Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abdominal computed tomography was performed on seven patients with primary hepatocellular carcinoma. The liver appeared normal in one patient, while in the other six patients the tumor was identified as an area of decreased attenuation. In four cases, the tumor was seen better following intravenous administration of a contrast agent, and, in two of these cases, it was not seen on the precontrast scans. In only one case was the hepatoma better seen on the precontrast examination, and it could still be identified following contrast enhancement. Hepatomegaly and an irregular hepatic contour were other findings in these patients.
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PMID:Computed tomography in primary hepatocellular carcinoma. 624 79

The authors report a series of 13 cases of bony metastases leading to the discovery of a hepatoma. They were subjects of male sex, average age 64 years. Nine were severe alcoholics. The presenting symptoms were in 7 cases neurological, in four cases an isolated bone tumour, finally, one spontaneous fracture, and one case with pain alone. Severe loss of weight was frequent; in 10 cases out of 13 it was greater than 5 kg. Hepatomegaly was found in 8 cases, but in 3 cases there was no sign suggesting liver disease. In 7 cases out of nine, the metastases were already numerous at the time of diagnosis. The diagnosis of metastases from a hepatoma was made on the bone histology 11 times and from the hepatic histology in 6 cases. The histological of the bone metastasis reproduces very well that of the liver. In four cases there was local secretion of bile, in one case the metastatic liver cells underwent steatonecrosis.
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PMID:[Bone metastasis revealing a hepatoma. 13 cases]. 626 7

This report describes four siblings affected with familial intrahepatic cholestasis detected in early infancy. In the two male siblings, biliary cirrhosis and fatal hepatocellular carcinoma later developed, whereas the female siblings have had persistent hepatomegaly and recurrent episodes of cholestasis. Sequential biopsies show that this rare disorder of unknown etiology must be added to the many causes of giant cell transformation of the liver in infancy. Its oncogenic risk, particularly in males, has not been generally appreciated.
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PMID:Hepatoma in siblings with progressive familial cholestatic cirrhosis of childhood. 626 30

The hormonal milieu that follows the ingestion of contraceptive agents promotes the growth of hepatic tumors, particularly hepatocellular adenomas. Evidence that the use of contraceptive drugs can also cause carcinoma of the liver is less convincing; this article describes the cases of 2 young women who had taken contraceptives and contracted hepatocellular carcinoma. Both women had no prior history of liver disease and died as a result of the carcinoma. Hepatocellular carcinoma has been a distinctly uncommon disease in the U.S. ranging in incidence from 0.23-0.47% in reported autopsy cases and being typically described as occurring mostly in men over 50 and associated with preexisting cirrhosis. Recent surveys show a greater proportion of female patients; in the U.S. patients at risk now include women in the reproductive age group with no history of prior liver disease. Some recorded changes in the human liver caused by oral contraceptives (OCs) include: 1) impairment of bile secretory function, 2) hepatomegaly associated with peripheral and midzonal sinusoidal congestion, and 3) peliosis hepatis. Significant risk factors in the occurrence of hepatic tumors in OC users are: 1) prolonged usage (1-3 years), 2) age over 30, and 3) use of compounds of high hormonal potency. Products containing mestranol have been implicated to a greater degree than those containing ethinyl estradiol. The link between use of OCs and development of hepatocellular carcinoma is not certain; however, the latter has been firmly linked with the use of anabolic steroids in men. Specifically only the C-17 substituted anabolic steroids oxymetholone and methyltestosterone have been implicated which are closely related to the C-17 substituted 19-norsteroids used in OCs. The following observations have also been made: 1) when hepatocellular carcinoma occurs in women it is mostly in those of reproductive age, and 2) OCs are associated with the development of benign hepatic tumors. Withdrawal from OCs is almost uniformly recommended after definitive diagnosis of a hepatic tumor along with surgery to avoid the risk of rupture and possible mortality.
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PMID:Oral contraceptives and cancer of the liver: a review with two additional cases. 628 82

Erythroblastopenia occurred in the course of chronic B cell lymphocytic leukemia. The failure of chlorambucil therapy prompted the decision of thymic irradiation. This was effective on the lymphoid proliferation but did not modify the erythroblastopenia. Progressive hepatomegaly led to the diagnosis of hepatoma.
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PMID:[Chronic lymphoid leukemia with erythroblastopenia and primary liver tumor]. 629 69

