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)

Administration of galbanic acid isolated from the roots of Ferula kopetdaghensis Eug. Kor. to rats orally in a dose of 50 mg/kg was found to improve the course of toxic hepatitis induced by fourfold subcutaneous injections of a 50% oil solution of CCl4. Galbanic acid produced much more earlier than in control normalization of the activity of the enzymes alanine- and aspartataminotransferase in blood serum, increased glycogen content and improved the parameters of the redox potential of lactic acid-pyruvic acid system in the liver. Galbanic acid exerted the antioxidant effect. In the animals with a developed hepatitis receiving galbanic acid there was a more rapid restoration of intensity of bile secretion, synthesis of bile acids and bilirubin, cholesterol excretion as compared with control.
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PMID:[The effect of galbanic acid on the course of experimental hepatitis]. 236 53

11 women with chronic non-A, non-B hepatitis (NANBH) were studied during 14 pregnancies. All women remained well, without signs of deterioration of liver function. On the contrary, serum transaminase levels were significantly lower in the latter part of the pregnancy compared to before and after. 12 children were born at full term. One child was born preterm and 1 child was stillborn after 36 gestational weeks. During follow-up, 8 of the children had elevated alanine amino transferase (ALT) levels in serum at least at one sampling occasion. Four children had ALT elevation in consecutive blood samples, 2 of whom had a longlasting ALT elevation, probably due to mother-to-infant transmission of NANBH virus(es).
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PMID:Chronic non-A, non-B hepatitis in pregnancy: outcome and possible transmission to the offspring. 251 24

Two chimpanzees were born to parents with chronic non-A, non-B hepatitis and remained with their mothers until 12 and 18 months, respectively. The infants were followed from 7 to 8 weeks of age with biweekly or monthly blood samples and with monthly liver biopsies from 4 to 7 months after birth. Another chimpanzee, along with both of its parents, was held throughout the parents' acute infection with non-A, non-B hepatitis; at this time the infant was 14-16 months of age, and it was followed with bi-weekly blood samples and monthly biopsies from the time of potential exposure for 20 months. No abnormalities indicative of non-A, non-B hepatitis were detected in these animals. During the 29 to 35 months of follow-up, alanine aminotransferases and gamma glutamyl-transferases (GGPT) levels remained well within normal range for animals held in the same facility. Histologic and electron microscopic examination of liver tissue revealed no abnormalities.
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PMID:Absence of perinatal transmission of blood-borne non-A, non-B hepatitis virus by chimpanzees with acute and chronic infection. 256 45

Forty four patients with various forms of pulmonary tuberculosis in association with virus hepatitis B (21) and toxic-allergic hepatitis (23) were followed up in the time course of the diseases. There was a marked clinical similarity between toxic-allergic hepatitis and virus hepatitis B which differed in their qualitative indices and duration. Differential diagnosis of virus hepatitis B and toxic-allergic hepatitis was possible on the basis of the clinical signs and routine tests: determination of bilirubin and its fractions in blood, estimation of activity of alanine and aspartate aminotransferases and case follow-up with an account of the epidemiological situation.
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PMID:[Toxic-allergic and viral hepatitis in patients with pulmonary tuberculosis]. 262 75

The incidence of post-transfusion hepatitis (PTH) in recipients of blood products is reviewed. PTH was observed in 10%-12% of recipients of blood products in the United States, 2%-4% in northern Europe and 15%-20% in southern Europe. All studies indicate that 80%-90% of all PTH cases are attributed to non-A/non-B. At least 40% of the patients with PTH non-A/non-B will develop chronic hepatitis or cirrhosis. No specific tests for the detection of the non-A/non-B agent(s) exist. However, several independent studies indicate that part of the donors carrying the infectious non-A/non-B agent have increased levels of alanine amino transferase (ALT). When donors are excluded with elevated ALT values, it is estimated that about 30% of the PTH non-A/non-B cases would be prevented. Some studies indicate that anti-hepatitis B core (anti-HBc) positive donors may carry an increased risk to transmit the non-A/non-B agent, but more recent studies do not confirm this. There is hope that a specific non-A/non-B test will be developed soon.
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PMID:Blood transfusion and hepatitis: still a threat? 264 93

Amino sugars such as galactosamine are hepatotoxic. It has been verified that toxic hepatitis induced by galactosamine is similar to that of CCl4 poisoning, and that both were inhibited by O2* scavengers. Fructosamine results from the union of glucose with the epsilon-amine of lysine. A test for fructosamine quantification is based on nitroblue tetrazolium (NBT) reduction, in which O2- is involved, the reduction being inhibited in the presence of superoxide dismutase (SOD). Given these facts, we attempted to elucidate if galactosamine and glucosamine reduce NBT and if that reduction is inhibited by SOD. This was confirmed. Subsequently, we incubated aminoacids (glycine, lysine, alanine) with glucose and galactose for 7 days and studied the action of the incubation products on NBT, using amino acids and sugars as controls. We found that NBT reduction increases proportionally to the length of incubation time of glucose/galactose with lysine, but not with other amino acids. Reduction of NBT by the Amadori compounds formed is inhibited by SOD. We suggest that oxygen radical generation by Amadori compounds must be taken into consideration as one cause of damage in diabetes of long duration.
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PMID:Oxygen radical generation by Maillard compounds. 283 94

