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 case of hepatoma in a 79-year old woman is reported. The patient had an enlarged liver and a pathological liver scintigram. Percutaneous liver biopsies were performed both with Menghini-and fine needles. The most prominent feature was the presence of hyaline cytoplasmic PAS-negative inclusions in liver parenchymal cells. There was no nuclear atypia. Electron microscopy disclosed two types of cytoplasmic changes. One consisted of a lamellar ultrastructure and was interpreted as a hyperplasia of smooth-surfaced endoplasmic reticulum. The other change consisted of smooth globular non-membrane limited regions containing amorphous or finely fibrillar material. This was interpreted as corresponding to the hyaline inclusions visible in the light microscope. The presence of PAS-negative hyaline cytoplasmic inclusions may thus be a sign of hepatoma. This may be of relevance for the diagnostic considerations of material obtained by fine needle biopsy.
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PMID:Hyaline cytoplasmic inclusions in human hepatoma. A case report. 19 65

Angio-immunoblastic lymphadenopathies with dysproteinemia represent a new entity characterised clinically by superficial lymphadenopathy splenomegaly more frequent than hepatomegaly, marked general signs and skin manifestations often triggered off by drugs. The laboratory disturbances include immue disorders, polyclonal dysproteinemia, anti-red cell autoimmunity. It is above all the histology which makes this entity original: polymorphic cellular proliferation with immunoblasts, plasmablasts and plasma cell disturbing the normal lymph node architecutre, intense vascular neogenesis and deposits of extra-cellular amorphous substances. This histology corresponds to a non-sarcomatous lymph node hyperplasia, probably due to a deficit in T suppressive function on the production of antibodies.
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PMID:[Angio-immunoblastic lymphadenopathy with dysproteinemia. Apropos of 5 cases]. 19 32

A consecutive series of 24 cases of primary carcinoma of the liver in Malawi has been investigated. Histologically, all were hepatocellular carcinomas (HCC). All patients were African Bantus, the average age was 42.7, and the sex ratio was men 3.5:women 1. The duration of symptoms attributable to HCC was about 5 months previous to admission to hospital and was in no case preceded by clinically manifest cirrhosis. The clinical picture was rather uniform with pain in the region of the liver, emaciation and nodular hepatomegaly as the most important features. One of the patients had repeated attacks of hypoglycaemic coma. Sera from 11 out of 13 patients contained alpha-feto-protein. Hepatitis-associated antigen and antibody in the serum were found in 7 and 6 out of 16 and 14 cases respectively. Serum B12 and serum unsaturated B12 binding capacity were moderately raised in most patients. The prognosis was poor, the average time of survival was 4.8 weeks after admission. The cause of death was most frequently hepatic coma. HCC in the African Bantu shows some different features from the same disease in the Western Hemisphere: The incidence is much higher; the patients are younger. The neoplasm commonly develops in a clinically latent cirrhosis. The latter is not caused by alcohol, but is presumably a sequel of hepatitis. It is possible that aflatoxin is the carcinogenic factor, acting more readily in a cirrhotic than in a normal liver.
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PMID:Primary carcinoma of the liver in Malawi: a review of 24 cases. 19 21

The patients was a 3-year-old boy with psychomotor retardation and attacked by seizures since 8 months of age. On funduscopy, the maculla presented a cherry-red spot. Serum hexosaminidase A activities were as low as 8.2 percent. Both parents were carriers. The patient was diagnosed as classical Tay-Sachs disease by neurological examination. Diphenylhydantoin was continuously given for 2 years and 2 months till his death. Autopsy revealed swelling of the cerebrum, atrophy and sclerosis of the cerebellum, hepatomegaly and mild enlargement of the lymph nodes. Histologically, the cerebrum showed ballooned swelling of nerve cells, slight gliosis and demyelination, while cerebellar Purkinje's cells and granular cells were degenerated and disappeared. The cerebellar cortex showed small focal spongy degeneration. By electron microscopy, membranous cytoplasmic bodies were found in the nerve cells. The change of brain observed in this case were interpreted as a combined result of (i) essential change to classical Tay-Sachs disease, (ii) ischemic change due to frequently repeated seizures, (iii) chronic toxicity by long-term anticonvulsant administration.
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PMID:Histological observation of the brain of Tay-Sachs disease with seizure and chronic DPH intoxication--report of an autopsy case. 20 60

In a 12-year-old female patients with HBAg phi hepatitis a differential diagnosis of the diseases has been considered. The CMV etiology of the hepatitis was suspected on the basis of a persistent temperature, hepatomegaly, a mild icterus, enlarged glands in the neck, predominantly mononuclear cells in the peripheral blood, a negative Paul-Bunnell test, and insufficiently characteristic biochemical analyses for virus A hepatitis. The CMV etiology of the disease was virologically confirmed. On the basis of the clinical picture without virological results, the diagnosis could not have been made with certainty.
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PMID:Cytomegalovirus hepatitis (diagnosis and differential diagnosis). 20 Nov 33

