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

The chief causes of liver disease in Ethiopia are reviewed, considering hospital data on admissions for hepatitis, cirrhosis, ascites and hepatoma. Liver diseases account for 11.4% of all medical admissions in 3 medical wards in Addis Ababa. The causes are viral hepatitis, post- hepatic and post necrotic and mixed cirrhosis and hepatocellular carcinoma. Alcoholic cirrhosis is rare. Viral hepatitis with shivering, rigor and fever and elevated direct bilirubin levels are common in Ethiopians, especially in child-bearing women. The hepatitis B surface antigen (HBsAg) is often associated with hepatitis. The disease may be transmitted by several species of mosquitoes, placental transmission, or feces, urine, saliva or semen. Blood products are not screened for hepatitis B. Cirrhosis is common, and causes significant mortality, usually from esophageal varices and hepatic coma. Chronic active hepatitis patients may live for a time, especially if they are near a hospital and are treated with steroids. In Ethiopia presenting symptoms for hepatoma are anorexia, weight loss, persistent, burning, right upper quadrant pain, and a hard, nodular, tender RUQ mass. Over 5% of malignancies seen are primary hepatocellular carcinomas. 50% have HBsAG, compared to 3.8% of controls. 65% have alpha-fetoglobulins. It is suggested that some viral hepatitis cases progress to cirrhosis, of which some go on to hepatocellular carcinoma. Herbal medicines, aflatoxins and other toxins may also contribute to liver disease.
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PMID:Current views on liver diseases in Ethiopia. 20 62

In patients who have impaired hepatic reserve, the Warren shunt has been proposed as an effective operation because it decompresses the esophageal varices without disturbing portal perfusion of the liver. However, early reports of high operative mortality and technical difficulties have impeded acceptance of the procedure. The operation was done in a series of 17 patients. All patients in whom elective variceal decompression with a patent splenic vein was required and without clinical ascites were candidates for this operation. Follow-up ranged from 2 to 48 months. Six patients had alcoholic cirrhosis, two had primary biliary cirrhosis and seven had postnecrotic cirrhosis; in two the cause of the liver disease was unknown. Five patients were categorized as Child's class A, nine as class B and three as class C. No intraoperative or early postoperative deaths owing to hemorrhage occurred. However, there was one death two weeks postoperatively from pulmonary sepsis and one death five weeks postoperatively due to antigen-positive hepatitis. Two patients died from hepatic failure six weeks and five months after operation, respectively; in the first of these, chronic active hepatitis was diagnosed at the time of operation. In one patient hemorrhage recurred and transfusion was required. Although ascites, which eventually resolved, developed in eight patients after operation, the results in 76 percent of patients have been good without new episodes of hemorrhage or encephalopathy. We conclude that the Warren shunt is a safe and effective elective operation for the treatment of patients in whom hemorrhage from esophageal varices has occurred.
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PMID:The Warren shunt in treating bleeding esophageal varices. 31 64

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

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

A total of 80 patients with asymptomatic small hepatocellular carcinoma (HCC) associated with liver cirrhosis underwent a liver resection. The patients were divided into 4 groups according to the location of their tumor: group A (n = 9): left lateral segmentectomy or left hepatectomy, group B (n = 42): atypical partial hepatectomy on the lateral aspect of the right lobe, group C (n = 25): subsegmentectomy on either the anterior or the posterior surface of the right lobe, group D (n = 4): subsegmentectomy in the hilar area. There were two postoperative deaths (both in group D) and five cases of hospital mortality (1 case due to myocardial infarction in group C; 1 case due to bleeding esophageal varices in group B and 2 cases in group C; and 1 case due to fulminating hepatitis in group B). There was no any significant difference in tumor size, the preoperative serum bromosulfaphthalein retention rate or the postoperative peak serum conjugated bilirubin level among all the groups (p less than 0.05). The weights of the resected specimens were higher in groups A and B (259 +/- 58 g, 230 +/- 154 g) than in groups C and D (54 +/- 32 g, 37.5 +/- 15.0 g) (p less than 0.05). The amount of blood required for transfusion during surgery in group D (3,625 +/- 3,146 mL) was significantly greater than in the other three, groups (p less than 0.05); and was also greater in groups B and C (1,649 +/- 880 mL, 1,635 +/- 1,156 mL), than in group A (444 +/- 273 mL; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Surgical resection of hepatocellular carcinoma in the cirrhotic liver. 168 51

