Predictive factors for successful sperm retrieval by microdissection testicular sperm extraction in men with nonobstructive azoospermia and a history of cryptorchidism.

This study aims to explore the factors influencing the success rate of the microdissection testicular sperm extraction (Micro-TESE) in patients with nonobstructive azoospermia (NOA) and cryptorchidism. Clinical data of 162 patients with cryptorchidism who underwent Micro-TESE due to infertility from December 2015 to May 2020 in the First Affiliated Hospital of Nanjing Medical University were analyzed retrospectively. In the univariate analysis, significant differences in the age of patient at the time of orchidopexy (median [interquartile range, IQR]: 7.0 [4.0-11.0] years vs 11.5 [9.0-14.5] years, P < 0.001), interval between orchidopexy and Micro-TESE (mean ± standard deviation: 17.5 ± 5.0 years vs 14.4 ± 4.4 years, P < 0.001), severity of cryptorchidism (unilateral [62.8%] vs bilateral [31.6%], P < 0.001; location of cryptorchidism, intra-abdominal [27.3%] vs inguinal [44.8%] vs suprascrotal [66.7%], P < 0.001), volume of the dominant testis (median [IQR]: 17.00 [15.00-19.00] ml vs 14.50 [11.75-16.25] ml, P < 0.001), and levels of follicle-stimulating hormone (FSH; P = 0.004) and testosterone (P = 0.006) were observed between the successful and failed sperm extraction groups. After conducting the multivariate analysis, four of these factors, including unilateral/bilateral cryptorchidism (P < 0.001), location of cryptorchidism (P = 0.032), age of orchidopexy (P < 0.001), and dominant testicular volume, were adopted in the clinical prediction model to evaluate preoperatively the success rate of Micro-TESE for patients with NOA and cryptorchidism. The likelihood of successful sperm retrieval by Micro-TESE in men with NOA and cryptorchidism increased in patients with mild forms of cryptorchidism.

[A case of complete androgen insensitivity syndrome with special family history and its genetic analysis].

OBJECTIVE: To report a case of complete androgen insensitivity syndrome with a special family history and its genetic analysis. METHODS: We studied the medical history, diagnosis and treatment of a case of complete androgen insensitivity syndrome, collected blood samples from the patient and his mother for whole exome sequencing, and analyzed the genetic etiology. RESULTS: The patient presented with "primary amenorrhea" and diagnosed with male pseudohermaphroditism, with the karyotype as 46, XY. Surgery confirmed undescended testes in the abdominal cavity. The androgen level was higher than normal. Whole exome sequencing of the patient and his mother found c.2678C>T (p.P893L) but no other abnormalities, which was considered as a suspected pathogenic mutation of complete androgen insensitivity syndrome. The patient had a "sister" with a similar medical history. CONCLUSION: c.2678C>T (p.P893L) is a suspected pathogenic mutation of complete androgen insensitivity syndrome, which usually cannot be detected until puberty, making it easy to delay the diagnosis.

A mixed-method evaluation of the relationship between Oxford classification scores and longitudinal changes in proteinuria in patients with immunoglobulin A nephropathy.

