Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibrosing cholestatic hepatitis is an aggressive and usually fatal form of viral hepatitis in immunosuppressed patients. We report three cases of fibrosing cholestatic hepatitis in various clinical situations. Case 1 was a 50-year-old man who underwent a liver transplant for hepatitis B virus (HBV)-associated liver cirrhosis. Two and a half years after the transplant, he complained of fever and jaundice, and liver enzymes were slightly elevated. Serum HBsAg was positive. Case 2 was a 30-year-old man in an immunosuppressed state after chemotherapy for acute lymphoblastic leukemia. He was a HBV carrier. Liver enzymes and total bilirubin were markedly elevated. Case 3 was a 50-year-old man who underwent renal transplantation as a known HBV carrier. One year after the transplant, jaundice developed abruptly, but liver enzymes were not significantly elevated. Microscopically lobules were markedly disarrayed, showing ballooning degeneration of hepatocytes, prominent pericellular fibrosis, and marked canalicular or intracytoplasmic cholestasis. Portal inflammation was mild, but interphase activity was definite and cholangiolar proliferation was prominent. Hepatocytes were diffusely positive for HBsAg and HBcAg in various patterns. Patients died of liver failure within 1 to 3 months after liver biopsy in spite of anti-viral treatment.
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PMID:Fibrosing cholestatic hepatitis: a report of three cases. 1071 21

Autoimmune hepatitis (AIH) after liver transplantation (LT) may recur and is difficult to diagnose. Our aims were to define the histopathology of and factors related to AIH recurrence. Fourteen of 475 patients received LT for AIH; 2 died perioperatively. Liver specimens (native and post-LT biopsies) from 12 other patients were reviewed and correlated with pre- and post-LT clinical course and outcome. Recurrent AIH was seen in 5 of 12 patients, 35 to 280 days post-LT as lobular hepatitis with acidophil bodies and lymphoplasmacytic infiltrate. Portal/interface hepatitis was seen with disease progression and 2 of 5 patients developed cirrhosis. Of 7 nonrecurrent patients, 1 had acquired hepatitis C with lobular/portal hepatitis and none developed cirrhosis. Histology suggestive of overlap syndrome was seen in 3 of 12 native livers with no effect on post-LT course or pathology. High-grade necroinflammation was present in native livers at LT in 5 of 5 cases with recurrent AIH and in 1 of 7 without recurrence (P <.01). Pre-LT disease duration, donor/recipient gender distribution, HLA studies, and rejection episodes did not correlate with AIH recurrence. We conclude that (1) recurrent AIH is not uncommon and was seen in 42% of patients with lymphoplasmacytic lobular, portal, and interface hepatitis; (2) acidophil bodies with lymphoplasmacytic cells are seen in early recurrent AIH; (3) recurrent AIH appears at variable time periods post-LT, and the progression is slow; and (4) high-grade inflammation in native liver at LT is a strong predictor of recurrent AIH.
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PMID:Liver transplantation for autoimmune hepatitis: a long-term pathologic study. 1091 22

We present a rare case of eight multicentric hepatocellular carcinomas (HCCs) occurring in the same segment of the liver. In a 66-year-old Japanese man, multiple liver tumors were detected during follow-up of chronic hepatitis C infection, and he was admitted to our hospital in 1995. Ultrasonography (US) showed eight tumors, each measuring between 10 and 15 mm in diameter, in the right lobe, and a 10-mm tumor in the left lobe. Angio-ultrasonography (US) showed no enhancement of the tumors, and multicentric occurrence was suspected. Portal angio-US showed eight tumors in the right lobe located in the anterior segment. Accordingly, anterior segmentectomy and partial resection of the S3 subsegment were performed, in December, 1995. On histological examination, all eight tumors in the anterior segment and the tumor in the S3 subsegment were well differentiated HCC. The liver parenchyma showed cirrhosis. The grade and stage of hepatitis did not differ between the anterior segment and the S3 subsegment, but irregular regeneration of hepatocytes was more prominent in the anterior segment. The multicentric occurrence of HCCs in the anterior segment may be related to the more severe damage caused by chronic hepatitis in the anterior segment than in the left lobe of the liver.
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PMID:Eight multicentric hepatocellular carcinomas occurring in the same segment of the liver. 1152 Nov 86

