Currently, the cornerstone for NAFLD management is weight reduction, mainly a decrease in central obesity, and reversal of IR [8,9]. In our study, however, despite 23/24 placebo and 21/24 D-002-treated patients being advised to follow a specific diet, no body weight reduction was observed during the trial [8,9]. Thus, the improvement in liver fat accumulation, HOMA index and insulin levels selleckchem Pacritinib observed in the D-002-treated group seems not to be strongly influenced by dietary intervention, but rather is attributable to D-002 treatment. Transaminase levels did not change significantly during the treatment. Although this seems to disagree with our efficacy hypothesis, it could be related to the fact that most patients had normal or relatively low baseline transaminase levels, the most frequent being high GGT values (�� 55 UI/L) (GGT, 41/50, 82%; ALT, 47/50, 94.
0%; AST, 50/50, 100%). In conclusion, treatment of NAFLD with D-002 seems to be effective and safe, and may ameliorate liver fat accumulation and clinical evolution of subjects, may reduce the HOMA index and insulin levels, and may increase the antioxidant response of the body, as assessed by plasma TAS. Nevertheless, further studies are needed to confirm the efficacy, safety, and tolerability of D-002 in NAFLD patients. KEY MESSAGE 1. Oral administration of D-002 (100 mg/day) for 6 months may ameliorate liver fat accumulation and insulin resistance, meanwhile improve clinical evolution and antioxidant response in subjects with nonalcoholic fatty liver disease (NAFLD). 2. D-002 seems to be safe and well tolerated in subjects with NAFLD.
Footnotes No potential conflict of interest relevant to this article is reported.
Hepatitis delta virus (HDV) superinfection of hepatitis B virus (HBV) carriers causes the most severe hepatitis in humans. Nearly all patients develop chronic HDV infection that has a high probability of progressing to liver cirrhosis and hepatocellular carcinoma (1, 2). Worldwide, approximately 15 million patients are affected with HDV. About 8% of HBV surface antigen (HBsAg)-positive patients in several European countries have tested positive for antibodies against HDV (2). Therapeutic options for HBV/HDV carriers are limited. Only in about 25% of the patients does alpha interferon therapy result in sustained viral clearance (3). HBV carriers are at risk of being superinfected with HDV.
Therefore, a vaccine protecting HBV carriers from HDV superinfection would be eligible. A main obstacle for the design of a vaccine against HDV infection is the fact that antibodies to the two proteins of HDV, p24 and p27, do not neutralize the HDV particle. The HDV protein/RNA complex is covered by the envelope protein of HBV (HBsAg). Therefore, classical vaccines which induce Cilengitide neutralizing antibodies cannot be expected to prevent HDV infection. Immunizations with nucleoproteins of, e.g.