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Hong-Miao Li,1 Fei Tang,2 Qian Huang,3 Hai-Feng Pan,1 Tian-Ping Zhang4 1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, People’s Republic of China; 2Department of Interventional Pulmonology and Endoscopic Diagnosis and Treatment Center, Anhui Chest Hospital, Hefei, People’s Republic of China; 3Department of Public Health, Medical Department, Qinghai University, Xining, People’s Republic of China; 4The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, People’s Republic of ChinaCorrespondence: Tian-Ping Zhang, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, People’s Republic of China, Email zhangtianping@ustc.edu.cn Hai-Feng Pan, Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, People’s Republic of China, Email panhaifeng1982@sina.comObjective: Our study aimed to explore the association of IL-13, IL-13RA1, and IL-13RA2 genes polymorphisms with PTB susceptibility and its clinical features.Methods: Nine SNPs were genotyped by improved multiple ligase detection reaction (iMLDR) in 476 PTB patients and 473 controls. The association between these SNPs and PTB risk was analyzed using SPSS software and haplotype analysis was assessed using SHEsis software.Results: The IL-13RA1 rs2495636 GA genotype frequency in PTB patients was significantly decreased, and IL-13RA2 rs5946039 A allele was related to the lower risk of PTB. In IL-13 gene, rs20541 variant was found to be associated with PTB risk under recessive mode. Moreover, IL-13RA1 rs141573089 C allele was significantly lower in PTB presenting with fever, drug resistance, and CC genotype was decreased in PTB presenting with leukopenia. IL-13RA1 rs2495636 polymorphism was associated with drug resistance, pulmonary infection, and IL-13RA2 rs3795175, rs638376 polymorphisms were related to drug resistance in PTB patients.Conclusion: IL-13 rs20541, IL-13RA1 rs2495636, IL-13RA2 rs5946039 polymorphisms might be contributed to the genetic background of PTB in Chinese population.Keywords: pulmonary tuberculosis, Mycobacterium tuberculosis, interleukin-13, single nucleotide polymorphisms

Hong-Miao Li,1,2 Qian Huang,1 Fen Tang,2 Tian-Ping Zhang3 1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, 230032, Anhui, People’s Republic of China; 2Anhui Chest Hospital (Anhui Provincial TB Institute), Hefei, 230022, Anhui, People’s Republic of China; 3The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, People’s Republic of ChinaCorrespondence: Tian-Ping ZhangThe First Affiliated Hospital of University of Science and Technology of China, 17 Lujiang Road, Hefei, Anhui, 230001, People’s Republic of ChinaEmail zhangtianping@ustc.edu.cnBackground: Reactive oxygen species (ROS) generated by NADPH oxidase has a pivotal role in the nonspecific innate immune response to invading microorganisms including M. tuberculosis (MTB). NCF2 and NOX2 were considered as important functional subunits of NADPH oxidase complex; hence, this study aimed to evaluate the NCF2, NOX2 mRNA expressions in PBMC of pulmonary tuberculosis (PTB) patients.Methods: A total of 79 PTB patients and 73 controls were included in our study. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was used to measure the NCF2, NOX2 mRNA levels, and receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic value of NCF2, NOX2 in PTB patients.Results: When compared to controls, the NCF2, NOX2 mRNA levels were significantly increased in PBMC from PTB patients (P < 0.001). However, the NCF2, NOX2 mRNA levels were not associated with major clinical and laboratory data of PTB patients. Area under curve (AUC) of ROC curve analysis for NCF2 and NOX2 were 0.686 (95% CI: 0.601, 0.770) and 0.705 (95% CI: 0.623, 0.787), respectively.Conclusion: Altered NCF2, NOX2 mRNA levels in PTB patients implied that these genes might play roles in PTB, and their expression levels might be potential biomarkers for the diagnosis of PTB.Keywords: pulmonary tuberculosis, NADPH oxidase complex, NCF2, NOX2, peripheral blood mononuclear cells