135 children with hepatitis and 179 patients with hepatomegaly of undetermined etiology were investigated for complement fixing antibodies to cytomegalovirus. 69 patients with hepatitis (51%) and 74 patients with hepatomegaly (41%) had a titer of 1:4 or above as compared with a control group of children without hepatic pathology in whom positive response occurred in only 20 resp. 18%. The mean titer found in the sero-positive patients was also significantly higher than that in the control group. In contrast, the incidence of positive sera in newborns with hyperbilirubinemia of unknown etiology did not differ significantly from that in a healthy control collective. Of 57 patients with liver disease, 20 excreted cytomegalovirus which was isolated 55 times from 103 urine specimens. These patients included 9 with hepatitis and 11 with hepatomegaly. Of 129 children without any indication of liver disease, cytomegalovirus could be demonstrated in only 3. Our results point toward a causal connection between the presence of cytomegalovirus and the development of hepatic disease in childhood.
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PMID:[Hepatic disease in childhood and cytomegalovirus infection (author's transl)]. 20 47

Fifteen patients with glycogen-storage disease type 1 (von Gierke's disease) were evaluated by serial scintigraphy, with a clearly recognizable pattern of an enlarged liver with diminished radionuclide accumulation, splenomegaly with considerably increased uptake and renomegaly. In seven of these patients with GSD-1 scintigraphy demonstrated focal defects of varying size. Small or stable defects suggest benign hepatic adenomata, whereas malignant change occurred in growing large lesions. The potential malignant end-point of hepatic-cell carcinoma in GSD-1 warrants careful serial liver scintigraphy with scintiangiography on a routine basis.
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PMID:Scintigraphic abnormalities in glycogen storage disease. 20 58

A 45-year-old man with hepatocellular carcinoma who developed intravascular coagulation following complete tumor regression by chemotherapy is described. After 2 doses of 10 mg of Mitomycin C given into the hepatic artery at the time of selective angiography, and 16 intravenous doses of 5-fluorouracil and Mitomycin C, 2 doses per week, subjective symptoms and hepatomegaly disappeared. Alpha-fetoprotein became negative and a remarkable change in tumor size and vasculature was noted in the arteriogram. Three months after chemotherapy, the patient developed thrombocytopenia, intravascular hemolysis, and acute renal failure. Autopsy disclosed a 8 X 7 X 5 cm solitary, encapsulated hepatocellular carcinoma in the right lobe. The tumor was surrounded by a thick capsule and completely necrotized. Neither intrahepatic invasion nor extrahepatic metastasis was observed. In the kidney, generalized fibrin thrombi were seen in the afferent arterioles of glomeruli as accounted for by intravascular coagulation.
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PMID:Complete necrotization of hepatocellular carcinoma by chemotherapy and subsequent intravascular coagulation: a case report. 20 57

Experimental models for hyper-beta-lipoproteinemia were established in rats and the effects of certain hypolipidemic drugs were studied with these models. In the hyperlipemia induced in rats by feeding a high cholesterol diet, Y-9738 [ethyl 2(4-chlorophenyl)-5-ethoxy-4-oxazoleacetate] produced a dose-dependent reduction of serum cholesterol: such hypolipidemic activity was estimated to be about 7 times as great as that of clofibrate. On the other hand, clofibrate induced hepatomegaly at 100 mg/kg, whereas Y-9738 did not at this dosage, which is about 10 times the effective dose. Hyperlipemia induced by high cholesterol and thiouracil was characterized by increased beta-lipoprotein (heparin-calcium and disc electrophoresis). In this model, Y-9738 showed a dose-dependent lowering effect on beta-lipoprotein cholesterol with a marked decrease in the beta/alpha lipoprotein ratio. A tendency was noted for alpha-lipoprotein to be increased. In contrast, clofibrate exerted no effect on this hyper-beta-lipoproteinemia. These results suggest that the above models may be of value in exploring hyper-beta-lipoproteinemia and that Y-9738 may be more useful than clofibrate in the therapy of hyperlipemia.
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PMID:Experimental hyper-beta-lipoproteinemia and its amelioration by a novel hypolipidemic agent. 20 4

A girl with hereditary tyrosinemia, diagnosed at 6 months of age, was treated with a diet restricted in phenylalanine and tyrosine. At 9 1/2 years of age she developed an acutely enlarged liver and spleen, and the diagnosis of hepatocarcinoma was made. The patient received a liver transplant and tyrosine metabolites became normal while she was receiving a regular diet. Three months later, an infected thrombosis of the portal vein caused her death. Liver transplant appears to be an effective method of enzyme replacement in tyrosinemia and should be considered for prevention of hepatoma.
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PMID:Homotransplantation of the liver in a patient with hepatoma and hereditary tyrosinemia. 21 42


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