The purpose of this study was to describe the magnetic resonance imaging findings of granulomatous hepatitis on T1-weighted, T2-weighted and postgadolinium images. Eight patients with histopathological diagnosis of granulomatous hepatitis were evaluated in this study. MRI examinations included precontrast T1-weighted breath-hold spoiled gradient echo, breathing independent STIR sequences, and T1-weighted breath-hold spoiled gradient-echo sequence following after i.v. gadolinium administration in arterial, intermediate and late phases. Diffuse nodular liver involvement was visualized in all patients. Nodules were consistent with granulomas and were 0.5-4.5 cm in diameter. Caseating granulomas were intermediate and high signal on T2-weighted, low signal on T1-weighted images. They revealed no enhancement in two patients, and enhanced in one patient. Noncaseating granulomas revealed intermediate signal on T1, and T2-weighted images and increased enhancement on arterial phase images with persisting enhancement in late phase images. Portal lymph nodes were visible in five patients. Splenomegaly was present in five patients. Granulomatous hepatitis has spectrum of MRI features, to be considered in differential diagnosis with other diffuse nodular liver pathologies.
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PMID:Granulomatous hepatitis: MRI findings. 1171 Dec 35

We studied nondiagnostic liver biopsy specimens from 20 patients with definite primary biliary cirrhosis (PBC) and 18 with definite autoimmune hepatitis (AIH) to identify distinguishing features. All patients had early-stage disease; biopsy specimens were devoid of granulomas or diagnostic features of PBC or AIH. Diagnoses were based on serologic and clinical variables. Sixteen specimens from each group were immunostained with cytokeratin 7. The density of portal tract eosinophils and number with cytokeratin 7-reactive periportal hepatocytes were quantified. Sixteen of 18 patients with AIH and 13 of 20 with PBC had no or minimal bile duct injury. Histologic activity index scores were 5.8 in AIH and 5.7 in PBC. The mean portal eosinophil score was greater in PBC than in AIH. Cytokeratin 7 identified many central bile ducts that were obscured by portal inflammation. The mean periportal cytokeratin 7-reactive hepatocyte score was greater in PBC than in AIH. Portal eosinophils and cytokeratin 7 reactivity in periportal hepatocytes are supportive of PBC rather than AIH. No morphologic features were supportive of AIH. Cytokeratin 7 reactivity in periportal hepatocytes may be an early response to PBC-induced biliary obstruction in other regions of the liver.
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PMID:Portal tract eosinophils and hepatocyte cytokeratin 7 immunoreactivity helps distinguish early-stage, mildly active primary biliary cirrhosis and autoimmune hepatitis. 1176 73

A 49-year-old woman was admitted to our hospital because of hepatocellular carcinoma (HCC). She had no hepatitis virus. Serum AFP and PIVKA-II levels were as high as AFP 329.4 ng/ml (AFP-L3% 73.1%) and 281 AU, respectively. Portal venous thrombus was observed from the right portal branch to left portal branch and superior mesenteric vein. An extended right hemihepatectomy with extraction of portal venous thrombus was performed. On postoperative day 8, low-dose cisplatin (10 mg/day for 5 days/week) and 5-fluorouracil (250 mg/day for 5 days/week) were administered through the hepatic artery for 4 weeks. After chemotherapy, one intrahepatic metastasis appeared and RFA was performed for this tumor. At 16 months after surgery, she had multiple lymph node metastases and died at 20 months after the surgery without intrahepatic metastasis. Low-dose CDDP/5-FU intra-hepatic artery infusion chemotherapy was effective for prevention of intrahepatic recurrence after resection of HCC with portal venous thrombus.
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PMID:[A case of Vp4 hepatocellular carcinoma treated with surgical resection and continuous intrahepatic artery infusion chemotherapy of low-dose cisplatin and 5-fluorouracil]. 1461 15

Autoimmune hepatitis (AIH) is usually a chronic portal-based hepatitis with prominent plasma cells. Although necroinflammatory activity throughout the lobule is described, centrilobular necrosis (CN) is only rarely the predominant pattern of injury. Recognition of the possibility of AIH in zone 3 hepatitis will lead to prompt steroid therapy and may avert cirrhosis. We report the clinicopathologic features of 6 cases of AIH with CN. The 3 females and 3 males averaged 48 years of age (range 32-66 years). Four patients had a history of autoimmune disorders. All had elevated transaminases and negative serology for viral hepatitis B and C. One had a history of ethanol use. One patient was taking interferon-beta and 1 patient was taking atorvastatin, but none of the patients was taking medication with a temporal relationship to suggest a drug hypersensitivity hepatitis. All patients had positive antinuclear antibody, anti-smooth muscle antibody, or both, although 1 patient was negative for autoantibodies at initial laboratory testing. Four biopsies showed confluent zone 3 necrosis, whereas two biopsies showed spotty CN. Portal inflammation was relatively mild in all cases. Plasma cells were few to numerous in both zone 3 and portal tracts in four biopsies; they were absent in 2 cases. All patients responded to steroid therapy. Two patients relapsed, and rebiopsy in 1 of them showed CN, bridging necrosis, and an increase in the degree of portal-based hepatitis. Another patient was not treated initially; a second biopsy 35 months after presenting revealed periportal hepatitis as well as CN. The histologic spectrum of AIH should be expanded to include zone 3 hepatitis. As with classic AIH, most patients with CN demonstrate serologic and clinical evidence of autoimmunity. Subsequent biopsies in patients with a centrilobular pattern may show evolution to portal-based hepatitis characteristic of AIH but may also show persistence of the zone 3 hepatitis. Unlike other causes of zone 3 hepatitis, AIH is steroid responsive; therefore, timely diagnosis is important.
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PMID:Autoimmune hepatitis with centrilobular necrosis. 1508 66

