A randomized, placebo-controlled trial of thymosin-alpha1 and lymphoblastoid interferon for HBeAg-positive chronic hepatitis B.
Lim. Seng Gee SG; Wai. Chun-too CT; Lee. Yin Mei YM; Dan. Yock Young YY; Sutedja. Dede Selamat DS; Wee. Aileen A; Suresh. Shirley S; Wu. Ying Juan YJ; Machin. David D; Lim. Chee Chian CC; Fock. Kwong Ming KM; Koay. Evelyn E; Bowden. Scott S; Locarnini. Steven S; Ishaque. Shamsuddin Mohammed SM
Key Findings
- Combination of thymosin‑alpha‑1 (1.6 µg three times weekly) with interferon gave a 45.8% HBeAg loss vs 28% with interferon alone
- The 17.8% improvement was not statistically significant (p=0.067)
- No significant differences were seen in HBeAg seroconversion, ALT normalization, HBV DNA loss, or liver histology
Practical Outcomes
- The trial suggests a possible benefit of adding thymosin‑alpha‑1 for hepatitis B, but the data are inconclusive. For most biohackers without chronic HBV, it isn’t a useful protocol, and even for patients it should only be considered under medical supervision or in further clinical trials.
Summary
A study tested adding the immune‑boosting peptide thymosin‑alpha‑1 to standard interferon treatment in people with chronic hepatitis B. The combo showed a higher rate of losing a viral marker (45.8% vs 28%) but the difference wasn’t statistically solid, and other health measures didn’t improve. So while there’s a hint it might help, the evidence isn’t strong enough to change how you’d use it on your own.
Abstract
Combination therapy between two immunomodulators used for treatment of chronic hepatitis B was explored based on reported therapeutic efficacy of interferon-alpha, and thymosin-alpha1 as monotherapeutic agents to determine if combination therapy was superior to interferon alone. This double-blinded, randomized, placebo-controlled trial compares the addition of thymosin-alpha1, 1.6 microg taken three times per week (combination therapy) or thymosin placebo (monotherapy) to lymphoblastoid interferon (Wellferon), 5 million international units (MIU) taken three times per week, for 24 weeks. Entry criteria included positive hepatitis B e antigen (HBeAg); alanine aminotransferease (ALT) > or = 1.5 x upper normal limit, but < or = 10 x upper normal limit; positive HBV DNA; absence of cirrhosis; treatment naivety and no co-morbid factors. A total of 98 HBeAg-positive patients were recruited, of which 48 were randomized to combination therapy and 50 to monotherapy. The primary endpoint was the loss of HBeAg at 72 weeks. The secondary endpoints were HBeAg seroconversion, normalization of ALT, loss of HBV DNA and improvement in histology. The HBeAg loss was 45.8% and 28.0% for combination therapy and monotherapy, respectively (difference, 17.8%; 95% CI -1.2%-35.3%, P = 0.067). There was a trend towards HBeAg loss when using combination therapy. There were also no statistically significant differences between the different therapies with respect to the secondary endpoints of HBeAg seroconversion, changes in histology, normalization of ALT or loss of HBV DNA. In conclusion, this trial showed a 17.8% improvement in HBeAg loss rates using combination therapy over interferon monotherapy. This could clinically indicate a potential important difference that would need confirmation in subsequent trials.
Study Information
pubmed
2006