Introduction: This study aimed to investigate the relationship between Oxford Classification scores and longitudinal changes in proteinuria in patients with immunoglobulin A nephropathy (IgAN). Methods: The study was a single-center retrospective cohort study involving 358 patients with primary IgAN who were treated at the Shenzhen Second People's Hospital, China, between January 2011 and May 2021. Multivariate linear regression and generalized additive mixed models (GAMMs), adjusted for traditional risk confounders, were used to evaluate the correlation between scores for mesangial hypercellularity (M), endocapillary hypercellularity (E), segmental glomerulosclerosis (S), tubular atrophy/interstitial fibrosis (T), and crescents (C) (known as the Oxford Classification MEST-C score system), with proteinuria/creatinine ratio (PCR) at the time of renal biopsy and longitudinal changes in PCR, respectively. Results: The median PCR was 1061 mg/g, and it increased on average by 68.82 mg/g per year in these patients. Among patients with renal insufficiency, compared with patients without relative lesions, those with E present (E1) (1153.44; 95% confidence interval [CI], 188.99-2117.89 mg/g) and C > 0 (C1/2) (1063.58; 95% CI, 185.25-1941.90 mg/g) were associated with increased PCR levels at the time of renal biopsy. What's more, S present (S1) (194.96; 95% CI, 54.50-335.43 mg/g per year) was associated with the fastest PCR increase; C > 0 (C1/2) (147.59; 95% CI, 8.32-286.86 mg/g per year) and T >25% (T1/2) (77.04; 95% CI, 7.18-146.89 mg/g per year), were also correlated with a faster PCR increase. In patients with normal kidney function, associations between S1 (55.46; 95% CI, 8.93-101.99 mg/g per year) and E1 (94.02; 95% CI, 21.47-166.58 mg/g per year) and PCR change could be observed. Additionally, in patients with overweight/obesity, S1 (156.09; 95% CI, 52.41-259.77 mg/g per year), E1 (143.34; 95% CI, 35.30-251.38 mg/g per year), T1/2 (116.04; 95% CI, 22.58-209.51 mg/g per year), as well as C1/2 (134.03; 95% CI, 41.73-226.32 mg/g per year) were associated with noticeably quicker PCR increase. Conclusions: Overall, E1 and C1/2 were independently associated with raised proteinuria levels at the time of renal biopsy, and S1, E1, T1/2, C1/2 were independently associated with a longitudinal increase in proteinuria in the patients with IgAN, especially in those with renal insufficiency or overweight/obesity, suggesting that currently available treatments might not be satisfactory, and weight control might be beneficial. Individual therapy development might benefit from the use of the Oxford Classification system.

[Clinical characteristics and treatment strategies of prostatic mucinous adenocarcinoma: A report of 10 cases and literature review].

OBJECTIVE: To investigate the clinical characteristics and treatment strategies of prostatic mucinous adenocarcinoma (PMAC). METHODS: We retrospectively analyzed the clinical data on 10 cases of PMAC treated in the First Affiliated Hospital of Nanjing Medical University from January 2014 to June 2018. The patients were aged 51－79 (65 ± 14) years, with a medium PSA level of 89 (14.63－128.05) µg/L and Gleason scores of 3 + 3 in 1 case, 3 + 4 in 2, 4 + 3 in 1 and 8 in 6 cases preoperatively, 1 treated by robot-assisted radical prostatectomy and the other 9 by laparoscopic radical prostatectomy. We conducted pelvic cavity lymph node dissection for all the patients and analyzed their prognosis and survival. RESULTS: Operations were successfully completed in all the cases. Pathological examination revealed 2 cases of mucinous adenocarcinoma with signet ring cell carcinoma in the 10 PMAC patients, 2 at stage ≤T2b, 5 at stage ≥T2c, 3 positive at pelvic lymph node dissection and 5 positive at the incision margin. The patients were followed up for 6－48 (median 26) months. Four of the patients were found with biochemical recurrence within 2 years after operation and treated by androgen-deprivation therapy, radiotherapy and chemotherapy, which reduced the PSA level to <1.0 µg/ml in all the 4 cases. CONCLUSIONS: PMAC has a good prognosis. Radical surgery is recommended for moderate and low-risk PMAC and the patients with postoperative biochemical recurrence can benefit from comprehensive treatment of total androgen blockade.

Metabolic Syndrome and Its Components Predict the Risk of Type 2 Diabetes Mellitus in the Mainland Chinese: A 3-Year Cohort Study.

INTRODUCTION: It has well established that metabolic syndrome (MetS) can predict the risk of type 2 diabetes mellitus (T2DM) in some population groups. However, limited evidence is available regarding the predictive effect of MetS for incident T2DM in mainland Chinese population. METHODS: A 3-year cohort study was performed for 9735 Chinese without diabetes at baseline. MetS and its components were assessed by multivariable analysis using Cox regression. Prediction models were developed. Discrimination was assessed with area under the receiver operating characteristic curves (AUCs), and performance was assessed by a calibration curve. RESULTS: The 3-year cumulative incidence of T2DM was 11.29%. Baseline MetS was associated with an increased risk of T2DM after adjusting for age (HR = 2.68, 95% CI, 2.27-3.17 in males; HR = 2.59, 95% CI, 1.83-3.65 in females). Baseline MetS exhibited relatively high specificity (88% in males, 94% in females) and high negative predictive value (90% in males, 94% in females) but low sensitivity (36% in males, 23% in females) and low positive predictive value (31% in males and females) for predicting the 3-year risk of T2DM. AUCs, including age and components of MetS, for the prediction model were 0.779 (95% CI: 0.759-0.799) in males and 0.860 (95% CI: 0.836-0.883) in females. Calibration curves revealed good agreement between prediction and observation results in males; however, the model could overestimate the risk when the predicted probability is >40% in females. CONCLUSIONS: MetS predicts the risk of T2DM. The quantitative MetS-based prediction model for T2DM risk may improve preventive strategies for T2DM and present considerable public health benefits for the people in mainland China.