Hepatic morphology and immunocytology were evaluated in 4 children with clinical and immunologic characteristics of the acquired immune deficiency syndrome or acquired immune deficiency syndrome related complex. All 4 children had hepatomegaly and increased serum alanine and aspartate aminotransferase activity. Both lobular and portal changes were noted. Lymphocytic infiltration, piecemeal necrosis, hepatocellular and bile duct damage, sinusoidal cell hyperplasia, and endothelialitis were prominent. Vesicular rosettes in sinusoidal lymphocytes and tubuloreticular structures in sinusoidal endothelial cells were demonstrated by electron microscopy. The lymphocytic infiltrate in both the lobular and portal spaces was characterized by a relative increase of cytotoxic/suppressor (T8) cells. Hepatitis may be a common feature of pediatric acquired immune deficiency syndrome and acquired immune deficiency syndrome-related complex. Although the histopathologic changes are consistent with chronic active hepatitis, the specific pathogenesis remains to be determined.
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PMID:Hepatitis in children with acquired immune deficiency syndrome. Histopathologic and immunocytologic features. 293 90

Sequences encoding the surface projection glycoprotein of the coronavirus, murine hepatitis virus (MHV), strain JHM, have been cloned into pAT153 using cDNA produced by priming with specific oligonucleotides on infected cell RNA. The regions of three clones pJMS1010, pJS112 and pJS92, which together encompass the surface protein gene have been sequenced by the chain termination method. The sequence of the primary translation product, deduced from the DNA sequence, predicts a polypeptide of 1,235 amino acids with a molecular weight of 136,600. This polypeptide displays the features characteristic of a group 1 membrane protein; an amino-terminal signal sequence and carboxy-terminal membrane and cytoplasmic domains. There are 21 potential glycosylation sites in the polypeptide and a cysteine-rich region in the vicinity of the transmembrane domain. During maturation proteolytic processing of the polypeptide occurs and at positions 624 to 628 the sequence Arg-Arg-Ala-Arg-Arg is found, which is similar to a number of basic sequences involved in the cleavage of enveloped RNA virus glycoproteins. The fusogenic properties of the MHV surface protein do not appear to correlate with a strongly hydrophobic region at the putative amino terminus of the carboxy-terminal cleavage product.
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PMID:Nucleotide sequence of the gene encoding the surface projection glycoprotein of coronavirus MHV-JHM. 302 48

A community survey was undertaken in order to determine the seroepidemiologic pattern of acute viral hepatitis in Auckland. As hospital records and Health Department notifications underestimate the problem, all patients with a serum alanine transpeptidase (ALT) level of greater than 200 mu/l (X 5 normal) were investigated for viral liver disease. Over a four month period a total of 303 cases of acute viral hepatitis were identified, 49 (16.2%) were hepatitis A, 11 with coincident hepatitis B, 88 (29%) were hepatitis B, 80 (26.4%) nonA nonB hepatitis, 81 (26.7%) Epstein Barr virus hepatitis and 5 (1.6%) cytomegalovirus hepatitis. Hepatitis A and hepatitis B occurred with increased frequency among Maoris and Polynesians, while Epstein Barr virus, cytomegalovirus and nonA nonB hepatitis occurred more frequently among Europeans. The incidence of acute symptomatic viral hepatitis (excluding cytomegalovirus and Epstein Barr virus infections) was 78 cases/10(5)/per year for the Auckland region in this survey.
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PMID:Acute viral hepatitis in Auckland. 303 65

The ratio of the serum aspartate to alanine amino-transferase levels (AST/ALT) is often used as a clue to the etiology of the underlying liver disease. This ratio is usually greater than 2.0 in alcoholic liver disease and less than 1.0 in patients with chronic hepatitis and chronic cholestatic syndromes. We analyzed the AST/ALT ratio in 177 patients with various forms of nonalcoholic chronic liver disease who underwent medical evaluation and percutaneous liver biopsy. In the majority of cases of chronic viral hepatitis, the AST/ALT ratio was less than 1.0. However, there was a statistically significant correlation between the AST/ALT ratio and the presence of cirrhosis. Among 100 patients with chronic type B hepatitis, the mean AST/ALT ratio was 0.59 in those without cirrhosis and 1.02 in those with cirrhosis. Furthermore, the AST/ALT ratio often rose to greater than 1.0 when cirrhosis first became manifest. Thus, the finding of an AST/ALT ratio of greater than 1.0 in a patient with nonalcoholic liver disease should suggest the presence of cirrhosis. In addition, the use of the AST/ALT ratio as a means of separating alcoholic and nonalcoholic liver disease must be tempered with the knowledge that this ratio may be less helpful in the presence of cirrhosis.
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PMID:Ratio of serum aspartate to alanine aminotransferase in chronic hepatitis. Relationship to cirrhosis. 313 26


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