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)

In rats treated with the hypolipidemic drug, nafenopin (NP), for 2 days the biliary excretion of phenolphthalein glucuronide (PPG) was markedly decreased, while in contrast that of chlorothiazide (CTZ) was enhanced. This suggests the existence of independent hepatic transport mechanisms for these two anions. For both PPG and CTZ blood disappearance curves showed an initial, rapid phase followed by a second, slow phase. The rapid phase for both compounds is affected only slightly by pretreatment with NP. Therefore, it is inferred that suppression of biliary excretion was attributable mainly to impairment of the liver-to-bile transport process. The increased bile flow induced by NP treatment was previously shown to be related to the biliary excretion of NP and its metabolites. Inhibition of NP choleresis by PPG may involve competition for biliary transport of these compounds. The marked hepatomegaly and choleresis seen after NP pretreatment was more evident in male rats than in females.
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PMID:Effect of nafenopin (SU-13437) on liver function. Influence on the hepatic transport of phenolphthalein glucuronide and chlorothiazide. 0 53

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

During the recovery stage of the hemolytic uremic syndrome in 2 cases an increase of serum levels of GOT, GPT, LDH, gammaGT, 5'ND and AP was noticed, without signs of a recurrence of the disease. In one patient also jaundice and hepatomegaly were found. The observations suggest a parenchymal damage of the liver.
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PMID:Liver damage in the hemolytic uremic syndrome. 3 33

Two infants with lethargy, vomiting, convulsions, coma and marked metabolic acidosis were found to have very high concentrations of methylmalonic acid in their serum and urine. In vitro studies of fibroblasts demonstrated that the infants had different variants of methylmalonic acidemia.Vitamin B(12) was given in two different forms at 1 month of age and at 12 months of age. Each trial continued for 4 months but neither infant showed a clinical or biochemical response.In both infants hyperglycinemia, neutropenia and thrombocytopenia developed during acute metabolic crises only. Hypoglycemia was found in patient 2. Hyperammonemia was severe in patient 2 during acute crises but never appeared in patient 1. When clinically well, both infants continued to excrete abnormal amounts of methylmalonic acid in the urine and both had persistent compensated metabolic acidosis.Marked hyperuricemia developed in patient 1 at 18 months of age and led to progressive renal failure. Allopurinol therapy was necessary to keep the uric acid concentration within the normal range. Renal function returned to normal, as indicated by a marked increase in the renal clearance of creatinine and uric acid.Patient 1 is physically and mentally retarded, and has moderate hypotonia, hepatomegaly and persistent vomiting. Patient 2 has developed normally.The urine concentrations of methylmalonic acid in the four parents were normal.
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PMID:Methylmalonic acidemia: 6 years' clinical experience with two variants unresponsive to vitamin B12 therapy. 3 17

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

A 65-year-old black female with Sezary syndrome had generalized intractable pruritus, erythroderma, alopecia, onychogryphosis, lumphadenopathy and hepatomegaly. Abnormal lymphocytes with large, convoluted and grooved nuclei (Sezary cells) were identified in the skin and peripheral blood. A striking feature of her disease was severe, deforming arthropathy of the hands and knees, a clinical finding which has been described previously in only one patient with Sezary syndrome. At necropsy no associated lymphoma was found.
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PMID:Sezary syndrome with arthropathy. Report of a case. 5 75

Eght dogs were orally superinfected for 1 month with 50,000 embryonated Toxocara canis ova. Results of laboratory examinations during inoculation and for 2 weeks postinoculation revealed moderate leukocytosis, marked absolute eosinophilia, hypoalbuminemia, increased concentrations of serum glutamic pyruvate transaminase, and in 2 dogs, precipitating humoral antibodies. Other changes were moderate ascites, hepatomegaly, lymphadenopathy, and focal lesions (0.5 to 3.0 mm) in liver, lung, kidney, intestine, abdominal lymph node, heart, diaphragm, and spleen. Microscopically, focal eosinophilic gastroenteritis was produced. Eosinophils and globule leukocytes were increased throughout the intestinal mucosa. Eosinophil-infiltrated and granulomatous lesions were in the same organs listed as having focal lesions, as well as in the pancreas. The importance of serum beta-globulin content as a potential diagnostic tool was emphasized, and the experimentally induced infection was compared with naturally occurring eosinophilic gastroenteritis in the dog.
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PMID:Experimentally induced canine toxocariasis: laboratory examinations and pathologic changes, with emphasis on the gastrointestinal tract. 5 22

The clinical and immunological features of fifteen cases of cryptogenic pulmonary eosinophilia are reported. There were ten women (mean age 35.4 years) and five men (mean age 42 years). Eight gave a previous history of asthma and seven had none. Thirteen of the fifteen patients had negative skin test to common allergens. Many features of a systemic illness were present in the asthmatic and non-asthmatic groups including anaemia, weight loss, fever and a grossly raised ESR. An absolute polymorphonuclear leucocytosis was frequent as well as the obligatory increase in blood eosinophils used as one of our criteria for inclusion. Hepatomegaly (three cases), splenomegaly (four cases) and hilar node enlargement (one case) were seen in the group without asthma. Evidence of renal involvement or necrotizing vasculitis was notably absent and the response to small doses of corticosteroids was dramatic. Immunologically the striking feature was a disproportionate increase in blood eosinophils compared with only minor elevations in the total serum IgE levels. This stands in contrast to patients with bronchopulmonary aspergillosis and helminth infestation. Studies of cytophilic antibodies using histamine liberation after challenge with antibodies to immunoglobulin sub-classes in six patients showed a marked increase in IgG2 and lesser increases of IgE and IgG3. No evidence of antibodies specific to A. fumigatus was found. The amount of cytophilic antibody was also in contrast to that found in bronchopulmonary aspergillosis.
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PMID:Cryptogenic pulmonary eosinophilia. 5 41


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