Background: Thyroid dysfunction seems to be common among rheumatoid arthritis (RA) patients, but the risk of thyroid dysfunction in RA has not been well-defined. Methods:We performed a case-control study of 65 RA patients and 550 matched non-RA subjects to assess the risk of thyroid dysfunction among Chinese RA patients. A systematic review and meta-analysis was also conducted to comprehensively define the relationship between RA and thyroid dysfunction. Results:The case-control study indicated that the prevalence of thyroid dysfunction was significantly higher in RA patients than controls (OR = 2.89, P < 0.001). Further subgroup analyses revealed positive correlations of RA with hypothyroidism (OR = 2.28, P = 0.006) and hyperthyroidism (OR = 8.95, P < 0.001). Multivariate logistic regression analysis revealed an independent association between RA and thyroid dysfunction (Adjusted OR = 2.89, 95%CI 1.63-5.12, P < 0.001). Meta-analysis of 15 independent studies also showed an obviously increased risk of thyroid dysfunction among RA patients (RR = 2.86, 95%CI 1.78-4.58, P < 0.001). Further subgroup analysis showed RA could obviously increase risk of hyperthyroidism (RR = 2.73, 95%CI 1.29-5.77, P = 0.043) and hypothyroidism (RR = 2.02, 95%CI 1.49-2.74, P < 0.001). Conclusion:Our study provides strong evidence for the increased risk of thyroid dysfunction among RA patients. Screening of thyroid dysfunction may be recommended for RA patients.

Background Accumulating data have shown that interleukin-27 (IL27) polymorphisms are linked to the susceptibility of some autoimmune diseases. We assessed whether there was an association between three single-nucleotide polymorphisms (SNPs) of IL27 gene and autoimmune thyroid diseases (AITDs). Methods Three SNPs (rs153109, rs17855750 and rs181206) of IL27 gene were genotyped by Hi-SNP high-throughput genotyping in 843 patients with AITDs (516 Graves’ disease (GD) and 327 Hashimoto’s thyroiditis (HT)) and 677 healthy controls in Chinese Han population. Results Compared with controls, rs153109 displayed significant associations with GD in allele and genotype frequencies (P = 0.002 and P = 0.008, respectively) and rs17855750 displayed significant associations with HT in allele frequencies (P = 0.02), whereas no differences in genotype or allele frequencies were found between AITD patients and controls at rs181206. Conclusion Our study, for the first time, showed the significant association of the IL27 gene SNPs with AITD.

S1. Haplotype association analysis of rs3130983, rs3778638, rs3815087, and rs4959053 in PSORS1C1. Haplotype associations Frequency χ 2 P CG 55.2% 0.987 0.321 TG 34.7% 0.359 0.549 CA 10.1% 0.481 0.488 Categorical data are presented as n (%) and were analyzed using the chi-square test. P-values <0.05 were considered statistically significant.

Objective. Hashimoto’s thyroiditis (HT) is one of the most common clinical autoimmune diseases. Recent studies have found that HT pathogenesis is associated with macrophage polarization. Saikosaponin-d (SSd) is an active component in the Chinese medicine Bupleurum, which has anti-inflammatory and immunomodulatory effects. The purpose of this study was to verify the therapeutic effect of SSd on HT and to investigate the regulatory effect of SSd on macrophage polarization in HT. Methods. Network pharmacology analysis was used to predict the relevant targets and signaling pathways of SSd for HT treatment. The therapeutic effect of SSd on HT model mice and the effect on macrophage polarization were detected by animal experiment. Results. Network pharmacological analysis showed that SSd can alleviate HT against multiple targets such as IL-6 and IL-10 and can act on macrophage polarization-related signaling pathways such as MAPK and JAK-STAT signaling pathways. Animal experiments showed that SSd intervention attenuated the lymphocytic infiltration in thyroid tissues of HT mice ( P = 0.044 ); SSd intervention reduced serum TPOAb antibody level in HT mice ( P < 0.001 ); SSd adjusted M1/M2 imbalance towards M2-type macrophage polarization in the spleen of HT mice ( P = 0.003 ); SSd inhibited the expressions of Th1-type cytokine IFN-γ and Th17-type cytokine IL-17 systemically and locally in the thyroid of HT mice ( P < 0.05 ). Conclusion. SSd treatment can regulate Th1/Th2 and Th17/Treg imbalances and reduce the severity of HT in mice by promoting the polarization of M2 macrophages.

Objective Hydroxychloroquine (HCQ) is widely used in patients with systemic lupus erythematosus (SLE), but its effects on the mortality have not reached a definite conclusion. In this systematic review and meta-analysis, we aimed to assess whether HCQ use could reduce the risk of mortality in SLE patients. Methods PubMed, Embase, Web of Science, and Cochrane database were searched from inception to April 17, 2022 without language restrictions to explore the relationship between HCQ use and SLE mortality. The relative risk (HR) was pooled using the STATA software. Results A total of 21 studies with a pooled patient population of 26,037 were included in the study, including 14 studies on the association between HCQ alone and mortality risk and seven studies on the association between HCQ/chloroquine (CQ) and mortality risk. The pooled findings suggested that HCQ significantly reduced the overall mortality risk of SLE (pooled HR 0.46, 95% CI 0.38–0.57, p < 0.001). In subgroup analysis of SLE complications, HCQ use also decreased the risk of death in SLE patients with renal (HR=0.43, 95% CI 0.26–0.70, p = 0.001) and cardiopulmonary involvement (HR=0.37, 95% CI= 0.25–0.54, p < 0.001). In addition, HCQ use was also protective against the risk of mortality in SLE patients in different regions, such as Asia (HR=0.46, 95% CI=0.33–0.64, p < 0.001), Europe (HR= 0.40, 95% CI = 0.22–0.71, p = 0.002), and America (HR=0.52, 95% CI= 0.42–0.64, p < 0.001). Conclusion Our data suggested that HCQ use was associated with a reduced risk of mortality in patients with SLE.

Objective Autoimmune thyroid disease(AITD) is not only an immune-related disorder, but also inherited as a complex gene-related disease. The psoriasis susceptibility 1 candidate 1(PSORS1C1) gene is a susceptibility locusin autoimmune diseases. Many autoimmune diseases have been proved to be related with the PSORS1C1 gene. However, whether the PSORS1C1 gene plays a role in affecting the predisposition to AITD remains unknown.Methods In this study, we included 1056 Chinese Han AITD patients and 954 matched healthy controls. Multiplex polymerase chain reaction (PCR) technology was used to genotype SNPs (rs3130983, rs3778638, rs3815087, rs4959053)in PSORS1C1 gene. Results An association between rs3778683 and Graves' disease (GD) was observed with statistical significance (p=0.039). The allele and genotype of single nucleotide polymorphism (SNP) rs3130983, rs3815087 and rs4959053 showed no significant association with AITDs. In addition, no linkage disequilibrium for rs3130983, rs3815087, rs3778638 and rs4959053 in PSORS1C1 gene was found between AITD patients and controls.Conclusion These data revealed the influence of PSORS1C1 on the susceptibility to AITDs and reinforced this locus as a common autoimmunity risk factor.

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