Hong-Miao Li,1,2,&ast; Li-Jun Wang,2,&ast; Fei Tang,3 Hai-Feng Pan,1 Tian-Ping Zhang4 1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, People’s Republic of China; 2Department of Infectious Diseases, The First Affiliated Hospital of Anhui Medical University, Hefei, People’s Republic of China; 3Anhui Chest Hospital (Anhui Provincial TB Institute), Hefei, Anhui, People’s Republic of China; 4The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Tian-Ping Zhang, The First Affiliated Hospital of USTC, 17 Lujiang Road, Hefei, Anhui, 230001, People’s Republic of China, Email zhangtianping@ustc.edu.cn Hai-Feng Pan, School of Public Health, Anhui Medical University, Hefei, 230032, Anhui, People’s Republic of China, Email panhaifeng@ahmu.edu.cnBackground: Recent studies have shown that abnormal expression of lncRNA NEAT1 is associated with the progression of pulmonary tuberculosis (PTB). The aim of our study was to analyze the relationship between single nucleotide polymorphisms (SNPs) of NEAT1 gene and susceptibility to PTB.Methods: Four SNPs (rs2239895, rs3741384, rs3825071, rs512715) in NEAT1 gene were genotyped in 479 patients with PTB and 476 controls by improved multiple ligase detection reaction (iMLDR) in a Chinese population.Results: We found no significant differences in allele and genotype frequencies of NEAT1 gene rs2239895, rs3741384, rs3825071, rs512715 between PTB patients and controls (all P > 0.05). There was no statistically significant association between genotype frequency distribution of dominant model, as well as recessive model, and genetic susceptibility to PTB patients (all P > 0.05). The TT genotype, T allele frequencies of rs3825071 were significantly increased in sputum smear-positive PTB patients when compared to sputum smear-negative PTB patients (P = 0.010, P = 0.003, respectively). Haplotype analysis shown that NEAT1 haplotype frequency was not associated with PTB susceptibility.Conclusion: NEAT1 gene polymorphisms were not associated with the risk of PTB in Chinese population, and rs3825071 polymorphism might be related to sputum smear-positive in PTB patients.Keywords: long non-coding RNA, NEAT1, pulmonary tuberculosis, single nucleotide polymorphisms

Recent studies have shown that abnormal expression of lncRNA NEAT1 is associated with the progression of pulmonary tuberculosis (PTB). The aim of our study was to analyze the relationship between single nucleotide polymorphisms (SNPs) ofFour SNPs (rs2239895, rs3741384, rs3825071, rs512715) inWe found no significant differences in allele and genotype frequencies of

The aim of our study was to investigate the association of leptin (LEP) gene (rs11761556, rs12706832, rs2167270), leptin receptor (LEPR) gene (rs1137100, rs1137101, rs1805096) variants and pulmonary tuberculosis (PTB) susceptibility, as well as their several clinical manifestations, in a Chinese population.This study included a cohort of 489 PTB patients and 489 healthy controls, and six SNPs were genotyped by improved multiple ligase detection reaction (iMLDR).We found that there were no significant differences regarding the allele and genotype frequencies of LEP rs11761556, rs12706832, rs2167270, LEPR rs1137100, rs1137101, rs1805096 between PTB patients and healthy controls (all P 0.05), as well as the results of the dominant model and recessive model (all P 0.05). In the LEP gene, the rs11761556 AA genotype frequency was significantly associated with the development of fever and pulmonary infection in PTB patients (P = 0.035, P = 0.049). In addition, the relation between main haplotypes and PTB patients was also analyzed, but only haplotype CAG in LEP was significantly associated with PTB susceptibility (P = 0.012).LEP and LEPR heritable variation were not contribute to the pathogenesis of PTB in Chinese. While rs11761556 variant might associate with several clinical features of PTB.

