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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure of mice to 1000 ppm of vinyl chloride (VC), 6 hr/day, 5 days/week, caused some acute deaths with toxic hepatitis and marked tubular necrosis of the renal cortex. Starting the sixth month, mice exposed to 1000, 250, or 50 ppm of VC became lethargic, lost weight quickly, and died. Only a few mice exposed to 50 ppm survived for 12 months. Pulmonary macrophage count was elevated in some mice. There was a high incidence of bronchiolo-alveolar adenoma, mammary gland tumors including ductular adenocarcinoma, squamous and anaplastic cell carcinomas with metastasis to the lung, and hemangiosarcoma in the liver, and, to a lesser extent, in some other organs. The incidence of these tumors quickly increased, and the severity was in direct proportion to the levels of VC and the length of exposure. Malignant lymphoma involving various organs was observed in a few mice. Rats were more resistant to the toxic effects of VC. Exposure to 1000 ppm slightly depressed the body weight of the females. Exposures of 250 or 1000 ppm caused a number of deaths and hemangiosarcoma in the liver starting the ninth month. Most rats with hepatic hemangiosarcoma also developed hemangiosarcoma in the lung. Hemangiosarcoma occasionally occurred in other tissues of one or two rats exposed to 50 ppm or higher level of VC. Exposure of mice to 55 ppm of vinylidene chloride (VDC) also caused a few acute deaths and a few hepatic hemangiosarcomas. Inflammatory, degenerative, and mitotic changes occurred in the liver. No mouse exposed to VDC developed any mammary gland tumors. Several mice had bronchioloalveolar adenoma. Exposure of rats to 55 ppm of VDC slightly depressed the body weight. Hemangiosarcoma occurred in the mesenteric lymph node or subcutaneous tissue in two rats.
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PMID:Inhalation toxicity of vinyl chloride and vinylidene chloride. 56 2

A variety of neoplasms and nonneoplastic hepatic lesions have been noted in winter flounder, Pseudopleuronectes americanus, from Boston Harbor, Massachusetts. Inflammatory lesions include cholangiitis, pericholangiitis, pericholangial fibrosis, hepatitis, and pancreatitis. Necrotic lesions consist essentially of focal coagulative necrosis and a distinctive vacuolated cell lesion of the hepatic parenchyma. The most conspicuous and numerous proliferative lesion is macrophage aggregate hyperplasia and hypertrophy. Preneoplastic lesions include principally basophilic foci of cellular alteration and hepatocellular adenoma. Carcinomas consist of several morphologic varieties: hepatocarcinoma, cholangiocarcinoma, and anaplastic adenocarcinoma. The pathogenesis of the lesions observed is discussed with respect to anthropogenically introduced chemical contaminants and the resistant hepatocyte model of hepatocarcinogenesis. This study, and others of bottom-living food fish with enzootic neoplastic disease, warrants further evaluation, particularly with respect to possible bioaccumulation of chemical contaminants in edible tissues.
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PMID:Neoplasms and nonneoplastic liver lesions in winter flounder, Pseudopleuronectes americanus, from Boston Harbor, Massachusetts. 164 9

In March 1989, ultrasonography revealed a hepatic mass in a 40 year old nulliparous woman who was then referred to the University of Southern California--Los Angeles (UCLA) Liver Unit. She exhibited no symptoms of a liver condition. From 19-28 years old, she took the combined oral contraceptive (OC) Ovulen 21 for irregular menses. After a brief period of taking Ortho Novum 1/80, she took Demulen 1/35-24 between ages 28-34. Her physician diagnoses endometriosis at 34. He stopped OC therapy and prescribed the progestin Norlutate. She had no history of hepatitis, toxin exposure, and previous liver disease. Further no one in her family had had liver disease or neoplasms. Computer tomography identified a 6.5 cm x 3.5 cm mass in the right lobe of the liver which matched a cold defect on a liver scan using technetium Tc 99m sulfur colloid. The mass selectively took up gallium. Arteriography revealed the mass to be a vascular tumor, but it did not exhibit a typical vascular pattern of an adenoma or the neovascularity of hepatocellular carcinoma. Physicians at UCLA used peritoneoscopy to take percutaneous needle biopsies of the right lobe which confirmed a hepatic adenoma. they then removed the right lobe of the liver. The remaining part of the liver was normal. Histologic examinations of the removed section showed features of a well differentiated hepatocellular carcinoma. Further tumor cells had invaded normal hepatic parenchyma. The physicians believed that hepatic adenoma was in the process of transforming into hepatocellular carcinoma in this patient. They thought that long term OC use, and possibly long term progestin use, may have contributed to the formation of the liver neoplasms. They emphasized the need for a pilot study to develop guidelines on surveillance ultrasonography of women taking OCs over a long period.
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PMID:Hepatocellular carcinoma coexisting with hepatic adenoma. Incidental discovery after long-term oral contraceptive use. 166 98

