleen weights were elevated 2.5- and 4.5-fold, respectively, after 12 weeks of treatment. Liver damage was indicated by hyperbilirubinaemia and a progressive rise in the activity in plasma of sorbitol dehydrogenase, alkaline phosphatase, and gamma-glutamyltransferase. Examination by light and electron microscopy showed increasing numbers of vacuoles, surrounded by a single membrane, in hepatocytes, sinusoidal endothelial cells, and Kupffer cells. Focal cytoplasmic degeneration in hepatocytes was occasionally indicated by formation of autophagic vacuoles and finger print lysosomes. Hepatocytes of 2-deoxy-D-galactose-treated rats showed a dissociation and fragmentation of the rough endoplasmic reticulum. Sinusoidal endothelial cells and Kupffer cells were markedly enlarged, the latter contained a PAS-positive but amylase resistant substance. Extrahepatic changes included an increased occurrence of vacuolated cells in thymus. Phosphate trapping and its metabolic consequences are common phenomena in the experimental injury induced b 2-deoxy-D-galactose and in some hereditary diseases such as uridylyltransferase deficiency galactosaemia, fructose intolerance and glucose-6-phosphatase deficiency.
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PMID:Consequences of recurrent phosphate trapping induced by repeated injections of 2-deoxy-D-galactose. Biochemical and morphological studies in rats. 4 10

Clinical, histological (including electron-microscopic), immunohistochemical and genetic studies were performed on two infants with alpha1-antitrypsin deficiency. The clinical picture was one of neonatal biliary stasis. Liver biopsies revealed multiple cytoplasmic acidophilic bodies within many cells of the liver parenchyma which were strongly periodic acid-Schiff-positive, diastase-resistant and stained selectively with fluorescein-labelled rabbit antihuman alpha1-antitrypsin. Ultrastructurally, the bodies were situated within enlarged cisterns of the endoplasmatic reticulum. Both infants were of the protease inhibitor (Pi) phenotype ZZ, having inherited on PiZ gene from each parent. Results of Pi typing of both families were consistent with an autosomal co-dominant inheritance. Both infants are clinically well except for slight hepatomegaly at one year of age. But transaminase and gamma-glutamyl transpeptidase activities have remained elevated.
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PMID:[Alpha-antitrypsin deficiency in infancy]. 23 76

This paper is a progress report of the epidemiologic work carried out under the supervision of the Lombardy Regional Authority during the two years elapsed from the accident in a TCP-producing factory (ICMESA) in Meda (Italy), which resulted in the contamination of several towns of a large, densely populated area called the Brianza di Seveso with a total population of 220,000 inhabitants. A wide follow-up program is in progress in the Seveso area; it includes a clinical screening of the population living in the contaminated area and longitudinal and systematic health control of different groups at risk; a long-term morbidity cohort study has been also undertaken. TCDD exposure following the ICMESA accident resulted in an increased chloracne frequency. Neurologic examinations showed both signs of idiopathic subclinical neurologic damage and cases of clinically detectable idiopathic polyneuropathy in adults. A limited percentage of idiopathic hepatomegaly was reported to be present on clinical investigation; no information, however, is given on the criteria by which the hepatomegaly was investigated. Some alterations were observed in some exposed people in one or more liver tests (mainly transaminases and gamma-GT). So far, immunologic investigations, cytogenetic examination and embryomorphology analysis on cases of therapeutical or spontaneous abortions have not given abnormal results.
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PMID:Human health effects from accidental release of tetrachlorodibenzo-p-dioxin (TCDD) at Seveso, Italy. 28 95

Report of a 10-year-old boy with congenital hypoplasia of the intrahepatic bile ducts, the socalled MacMahon-Thannhauser-Syndrome. The patient had been suffering from a varying degree of jaundice since his 2nd day of life and from pruritus since his 21st month of life. Furthermore, he had hepatomegaly, a systolic cardiac murmur, hypogenitalism, retarded growth, and finally hypertension. Transitory xanthomas existed between 1 3/4 and 2 3/4 years of age. Signs of persistent intrahepatic cholestasis was manifested by increased levels of bilirubin and bile acids in serum as well as raised activities of leucine aminopeptidase, gamma-glutamyl transpeptidase and alkaline phosphatase. Pathological values of serum glutamic dehydrogenase pointed to a persistent destruction of liver cells. Without treatment, the activities of vitamin K dependent clotting factors were decreased. Cholesterol, phosphatides and triglycerides in serum were increased and lipoprotein-X was detectable. Aortography revealed stenosis of both renal arteries. An exploratory laparotomy and 5 liver biopsies led to the diagnosis of hypoplasia of the intrahepatic bile ducts. Therapeutic trials with steroids and the anion exchange resin "cholestyramine" were ineffective. Phenobarbital relieved the pruritus. Parenteral administration of fat soluble vitamins restored the activity of vitamin K dependent clotting factors to normal. The high blood pressure fell significantly due to treatment with adelphan. The etiology of hypoplasia of the intrahepatic bile ducts is unknown. It may be a malformation or an obliteration secondary to inflammation. In our patient, narrowing of the renal arteries, increase of plasma-renin activity and hypertension were probably secondary to hyperlipidemia. It has been suggested that hyperlipemia secondary to cholestasis may be due to a disturbance of lipoprotein metabolism. A review of reports on 118 patients suffering from intrahepatic bile ducts hypoplasia is included.
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PMID:[Hypertension and bilateral stenosis of the renal artery associated with congenital hypoplasia of the intrahepatic bile ducts (author's transl)]. 124 84