Primary malignancies of the liver include tumors arising from the hepatocytes (hepatocellular carcinoma and the fibrolamellar variant) and the intrahepatic bile ducts (intrahepatic cholangiocarcinoma). Hepatocellular carcinoma is the most common primary cancer of the liver and is a leading cause of death from cancer worldwide. Although it is uncommon in the United States, the incidence of hepatocellular carcinoma is rising. Hepatitis, ethanol use, and cirrhosis often dominate the clinical picture and may dictate prognosis. New clinical and pathological staging systems have allowed for the more accurate stratification of patients to more appropriately identify patients for resection, transplantation, and percutaneous ablation therapies. A correlation between liver volume and surgical outcome has recently been demonstrated, with small liver remnant size being associated with increased morbidity. Portal vein embolization has therefore been proposed as one way to induce hypertrophy of the anticipated liver remnant before resection. Initial reports have shown that portal vein embolization decreases the incidence of postoperative complications. More recently, systemic chemotherapy and chemoembolization have been investigated as both primary and neoadjuvant therapy. Chemoimmunotherapy with 5-fluorouracil and interferon may be associated with a superior response rate in the fibrolamellar variant of hepatocellular carcinoma. Two recent randomized studies have also indicated improved survival after hepatic artery embolization in selected patients.
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PMID:Advances in the surgical management of liver malignancies. 1513 Feb 67

Helicobacter hepaticus infection induces sustained inflammation and carcinoma of the liver in A/JCr mice, and serves as a model of human cancers associated with viral hepatitis and H. pylorichronic gastritis. Here we describe the pathogenesis of premalignant disease in A/JCr mice infected with H. hepaticus. We inoculated dams intragestationally and/or pups postnatally, and evaluated offspring at 3, 6, or 12 months. Mice infected at or before 3 weeks of age, but not at 12 weeks, developed disease. Male mice were most affected, but expressed a bimodal pattern of susceptibility. Males exhibited lobular necrogranulomatous and interface (chronic active) hepatitis, while females usually developed intraportal (chronic persistent) hepatitis. Portal inflammation was slowly progressive, with tertiary lymphoid nodule development by 12 months. Hepatic bacterial load and preneoplastic lesions, including clear and tigroid cell foci of cellular alteration, were correlated with lobular hepatitis severity. No extrahepatic surrogate disease marker reliably predicted individual hepatitis grade. In conclusion, gender and bacterial exposure timing are key determinants of H. hepaticus disease outcomes. Intrahepatic inflammation is driven by local signals characterized by a vigorous but nonsterilizing immune response. Continued study of chronic hepatitis progression may reveal therapeutic targets to reduce the risk of hepatocellular carcinoma.
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PMID:Progression of chronic hepatitis and preneoplasia in Helicobacter hepaticus-infected A/JCr mice. 1551 10

The aim of the present study was to investigate the impact of the combined administration of Vitamin C and silymarin on lead toxicity. Male albino rats were subdivided into three groups: the first was a control group, the second received lead acetate in diet as 500 mg/kg diet daily, the third received the same lead acetate dose and supplemented with Vitamin C (1 mg/100g body weight) and silymarin (1 mg/100g body weight) by gastric tube three times per week. Blood samples were taken after 2, 4 and 6 weeks of treatment. Significant lead-induced elevations in serum ALT, AST, GGT and ALP activities were observed after different periods of treatment. However, serum LDLc was decreased. The intensities of RNA and apoptotic fragments of DNA were measured as optical density by Gel-pro program. Lead acetate decreased the intensity of DNA at 6 weeks and induced apoptotic DNA fragments reversibly with time. After 2 weeks of lead administration dilation and congestion of terminal hepatic veins and portal vein branches were observed. Lead also induced hepatocyte proliferation without any localized distribution among zones 1-3. Portal inflammatory infiltrate with disruption of the limiting plates (interface hepatitis), steatosis, apoptosis and mild fibrosis were detected especially by sixth week of lead administration. Combined treatment of lead-exposed animals with Vitamin C and silymarin showed marked improvement of the biochemical, molecular and histopathological findings. These experimental results strongly indicate the protective effect of Vitamin C and silymarin against toxic effects of lead on liver tissue.
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PMID:Amelioration of lead toxicity on rat liver with Vitamin C and silymarin supplements. 1559 Jan 5


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