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 child with hemihypertrophy presented with Wilm's tumor at 3 years of age. History included neonatal hypoglycemia and the discovery of hepatomegaly and renal dysplasia. This case report emphasizes the close relation of body hemihypertrophy to Beckwith's syndrome, as well as the high degree to which both predispose to certain tumors.
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PMID:[Nephroblastoma and whole-body hemihypertrophy. Relation to Wiedemann-Beckwith's syndrome]. 23 62

Fifteen males and 17 females with adrenal cortical carcinoma were reviewed. Their average age at diagnosis was 50.33 years plus or minus 12.26 SD for males and 39.76 years plus or minus 12.02 SD for females. The 5-year survival rate in this series was 31.25%. Abdominal pain, weakness, and weight loss were the primary presenting symptoms, whereas abdominal mass, distant lymphadenopathy, hepatomegaly, and edema of the lower extremities were the main presenting signs. The major sites of distant metastatic involvement were the lungs, liver, lymph nodes, and bones. The best available mode of therapy was surgery. The use of ortho para 'DDD (o,p'DDD), either in addition to surgery or as the only mode of therapy, was not associated with any significant advantage to the patient. Female patients had a longer survival than males, probably because of their younger age at diagnosis.
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PMID:Adrenal cortical carcinoma. A study of 32 patients. 23 92

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

After oral administration of bromazepam, 50 mg/kg/day for 14-28 days to rats, the rate of elimination of the unchanged drug from the blood increased by 20-40%, as determined from the half-lives of the blood decay curves during the first 4 hr after administration of an oral or intravenous test dose of bromazepam. During the chronic administration, the liver weight increased 30-40%, with concomitant enlargement of the liver. The hepatomegaly was associated with elevation of microsomal drug-metabolizing enzyme activities, including that responsible for the oxidation of bromazepam itself. Spectral characteristics of the isolated microsomes indicated that the manner by which bromazepam caused the elevation (induction) of the enzyme activities was of the "phenobarbital type" rather than the "methylcholanthrene type." Since certain steps of bromazepam metabolism take place in the liver, it appears reasonable to assume that the increase in the elimination rate found after chronic administration may depend upon the enhanced drug-metabolizing activities in the liver. The hepatomegaly and the associated elevation of enzyme activities returned to the normal states within 7 days after withdrawal of the drug. Neither the increase in the elimination rate nor the enzyme induction was observed with doses lower than 5 mg/kg.
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PMID:Effects of chronic administration of bromazepam on its blood level profile and on the hepatic microsomal drug-metabolizing enzymes in the rat. 24 Jun 52

The paper presents the case of a patient with borderline hanseniasis. After a long period of illness, he presented an outbreak with new lesions, that showed reactional tuberculoid aspects; he later presented lesions with clinical and histological aspects of Virchowian hanseniasis. This evolutional type is compatible with the pseudo-exacerbations outbreaks reported by Souza Lima. This patient also presented an Erythema Nodosum outbreak with cutaneous and visceral lesions, the latter occurring with great intensity in the liver parenchyma with clinical manifestations of icterus and hepatomegaly. The pathogenesis of the pseudo-exacerbations outbreaks is discussed, also the special situation of Borderline patients, subject to neurologic injuries during the pseudo-exacerbations outbreaks, and cutaneous, neurological and visceral lesions during the Erythema Nodosum Hansenicum outbreaks.
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PMID:[Dimorphous Hansen's disease with outbreaks of Hansen reactions and visceral lesions]. 26 77

An infant presented with congenital hemihypertrophy, hepatomegaly, and a low thoracic paraspinal mass. Liver scan showed multiple defects in the uptake of radioisotope. Surgical exploration revealed multiple infantile hemangioendotheliomas of the liver and a paraspinal hemangioendothelioma. In review of 69 reported cases of infantile hemangioendothelioma of the liver and viscera, there has been no previous note of hemihypertrophy associated with this abnormality.
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PMID:Infantile hepatic hemangioendotheliomas associated with hemihypertrophy. 26 14

