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

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.
 ...
PMID:Metabolic changes during prolonged total parenteral nutrition in intensive care. 3 24

Twelve patients with liver disease related to methyldopa were seen between 1967 and 1977. Illness occurred within 1--9 weeks of commencement of therapy in 9 patients, the remaining 3 patients having received the drug for 13 months, 15 months and 7 years before experiencing symptoms. Jaundice with tender hepatomegaly, usually preceded by symptoms of malaise, anorexia, nausea and vomiting, and associated with upper abdominal pain, was an invariable finding in all patients. Biochemical liver function tests indicated hepatocellular necrosis and correlated with histopathological evidence of hepatic injury, the spectrum of which ranged from fatty change and focal hepatocellular necrosis to massive hepatic necrosis. Most patients showed moderate to severe acute hepatitis or chronic active hepatitis with associated cholestasis. The drug was withdrawn on presentation to hospital in 11 patients, with rapid clinical improvement in 9. One patient died, having presented in hepatic failure, and another, who had been taking methyldopa for 7 years, showed slower clinical and biochemical resolution over a period of several months. The remaining patient in the series developed fulminant hepatitis when the drug was accidentally recommenced 1 year after a prior episode of methyldopa-induced hepatitis. In this latter patient, and in 2 others, the causal relationship between methyldopa and hepatic dysfunction was proved with the recurrence of hepatitis within 2 weeks of re-exposure to the drug.
 ...
PMID:Patterns of hepatic injury induced by methyldopa. 42 37

This is a report on the clinical signs of Wesselsbron disease in 37 lambs and the pathology of 4 natural and 12 experimental cases. Generally the symptoms were ill-defined. At autopsy 13 of the 14 lambs revealed a mild to severe icterus and a slight to moderate hepatomegaly with discoloration of the liver. No foci of hepatic necrosis were observed macroscopically and, except for petechial and ecchymotic haemorrhages in the mucosa of the abomasum and generalized lymphadenopathy, no other obvious macroscopic lesions were noted. Perforation of the abomasum occurred in one lamb only. Microscopy on the liver showed mild to extensive necrosis of the parenchyma. Degenerated and necrotic hepatocytes were diffusely scattered throughout the liver, but no definite well-circumscribed foci of necrosis were seen. Mitotic figures and hepatocytes with large nuclei indicated that active regeneration of parenchymal cells had occurred in some of the livers. Other changes, for example, Kupffer cell proliferation, sinusoidal leucostasis, bile duct proliferation and infiltration of mononuclear cells in the portal triads, were frequently encountered. Moderate to severe cholestasis was a feature in 66% of the livers examined, while intranuclear inclusions and intracytoplasmic acidophilic or Councilman-like bodies were frequently observed. A complete haematological study was carried out on 4 experimentally produced cases. The gross and histopathological lesions in the liver are compared with those of Rift Valley fever in the new-born lamb.
 ...
PMID:Wesselsbron disease, pathological, haematological and clinical studies in natural cases and experimentally infected new-born lambs. 71 95

An epidemic of jaundice probably due to toxic hepatitis occurred in three adjoining districts of Northwest India during the period November and December, 1974. The dogs of the villages were affected first, then the human beings. Detailed clinical features, appropriate laboratory tests, and liver biopsies were studied. A retrospective epidemiological survey was carried out. The disease had a subacute onset starting with high fever, followed by rapidly progressive jaundice. Ascites appeared simultaneously and soon became quite massive. Hepatomegaly was recorded when ascites decreased. Liver function tests suggested cholestatic jaundice. The mortality rate in the hospital was 10%. Clinical features in dogs were similar, but mortality was almost 100%. Liver histology was characterized by (1) edema and collagenization of the central veins, never with thrombosis, (2) cholangiolar proliferation, (3) moderate to severe ballooning of the hepatocytes, (4) perisinusoidal fibrosis, (5) cholestasis, and finally, (6) cirrhosis with reverse lobulation. Etiology of this epidemic of hepatitis could not be unequivocally established. Critical analysis of the data suggests that some food toxin may have been a factor in the outbreak of this unusual epidemic of toxic hepatitis.
 ...
PMID:Study of an epidemic of jaundice, presumably due to toxic hepatitis, in Northwest India. 83 97