Pentraxin 3 (PTX3) promoter methylation associated with PTX3 plasma levels and neutrophil to lymphocyte ratio in coronary artery disease.

BACKGROUND: Pentraxin 3 (PTX3) is expressed in the heart under inflammatory conditions and plays an important role in atherogenesis. Patients with increased PTX3 levels may suffer from higher rates of cardiac events. Regulation of specific genes by promoter methylation is important in atherogenesis. The factors influencing PTX3 levels and the association between epigenetics and PTX3 levels have not been investigated. METHODS: Blood samples were collected from 64 patients admitted to the Department of Cardiology, 35 who had coronary artery disease (CAD), and 29 who were CAD-free. Plasma levels of PTX3 were measured by ELISA. PTX3 promoter methylation was evaluated via methyl-specific PCR. The severity of coronary artery lesion was evaluated by angiography. RESULTS: The level of PTX3 promoter methylation in the CAD group was 62.69% ± 20.57%, significantly lower than that of the CAD-free group, which was 72.45% ± 11.84% (P = 0.03). Lower PTX3 promoter methylation levels in the CAD group were associated with higher plasma PTX3 concentrations (r = -0.29, P = 0.02). Furthermore, lower PTX3 promoter methylation levels were associated with higher neutrophil to lymphocyte ratio (NLR) in men (r = -0.58, P = 0.002). CONCLUSIONS: The present study provides new evidence that methylation of the PTX3 promoter is associated with PTX3 plasma levels and NLR in coronary artery disease. This study also shows that modification of epigenetics by chronic inflammation might be a significant molecular mechanism in the atherosclerotic processes that influence plasma PTX3 concentrations.

Expression and Characterization of a Novel Thermostable and pH-Stable ß-Agarase from Deep-Sea Bacterium Flammeovirga Sp. OC4.

A novel gene (aga4436), encoding a potential agarase of 456 amino acids, was identified in the genome of deep-sea bacterium Flammeovirga sp. OC4. Aga4436 belongs to the glycoside hydrolase 16 ß-agarase family. Aga4436 was expressed in Escherichia coli as a fusion protein and purified. Recombinant Aga4436 showed an optimum agarase activity at 50-55 °C and pH 6.5, with a wide active range of temperatures (30-80 °C) and pHs (5.0-10.0). Notably, Aga4436 retained more than 90%, 80%, and 35% of its maximum activity after incubation at 30 °C, 40 °C, and 50 °C for 144 h, respectively, which exhibited an excellent thermostability in medium-high temperatures. Besides, Aga4436 displayed a remarkable tolerance to acid and alkaline environments, as it retained more than 70% of its maximum activity at a wide range of pHs from 3.0 to 10.0 after incubation in tested pHs for 60 min. These desirable properties of Aga4436 could make Aga4436 attractive in the food and nutraceutical industries.

Higher spherical equivalent refractive errors is associated with slower axial elongation wearing orthokeratology.

PURPOSE: To investigate the relationship between axial length (AL) increase and baseline spherical equivalent refractive errors (SER) in myopic children wearing orthokeratology contact lenses (OK). METHODS: One hundred fifteen Chinese (115 right eyes) children wearing OK were enrolled in this cohort study. Gender, age, baseline SER, corneal power, corneal astigmatism, and AL at baseline and 2 years after wearing OK were collected. Univariate analysis and trend test were used to estimate the relationship between change in AL and baseline SER. RESULTS: After univariate analysis, a statistically significant relationship was found between change in AL and baseline SER (ß=0.061, 95% CI: 0.015-0.111, P=0.015). In the trend test, after adjusting for potential confounders, higher SER was associated with smaller increases in AL (P trend=0.041). CONCLUSIONS: The SER at baseline was associated with AL growth in myopic children wearing OK. The higher SER was associated with slower AL growth and control the development of myopia.