Abnormal vitamin D metabolism is involved in the pathogenesis of rheumatoid arthritis (RA). In this study, we evaluated the association of single nucleotide polymorphisms (SNPs) and methylation levels in vitamin D metabolic pathway genes with RA susceptibility. Ten SNPs in vitamin D metabolic pathway genes (CYP2R1, CYP24A1, VDR, CYP27B1) were genotyped in 477 RA patients and 496 controls by improved multiple ligase detection reaction (iMLDR). The methylation levels of the promoter regions of these genes were detected in 122 RA patients and 123 controls using Illumina Hiseq platform. We found that the CYP2R1 rs1993116 GA genotype, CYP27B1 rs4646536 GA genotype, rs4646536 A allele frequencies were significantly increased in RA patients when compared to controls. The decreased risk of rs1993116, rs4646536 was found under the dominant mode in RA patients. However, no significant association was found between CYP2R1 rs7936142, rs12794714, CYP24A1 rs2762934, rs6068816, rs2296239, rs2296241, VDR rs11574129, rs3847987 polymorphism, and RA susceptibility. The VDR, CYP27B1 methylation levels in RA patients were significantly lower than those in controls, while CYP2R1, CYP24A1 methylation levels were not associated with RA. There were no statistical associations between CYP2R1, CYP24A1, VDR, CYP27B1 methylation levels and their respective genotype in RA patients. In addition, plasma 25OHD level in RA patients was significantly lower than that in healthy controls. In summary, our results showed that CYP2R1, CYP27B1 genetic variations were associated with the genetic background of RA, while altered VDR, CYP27B1 methylation levels were related to the risk of RA.

Dickkopf-1 (DKK-1) is mostly known as a mature inhibitor of classic Wnt signaling pathways, which plays a critically role in regulating bone formation and bone metastasis. In recent years, the roles of DKK-1 played in bone resorption, bone formation, immune homeostasis and inflammation have been investigated. The role of DKK-1 in the pathogenesis and treatment of autoimmune diseases (ADs), including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), etc, has attracted widespread attention. Various studies have found that DKK-1 may be used as a biomarker for the occurrence and development of ADs, and as a potential target for the treatment of ADs. In this review, we have briefly summed up the intricate immunological functions and regulatory mechanisms of DKK-1 in ADs, aiming to further learning more about the role of DKK-1 involved in the pathogenesis of ADs and provide an outlook for the potential future researches.

Objective This study aimed to evaluate the association of single nucleotide polymorphisms (SNPs) of vitamin D metabolic pathway genes with susceptibility to pulmonary tuberculosis (PTB). Methods Nine hundred seventy-nine patients (490 PTB cases and 489 healthy controls) were included in this study. Seventeen SNPs of vitamin D metabolic pathway genes, including CYP24A1, CYP27A1, CYP27B1, CYP2R1, GC, and DHCR7, were genotyped with improved multiple ligase detection reaction (iMLDR). Results The GC rs3733359 GA, rs16847024 CT genotypes were significantly associated with the reduced risk of PTB, and the rs3733359 A, rs16847024 T alleles were also associated with the decreased PTB susceptibility. The GT genotype of GC rs4588 variant was significantly higher in patients with PTB when compared to controls. Moreover, the increased risk of rs3733359 and rs16847024 variants, and a decreased risk of rs4588, were found under the dominant mode among the PTB patients. However, there was no significant relationship of CYP24A1, CYP27A1, CYP27B1, CYP2R1, and DHCR7 polymorphisms with the risk of PTB. In CYP27A1, the rs17470271 T and rs933994 T alleles were significantly associated with leukopenia, drug resistance in the PTB patients, respectively. In GC gene, the rs7041 and rs3733359 variants were found to be associated with pulmonary infection, fever in the PTB patients, respectively. The increased frequency of rs16847024 TT genotype was found in the PTB patients with fever and drug-induced liver damage. DHCR7 rs12785878 TT genotype, and T allele frequencies were both significantly associated with pulmonary infection in the PTB patients. The haplotype analysis showed that CYP24A1 TACT, CYP2R1 GGCT, GGAT, GC AATG haplotypes were related to PTB susceptibility. Conclusion Our study suggested that GC SNPs were associated with the genetic background of PTB. CYP27A1, GC, and DHCR7 genetic variations might contribute to several clinical phenotypes of PTB in Chinese.

