The effect of indomethacin on hepatitis B virus replication in chronic healthy carriers

Citation
S. Kapicioglu et al., The effect of indomethacin on hepatitis B virus replication in chronic healthy carriers, SC J GASTR, 35(9), 2000, pp. 957-959
Citations number
15
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
ISSN journal
00365521 → ACNP
Volume
35
Issue
9
Year of publication
2000
Pages
957 - 959
Database
ISI
SICI code
0036-5521(200009)35:9<957:TEOIOH>2.0.ZU;2-6
Abstract
Background: A chronic HBsAg carrier state, a major cause of viral spread in a community, is one of the consequences of hepatitis B virus (HBV) infecti on. Although successful immunization programs have been initiated to elimin ate the virus, there is still a large number of people with HBV infection w orldwide. This study was designed to investigate the effect of indomethacin treatment on HBV markers in humans, in comparison with a control group. Me thods: In total, 65 chronic 'healthy' HBV carriers were involved in the stu dy. Patients were divided randomly into two groups. Group I (n = 42) receiv ed oral indomethacin 75 mg daily for 6 months. Group II (n = 23) acted as c ontrol. Patients in both groups were followed up for 6 months, during which laboratory tests, including viral parameters, were performed periodically. Liver biopsy was done in 17 patients (11/42 of the indomethacin group and 6/23 of the control group). Results: All liver biopsies showed grade 0-2 an d stage 0-1 HBV in both groups (P > 0.05). HBsAg positivity did not change in any patient in either group. Five patients who had positive HBeAg in gro up I became negative 4 months later, while patients in group II continued t o be positive at 6 months (P < 0.001). Similarly, all patients receiving in domethacin exhibited a total anti-HBeAg immunoglobulin response at 6 months , while the control group remained the same during this period (P < 0.05). HBV DNA, as detected by polymerase chain reaction in 20/22 (91%), was negat ive in group I at the end of 6 months. No change was observed in group II ( P = 0.007). Conclusions: Although no biochemical analyses were performed on prostaglandins in the present study, the results suggest that the prostagl andin pathway may be involved in the pathogenesis of the immune response ag ainst HBV, and that the suppression of viral replication is achieved as ind icated by the disappearance of HBeAg and HBV DNA in healthy chronic HBV car riers.