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)

Adverse drug reactions may mimic almost any kind of liver disease. Acute hepatitis is often due to the formation of reactive metabolites in the liver. Despite several protective mechanisms (epoxide hydrolases, conjugation with glutathione), this formation may lead to predictable toxic hepatitis after hugh overdoses (e.g. paracetamol), or to idiosyncratic toxic hepatitis after therapeutic doses (e.g. isoniazid). Both genetic factors (e.g. constitutive levels of cytochrome P-450 isoenzymes, or defects in protective mechanisms) and acquired factors (e.g. malnutrition, or chronic intake of alcohol or other microsomal enzyme inducers) may explain the unique susceptibility of some patients. Formation of chemically reactive metabolites may also lead to allergic hepatitis, probably through immunization against plasma membrane protein epitopes modified by the covalent binding of the reactive metabolites. This may be the mechanism for acute hepatitis produced by many drugs (e.g. amineptine, erythromycin derivatives, halothane, imipramine, isaxonine, alpha-methyldopa, tienilic acid, etc.). Genetic defects in several protective mechanisms (e.g. epoxide hydrolase, acetylation) may explain the unique susceptibility of some patients, possibly by increasing exposure to allergenic, metabolite-altered plasma membrane protein epitopes. Like toxic idiosyncratic hepatitis, allergic hepatitis occurs in a few patients only. Unlike toxic hepatitis, allergic hepatitis is frequently associated with fever, rash or other hypersensitivity manifestations; it may be hepatocellular, mixed or cholestatic; it promptly recurs after inadvertent drug rechallenge. Lysosomal phospholipidosis occurs frequently with three antianginal drugs (diethylaminoethoxyhexestrol, amiodarone and perhexiline). These cationic, amphiphilic drugs may form phospholipid-drug complexes within lysosomes. Such complexes resist phospholipases and accumulate within enlarged lysosomes, forming myeloid figures. This phospholipidosis has little clinical importance. In a few patients, however, it is associated with alcoholic-like liver lesions leading to overt liver disease and, at times, cirrhosis. Subjects with a deficiency in a particular isoenzyme of cytochrome P-450 poorly metabolize perhexiline and are at higher risk of developing liver lesions. Prolonged, drug-induced liver-cell necrosis may also lead to subacute hepatitis, chronic hepatitis or even cirrhosis. This usually occurs when the drug administration is continued, either because the liver disease remains undetected or because its drug aetiology is overlooked. Several autoantibodies may be present.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute and chronic drug-induced hepatitis. 304 68

Aflatoxin analysis of 40 percutaneous needle liver biopsies in 27 children with protein-energy malnutrition and 13 children with miscellaneous liver disease in The Sudan is reported. Aflatoxins B1, B2 and aflatoxicol were detected in 5 of the 16 biopsies from kwashiorkor but in none of 11 biopsies from marasmus or marasmic kwashiorkor. Aflatoxins G1, G2 and M2 were detected in 5 of 12 children with chronic liver disease. A very high concentration of aflatoxicol was found in a breast-fed infant with neonatal hepatitis of unknown etiology.
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PMID:Aflatoxins in liver biopsies from Sudanese children. 308 33

The vast majority of pediatric RBC hypoplastic anemias are accounted for by red blood cell aplasia associated with chronic hemolysis, Diamond-Blackfan anemia, and transient erythroblastopenia of childhood. However, other causes of hypoplastic anemia occur in children, and some of these are similar to what is seen in adult RBC aplasia. For example, it has been reported that a 5-year-old girl with an aregenerative anemia had a thymoma and later developed pancytopenia. RBC aplasia also has been seen in children receiving anticonvulsant drug therapy, children recovering from severe protein malnutrition, children with hepatitis, and in children with leukemia during maintenance therapy. In addition, it is not uncommon for pediatric hematologists to observe children with RBC aplasia where there is no obvious diagnosis, although many are considered to be variants of Diamond-Blackfan anemia. Several important questions about RBC hypoplastic anemias in children need to be resolved; it is hoped that this will be accomplished in the next decade. Do RBC hypoplastic crises associated with hemolytic anemia occur with viral infections other than HPV? What is the cellular pathophysiology in DBA and TEC? Does the apparent heterogeneity of these disorders reflect limitations of laboratory techniques or are we looking at several different diseases? Is acute leukemia a real complication of Diamond-Blackfan anemia? Is TEC a completely benign entity or will we see other long-term problems in these children? Is the incidence of TEC actually increasing? Will TEC-like problems be seen in other aged children? As a case in point, we recently observed a 16-year-old girl who presented with pure RBC aplasia that required RBC transfusion support for 5 months; she also received prednisone therapy. After 7 months, however, this young lady had a spontaneous remission, and now 4 years later she is normal and free of any hematologic abnormalities. This was a most unusual event in our experience and, in view of the apparent increasing incidence of TEC in young children, we queried whether we were observing an adolescent equivalent of this disorder. During the next several years the answer to this and the other questions posed herein should be available.
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PMID:Diagnosis and management of red cell aplasia in children. 312 94

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

Deficiency of factor XI (plasma thromboplastin antecedent) can result in severe bleeding in women undergoing obstetric or gynecologic procedures, with the highest risk in women of Ashkenazi Jewish background. Most patients do not bleed if treated with sufficient fresh frozen plasma to maintain a factor XI level of 30% or more but occasionally patients may require higher levels. Plasma infusion should be continued for several days, even if bleeding does not seem excessive, since delayed bleeding is not uncommon. The use of hepatitis B vaccine and of plasma from a single donor, may reduce the risk of hepatitis.
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PMID:Management of factor XI deficiency in gynecologic and obstetric patients. 348 57