Background The aim of our study was to estimate the association of ficolin‐1 (FCN1) gene (rs10120023, rs1071583) and ficolin‐3 (FCN3) gene (rs3813800, rs10794501) polymorphisms and pulmonary tuberculosis (PTB) susceptibility, as well as their several clinical features, in a Chinese population. Methods This study included a cohort of 489 PTB patients and 489 healthy controls, and the four SNPs were genotyped by improved multiple ligase detection reaction (iMLDR). Results We found that there were no significant differences regarding the allele and genotype frequencies of FCN1 rs10120023, rs1071583 and FCN3 rs3813800, rs10794501 between PTB patients and healthy controls (all p > 0.05). The association of three main haplotypes (CC, CT, and TC) in FCN1 and three main haplotypes (CT, GA, and GT) in FCN3 with PTB susceptibility was also analyzed, and no significant association was detected (all p > 0.05). In FCN1, the rs1071583 TT genotype was significantly associated with the occurrence of drug resistance in PTB patients (p = 0.040). In addition, the GG genotype and G allele frequencies of rs3813800 in FCN3 gene were significantly higher in PTB patients with pulmonary infection (p = 0.027, p = 0.020, respectively). Conclusions FCN1 and FCN3 genetic variation were not contributed to the pathogenesis of PTB in Chinese. While rs1071583 and rs3813800 variant might associate with several clinical characteristics of PTB., Our results found that there were no significant differences regarding the allele and genotype frequencies of FCN1 rs10120023, rs1071583, FCN3 rs3813800, and rs10794501 between PTB patients and healthy controls (all p > 0.05). While the FCN1 rs1071583 TT genotype was significantly associated with the occurrence of drug resistance in PTB patients (p = 0.040), in addition, the GG genotype and G allele frequencies of rs3813800 in FCN3 gene were significantly higher in PTB patients with pulmonary infection (p = 0.027, p = 0.020, respectively).

IntroductionThe vitamin D metabolic pathway has been shown to play a pivotal role in the pathogenesis of pulmonary tuberculosis (PTB), and vitamin D receptor (VDR) and CYP2R1 gene variation are known to affect vitamin D status. Hence, this study aimed to evaluate VDR and CYP2R1 mRNA expression in peripheral blood mononuclear cells (PBMCs) in PTB patients.Material and methodsWe measured VDR and CYP2R1 mRNA levels in 75 PTB patients and 63 healthy controls by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). The associations of VDR and CYP2R1 mRNA levels with clinical characteristics and laboratory indexes of PTB patients were also examined in this study.ResultsCompared to healthy controls, the VDR mRNA level was significantly higher, and the CYP2R1 mRNA level was significantly lower in PBMCs from PTB patients (p = 0.047, p = 0.008, respectively). The CYP2R1 mRNA level in PTB patients with drug-resistant, unilateral tuberculosis foci was significantly higher than that in PTB patients without these clinical characteristics (p = 0.005, p = 0.048, respectively). In addition, our results demonstrated that the VDR mRNA expression level was positively correlated with erythrocyte sedimentation rate (ESR) (p = 0.045), while the CYP2R1 mRNA level was negatively correlated with ESR in PTB patients (p = 0.020).ConclusionsAltered VDR and CYP2R1 mRNA expression levels among PTB patients suggest their involvement in this disease.

Background In this study, we aimed to assess mRNA expressions of visfatin and lipocalin‐2 in peripheral blood mononuclear cells (PBMCs) from patients with pulmonary tuberculosis (PTB). Methods Overall, 79 PTB patients and 71 healthy controls were enrolled. In PBMCs, mRNA expressions of visfatin and lipocalin‐2 were detected using real‐time quantitative polymerase chain reaction (qRT‐PCR), and the diagnostic value of these adipokine mRNAs in PTB patients was calculated through receiver operating characteristic (ROC) analysis. Results In PBMCs from PTB patients, the visfatin mRNA level was significantly higher than in healthy controls (P, In this study, we found that the visfatin mRNA expression level in PBMCs from PTB patients was significantly higher than that in healthy controls (P

