Related Experiment Videos
HBs antigen and blood glucose concentration
Insights
High blood glucose levels correlate with the absence of Hepatitis B surface antigen (HBsAg) in patients with liver cirrhosis and diabetes. This suggests hyperglycemia may inhibit Hepatitis B virus replication or HBsAg expression.
Area of Science:
- Hepatology
- Virology
- Endocrinology
Background:
- Hepatitis B virus (HBV) infection is a major cause of liver disease.
- The presence of Hepatitis B surface antigen (HBsAg) is a key indicator of HBV infection.
- The relationship between metabolic factors like hyperglycemia and HBV infection markers is not fully understood.
Purpose of the Study:
- To investigate the correlation between high blood glucose levels and the presence or absence of HBsAg.
- To explore the potential impact of hyperglycemia on HBV infection markers in patients with liver cirrhosis and diabetes mellitus.
Main Methods:
- Counterelectrophoresis (CEP) was used to detect HBsAg presence.
- HBsAg status was analyzed in 76 liver cirrhosis patients and 431 diabetes mellitus patients.
- Blood glucose levels (glycemia) were measured and compared between HBsAg-positive and HBsAg-negative groups.
Main Results:
- A significant correlation was observed between high blood glucose levels and HBsAg absence.
- HBsAg-negative cirrhotic patients exhibited significantly higher glycemia (95.75 +/- 6.36 ng/100 ml) than HBsAg-positive patients (78.30 +/- 10.2/100 ml).
- HBsAg absence was noted in all but one diabetic patient, with a very low incidence (0.2%) compared to general and non-hepatic disease populations.
Conclusions:
- Sustained high blood glucose concentrations appear to be a primary factor responsible for HBsAg negativity.
- Hyperglycemia may directly impede HBV replication or indirectly affect HBsAg secretion/excretion through metabolic hepatic dysfunction.
- The inhibitory effect of high glucose concentrations might explain failures in HBV culture experiments.
Abstract:
HBsAg presence was studied by counterelectrophoresis (CEP) in 76 patients with liver cirrhosis and in 431 patients with diabetes mellitus. A striking correlation was found between high blood glucose values and HBsAg absence. Thus, HBsAg-negative cirrhotics (53%) had significantly higher levels of glycemia than the HBsAg-positive patients of the same age group, i.e. 95.75 +/- 6.36 ng/100 ml compared to 78.30 +/- 10.2/100 ml. This absence of HBsAg was also observed in all diabetics but one. As the incidence of HBsAg (CEP) was found to be of 3.63% in 253,460 subjects from different areas of Romania and 6.84% in 14,690 subjects with various non-hepatic diseases included, the chance of finding the 0.2% HBsAg incidence observed in the diabetics would be less than 0.0002 and 0.0001, respectively. The serum HBsAg absence in cirrhotics with high glycemia and in diabetics strongly incriminates the constant high concentrations of blood glucose as the main factor responsible for this negativity. The effect may be direct on virus replication, or indirect, by metabolically-induced hepatic dysfunction interfering with HBsAg secretion or excretion. The presence of high concentrations of glucose in cell culture media might explain the repeated failure of hepatitis B virus serial passage in tissue or organ culture.