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)

We report three cases of nodular regenerative hyperplasia of the liver: the clinical onset of hepatic disease occurred between 24 and 30 months after renal transplantation. Nodular regenerative hyperplasia was associated with peliosis hepatitis in two cases, and with veno-occlusive disease in one case. Two patients developed portal hypertension, but are doing well. The third patient developed jaundice and died of septic shock. We discuss the aetiological role of renal transplantation, cytomegalovirus infection, and azathioprine in the development of nodular regenerative hyperplasia of the liver.
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PMID:Three cases of nodular regenerative hyperplasia of the liver following renal transplantation. 314 Jan 8

Liver biopsy specimens previously taken from 16 haemophilic patients with chronic non-A, non-B hepatitis were reviewed. The degree of fibrosis correlated with serum procollagen III peptide (sPIIIP) concentrations, measured both at the time of biopsy and 4.25 years later. Two patients with extremely high sPIIIP concentrations had collateral veins on computed tomography, suggesting portal hypertension. Twenty eight of 47 patients (60%) had splenomegaly on computed tomography, and of 28 patients in whom intravenous contrast medium was used, seven (25%) had collateral oesophageal veins. Serum procollagen III peptide estimations and computed tomography, both non-invasive investigations, indicated that hepatic fibrosis and portal hypertension had developed in a proportion of haemophilic patients with non-A, non-B hepatitis. Infection with the human immunodeficiency virus (HIV) may modify the course of this presumably cytopathic virus infection of the liver.
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PMID:Non-invasive investigation of liver disease in haemophilic patients. 314 33

The liver in an infant or child is as liable to the same pathologies afflicting the adult liver but with certain differences in prevalence and causes. Genetic disorders are more likely to present in the paediatric age group where many involve metabolic processes such as galactosemia, phenylketonuria, glycogen storage disease and others. Many of these present in the newborn period. However, neoplasms and hamartomas also present in the newborn period, such as congenital neuroblastoma with an enormously enlarged liver, hepatoblastoma and haemangioma. The latter may present with intractable cardiac failure as a result of considerable shunting of blood. Acquired liver lesions often present in the newborn period or early infancy and this includes hepatitis and biliary atresia. The difficulties in the differentiation of the two lesions will be discussed together with the management of biliary atresia. As the child grows older, Reyes encephalopathy with microvesicular fat in the liver is not uncommon. The pathophysiology of Reyes encephalopathy as seen locally will be described. The choledochal cyst with direct (Caroli's disease) or indirect effect on the liver will be described. Problems of childhood portal hypertension as well as congenital hepatic fibrosis will be described. Hemosiderosis of the liver is chiefly seen in homozygous beta-thalassaemia patients who have been kept alive with repeated blood transfusions. Amoebic and pyogenic hepatitis, fatty liver due to protein malnutrition, biliary ascariasis, etc, which are common in tropical and subtropical countries are rarely seen now in Singapore children.
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PMID:Paediatric liver disorders in Singapore. 346 38

A total of 26 children aged 2 to 14 with the initial (6), formed (14) and terminal (6) stages of liver cirrhosis were examined by a method of radionuclide scintigraphy with 99mTc-colloid. 34 children aged 7 to 14 examined in the catamnesis of virus hepatitis, were controls. A set of indices characterizing function of the reticuloendothelial system (RES), the effective hepatic blood flow, metric parameters of the liver and spleen were obtained from an analysis of the curves of the heart, liver and spleen area, and digital imaging of the liver with the marked costal arch. It was shown that at the initial stage of disease indices of the time course of the radioactive colloid were of compensated nature. Spleen function was elevated, liver and spleen sizes were increased. The formed stage was characterized by the signs of subcompensation of liver function: changes of indices of RP retention in the blood, a decrease in the indices of the total and hepatic radioactive colloid. The terminal stage was characterized by marked disorder of liver RES function which was not compensated for by a high splenic uptake, image deformation and focal RP distribution. Irrespective of a stage of disease the syndrome of portal hypertension was shown to manifest itself in splenomegaly and an increase in the radioactive colloid uptake by the liver over 15%. The accuracy of the set of signs was 90%.
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PMID:[Hepatic scintigraphy using 99mTc-colloid in liver cirrhosis in children]. 349 80

Over a 6-year period 26 infants and children with homozygous (2 Z and 6 ZZ) or heterozygous alpha 1-antitrypsin deficiency (12 MZ, 6 MS) were observed prospectively and their families investigated. 7 of 8 homozygous patients had neonatal hepatitis, whereby 3 of these showed maximum transferase activities during the 5th to 9th months of life. At the age of 7 years 2 of these patients were clinically normal, but only one patient had normal transferases. One patient had cirrhosis with portal hypertension at the age of 16 years 6 months; her nephew showed hypersplenism. Family studies revealed a further 5 relatives of phenotype Z, 16 of phenotype MZ, 3 of phenotype SZ and 1 of phenotype MS; 6 of these had slightly elevated serum transferase activities. 6 patients of phenotype MZ and 2 patients of phenotype MS had neonatal hepatitis but generally with a much better prognosis than in homozygous patients. The other heterozygous patients (6 MZ and 4 MS) had a variety of additional factors determining the disease and the prognosis. Family studies showed a further 7 family members of phenotype MZ, and 2 of phenotype MS; 2 of these had slightly elevated transferase activities, 3 parents had hereditary hyperbilirubinaemia.
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PMID:[Liver diseases in children and their relatives with homozygous and heterozygous alpha 1-antitrypsin deficiency]. 349 72