Objective An increasing number of studies have demonstrated the roles of adipokines in systemic lupus erythematosus (SLE). We aimed to investigate the association of genetic variations of omentin-1, adiponectin, and resistin with SLE susceptibility. Methods We selected 623 SLE patients and 665 normal controls in the present study. Genotyping of omentin-1 rs2274907, rs35779394, rs79209815, and rs13376023; adiponectin rs16861194 and rs266729; and resistin rs1862513, rs3745368, and rs3745367 was conducted by TaqMan SNP genotyping assays. Results Overall, we found no significant differences in the allele or genotype frequencies of the nine studied SNPs between the SLE patients and controls. However, an increased frequency of the resistin rs3745368 variant was observed in the SLE patients under the dominant model (P = 0.024). In omentin-1, the rs13376023 A allele was found to be related to oral ulcers in SLE patients (P = 0.013), and the rs35779394 C and rs13376023 A allele frequencies were significantly lower in SLE patients with BMI ≥ 24 kg/m2 (P = 0.019, P = 0.033, respectively). For resistin, the frequencies of the rs3745368 AA genotype and A allele were lower in SLE patients with discoid rash (P = 0.036, P = 0.011), and the rs3745368 A allele frequency was higher in SLE patients with lupus nephritis (P = 0.018). The resistin rs3745367 AA genotype and A allele frequencies were related to the occurrence of renal disorder in SLE patients (P = 0.024, P = 0.009). The haplotype analysis showed that the CGA haplotype of resistin was associated with susceptibility to SLE (P = 0.005). No significant associations of plasma omentin-1, adiponectin or resistin levels with their respective genotypes were found in SLE patients. Conclusions In summary, omentin-1, adiponectin and resistin SNPs are not associated with the genetic background of SLE in Chinese patients. However, omentin-1 and resistin genetic variations might contribute to several clinical phenotypes of SLE.

To explore the association of LEP and leptin receptor (LEPR) gene single‐nucleotide polymorphisms (SNPs) with susceptibility to systemic lupus erythematosus (SLE) in a Chinese population. Four LEP SNPs (rs11761556, rs12706832, rs2071045 and rs2167270) and nine LEPR SNPs (rs10749754, rs1137100, rs1137101, rs13306519, rs8179183, rs1805096, rs3790434, rs3806318 and rs7518632) were genotyped in a cohort of 633 patients with SLE and 559 healthy controls. Genotyping of SNPs was performed with improved multiple ligase detection reaction (iMLDR). No significant differences were detected for the distribution of allele and genotype frequencies of all 13 SNPs between patients with SLE and controls. The genotype effects of recessive, dominant and additive models were also analysed, but no significant evidence for association was detected. However, further analysis in patients with SLE showed that the TT genotype and T allele frequencies of the LEP rs2071045 polymorphism were nominally significantly higher in patients with pericarditis (P = 0.012, P = 0.011, respectively). In LEPR, the GA/AA genotype and A allele frequencies of the rs1137100 polymorphism were both nominally associated with photosensitivity in patients with SLE (P = 0.043, P = 0.018, respectively). Moreover, the genotype and allele distribution of rs3806318 were also nominally associated with photosensitivity in patients with SLE (P = 0.013, P = 0.008, respectively). No significant differences in serum leptin levels were observed in patients with SLE with different genotypes. In summary, LEP and LEPR SNPs are not associated with genetic susceptibility to SLE, but may contribute to some specific clinical phenotype of this disease; further studies are necessary to elucidate the exact role of LEP and LEPR genes in the pathogenesis of SLE.

Objective To evaluate the plasma levels of six adipokines, including chemerin, omentin-1, lipocalin-2, cathepsin-S, cathepsin-L and adipsin, in patients with SLE. Methods Ninety SLE patients and ninety control subjects were recruited, plasma adipokines levels were measured by enzyme-linked immunosorbent assay, and their associations with major clinical and laboratory indexes were analyzed. Results There were no significant differences in plasma chemerin, omentin-1, lipocalin-2, cathepsin-S, cathepsin-L and adipsin levels between SLE patients and controls. Further subgroup analyses by major clinical and laboratory indexes showed that plasma omentin-1 level was significantly lower in SLE patients without nephritis when compared with those patients with nephritis ( P = 0.002). Plasma chemerin, cathepsin-S levels in SLE patients without nervous system disorder were significantly lower in comparison with SLE patients with nervous system disorder ( P = 0.035, P = 0.029). No significant associations of other adipokines with any major clinical and laboratory indexes were observed. Conclusions Plasma levels of chemerin, omentin-1, lipocalin-2, cathepsin-S, cathepsin-L and adipsin in SLE patients were not markedly different from the normal controls. The presence of nephritis was connected with higher plasma omentin-1 levels in SLE patients, and the presence of nervous system disorder was associated with higher plasma chemerin, cathepsin-S levels in SLE patients. However, functional studies are awaited to further explore the potential roles of these cytokines in SLE.