Is there comparable morbidity in pylorus-preserving and pylorus-resecting pancreaticoduodenectomy? A meta-analysis.

Pancreaticoduodenectomy (PD) is the most effective treatment for patients with pancreatic head or periampullary lesions. Two major strategies exist: pylorus-preserving pancreaticoduodenectomy (PPPD) and pylorus-resecting pancreaticoduodenectomy (PRPD). However, it is yet unclear regarding the morbidity after PPPD and PRPD. This study analyzed the morbidity after PPPD and PRPD to determine the optimal surgical treatment of masses in the pancreatic head or periampullary region. A systematic search of databases identifying randomized controlled trials (RCTs) from the Cochrane Library, PubMed, EMBASE and Web of Science was performed. Outcome was compared by postoperative morbidity including overall morbidity, pancreatic fistulas, wound infections, postoperative bleeding, biliary leakage, ascites and delayed gastric emptying (DGE) rate between PPPD and PRPD. The DGE rate in the PRPD subgroups (conventional PD [CPD] and subtotal stomach-preserving PD [SSPPD], respectively) was also analyzed. The results showed that 9 RCTs including 722 participants were included for meta-analysis. Among these RCTs, 7 manuscripts described PRPD as CPD, and 2 manuscripts described PRPD as SSPPD. There were no significant differences in the overall morbidity, pancreatic fistulas, wound infections, postoperative bleeding, or biliary leakage between PPPD and PRPD. There was a lower rate of DGE with PRPD than that with PPPD (RR=2.15, P=0.03, 95% CI, 1.09-4.23). Further subgroup analysis indicated a comparable DGE rate for the CPD but a lower DGE rate for the SSPPD group than the PPPD group. However, the result did not indicate any difference between CPD and SSPPD regarding the DGE rate (P=0.92). It is suggested that PPPD is comparable to PRPD in overall morbidity, pancreatic fistulas, wound infections, postoperative bleeding and biliary leakage. The current data are not sufficient to draw a conclusion regarding which surgical procedure is associated with a lower postoperative DGE rate. Our conclusions were limited by the available data. Further evaluations of RCTs are needed.

Octacosanol enhances the proliferation and migration of human umbilical vein endothelial cells via activation of the PI3K/Akt and MAPK/Erk pathways.

Atherosclerosis is characterized by endothelial dysfunction, lipid deposition, fibro-proliferative reactions and inflammation. Octacosanol is a high-molecular-weight primary aliphatic alcohol. As the main component of a cholesterol-lowering drug, octacosanol could inhibit lipids accumulation and cholesterol metabolism. To explore the indication of octacosanol on endothelial protection, we evaluated its effects on the proliferation and migration of human umbilical vein endothelial cells (HUVEC). Cell viability assay using methyl thiazolyl tetrazolium and 5-ethynyl-2'-deoxyuridine revealed that 3.125 µg/ml octacosanol promoted the proliferation of HUVEC. A cell migration assay indicated that 0.781 and 3.125 µg/ml octacosanol increased the migration of HUVEC. Moreover, the phosphorylation levels of Akt and Erk1/2 were significantly elevated under exposure to octacosanol. Blocking the activation of Akt and Erk with their potent inhibitors LY294002 and PD98059, respectively, markedly attenuated the octacosanol-induced proliferation and migration of HUVEC. These findings demonstrated for the first time that octacosanol enhanced the proliferation and migration of HUVEC and mediated these effects through activation of the PI3K/Akt and MAPK/Erk1/2 signaling pathways.

Elevated serum levels of soluble Axl in acute coronary syndrome.