Clinical and laboratory evidence of an association of oral contraceptive (OC) use with the subsequent development of benign and malignant hepatobiliary neoplasia is growing. The authors present a case in which an adenoma within a large, multicentric anaplastic spindle cell carcinoma occurred in a woman with a long history of OC use. The patient, a 38-year-old gravida 2, para 2, was diagnosed following low-grade fevers and right upper quadrant pain. A partial hepatectomy was performed with no complications; however, a follow-up examination 2 months later revealed widespread intra-abdominal tumor recurrence histologically identical to the original tumor. Immunostaining for alpha 1 antitrypsin and keratin was strongly positive in tumor cells, indicating a biliary derivation. Electron microscopy indicated an epithelial derivation as well, including the presence of intracellular lumens, intermediary filaments, and numerous intercellular junctions. Estrogen and progesterone receptors were negative in the tumor. The tritiated thymidine labeling index was 5.05%, with an estimated potential doubling time of 11 days. This woman had no history of hepatitis, no family or personal history of neoplasms, and no known hepatotoxin exposure. The only medication used by the patient was Norlestrin, an OC containing 1 mg norethindrone and 50 mcg ethinyl estradiol that she had taken continuously for the past 8 years.
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PMID:Hepatic adenoma within a spindle cell carcinoma in a woman with a long history of oral contraceptives. 243 48

Hepatocellular carcinoma (hepatoma) accounts for over 80% of primary liver tumors. Although relatively uncommon in North America and Europe, hepatocellular carcinoma is the dominant malignant carcinoma in Southeast Asia and South and West Africa. About 80% of the patients have cirrhosis. The tumor has a grim prognosis with an average survival time of 4.5-13 months after the onset of complaints. Beginning with the observation of the striking coincidence of the geographic distribution of hepatocellular carcinoma with the endemic distribution of virus hepatitis, many studies have demonstrated the close correlation of the carcinoma with chronic hepatitis B. In the endemic areas vertical perinatal transmission of the virus from mother to the newborn is an important route of transmission. While only about 10% of infected adults develop HBs antigen carrier status, the carrier rate of perinatal infections is about 95%. In chronic infection the virus DNA can be integrated into the host genome and may become carcinogenic with time. Many studies have substantiated an increased incidence of liver adenoma and resulting complications among women taking oral contraceptives; evidence for a relationship between oral contraceptives and hepatoma has not been established. No increase in hepatoma has been observed among young women following the introduction of oral contraceptives in the USA and in Denmark.
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PMID:[Hepatocellular carcinoma]. 246 47

The livers of 16 woodchucks with naturally acquired chronic infection with woodchuck hepatitis virus were examined both grossly and histologically in 14 biopsy specimens and seven necropsy specimens. Fifteen woodchucks had lesions characteristic of chronic hepatitis; ten of these had chronic active hepatitis, four had chronic persistent hepatitis, and one had cirrhosis with nodular regeneration. In one woodchuck there was massive hepatic necrosis attributed to infection with an unclassified protozoan. Thirteen woodchucks had primary hepatocellular carcinoma. Metastasis to the lung was observed in only one woodchuck. These results were compared to liver lesions in 149 woodchuck hepatitis virus-negative woodchucks. Chronic hepatitis comparable to that associated with woodchuck hepatitis virus infection was not observed in woodchuck hepatitis virus-negative woodchucks although in one, a single, small hepatocellular adenoma was found.
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PMID:Chronic hepatitis and hepatocellular carcinoma associated with persistent woodchuck hepatitis virus infection. 299 74