Hepatomegaly and abnormal liver function can occur in nonmetastatic malignancies. A patient with metastatic prostatic adenocarcinoma that had spared the liver and extrahepatic biliary tree is described. He had puzzling episodes of jaundice for a period of 2 1/2 years. The results of appropriate investigations and an exploratory laparotomy performed dlring the patient's four antemortem hospitalizations were indicative of "recurrent intrahepatic cholestasis," the cause of which remained an enigma even after exploratory laparotomy. At autopsy, no evidence of hepatic metastases or extrahepatic biliary obstruction was found. Alcohol, hepatotoxic drugs, toxins, viral and chronic active hepatitis, hemolysis, and extrahepatic biliary obstruction were eliminated as causes of the jaundice. We believe that the intermittent intrahepatic cholestasis is one of the nonmetastatic manifestations (nonmetastatic hepatopathy of malignancy) of the prostatic adenocarcinoma.
 ...
PMID:Intermittent cholestatic jaundice and nonmetastatic prostatic carcinoma. 92 51

Among 424 children with liver disease, 20 had alpha1-antitrypsin deficiency associated with protease inhibitor ZZ phenotype. This disorder manifested itself as cholestasis in early infancy in 19 children. Jaundice and pruritus cleared in 16 of these by 7 months of age, but hepatomegaly and laboratory evidence of mild hepatic dysfunction persisted in all. Biliary cirrhosis and portal hypertension eventually developed or was suspected in eight, and hypoplasia of intraheptic bile ducts was demonstrated in another four. Routine screening revealed intermediate alpha1-antitrypsin deficiency in 16 other children with various types of liver disease. The phenotype in these patients was MZ, MS, or SZ. PAS-positive granules were present in liver of all patients with the ZZ phenotype and in none with other phenotypes. The findings indicate that manifestations and prognosis of this inherited liver disease are extremely variable.
 ...
PMID:Alpha1-antitrypsin deficiency and liver disease in children: phenotypes, manifestations, and prognosis. 108 71

A total of 240 cases of a bleeding syndrome in infants due to prothrombin complex deficiency of unknown aetiology were reviewed. The majority of patients were breast fed, aged 1-2 months and the syndrome was more prevalent in males. Clinical manifestations consisted of bleeding, pallor and mild hepatomegaly in the majority of cases. Mild fever, diarrhoea, jaundice, and upper respiratory tract infection were associated in a few patients. Acute onset, short course and a high rate of intracranial bleeding (65%), particularly subdural and subarachnoid, were observed. The haemostatic defects appeared to be a marked reduction in factor II, VII, IX, and X. Complete blood counts remained relatively normal, with the exception of some changes (anaemia, leukocytosis), in response to the acute bleeding. Liver chemistry was normal or slightly impaired. No specific pathological changes were noted at autopsy, there were mild changes of liver cells, such as rare focal necrosis of liver cells, the proliferation of Kupffer cells, extramedullary haemopoeisis and mild cholestasis. Clinical improvement and correction of hemostatic defects were noted after vitamin K therapy alone or with fresh blood transfusion. Mortality rates were high in infants with intracranial bleeding (40-55%), while the overall mortality rate was 25%. The pathogenesis and the possibility of prevention of the syndrome were discussed.
 ...
PMID:A bleeding syndrome in infants: acquired prothrombin complex deficiency of unknown aetiology. 108 22

The development of the syndrome of chronic intrahepatic cholestasis in five young, black men who had systemic granulomatous disease and clinical features consistent with those of sarcoidosis is described. Clinical and biochemical aspects, similar to those of primary biliary cirrhosis, included pruritus, jaundice, hepatomegaly and striking elevations of serum levels of alkaline phosphatase and cholesterol. (One patient had skin xanthomas.) Mitochondrial antibodies were not found; and survival of the patients (7 to 18 years) exceeded the usual survival of patients with primary biliary cirrhosis. The histologic abnormalities included noncaseating granulomas, chronic intrahepatic cholestasis, increased copper in hepatocytes, progressive diminution in number of interiobular bile ducts, periportal fibrosis and the eventual development of a micronodular "biliary" cirrhosis. The histologic evolution of the disease suggests a slow, progressive destruction of the bile ducts by granulomas. Although the end stage of this syndrome resembles primary biliary cirrhosis, the characteristic nonsuppurative, destructive cholangitis of primary biliary cirrhosis was not present.
 ...
PMID:Chronic intrahepatic cholestasis of sarcoidosis. 116 46

Carbenicillin disodium was temporally associated with eight episodes of a mild reversible anicteric hepatitis characterized by nausea, vomiting, and a tender, somewhat enlarged liver. Serum glutamic and oxaloacetic transaminase as well as alkaline phosphatase levels rose, but serum bilirubin values remained normal. There usually were no signs of concomitant allergy to penicillin, and other penicillins could be given subsequently without ill effects. Biopsy specimens of the liver showed spotty liver cell necrosis with no cholestasis.
 ...
PMID:Anicteric carbenicillin hepatitis. Eight episodes in four patients. 117 85

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.
 ...
PMID:[Hypertension and bilateral stenosis of the renal artery associated with congenital hypoplasia of the intrahepatic bile ducts (author's transl)]. 124 84


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