This study aims to evaluate the plasma interleukin (IL)-37 levels in systemic lupus erythematosus (SLE) patients, as well as its association with major clinical and laboratory features. Ninety consecutively selected SLE patients and 78 community-based healthy controls were recruited. Plasma IL-37 levels were detected by enzyme-linked immunosorbent assay (ELISA). The major clinical and laboratory data of SLE patients were also recorded. The results showed that IL-37 level was significantly higher in the plasma of patients with SLE compared with controls ( p = 0.028). The correlation of plasma IL-37 levels with major clinical and laboratory data of SLE patients was also analyzed, and the results showed that anti-Sm and anti-RNP were negatively associated with plasma IL-37 levels of SLE patients, while C3 was positively associated with plasma IL-37 levels of SLE patients. No significant associations of IL-37 with other clinical and laboratory parameters were observed (all p > 0.05). In conclusion, elevated plasma IL-37 level and its associations with anti-Sm, anti-RNP and C3 in SLE patients suggest that IL-37 may be implicated in this disease.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by multisystem organ involvement and unclear pathogenesis. Several adipokines synthesized in the adipose tissue, including leptin, adiponectin, resistin, and chemerin, have been explored in autoimmune rheumatic diseases, especially SLE, and results suggest that these mediators may be implicated in the pathogenesis of SLE. However, the current results are controversial. In this review, we will briefly discuss the expression and possible pathogenic role of several important adipokines, including leptin, adiponectin, resistin, and chemerin in SLE.

This study aims to derive a more precise estimation on carotid intima-media thickness (CIMT) level in patients with rheumatoid arthritis (RA) and related factors. Studies published from January 1, 1982 to December 31, 2014 in English, which comparing CIMT between RA group and control group were searched in PubMed, Embase, and Cochrane Library databases. Heterogeneity test was performed, and publication bias was evaluated. Stata software 12.0 was used to perform the meta-analysis. Two-thousand one hundred sixty-three articles were obtained after searching databases, and 47 studies were finally included in the meta-analysis. The result of the analysis in random effect model showed that RA group had significantly higher CIMT than control group, with the standardized mean difference (SMD) of 1.04 and 95% CI (0.81,1.27). To evaluate the stability of our results, sensitivity analyses were performed, and the results showed no significant change when any one study was excluded. Subgroup analyses showed that region, race, age, BMI, and disease duration were associated with CIMT in RA patients. In summary, CIMT in RA patients is thicker than healthy controls, and it is influenced by region, race, age, BMI, and disease duration.

Currently published data regarding the relationship between plasma/serum leptin levels and systemic lupus erythematosus (SLE) are contradictory. To derive a more precise evaluation of this relationship, a meta-analysis was performed.Published literature from PubMed, Embase and Cochrane Library were obtained. The study quality was assessed by the Newcastle-Ottawa scale. Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by fixed-effects or random-effect model analysis. Heterogeneity among studies was estimated using the Cochran Q and I(2) statistics.A total of 11 studies including 868 SLE patients and 591 controls were finally included in the meta-analysis. No significant differences in plasma/serum leptin levels was found between SLE patients and healthy controls when all studies were pooled into the meta-analysis (pooled SMD = 0.269, 95% CI = -0.188 to 0.726). However, subgroup analyses showed that SLE patients from an Asian population, age ≥40 years and BMI25 had higher plasma/serum leptin levels when compared with controls.There is no significant difference in plasma/serum leptin levels between the entire group of SLE patients and controls. However, plasma/serum leptin levels are significantly higher in the subgroup of SLE patients from an Asian population ≥40 years of age and with a BMI25.