A case report is presented of a 43-year-old woman with generalized peliosis hepatitis that developed during longterm use of oral contraceptives (OCs). The patient had been in good health until the last 2 years when she began to experience vague epigastric pains and a feeling of abdominal distension. Several months prior to admission, she had started to complain of itching and fatigue. There was no history of dark urine, white stools, or hepatitis. On physical examination, no jaundice or cutaneous stigmata of chronic liver disease were observed. Laboratory studies showed a normal erythrocyte sedimentation rate and hematological blood count. A radionuclide study of the liver showed hepatomegaly; especially the left lobe was enlarged. A computerized tomographic scan of the liver showed multiple areas of decreased density in both of the enlarged lobes. There was no evidence of a tumor. Selective transfemoral angiography of the celiac artery also showed hepatic enlargement but no signs of a space-occupying lesion. At laparoscopy, the liver was grossly enlarged and had a lumpy appearance, but again there were no signs of a tumor. No evidence of veno-occlusive disease or hepatocellular adenoma was found. The diagnosis was peliosis hepatitis. The OCs were withdrawn, and the patient was discharged. Regular follow-up in the outpatient department showed no decrease in the size of the liver. The alkaline phosphatase level rose. The fatigue became worse, and cholestyramine was prescribed for progressive itching. In September 1980, the patient was admitted for reevaluation. A repeated CT scan and angiography of the liver again yielded no evidence of a tumor. Esophagoscopy showed the presence of varices grade 2. The liver at laparoscopy had the same appearance as it had in 1976. Histological examination of a biopsy specimen showed occasional dilated sinusoids and locally marked periportal and intralobular fibrosis. No regeneration nodules were found. The diagnosis was liver fibrosis. The patient's condition deteriorated gradually in the following years. She experienced increasing fatigue. Steatorrhea developed, and the patient lost weight. She needed increasing doses of cholestyramine and oral supplementation of vitamins A, D, and K. She was admitted for a 3rd time in February 1985. Esophagoscopy revealed varices grade 4. A CT scan of the liver showed no change. The patient successfully underwent an orthotopic liver transplantation in January 1987. The diagnosis of peliosis hepatis was well documented in this patient.
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PMID:Generalized peliosis hepatis and cirrhosis after long-term use of oral contraceptives. 312 33

Morphometric study of liver biopsies from six entities (normal tissue, post-hepatitis cirrhosis, post-alcoholic cirrhosis, cancer-related cirrhosis, hepatocellular adenoma and hepatocellular adenocarcinoma) confirmed that this technique can be a valuable adjunct to histopathologic study in the examination of such specimens. As expected, measurements in cirrhotic nodules showed two populations of cells. The so-called "large dysplastic cells" had nuclear and cellular areas close to those of normal hepatocytes and should thus be considered to be hyperplastic elements, not precancerous elements. The smaller dysplastic cells had morphometric values close to those of the corresponding hepatocellular carcinomas, indicating that these cells are the truly precancerous ones. Therefore, while the study confirmed that hepatic cirrhosis is a precancerous lesion, it also showed that the term hepatocellular dysplasia must be restricted to the smaller type of cells found in such nodules.
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PMID:Morphometric characteristics of hepatocellular dysplasia. 320 57

This is a broad review (140 literature citations) of the possible effects of oral contraceptives on the liver. The oral contraceptives considered consist of combined preparations of estrogens and progestogens although the so-called "minipills" contain only a progestogen. The effects are divided into 1) decrease in excretory liver function; 2) influence on bile acid formation, including cholesterol metabolism; 3) increased synthesis of various transport proteins (ceruloplasmin, transferrin, thyroxine-binding protein, and cortisol-binding protein); 4) the effects of increased tissue circulation caused by sexual hormones and anabolic steroids as a cause for more frequent cavernous angiomas and peliosis hepatis; 5) interference with the metabolism of other drugs by the competitive action of the hepatic metabolites of steroid hormones. This includes the increased formation of delta amino levulinic-acid synthetase, the key enzyme for porphyrin synthesis. The gestagen component of oral contraceptives is responsible for enzyme induction in the smooth endoplasmic reticulum. Morphological liver changes caused by oral contraceptives include parenchyma changes, hepatosis, reactive hepatitis, hepatitis resembling viral hepatitis, vascular changes, sinusoid ectasia, Budd-Chiari syndrome, hyperplasias and neoplasias, focal nodular hyperplasia, adenoma and liver cell carcinoma.
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PMID:[Effects of oral contraceptives on liver function and structure]. 332 30

The clinical and biochemical evolution of hepatic lesions in 124 patients with toxic oil syndrome from 1981 to 1986 has been reviewed. Most patients became asymptomatic during the early phase of the disease and abnormal liver function tests gradually normalized. In 1981, liver injury resembled drug-induced cholestatic hepatitis in 31 patients, and in 1 patient chronic destructive nonsuppurative cholangitis was evident. From 1982 to 1986 serial liver biopsies demonstrated toxic cholestatic hepatitis in 14 patients, chronic active hepatitis in 13, and nonalcoholic cirrhosis in 4. Nineteen patients showed lesions suggestive of alcoholic liver disease, but only 8 had a history of heavy alcohol intake. One patient developed biliary cirrhosis, another liver cell adenoma, and 8 nodular regenerative hyperplasia of the liver. We conclude that although liver injury had subsided in most patients, a significant number developed a variety of different liver diseases after follow-up for 5 yr.
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PMID:Clinico-biochemical evolution and late hepatic lesions in the toxic oil syndrome. 360 65


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