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)

A 39-year-old male with bleeding esophageal varices due to portal hypertension was observed. The patient had taken an arsenical preparation during a period of 12 yr because of psoriasis and subsequently developed keratotic changes of the palms and soles of his feet and an epithelioma of the scrotum. Physical examination was unremarkable except for splenomegaly and skin lesions. Liver function tests were normal; a needle biopsy of the liver (right lobe) showed nonspecific changes. Combined hepatic and umbilicoportal catheterization revealed, on splenography and portography, huge esophageal varices and patent portal vein; dilation, distortion, and cut-off of many intrahepatic portal branches were found. A marked gradient existed between the free portal venous pressure (25 mm Hg) and the wedged hepatic venous pressure (9.5 mm Hg). Hepatic blood flow, portal PO2, cardiac output, cardiac index, and blOOD volume were within normal range. Arteriographies did not reveal arteriovenous shunts in the splanchnic or splenic vessels. A splenorenal shunt were performed and a wedged biopsy of the liver (left lobe) revealed nonspecific changes. Three years later the patient had not experienced any episode of hemorrhage or hepatic encephalopathy but developed an epithelioma of the tongue. No known cause could be incriminated in the pathogenesis of the portal hypertension. However, there was unequivocal chronic arsenic intoxication. Toxic hepatitis, cirrhosis, noncirrhotic portal hypertension, and hemangiosarcoma of the liver have been reported with the intake of arsenicals. Thus, it is suggested that in this patient, presinusoidal portal hypertension was secondary to chronic arsenical intake associated with marked intrahepatic vascular changes seen on portography.
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PMID:Noncirrhotic presinusoidal portal hypertension associated with chronic arsenical intoxication. 112 3

The determination of plasma viscosity in 37 patients with liver disease allowed their subdivision into three groups. Firstly, decreased viscosity (hypoviscosity) was found in patients with cirrhosis, marked portal hypertension and esophageal varices. Secondly, normal viscosity (normoviscosity) was found in patients with inactive cirrhosis without portal hypertension, and thirdly, increased viscosity (hyperviscosity) was found in patients with active cirrhosis and chronic progressive hepatitis. The concentrations of total serum protein, of fibrinogen and of IgG were found to influence plasma viscosity. A detailed differentiation revealed that increased plasma viscosity is caused by increased levels of IgG while decreased viscosity correlates with low fibrinogen levels. Furthermore a close correlation exists between plasma viscosity and the enzymatic activity of SGOT, SGPT and GLDH. In 5 patients with chronic progressive hepatitis treated with corticosteroids the plasma viscosity normalized in parallel with improvement of the hepato-cellular damage. These findings will be discussed in detail. Hyperviscosity might possibly serve as an additional parameter to characterize chronic progressive hepatitis and to indicate steroid treatment.
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PMID:[Changes of blood-flow properties in patients with chronic liver disease (author's transl)]. 113 47

47 patients with chronic aggressive hepatitis were immunosuppressively treated on the average 33.8 months (daily dose 100 mg azathioprine and 10 mg prednisolone). The serochemical parameters thymol, ZnSO4, GOT and GPT statistically significantly improved themselves. In 36 patients bioptic controls in 61.1% resulted in an improvement, and in 27.8% of the cases they resulted in a constancy of the histological findings. 10.6% of the patients died of a liver cirrhosis with portal hypertension. Nearly half the patients is capable to work. No severe side-effects appeared. The present results correspond to the results mentioned in literature. The chronic aggressive hepatitis, furthermore, should be added to a prednisone monotherapy or to a combination therapy of azathioprine and prednisone.
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PMID:[Immunosuppressive long-term treatment of chronic aggressive hepatitis]. 122 50

One hundred and thirty-five patients who developed non-A, non-B post-transfusion hepatitis mostly after cardiac surgery, were followed for a mean (+/- S.D.) of 90 +/- 41 months (range: 13-180) to evaluate clinical and histological outcome. Thirty-one cases resolved within 12 months, while 104 (77%) progressed to chronicity. Twenty-one of 65 (32%) biopsied patients developed cirrhosis at the end of the follow-up, and one further progressed to hepatocellular carcinoma. One patient had a complete histological remission (1%). The remaining cases had chronic active (37%), chronic persistent (27%) or chronic lobular hepatitis (3%). About half of the cases with cirrhosis developed portal hypertension, and three of these died due to esophageal varices hemorrhage, one due to liver failure, and one due to hepatocellular carcinoma. Out of 26 patients with the initial histologic diagnosis of chronic hepatitis that were rebiopsied during follow-up, 13 (50%) progressed to cirrhosis. These patients were significantly older than patients who did not develop cirrhosis (mean age 57 and 45 years respectively; p < 0.01). During acute hepatitis anti-HCV was positive in all but one of the 114 patients tested. Percentages were similar for patients who recovered (95%) and those who developed chronic hepatitis (100%). However, during follow-up, 71% of the 1st generation and 21% of the 2nd generation ELISA test patients with acute resolved hepatitis became anti-HCV negative, while the same figures in chronic cases were only 8.5% (p < 0.0001) and 1.4% (p = 0.012). This suggests a correlation between anti-HCV antibody activity, hepatitis C virus replication, and the development of chronic liver disease.
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PMID:Long-term follow-up of non-A, non-B (type C) post-transfusion hepatitis. 148 3