Clinical and biochemical diagnostic studies concerned 17 cases of galactosemia coming from 15 not consauguineous families. Galactosemia was diagnosed between 1-st day and 11-th month of life. Tentative diagnosis based on clinical picture was made in 12 infants, others were detected through family history of galactosemia and/or biochemical newborn screening carried out at the National Research Institute of Mother and Child since 1969. Clinical symptoms of galactosemia occurred in most patients in the first week of life. They were the following (tab. II): hepatomegaly (in 94%), jaundice (81%), splenomegaly (79%), vomitus (62%) and diarrhoea in 56% of patients. Cataract was found in 6 infants (38%). Biochemical diagnosis was based on the results of enzymatic estimation of galactose-1-phosphate uridyl transferase activity in blood, galactose-1-phosphate in red blood cells and galactose in blood and urine. No activity of galactose-1-phosphate uridyl transferase was found in all patients, and the concentration of galactose-1-phosphate was higher than 25 mg/100 ml of red blood cells. High galactose level was observed in blood and urine in all patients with typical clinical course of galactosemia. In 2 patients however without clinical symptoms of the disease only trace amounts of galactose was detected in blood and urine. All these patients were treated with galactose free diet.
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PMID:[Clinical and biochemical diagnosis of galactosemia among our cases]. 26 27

This is a report of an unusual acetaminophen poisoning in a 3-year-old girl who, three days after the ingestion of an estimated thirty-five 325-mg tablets of acetaminophen, had the highest levels of hepatic enzymes ever recorded at Duke Hospital. Although she was only moderately ill with an enlarged liver, she was discharged from the hospital on the seventh day in good condition. The liver enzyme levels returned to normal when last assessed, 50 days after ingestion. The importance of determining acetaminophen plasma concentration at different times to evaluate more precisely the plasma half-life is discussed, along with the current suggested therapy now being recommended for acetaminophen poisoning.
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PMID:Acetaminophen: report of an unusual poisoning. 26 76

Eleven cases of myeloproliferative disease occurred in a group of 24 beagle dogs placed in a 60Co gamma-ray field at about 13 months of age and irradiated at an exposure rate of 5 R/22-hour day for duratior of life. Of these 11 dogs, 5 (described in this paper) were diagnosed as having erythroleukemia. The bone marrow showed marked erythroblastic hyperplasia, with maturation arrest of the erythroid elements, and increased numbers of myeloblasts and promyelocytes. The terminal peripheral blood was characterized by marked anemia and thrombocytopenia, with circulating erythrocytic precursors and abnormal erythrocyte morphology. Splenomegaly and hepatomegaly occurred in 4 of the 5 animals. In the spleens and livers of all 5, there was extensive leukemic infiltration and proliferation. The extent of leukemic involvement in other tissues and organs varied in individual dogs.
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PMID:Radiation-induced erythroleukemia in the beagle dog. A hematologic summary of five cases. 26 46

Bone marrow lymphoblasts from 109 children admitted with untreated acute lymphoblastic leukemia (ALL) were tested for spontaneous rosette formation with sheep erythrocytes. Twenty-six children (24%) had lymphoblasts that formed rosettes (E+). Of 13 initial clinical characteristics, 8 were significantly associated with E+ lymphoblasts: mediastinal enlargement (86% of patients E+), leukocyte counts over 100 X 10(9)/liter (65% E+), nodes greater than 2 cm in any diameter (65% E+), age over 5 yr (46% E+), hemoglobin over 8 g/dl (44% E+), hepatomegaly greater than 5 cm (38% E+), boys (35% E+), and lymph node enlargement outside of the cervical area (28% E+). Spleen size, initial platelet counts, and periodic acid-Schiff scores did not distinguish E+ from E- patients. Since few patients were black and few presented with central nervous system leukemia, the association of these two characteristics with E+ blasts could not be determined. A hierarchical classification scheme and a linear logistic regression model were used to define the patterns of characteristics associated with E+ lymphoblasts. The initial clinical characteristics and the poorer course of E+ patients suggest that ALL comprises at least two biologically and clinically distinct types. The E+ ALL may result from a leukemic transformation of a non-Hodgkin lymphoma.
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PMID:Initial prognostic factors and lymphoblast-erythrocyte rosette formation in 109 children with acute lymphoblastic leukemia. 26 81


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