Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Researchers compared data on 333 newborns with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency at 5 public and 5 private hospitals in Taiwan with data on 653 birth date, sex, and delivery hospital matched newborns to examine the peak serum bilirubin (PSB) level and incidence of neonatal jaundice of both G-6-PD deficient and G-6-PD normal newborns. They also wanted to determine whether an association exists between G-6-PD activity level and incidence of neonatal jaundice and associations between G-6-PD deficiency and other likely risk factors of neonatal jaundice. A significant association between G-6-PD deficiency and neonatal jaundice existed among male neonates but not female neonates. Male neonates had a considerably higher incidence of neonatal jaundice than did female neonates (11.6% vs. 6.2%). There was a significant inverse dose-response relationship between G-6-PD activity and neonatal jaundice among the male neonates (p.01). For example, the relative risk was 1.78 for 20.1-29.9 relative intensity, 2.01 for 15.1-20, 2.61 for 10.1-15, and 4.07 for 10. Maternal hepatitis B surface antigen (HBsAg) carrier status and hypoxia/asphyxia significantly increased the risk for G-6-PD deficiency in male neonates (p.05). The multiple regression analysis indicated a significant effect of G-6-PD deficiency on the PSB level and the incidence rate of severe neonatal jaundice. There was a similar significant interaction between G-6-PD deficiency and maternal HBsAg carrier status.
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PMID:Association between glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice: interaction with multiple risk factors. 146 58

As many as 160 patients with acute virus hepatitis B (AVHB) were examined over time. Spectroscopy was used to study the activity of glucose-6-phosphate dehydrogenase (G-6-PDH), glutathione peroxidase-1 (GP1), glutathione peroxidase-2 (GP2), glutathione reductase (GR), glutathione transferase (GT) and to measure the concentration of reduced glutathione (GSH) in the blood serum and in red blood cells. Within the first days of the icteric period, the activity of all the enzymes rose, followed by reduction of the activity of G-6-PDH, GP1, GP2, GR and the concentration of GSH at the height of the disease. The GT activity remained high throughout the entire disease period.
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PMID:[The functioning of the glutathione system in patients with acute viral hepatitis B]. 233 29

Hepatocarcinogenesis in hepatitis B virus transgenic mice was studied by means of a correlative cytomorphological and cytochemical approach at different time points in animals from 1 to 34 mo old. HBsAg-positive ground-glass hepatocytes emerged throughout the liver parenchyma in nearly all transgenic mice during the first 4 mo after birth. The panlobular expression of HBsAg persisted until foci of altered hepatocytes appeared (6 to 9 mo of age). Three different types of foci of altered hepatocytes-namely, glycogen-storage foci, mixed cell foci and glycogen-poor foci-developed. Hepatocellular adenomas and carcinomas appeared after 11 mo. Orcein staining revealed frequent transitions between ground-glass hepatocytes extensively expressing HBsAg and glycogen-storage (predominantly clear-cell) foci containing HBsAg-positive cytoplasmic components. Similar transitions between ground-glass hepatocytes and glycogenotic (clear) cells were often found in diffuse parenchymal glycogenosis at 11 or 12 mo. Remnants of HBsAg-positive material were also detected in mixed cell foci, glycogen-poor diffusely basophilic cell foci, hepatic adenoma and hepatocellular carcinoma. These findings suggest that ground-glass hepatocytes are the direct precursor of foci of altered hepatocytes and their neoplastic descendants. The extensive expression of HBsAg is gradually down-regulated during neoplastic transformation, just as the morphological the biochemical phenotypes of foci of altered hepatocytes, hepatic adenoma and hepatocellular carcinoma in transgenic mice resemble those described in chemical hepatocarcinogenesis. The predominant sequence of cellular changes leading from glycogen-storage (predominantly clear cell) foci to mixed cell foci, hepatic adenoma and hepatocellular carcinoma is characterized by a gradual decrease in the activities of glycogen synthase, phosphorylase, glucose-6-phosphatase and adenylate cyclase, whereas glucose-6-phosphate dehydrogenase and pyruvate kinase activities increase. These alterations indicate a shift from the glycogenotic state toward an increase in the pentose phosphate pathway and glycolysis.
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PMID:Hepatic preneoplasia in hepatitis B virus transgenic mice. 792 48

Haemolytic anaemia as a complication of acute hepatitis has been reported in up to 23% of patients. However, the incidence may rise up to 70-87% in patients who have glucose-6-phosphate dehydrogenase (G6PD) deficiency. Massive intravascular haemolysis with renal failure, hepatic encephalopathy and even death have been reported. In our retrospective study of patients with acute viral hepatitis, the overall incidence of acute haemolysis was 4% (17/434). Only 53% (9/17) of them had G6PD deficiency. Patients with acute haemolysis had a significantly higher peak bilirubin level and required more prolonged hospitalization. Since hepatitis A virus vaccination, unlike hepatitis B virus vaccination, is not yet recommended for routine immunization, we suggest subjects who are G6PD-deficient should be vaccinated against hepatitis A. In endemic areas of hepatitis A virus infection, universal immunization remains the definitive answer.
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PMID:Haemolysis complicating acute viral hepatitis in patients with normal or deficient glucose-6-phosphate dehydrogenase activity. 957 32