Nodular regenerative hyperplasia (NRH) is a rare lesion of the liver associated with portal hypertension in more than half of patients. We present two cases demonstrating complications and diagnostic problems of NRH and review the pathogenesis, clinical, radiologic, and pathologic features of 240 cases in the literature. Patient 1 died from variceal bleeding as a complication of NRH. Patient 2 presented with ascites. Sonographic, computed-tomographic and magnetic resonance findings did not differ from liver cirrhosis. Three needle biopsies showed nonspecific reactive hepatitis. Wedge liver biopsy provided the correct diagnosis of NRH and a shunt operation was performed. Non-Hodgkin's lymphoma (centroblastic type) was diagnosed three years after NRH. At present there is no clinical or radiologic evidence of progression of NRH in this patient. The diagnosis of NRH cannot be made without histologic examination. Correct diagnosis is difficult in percutaneous needle biopsy. Therefore, laparoscopically guided liver biopsy or wedge biopsy is often necessary for diagnosis. NRH should be included in the differential diagnosis of portal hypertension. Portal diversion can be considered.
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PMID:Diagnostic problems in nodular regenerative hyperplasia (nodular transformation) of the liver. Review of the literature and report of two cases. 159 15

Patients with portal hypertension without a demonstrable cause have been reported in the literature under several different terms, such as tropical splenomegaly, phlebosclerosis, obliterative portal venopathy of the liver, hepatoportal sclerosis, noncirrhotic portal fibrosis and idiopathic portal hypertension (IPH). Such patients have been described worldwide, with a greater frequency in India and Japan. The etiology of IPH is still unknown, although some of the theories that have been proposed are: exposure to toxic substances or drugs, relationship with the hepatitis-B virus, immunologic abnormalities, systemic or intra-abdominal infections and clotting abnormalities. The main histopathologic findings are periportal fibrosis, obliteration of small portal veins and sclerosis of the interhepatic portal system. Although these abnormalities could be secondary to portal hypertension, it has been proposed that the vascular changes are the primary event that leads to portal hypertension. The site of increased resistance in IPH is found at the presinusoidal level with some component at the sinusoidal and postsinusoidal level. The main symptoms and signs in IPH are upper gastrointestinal tract bleeding secondary to esophago-gastric varices, symptoms related to anemia, and splenomegaly. The long-term prognosis for patients with IPH is better than for cirrhotic patients, with a 77% survival at ten years. Variceal bleeding is the main cause of death, and some treatment to prevent bleeding or its recurrence is warranted. Although no comparative trial has been performed in IPH patients, the surgical management could be the first choice for elective treatment in these patient without liver failure, because of the high re-bleeding rates with chronic sclerotherapy. Pharmacologic management could be considered for prophylactic treatment of these patients.
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PMID:[Idiopathic portal hypertension]. 186 3

Out of 99 histologically verified carcinomas (HCC), 73 (73.7%) belonged to HCC with associated cirrhosis and 26 (26.2%) belonged to HCC without cirrhosis. The relatively high incidence of HBsAg in the serum of patients with non-cirrhotic HCC (57.6%) shows that HBV infection persistence could be, one of the very important bases for HCC development, more than cirrhosis itself. The negative finding of HBsAg in the serum couldn't exclude the possibility of an integrated HBV genome in the cirrhotic tissue. There is an alternative possibility of an induced infection with hepatitis NANB (transfusions). A non-significant inclination towards younger age groups exists in non-cirrhotic HCC. Males are predominant in both groups, but females are more present in non-cirrhotic HCC than in cirrhotic HCC. The clinical course of non-cirrhotic HCC is usually slower; often there are no signs of portal hypertension or surrounding organ involvement, which offers better prognostic prospects than cirrhotic HCC. In relation to cirrhotic HCC, patients with non-cirrhotic HCC had a less frequent history of hepatitis (19.2%), a higher albumin-globulin ratio (1.5) and lower values in serum alpha-1 fetoprotein elevation (53.8%). Ultrasonographically, HCC without cirrhosis is presented with a mono-nodular shape in the majority of cases, or as a primary and dominant form, with surrounding satellite lesions even within the other lobe. Pathoanatomic findings usually show massive, compact, solid tissue formation alone, or accompanied by satellite lesions. Histologically, there is low-degree evolution with minimal necrosis and mild mitotic activity with a presence of minimal fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Characteristics of hepatocellular carcinoma in the non-cirrhotic liver]. 196 51

We report two cases of children followed for many years with an original diagnosis of non-A/non-B hepatitis. One child developed serious cirrhosis with portal hypertension. Long-term observation of the course of their hepatic disease provided the diagnosis of cystic fibrosis. These cases demonstrate that cystic fibrosis though rarely presenting with initial hepatic signs, can manifest itself with only long-term hepatic symptoms. We therefore strongly recommend analysis of sweat chloride concentration in cases of hepatic disease of unknown origin.
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PMID:False diagnosis of non-A/non-B hepatitis hiding two cases of cystic fibrosis. 212 37

Fifty nine C.F. pts (38 males) aged 14-41 years have been considered, for all of them the following parameters were taken into account: Shwachman clinical score modified (radiological evaluation emended), steatorrhea, liver function tests (SGOT, SGPT, GT, Bilirubin, AP, Quick T.), A and B hepatitis markers and ultrasonographic scan of pancreas and hepatobiliary system. 23 pts (38%) presented well recognized hepatobiliary involvement: 2 pts (3%) evident cirrhosis, 3 pts (5%) cirrhosis with portal hypertension and esophageal varices, 5 pts (8%) were affected with signs of chronic hepatopathy, 13 pts (22%) presented gallbladder stones.
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PMID:Hepatobiliary involvement in adolescents and adults with cystic fibrosis. 213 Jun 90

Neonatal cytomegalovirus hepatitis usually recover completely. The authors report a case evolving toward fibrosis, mostly perisinusoidal and with mild biliary hypoplasia. Similar cases with portal hypertension previously published are reviewed.
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PMID:[Neonatal cytomegalovirus infection with development of liver fibrosis]. 216 67


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