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

We analyzed 31 patients with a diagnosis of primary biliary cirrhosis, 29 of them males, aged 23 to 72 years. Liver biopsy was diagnostic in all showing initial findings of the disease in 5. Echotomography and cholangiography demonstrated a patent biliary, tract. Anti-mitochondrial antibodies were present in 94% of patients. Alkaline phosphatase and biliary acid levels were useful for diagnosis. Pruritus was present with varying intensity in all patients, with premenstrual exacerbations in 5 females who had cholestasis of pregnancy or hepatitis caused by progestin drugs before developing cirrhosis. Recurrent urinary tract infection was present in 8 patients, osteoporosis in 24, Sjogren's syndrome in 24 and Crest syndrome in 4. Survival ranged from 1 to 12 years, death being caused by ruptured esophageal varices in 12 patients and by liver failure in 7. Persistence of pruritus and altered liver function tests after cholestasis of pregnancy or hepatitis caused by progestins should lead to investigation of biliary cirrhosis.
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PMID:[Primary biliary cirrhosis. The clinical experience in 31 patients]. 215 67

The present study was undertaken to elucidate clinicopathological findings and operative results of HCC with HB-associated cirrhosis, compared with those in HCC patients with alcoholic and post-transfusion cirrhosis. The number of the HBV group was 26 cases, consisting of 17 in sAg(+), 4 in eAg(+) and 5 in eAb(+) subgroups. The number of the post-transfusion group was 7 and that of alcoholic group was 12. A high incidence of hypersplenism and esophageal varix in the eAg(+) subgroup was found. ICG R15 was the highest, KICG and ICG Rmax were the lowest in the eAg(+) subgroup. The mean diameter of tumors was the largest, 6.6 +/- 3.9 cm, in the sAg(+) subgroup and was the smallest, 2.2 +/- 1.7 cm, in the eAg(+) subgroup. The incidence of postoperative jaundice, hyperammoninemia and live dysfunction were the highest in the sAg(+) and eAg(+) subgroup. One and three-year survival rate were 76.9% and 48.1% in the sAg(+) subgroup, 60.0% and 30.0% in the eAb(+) subgroup, and the one-year survival rate in the eAg(+) subgroup was 50.0%. The three-year survival rate could not be calculated because 3 years had not passed since the operation. The prognosis was the poorest in the HBV group among all groups. This study suggests that in HBV-associated cirrhosis, hepatectomy might induce "acute on chronic" changes (acute hepatitis and fulminant hepatitis). Therefore we should select operative procedures by considering surgical risk and the etiology of liver cirrhosis in hepatectomy.
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PMID:Clinicopathological studies and operative results of hepatocellular carcinoma with liver cirrhosis, comparing HB-associated cirrhosis to alcoholic and post-transfusion cirrhosis. 215 51

A case of idiopathic portal hypertension (IPH) developing after renal transplantation is reported. A 33-year-old Japanese male who had undergone renal transplantation 8 years previously was transferred to our hospital because of hematemesis from ruptured esophageal varices. He had no history of any liver disease before the renal transplantation, but had a history of receiving blood transfusion. Abdominal computed tomography (CT) and ultrasonography revealed marked splenomegaly and collateral channels, but no obliteration which might cause portal hypertension in the hepatic or portal vein. No findings suggestive of hepatitis or liver cirrhosis were found either macroscopically on laparoscopy or by liver biopsy. Light microscopic study of the liver biopsy specimen showed mild periportal fibrosis, inconspicuous portal branches in the most peripheral tracts, but no pseudolobule formation or piecemeal necrosis. However collagen deposition was found in the perisinusoidal space and partly in intercellular space on electron microscopy. We consider that the development of portal hypertension in this case is responsible for the collagen deposition, which may be related to the administration of azathioprine after renal transplantation. There are few reports on IPH after renal transplantation, and it is stressed that a lower amount of azathioprine than previously reported may induce IPH under such conditions.
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PMID:A case of idiopathic portal hypertension after renal transplantation. 222 56


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