What is known and objective: In the absence of head-to-head comparisons, the objective of this study was to conduct a network meta-analysis (NMA) to indirectly compare the relative efficacy and safety of Janus kinase (JAK) inhibitors for ulcerative colitis (UC). Methods:We searched PubMed, EMBASE, Web of Science and Cochrane Library from the database inception until 13 August 2021. No randomized controlled trials (RCTs) that directly compared these interventions were identified. Therefore, a fixedeffects Bayesian NMA was conducted by identifying a connected (via comparison to placebo) network of RCTs. Ranking was assessed using surface under the cumulative ranking (SUCRA) probabilities.Results and discussion: Seven RCTs including 3190 patients met the inclusion criteria.Filgotinib 100 mg was ranked highest for induction of endoscopic remission (SUCRA, 0.67) whereas peficitinib 75 mg BID was ranked highest for induction of clinical response (SUCRA, 0.72). Peficitinib 75 mg was ranked highest for induction of mucosal healing (SUCRA, 0.71), whereas peficitinib 150 mg was ranked highest for clinical remission (SUCRA, 0.74). Tofacitinib 3 mg had the highest probability of being the best treatment in terms of change from baseline in Mayo score (SUCRA, 0.78). Adverse events (AEs) and treatment discontinuations or withdrawals from the study due to AEs did not differ between JAK inhibitors and placebo groups.What is new and conclusion: Based on indirect comparisons, peficitinib 75 mg/75 mg BID/150 mg, tofacitinib 3 mg and filgotinib 100mg were the most efficacious JAK inhibitor interventions in patients with UC. However, head-to-head trials are warranted to inform clinical decision-making with greater confidence.
Background: Gouty arthritis (GA) is a chronic disease caused by monosodium urate crystal deposition. Repeated attacks of arthritis may lead to the deposition of urate to form gout stone, resulting in joint deformity and joint damage. Although GA is not fatal, it causes low work productivity and low quality of life. Western drug, such as febuxostat, colchicine, allopurinol, often cannot get satisfying curative effect, and may even lead to serious side effects, such as exfoliative dermatitis or uremia. However, the therapeutic effect of Traditional Chinese medicine is very satisfactory. The treatment effect of simiao powder, a Chinese patent medicine, combined with acupuncture was widely used on treatment of GA. Although it has been widely used in clinical practice, its relative effectiveness and safety have not been confirmed. Therefore, this study will use meta-analysis to verify the efficacy and safety of simiao powder combined with acupuncture in the treatment of GA. Methods: All randomized controlled trial of simiao powder combined with acupuncture for the treatment of RA from their inception 29 October, 2020 will be searched form the China National Knowledge Infrastructure, Wanfang Database, Chinese Science and Technology Periodical Database, Chinese Biomedical Literature Database, Pubmed, Embase, Web of Science, and the Cochrane library. Two authors will independently select studies, extract data based on pre-designed inclusion and exclusion criteria. Methodological quality assessment and risk of bias will be assessed using Cochrane bias risk tool. All data analysis will be conducted using Revman5.3, WinBUGS 1.4.3, and Stata14.2 software. Results: We will compare the different outcome indicators of various studies to provide a synthesis of the efficacy and safety of Simiao powder combined with acupuncture for GA patients. The main outcome measures included efficacy, remission rate (no drug symptoms), recurrence rate, clinical absolute score and relative score. Secondary outcome measures included related adverse reactions and uric acid concentration. Conclusion: The findings of the study will provide helpful evidence for the efficacy and safety of simiao powder combined with acupuncture in the treatment of GA. Registration number: This study protocol have been funded through a protocol registry. The registry number is INPLASY2020110028
and DNMT3B polymorphisms contribute to gout susceptibility. These polymorphisms were screened for in 336 gout patients and 306 healthy control subjects (from a South China population) for association with gout. The distribution frequencies of DNMT1 rs2228611 AA genotype (P=0.007) and A allele (P=0.002; odds ratio=1.508, 95% confidence �����v�l=1.158�1.964) w��� ����d �� b� ��g��fi����l� ��������d in the gout patients when compared with those in the healthy control subjects. The rs1550117 in DNMT3A and rs2424913 in DNMT3B �x��b���d �� ��g��fi���� ������������ w��� g��� susceptibility between the patients and control subjects. These results demonstrated that the DNMT1 rs2228611 polymorphism may be involved in the pathogenesis of gout, while DNMT3A rs1550117 and DNMT3B rs2424913 did not show any obvious ��g��fi����� �� ��� ������� ���d�; ����, ��� ��� b� ���d �� ���k factors to predict the susceptibility to gout. However, further studies are required to investigate the functions and regulatory mechanism of the polymorphisms of DNMTs in gout. Introduction���� ��������� �� ��� ���� ������ ����������� ��d ������ disease affecting 1-2% of adults worldwide, which is associated with elevated serum urate levels and the deposition of monosodium urate (MSU) in the joints (1). Previous studies show that gout is also associated with the genetic background, a purine rich diet and alcohol consumption (2-4), and epidemiological studies have suggested that the prevalence and incidence of gout are increasing globally (5,6). Over the past decade, signif-����� �������fi� �dv����� ��v� b��� ��d� �� ��d������d��g ��� �����g������ ��d ��������� �� g���. B���g � ����l�x d������, ��� �d����fi������ �� g������ ��d ��v���������l ���k ������� ��� gout may facilitate with investigating the pathogenesis of gout. As with other diseases, epigenetic events or heritable changes �� g��� �x�������� �������� w������ DNA ��q����� �l��������� may be evaluated to gain insight into the concrete pathogenesis of gout (7). DNA methylation is the most common epigenetic ��d�fi������, ��d �� ��������� �� ������������� ��d ��� ����-matin structure (8). The process of DNA methylation usually occurs at the CpG sites and the methyl group to the 5' position of a cytosine in a CpG dinucleotide conferred by DNA methyltransferases (DNMTs) (9). Three primary DNMTs, DNMT1, DNMT3A ��d DNMT3B, ��� �������� gl�b�l DNA ����-ylation (10). In addition, DNMT1 is a primary enzyme for maintaining methylation patterns during DNA replication, whereas DNMT3A and DNMT3B act predominantly as the de novo methyltransferases, and create novel methylation patterns (11-13).In addition, DNA methylation and its regulatory enzymes have been implicated in a diverse set of biological processes, including X chromosome inactivation, genomic imprinting, as well as autoimmunity (14)(15)(16)(17). Mutation of the human DNMTs �l���� g��� �x�������� ��d ��� ���v�d� ����g�� ���� ��� �����-nism of various diseases, such as centromere instability, acute ���l��d l��k���� ��d ������d�fi������ (18�20). T��...
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