Liver function tests were performed in 165 hospitalized patients suffering from P. falciparum malaria with complications. Serum bilirubin was found increased in 33 patients, and 22 of them had unconjugated hyperbilirubinaemia. Serum alanine aminotransferase was increased in 5 patients, but only to mild to moderate levels. Serum alkaline phosphatase was increased in 11 patients, gamma-glutamyl transpeptidase in 3 patients. Serum total protein and albumin were significantly decreased but these were considered more as indicator of acute phase response. Liver cell necrosis was observed in one patient, and oedema and mononuclear cell infiltration in two patients. Though hepatomegaly and mild elevation of enzymes can be observed in a significant proportion of patients, involvement of liver leading to acute hepatitis or liver cell necrosis is a relatively uncommon complication in P. falciparum malaria.
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PMID:Hepatic changes in P. falciparum malaria. 128 32

Twenty-two patients with clinical, biochemical, immunological and pathological characteristics compatible with primary biliary cirrhosis were studied. There were 17 women and 5 men with a mean age of 57.4 +/- 15.2 years and a mean follow-up of 24.1 +/- 20.1 months. Four of them expired during the follow-up and eighteen patients now survive. The most common complaints were fatigue (63.6%) and itching (59.1%). Only one case (4.5%) was asymptomatic in this series. The major physical findings were jaundice (50%) and hepatomegaly (50%). The significant laboratory findings were: elevation of alkaline phosphatase (91% of the cases greater than 3 times the upper limit of normal), gamma-glutamyl transpeptidase (100% of the cases greater than 4 times the upper limit of normal), aspartate transaminase (95%) and alanine transaminase (100%), presence of anti-mitochondrial antibodies (91%), antinuclear antibodies (73%) and the elevation of IgM (88%). One case was associated with ulcerative colitis. Pathological staging in this series revealed 57.9% of stage II, 26% of stage III, 10% of stage IV and 5.3% of stage I. All patients with granuloma survived but 4 of the 5 patients with cholestasis died during follow-up. The results show that the features in this series of PBC were similar to those observed in western countries. The very high ALP and gamma-GT level as well as only one asymptomatic case in this series, suggest that our patients were diagnosed at a late stage. The reason(s) for the higher positivity of ANA, particularly the speckled type and a lower rate of associated auto-immune disease requires further study. Liver biopsy in predicting a prognosis is valuable.
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PMID:[A clinicopathological study in primary biliary cirrhosis]. 135 58

Piperonyl butoxide, alpha-[2-(2-Butoxyethoxy)ethoxy]-4,5-methylenedioxy- 2-propyltoluene, is a pesticide synergist. F344 rats of both sex were maintained on diets containing 0, 0.6, 1.2 or 2.4% of piperonyl butoxide for 13 weeks. At the end of experimental period, they were necropsied. Selected organs were weighted and serum was analyzed by clinical chemistry. In male and female rats of the 2.4%-group, body weight gains were depressed, macroscopically, hepatomegaly was marked and liver weights were significantly higher than those of the control group. In male and female rats of all treated groups, relative kidney weights were significantly increased in a dose-dependent manner. Rats of the 2.4%-group had increased levels of albumin, cholesterol, urea nitrogen and gamma-glutamyl transpeptidase. Examination of livers of the male 2.4%-group by light microscopy showed enlarged hepatocytes with glassy cytoplasm and fatty deposition. On occasion, there was coagulative necrosis of a few hepatocytes in the periportal area and oval cell proliferation. The kidney of treated rats showed atrophy of epithelium in the proximal convoluted tubules. These results indicated that toxicity of piperonyl butoxide in rats was directed primarily to the liver and kidney.
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PMID:Sub-acute toxicity of piperonyl butoxide in F344 rats. 158 83


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