Twenty-eight consecutive unselected patients were treated for esophageal varices by means of a modified Sugiura procedure between 1978 and 1985. In accordance with Child's classification, 59% were considered as class A, 11% as class B, and 30% as class C. The etiology of the cirrhosis included alcohol abuse (42%), hepatitis (33%), granulomatous disease (7%), and cryptogenic disease (18%). One patient had extrahepatic portal hypertension from unknown causes. The surgical treatment included esophageal and gastric devascularization in all cases. The average operative time was 4 1/2 hours. The average blood replacement during surgery was 8 units. The operative mortality was 32% (2/16 class A, 1/3 class B, and 6/9 class C). Morbidity occurred in 33% of the patients. Significant causes of morbidity and mortality were related to complications of the esophageal transection, which was omitted in the later series. Six of the eighteen patients who survived surgery died later, but only one death was due to presumed recurrent variceal hemorrhage. Significant bleeding occurred in four patients--two due to recurrent varices and two due to peptic ulcer disease. Encephalopathy, which was present preoperatively in two patients, is still manifest but is well controlled. Encephalopathy did not develop in any other patients. At present, the 12 surviving patients have stable liver function.
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PMID:Experience with the esophagogastric devascularization procedure. 349 95

In a prospective study the impact of ultrasound tomography in the recognition and exclusion, respectively, of liver diseases was investigated. 646 patients with a suspected liver disease were sonographed in real-time procedure. The investigator was familiar with the history as well as with clinical and lab findings before the examination was started. The sonography was performed before a laparoscopy, liver blind punktion, scintigraphy, angiography, computerized tomography. The diagnoses were confirmed by sufficient, comparable methods (see above) or operatively; they were supported by a follow-up for one year. While liver cysts, cystic livers, liver abscesses, haematomas, metastases (with a diameter of more than 10-20 mm), stasis liver, cirrhoses with portal hypertension and fatty livers could be diagnosed with a high rate of confidence by sonography, healthy livers and the following disorders could not exactly be separated by ultrasound: acute hepatitis, reactive hepatitis hepatoses, chronically persisting hepatitis, chronic active hepatitis, and livers with a low incorporation of fat.
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PMID:[Results of ultrasound tomography in the diagnosis of liver diseases]. 353 Jul 8

Alcohol, hepatitis B, and Non A Non B hepatitis were the main aetiologies of 124 patients with hepatic encephalopathy (HE) due to histologically proven liver cirrhosis. All had severe portal hypertension (PH) and usually increased inflammatory activity of the liver. In stage I (n = 27) 7.4% died, in stage II (n = 28) 14.3%, in stage III (n = 32) 50% and in stage IV (n = 37) 94.6%. Even in cirrhotics without PH, serum albumin, cholinesterase activity and prothrombin time (PT) were significantly decreased. But only in the case of PT did the magnitude of the decrease parallel the stage of HE. Hyperammonaemia and serum creatinine were increased in parallel with the stage of HE. Therefore, in liver cirrhosis a quotient derived from decreased PT and increased serum creatinine has a good prognostic value. Early diagnosis of HE is possible on the basis of writing tests and the determination of free or toxic ammonia.
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PMID:The role of protein metabolism in 204 liver cirrhotics with and without hepatic encephalopathy. I. Clinical and general biochemical findings. 372 88

Fifty four infants with hepatobiliary disease and conjugated hyperbilirubinaemia of more than two weeks' duration were identified in a defined area of south east England in a prospective study between January 1971 and December 1973. The overall incidence was one case per 2500 live births. The cases were regularly reviewed and all survivors except one were assessed at age 10 years. Nine of 11 with extrahepatic biliary atresia died from liver disease by 2 years of age, one died at 5 years, and the survivor has cirrhosis with portal hypertension. Four out of seven with alpha 1 antitrypsin deficiency died aged 1 to 3 years from liver disease and one of the survivors has cirrhosis. All three infants with intrauterine infection and one with chromosomal abnormality died in infancy. Three children with other associated factors, choledochal cyst, galactosaemia, and rhesus isoimmunisation, recovered completely with no persisting liver disease. Two of 29 with cryptogenic hepatitis died, but only a further two have signs of persisting liver disease. Perinatal complications were more common in this group. Four of the 27 children surviving to the age of 10 years are educationally subnormal. Prognosis for infants with intrahepatic liver disease in the absence of known associated factors is good and every effort should be made to minimise the short term effects of cholestasis.
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PMID:Hepatitis syndrome in infancy--an epidemiological survey with 10 year follow up. 387 4

In patients with cirrhosis, superior portosystemic collateral circulation was evaluated by the continuous thermodilution method in the azygos vein. Azygos blood flow was 5 times higher in a group of patients with cirrhosis (alcoholic in 27, cryptogenic in 8, post-hepatitic in 2 and primary biliary cirrhosis in 1), than in a group of patients without portal hypertension (steatosis in 2, granulomatous hepatitis in 2, persistent chronic hepatitis in 2 and Hodgkin's disease in 1). Azygos blood flow was not different in cirrhotic patients with no visible, in those with small-sized, and in those with large sized oesophageal varices. Azygos blood flow was not different in cirrhotic patients with and without a previous episode of gastrointestinal bleeding. Fifteen min after intravenous administration of 15 mg of propranolol, azygos blood flow significantly decreased whereas azygos blood flow did not change after placebo. The decrease in azygos blood flow was significantly more marked than the reduction in cardiac output. It is concluded that superior portosystemic collateral blood flow is elevated in patients with cirrhosis and that the reduction in this collateral circulation might explain the efficiency of propranolol in the prevention of recurrent gastrointestinal bleeding.
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PMID:Superior portosystemic collateral circulation estimated by azygos blood flow in patients with cirrhosis. Lack of correlation with oesophageal varices and gastrointestinal bleeding. Effect of propranolol. 387 12


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