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INTRODUCTION: Currently, the cause of psoriatic arthritis (PsA) is unknown, and the effectiveness of current drug treatments is unsatisfactory. In March 2019, the US Food and Drug Administration (FDA) approved risankizumab, a humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting the p19 subunit of interleukin (IL)-23, for the treatment of PsA in adults. This study aimed to conduct a meta-analysis of double-blind, randomized, placebo-controlled trials to evaluate the effectiveness and safety of risankizumab in moderate-to-severe PsA. METHODS: We conducted a thorough search of relevant databases from the establishment of the databases to October 1, 2023. We conducted a meta-analysis using Stata 12.0 and utilized I2 and Egger tests to assess heterogeneity and publication bias among the studies. Bias assessment was performed using the risk bias map and bias risk summary diagram generated by Revman5.4 software. The review protocols were registered on PROSPERO (CRD42023451894) and adhered to the preferred reporting item of system evaluation (PRISMA) guideline. RESULTS: Six randomized controlled trials (RCTs) involving 5038 patients with PsA treated with either risankizumab or placebo were included in the analysis. At 24 weeks, the risankizumab group demonstrated a significantly higher American College of Rheumatology-20 (ACR20) response rate compared to the placebo group (RR 1.760, 95% CI 1.568-1.977, P < 0.001). Additionally, the risankizumab group showed a significantly higher Minimal Disease Activity (MDA) response rate compared to the placebo group (RR 1.827, 95% CI 1.048-3.184, P < 0.05). The risankizumab group also exhibited improvement in Short Form 36 Questionnaire (SF-36) score (SMD 0.51, 95% CI 0.33-0.69, P < 0.001), with significantly lower Health Assessment Questionnaire Disability Index (HAQ-DI) score (SMD - 0.27, 95% CI - 0.37 to - 0.17, P < 0.001) and higher Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F) score (SMD 0.27, 95% CI 0.20-0.35, P < 0.001) compared to the placebo group. Moreover, the risankizumab group had a significantly lower Psoriasis Area and Severity Index (PASI) score (SMD - 6.12, 95% CI - 10.02 to 2.23, P < 0.001). A study by Mease et al. indicated that patients receiving risankizumab generally demonstrated numerical improvements in the Leeds Enthesitis Index (LEI), although the small sample size limits the evidence. Further research is necessary to provide evidence-based guidelines. There were no significant differences in the incidence of serious adverse events (SAE) and serious treatment-emergent adverse events (STEAE) between the risankizumab and placebo groups (RR 0.76, 95% CI 0.45-1.28, P = 0.31; RR 0.99, 95% CI 0.49-1.99, P = 0.97, respectively), and the overall incidence of adverse events (AE) was not comparable (RR 1.10, 95% CI 0.63-1.94, P = 0.73). CONCLUSION: Risankizumab showed superior efficacy across multiple outcome measures compared to placebo, with no significant increase in adverse events. Our findings endorse risankizumab as an excellent treatment option for PsA, offering valuable insights for clinicians and patients when choosing appropriate therapeutic interventions. TRIAL REGISTRATION: Retrospectively registered (CRD42023451894, 16 August 2023).
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OBJECTIVE: To determine the relationship between IgG antibody against the C-terminal region of the preS1 protein of hepatitis B virus and the early response to interferon therapy in chronic hepatitis B. METHODS: 69 patients with chronic hepatitis B virus (genotype B) infection were recruited in this study. 42 patients were treated with interferon-a-1b or a-2b, and 27 patients were treated with PEG interferon (a-2a). Peptide mimicking the C-terminal region of the preS1 protein (94-117aa) of genotype B HBV were synthesised, and the IgG antibody against this peptide was measured by ELISA, and the early response to IFN-alpha therapy was judged by the effect on the viral kinetics, transaminase and the status of HBeAg at 12th week after the treatment. RESULTS: 21 patients were positive for anti-preS1 antibody, and 48 patients were negative for anti-preS1 antibody. After 12 weeks of the treatment, the average decrease in viral levels was 3.37log10 copies/ml and 0.33log10 copies/ml in anti-PreS1 positive patients and anti-preS1 negative patients, respectively, the difference between the two groups was significant (Z = -3.658, P = 0.000); the average decrease in ALT levels was 92 U/L and 30.5 U/L in these two groups, respectively (Z = -2.132, P = 0.033). The rate of hepatitis B e antigen (HBeAg) loss was 41.2% (7/17) and the rate of anti-HBe seroconversion was 5.9% (1/17) in anti-PreS1 positive group, however, the rate of hepatitis B e antigen loss was only 12.8% (5/39), and none of the patients in anti-PreS1 negative group showed anti-HBe seroconversion, the difference between the two groups was significant (Z = -5.110, P = 0.000). The rates of response were 71.4% (15/21) and 16.7% (8/48), respectively, in anti-PreS1 positive group and anti-PreS1 negative group. The rates of complete response were 23.8% (5/21) and 6.25% (3/48), respectively, in these two groups. The positive predictive value (PPV) of anti-C-terminal region of preS1 (94-117aa) antibody in predicting early response was 71.6% and the negative predictive value (NPV) was 83.3%. CONCLUCIONS: Detection of anti-C-terminal region of preS1 (94-117aa) antibody may help to improve the efficacy of INF-alpha therapy for chronic hepatitis B (CHB).