The possible association of hepatocellular carcinoma with oral contraceptive (OC) use is supported by the case of a 33-year old black female, gravida 5, para 4. She presented in April 1978 with right upper quadrant pain, nausea, vomiting, and fatty food intolerance. The case had been taking norethindrone, 1 mg with mestranol 0.05, for 2 years. There was no history of liver disease, alcohol abuse, or exposure to chemical toxins. The preoperative diagnosis was subacute cholecystitis; however, an unresectable primary liver tumor of both lobes was detected on surgery. OC use was discontinued, and the case refused chemotherapy. On December 1, 1978, she presented with a 9-week pregnancy which was aborted. Physical examination revealed an enlarged liver and mass in the upper right quadrant. The patient was readmitted December 11 with intractable pain and discharged. She died December 28, 1978. At autopsy the liver tumor appeared as a moderate to poorly differentiated hepatoma with irregular hyperchromatic nuclei. There was no evidence of coexistent benign lesions. The rapid progression of the disease following pregnancy suggests that hepatic growth was stimulated by the high estrogen levels of pregnancy. Earlier diagnosis and improved management are required in such cases. Ultrasonography can be used to confirm the presence of a mass, and liver scan or hepatic angiogram may be useful. Liver biopsy is required for definitive diagnosis. Treatment involves discontinuation of OC use and complete excision of the tumor where possible. If tumors have progressed beyond the stage of resectability, as in this case, the prognosis is poor.
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PMID:Hepatocellular carcinoma associated with oral contraceptive use and pregnancy. 629 72

Neocarzinostatin (NCZ), a new antitumor antibiotic, was administered to 19 patients with bladder cancer, 16 patients with prostatic cancer, and 3 patients with hepatoma. All patients had objectively measurable metastatic lesions including 21 with palpable nodes or subcutaneous nodules, 10 with pulmonary nodules as demonstrated by chest x-ray, 4 with malignant hepatomegaly, and 3 with bidimensional pelvic masses as demonstrated by CT scanning. Sixty-five courses of NCZ were administered via an intravenous bolus daily for five days with dosages ranging from 1500 to 3000 U/m2. Immediate toxicity was not dose-limiting except for 1 episode of anaphylaxis and 1 of acute renal failure. Myelotoxicity was delayed, dose-dependent, noncumulative, and dose-limiting. Thrombocytopenia was prolonged or irreversible in 5 cases. The maximally tolerated dose was 2750 U/m2. One patient with NCZ-associated pulmonary fibrosis and 1 with biopsy-proven hepatitis are discussed in detail. Neocarzinostatin demonstrated minimal therapeutic activity (1 partial remission) in patients with bladder cancer. There was no response in patients with prostatic cancer or hepatoma.
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PMID:Phase II trial of neocarzinostatin in patients with bladder and prostatic cancer: toxicity of a five-day iv bolus schedule. 644 76

Non-cystic cholangiodysplastic pseudocirrhosis of the liver was found in a 7 month old infant. Hepatomegaly was the first clinical sign. The cause of this disease entity ist believed to be a developmental disturbance of the small bile ducts. The etiology is unknown and the clinical course is hard to control. The transition to cirrhosis and the development of hepatocellular carcinoma are described.
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PMID:[Cholangiodysplastic pseudocirrhosis]. 651 31

Our results demonstrate that benfluorex at doses that are strongly hypotriglyceridemic does not increase hepatic peroxisomal enzyme activities, whereas fenofibrate at doses that are only slightly hypolipidemic induces a dramatic increase in the activity of these enzymes. Thus, the biochemical approach used in this study reveals that the hypolipidemic drug benfluorex does not belong to the class of hypolipidemic compounds known to induce hepatomegaly, hepatic peroxisome proliferation and hepatocarcinoma in rodents. Morphological studies should confirm the absence of peroxisomal induction.
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PMID:Effects of benfluorex and fenofibrate treatment on mitochondrial and peroxisomal marker enzymes in rat liver. 671 25

The administration of lipid-lowering drugs to rodents, notably those related to clofibrate, rapidly provokes a hepatic response characterized by hepatomegaly, proliferation of smooth endoplasmic reticulum and proliferation of peroxisomes in hepatocytes. In some studies hepatocellular carcinoma has been found in rats or mice exposed for their entire life-span to high dose levels of various fibrates. In the present study liver biopsy samples were obtained from 38 hyperlipidemic patients, 28 of whom had been receiving fenofibrate for between 2 months and approximately 3 years (mean values: males 1.79, females 1.98 years). The remaining 10 patients had never been treated with a lipid-lowering drug. Examination of the biopsy samples by a variety of optical techniques and by electron microscopy failed to reveal any difference between the groups. Peroxisomes were relatively rare, there being no evidence of the clear proliferation seen in rodent studies. Other microscopic features of interest were some variation of nuclear size, mitochondria containing paracrystalline inclusions, dilated endoplasmic reticulum associated with reduced amounts of rough endoplasmic reticulum, and the presence of lipid droplets in the liver cells. However, these variations from normal were in general not much more apparent in samples from the fenofibrate-treated patients than in the untreated group. Light- and electron-microscopic observations did not suggest liver intoxication or a carcinogenic pattern.
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PMID:Influence of fenofibrate on cellular and subcellular liver structure in hyperlipidemic patients. 683 87


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