Pulmonary hypertension (PH) has been suggested to be associated with systemic lupus erythematosus (SLE). However, the results of prevalence studies on PH in SLE vary substantially. To derive a more precise estimation on the prevalence of PH in SLE, a meta-analysis was performed. Relevant literatures were searched in PubMed and EMBASE until November 2017. A total of 1366 articles were obtained after searching databases, and 23 studies were finally included in the meta-analysis. Heterogeneity test was performed, and publication bias was evaluated. The result of analysis in random effect model showed that the pooled prevalence was 8% (95%CI 5–12%). There was no evidence of publication bias (p = 0.51). To evaluate the stability of our results, sensitivity analyses were performed, and the results showed no significant change when any one study was excluded. Subgroup analyses demonstrated that there were significant differences in PH prevalence in SLE patients of different gender, age, regions, year of publication, and diagnostic methods. PH is prevalent in SLE patients, but it was significantly different between different gender, age, regions, year of publication, and diagnostic methods.

Prolactin (PRL), a polypeptide hormone produced by the pituitary gland, is involved in the regulation of humoral and cell mediated immune responses. PRL levels have been investigated in several autoimmune diseases including systemic lupus erythematosus (SLE), however, yielded different and inconsistent results. This study aims to derive a more precise evaluation on plasma/serum PRL levels in SLE patients, as well as the potential influential factors.Studies published from 1 January 1987 to 31 December 2015 in English, which comparing plasma/serum PRL levels between SLE group and control group were searched in PubMed, EMBASE and The Cochrane Library databases. Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by fixed-effects or random-effect model analysis. Heterogeneity test was performed by the Q statistic and quantified using IFive-hundred and forty-seven articles were obtained after searching databases, and 12 studies with 429 SLE patients and 326 controls were finally included. Meta-analysis revealed that, compared with the control group, the SLE group had significantly higher plasma/serum PRL levels (P 0.001), with the SMD of 1.26 and 95%CI (0.70，1.82). Subgroup analyses showed that SLE patients from Asia and Europe had higher plasma/serum PRL levels. However, no significant change in plasma/serum PRL levels was observed in SLE patients from America (P 0.05).Overall, our study suggests that SLE patients have higher plasma/serum PRL level, but with a regional difference.

Objectives To derive a more precise comparison of flow-mediated dilatation (FMD%) of the brachial artery between patients with rheumatoid arthritis (RA) and normal controls by performing a meta-analysis of appropriate studies. Methods PubMed and EMBASE databases were searched for all relevant articles. STATA (V.12.0) software was used to perform the meta-analysis. Quality estimation of all appropriate studies was evaluated according to the Newcastle-Ottawa Scale (NOS). Standardised mean difference (SMD) with 95% CIs were calculated with a random-effects model. The Cochrane Q test and I2 statistic were used to evaluate the heterogeneity. Funnel plot and Egger’s test were conducted to assess the publication bias. Results In total, 464 articles were obtained after searching the two databases. Ten studies were included in the meta-analysis on the basis of the inclusion and exclusion criteria. Significant heterogeneity was observed among these 10 studies (Q=102.89, p Conclusions FMD% in patients with RA is significantly decreased compared with healthy controls. FMD% is an important early marker of atherosclerosis. It may be used as a parameter to forecast cardiovascular disease in patients with RA.

To derive a more precise estimation of carotid intima-media thickness (CIMT) levels in patients with type 1 diabetes mellitus (T1DM) by meta-analysis.PubMed and Embase databases were searched to identify all available studies comparing CIMT levels between T1DM group and control group. Meta-analysis was performed to compare the difference of overall mean CIMT levels between the two groups. Publication bias was evaluated by funnel plot, Begg' test and Egger' test. Meta-regression analysis was conducted to investigate the influential factors on CIMT difference. The meta-analysis was conducted by STATA 12.0 software.A total of 1840 articles were obtained after searching databases; 47 studies were finally included in the meta-analysis. Significant heterogeneity was observed among these studies (Q = 768.75, P0.001, I(2) = 94.0%). Compared with the control group, the T1DM group had significantly higher CIMT levels (standardized mean difference: 1.01, 95% CI: 0.75-1.28; P0.001). A likely source of heterogeneity was Newcastle-Ottawa Scale (NOS) scores and sample size ratio of patents and controls. The funnel plot did not show a skewed or asymmetrical shape, and the result of Begg' test and Egger' test was P = 0.178 and P = 0.145 respectively. Accordingly, it could be assumed that publication bias was not present.T1DM patients have significantly increased CIMT levels compared to control subjects.