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)

Abnormal serum aminotransferase activities with dominance of aspartate aminotransferase over alanine aminotransferase activity, and elevated serum adenosine deaminase activity and immunoglobulin. A concentration, were commonly encountered among patients with portal cirrhosis. The full triad was present in 31 of 49 cases (63%). As isolated abnormalities, these features were not uncommon in patients with other diseases of the liver and biliary tree, but the full triad was found only in 11 of 163 such cases (6.8%). The presence of this triad in a patient with unexplained hepatomegaly is indicative of portal cirrhosis.
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PMID:A diagnostic triad for portal cirrhosis. 97 89

The nonerythropoietic component of early labeled bilirubin in plasma and bile was studied in 7 patients with acute infectious hepatitis during the late convalescent stage, in 13 patients with Laennec-type liver cirrhosis, and in 7 control subjects after intravenous injection of a tracer dose (2.5 muCi) of 4-14C-delta-aminolevulinic acid (14C-deltaALA). All subjects were examined during the nonicteric stage. In control subjects, the mean cumulative radioactivity readings in 4 hours were 29.6 +/- 4.7 X 10(3) d.p.m. per milligram times 4 hours in plasma and 27.0 +/- 1.2 X 10(3) d.p.m. per milligram times 4 hours in bile. In acute infectious hepatitis patients, the mean cumulative radioactivity readings for both plasma and bile in 4 hours were approximately twice that found in control subjects. In mild cirrhotic patients with enlarged liver on scintigram, the mean cumulative radioactivity readings for both plasma and bile were approximately 1.4 times that in control subjects. In patients with more advanced cirrhosis and markedly small livers on scintigram, the mean cumulative radioactivity readings for both plasma and bile were as low as approximately 0.5 that of control subjects. These findings seem to indicate the important role of the liver in the production of the nonerythropoietic component of early bilirubin in man.
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PMID:The effects of acute infectious hepatitis and cirrhosis of the liver on the nonerythropoietic component of early bilirubin. 124 90

When larvae of C. sinensis reach the biliary system and mature, the flukes provoke pathological changes, both as a result of local trauma and of toxic irritation. The appearances vary with duration and severity of the infestation, but they are sufficiently distinctive and characteristic to allow a classification into four phases as follows; 1st phase, desquamation of epithelial cells, 2nd phase, hyperplasia and desquamation of epithelial cells, 3rd phase, hyperplasia and desquamation of epithelial cells, and adenomatous tissue formation, and 4th phase, marked proliferation of the periductal connective tissue with scattered abortive acini of epithelial cells and fibrosis of the wall of the bile duct. The onset of symptoms and signs is at times gradual, at times sudden. Chill and fever up to 40 degrees C occur during the acute stage, i.e. the period less than a month after parasite invasion. And a few weeks later, the chronic stage follows with the classical clinical features. In general, symptoms and signs can be classified as follows: mild, essentially symptomless, progressive, with irregular appetite, gastrointestinal disturbances, oedema, hepatomegaly, etc., and severe, with a syndrome associated with portal cirrhosis and hypertension. Pathogenic changes and complications are generally restricted to foci, but may eventually affect the whole liver. Calculi, acute suppurative cholangitis, recurrent pyogenic cholangitis, cholecystitis, hepatitis, and acute pancreatitis are important complications. Carcinoma of the liver is often found in association with clonorchiasis, too.
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PMID:Clonorchis sinensis: pathogenesis and clinical features of infection. 639 2

Post mortems of 2289 patients with liver cirrhosis revealed that 37% died of causes related directly to cirrhosis i.e. liver failure or hemorrhage from oesophageal varices. Patients who died of ruptured oesophageal varices in 82% have splenomegaly and most frequently hepatomegaly. Livercell carcinomas were recognized in 7,5% of cirrhotic livers, increasing to 10% in 1976-1978. This rise particularly is conspicuous in women. Liver carcinoma is 4,5 times more frequent in postnecrotic than in portal cirrhosis.
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PMID:[Liver cirrhosis in autopsy material within 48 years. II. Causes of death, liver cell carcinoma, weights of liver and spleen (author's transl)]. 708 May 73

Hepatic vein (HV) thrombosis causes ascites, hepatomegaly, and severe congestion of the liver (Budd-Chiari syndrome [BCS]). Severe hepatic fibrosis develops in this syndrome with a variety of histological patterns. Some livers have a pattern of cirrhosis in which there is fibrous bridging between HVs and portal tracts (veno-portal cirrhosis). Other livers have a pattern of "reversed-lobulation cirrhosis" (veno-centric cirrhosis), in which fibrous bridging between HVs and portal tracts is minimal. The prevalence and pathogenesis of these forms of cirrhosis and the effect of portal vein (PV) thrombosis in this disease have not been studied. We examined 15 resected livers from patients with BCS to determine the distribution of vascular obstruction and the character of the parenchymal response. Six livers had veno-portal cirrhosis, and all of these had severe PV obliteration caused by thrombosis. Three livers had veno-centric cirrhosis and had normal medium and large PVs. The remaining six livers had mixed veno-centric/veno-portal cirrhosis and had moderate PV obliteration. The nodules in veno-centric cirrhosis had evidence of an unusual circulation with small arteries supplying a midzonal venous plexus that appeared to drain retrogradely into patent small PVs. Nine livers had large regenerative nodules histologically similar to focal nodular hyperplasia. PV thrombosis is a frequent occurrence in BCS. The correlation between PV thrombosis and the pattern of cirrhosis suggests a role for PV obliteration in the genesis of veno-portal bridging fibrosis in this disease and possibly in other diseases leading to cirrhosis.
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PMID:Pathology of the liver in Budd-Chiari syndrome: portal vein thrombosis and the histogenesis of veno-centric cirrhosis, veno-portal cirrhosis, and large regenerative nodules. 946 48

The author reports the history of a family of six children, of whom two, the eldest and the fifth, are normal; three died, a boy when 6 months old and two girls when 9 and 10 years old, from the same familial disease that also attacked another boy now 7 years old. The essential features of this disease are hypertrophy of both liver and spleen, chronic icterus with evidence of salts and bile-pigments in the blood and urine, retardation of physical, mental, and sexual development, slight deafness in one case and clubbing of the fingers in another. This condition is a good example of biliary cirrhosis of the liver.After reviewing recent French observations, the author recalls the large contribution of English authors on the subject.HE THEN DISTINGUISHES THREE TYPES OF FAMILIAL CIRRHOSIS: Laennec's type with enlarged liver, the type of splenomegalic anascitic and anicteric cirrhosis, resembling Banti's syndrome, and the commonest type or biliary cirrhosis.The author describes particular histological lesions, and when dealing with differential diagnoses, excludes dyslipoidic, polycoric, and other acquired cirrhosis in children. He then summarizes the relationships between this disease and the obstructive cirrhosis to a congenital defect of the bile-ducts, the cirrhosis in young Indians, the syndrome of hepatic lenticular degeneration, and the syndrome of cirrhosis of the liver combined with haemangiomatosis. Finally, after recalling the close analogy of the condition with renal dwarfism, the author shows how the interpretation of these relationships may throw light on the pathogenesis of various progressive congenital diseases.
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PMID:Familial Hepatitis and Chronic Jaundice: (Section for the Study of Disease in Children). 1999 37