The aflatoxin B1 content of liver tissue was measured in patients who died from chronic liver disease [hepatocellular carcinoma (HCG) (5), schistosomal liver fibrosis (1), chronic aggressive hepatitis (1)] and compared with fifteen controls who died of motor traffic accidents (10), drowning (1), malnutrition (1), idiopathic cardiomegaly (1) and lung infection (2). Significant levels of aflatoxin B1 were found in hepatocellular carcinoma patients who were also hepatitis B surface antigen (HBsAg) negative. Histology showed HCC arising in macronodular cirrhosis.
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PMID:Aflatoxin B1 in hepatocellular carcinoma. 625 85

Most immunologically-mediated diseases are inflammatory in nature, as assessed by cellular infiltrates at the lesion site. Recent immunohistological studies using monoclonal antibodies on tissue sections and synovial or cerebrospinal fluid reveal that B- and T-lymphocytes (predominantly T) participate in this reaction, together with monocytes and macrophages. The etiopathogenesis of inflammatory diseases of immunological origin can be discussed at two levels. (1) Lesions may be secondary to the cytopathic effect of antibodies, either by direct cytolysis or by opsonization, antigenic modulation, or blockage of functionally-relevant molecules. Immune complexes formed in the circulation or locally at the lesion site may intervene. Direct cellular mechanisms are probably involved, as suggested by evidence in hepatitis (indirect) and in juvenile insulin-dependent diabetes (direct). K-cells may act by antibody-dependent cytotoxicity, particularly in autoimmune diabetes and thyroiditis where lymphocyte-dependent antibodies are demonstrated. Unfortunately, the absence of adequate markers does not permit adequate detection of K-cells in inflammatory reaction sites. (2) Etiological factors are multiple in a given disease and even in a single patient. Deficiency of suppressor T-cells, assessed using monoclonal anti T-cell antibodies, represents a major predisposing factor, although suppressor cell deficit may be restricted to some antigens (EBV) in certain patients. The deficiency of interleukin-2 production in lupus and rheumatoid arthritis is intriguing but the mechanism and its relationship to disease etiology are unknown. Other immunological factors include intrinsic B-cell hyperactivity, anti-T-cell auto-antibodies, and complement deficiencies, whereas non-immunological factors such as viruses, drugs or sex hormones are important but ill-defined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The immunological basis of inflammatory diseases. 648 71

The causes of hepatopathies were studied retrospectively in a group of 200 infants who were inpatients at the Paediatric Department of Ain Shams University, Cairo, over the period 1977-1981, and prospectively in 50 children who were outpatients of the Paediatric Hepatology Clinic over the period October 1982-March 1983. The main cause of hepatopathy in both groups was hepatitis, followed by protein-calorie malnutrition in infants and bilharziasis in children. Suggestions are made as to methods of prevention.
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PMID:Profile of liver disease in Egyptian infants and children. 653 15

Management of protein-calorie malnutrition found in 32 patients with severe liver diseases such as fulminant hepatitis and cirrhosis of the liver was carried out using 2 types of synthetic amino acid solution (Hep-OU and Fischer solution) for intravenous and enteral alimentations with rapid monitoring of serum aminogram. Intravenous hyperalimentation of these cases resulted in maintenance of nutritional status with improvement of nitrogen balance and normalization of impaired serum aminogram. During this study, however, nutritional support was initiated only when intractable ascites, upper gastrointestinal bleeding and hepatic encephalopathy were observed. In 2 cases of fulminant hepatitis with sepsis and 3 hepatoma patients with ascites, elemental diet containing maltose and amino acids was used to supply sufficient amounts of nutrients in a minimum volume of water. These techniques with simultaneous monitoring of urinary excretion of 3-methylhistidine and creatinine height index as nutritional parameters make nutritional management easy for patients with liver disease.
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PMID:Nutritional management of patients with severe liver disease by using intravenous hyperalimentation and elemental diet. 676 41

With the aim to evaluate the influence of gastric resection on the morphological and functional conditions of the liver and the eventual appearance of gallstones, 50 randomized patients with a resection of the stomach were clinically analysed at different period of time, together with 50 patients suffering from peptic ulcer. All patients underwent a liver biopsy, 26% of the patients with gastric resection and 20% of the patients with peptic ulcer showed pathological findings of the liver, which statistically is not a significant difference. The most frequent pathologic change in both groups was a persistent hepatitis, while gallstones rarely occurred. Further, a presence in the past of viral hepatitis and alcoholism in both groups has been analysed as possible factors for the mentioned changes in the liver. Hbs Antigen detection has also been drawn as important. People with gastric resection belong to the jeopardized groups of the population with a great risk-factor related to previous frequent blood transfusion and other medical procedures. Patients who underwent a gastric resection, were analysed for the influence of the time period, following operation, on proved lesions of the liver, which were also observed in relation to dumping syndrome, malnutrition and other postresection syndromes. The authors point out the importance of making an early detection of the lesions of the liver, during surgery, with the aim to prevent the development of severe chronic inflammation.
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PMID:[Gastric resection and the hepatobiliary tract]. 688 May 42


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