BACKGROUND: Morbidities related to atherosclerosis, such as acute coronary syndrome (ACS), remain the leading cause of mortality. Axl is a receptor tyrosine kinase that is expressed in mammalian vascular and immune cells. Axl signaling is involved in the regulation of the inflammatory response. A considerable amount of evidence indicates that inflammation is responsible for the development of atherosclerosis in patients with ACS. METHODS: To assess the relation of Axl and ACS, we recruited 64 patients with coronary heart disease: 34 with ACS, 30 with stable coronary heart disease, and 24 apparently healthy controls. Serum concentrations of soluble Axl (sAxl) were quantified by enzyme-linked immunosorbent assay. High-sensitivity C-reactive protein, tumor necrosis factor alpha, troponin I, and other routine biochemical markers were also measured. RESULTS: The levels of sAxl were significantly higher in patients with ACS than in the controls (P=0.005). Furthermore, correlation analysis indicated that sAxl was significantly associated with serum levels of high-sensitivity C-reactive protein (r=0.283, P=0.008), tumor necrosis factor alpha (r=0.565, P<0.001), and troponin I (r=0.264, P=0.013). Logistic regression analysis (odds ratio=1.038, 95% confidence interval, 1.008-1.069, P=0.012) indicated a significant association between sAxl and ACS. CONCLUSIONS: Serum levels of sAxl correlate to inflammatory biochemical markers. These findings demonstrate for the first time that sAxl does have a role in ACS, presumably connected to the inflammation.

Increased risk of cerebrovascular events in patients with cancer treated with bevacizumab: a meta-analysis.

Arterial ischemia and hemorrhage are associated with bevacizumab, an inhibitor of vascular endothelial growth factor that is widely used to treat many types of cancers. As specific types of arterial ischemia and hemorrhage, cerebrovascular events such as central nervous system (CNS) ischemic events and CNS hemorrhage are serious adverse events. However, increased cerebrovascular events have not been uniformly reported by previous studies. New randomized controlled trials (RCTs) have been reported in recent years and we therefore conducted an up-to-date meta-analysis of RCTs to fully characterize the risk of cerebrovascular events with bevacizumab. We searched the databases of PubMed, Web of Science, and the American Society of Clinical Oncology conferences to identify relevant clinical trials up to February 2014. Eligible studies included prospective RCTs that directly compared patients with cancer treated with and without bevacizumab. A total of 12,917 patients from 17 RCTs were included in our analysis. Patients treated with bevacizumab had a significantly increased risk of cerebrovascular events compared with patients treated with control medication, with a relative risk of 3.28 (95% CI, 1.97-5.48). The risks of CNS ischemic events and CNS hemorrhage were increased compared with control, with RRs of 3.22 (95% CI, 1.71-6.07) and 3.09 (95% CI, 1.36-6.99), respectively. Risk varied with the bevacizumab dose, with RRs of 3.97 (95% CI, 2.15-7.36) and 1.96 (95% CI, 0.76-5.06) at 5 and 2.5 mg/kg/week, respectively. Higher risks were observed in patients with metastatic colorectal cancer (RR, 6.42; 95% CI, 1.76-35.57), and no significant risk was observed in other types of tumors. In conclusion, the addition of bevacizumab significantly increased the risk of cerebrovascular events compared with controls, including CNS ischemic events and CNS hemorrhage. The risk may vary with bevacizumab dose and tumor type.

Growth arrest-specific gene 6 protein promotes the proliferation and migration of endothelial progenitor cells through the PI3K/AKT signaling pathway.

Endothelial progenitor cells (EPCs) play an important role in endothelial repair and vascular regeneration. Growth arrest-specific gene 6 (Gas6) is a novel key regulator of the vascular system, which is linked to a number of cardiovascular diseases. However, the effects of Gas6 on EPCs have not been elucidated to date. The present study was designed to determine the biological function of EPCs treated with Gas6 and to eludicate the underlying mechanisms. EPCs were isolated from umbilical cord blood and treated with various concentrations (25, 50, 100 and 200 ng/ml) of Gas6. The proliferation, migration and angiogenesis of the Gas6-treated EPCs were evaluated by MTT assay, Transwell assay and in vitro tube formation assay, respectively. The phosphorylation status of AKT and ERK was evaluated by western blot analysis. The results demonstrated that treatment with Gas6 enhanced the proliferation and migration of the EPCs in a dose-dependent manner. However, Gas6 did not promote the differentiation of EPCs on Matrigel. Gas6 induced the phosphorylation of AKT, but not that of ERK. The enhanced proliferation and migration induced by Gas6 was markedly suppressed by the inhibitor of PI3K but not by that of ERK. These results suggest that Gas6 activates the AKT signaling pathway, which, in turn, promotes the proliferation and migration of EPCs.

Pylorus-preserving versus pylorus-resecting pancreaticoduodenectomy for periampullary and pancreatic carcinoma: a meta-analysis.

BACKGROUND: The aim of this meta-analysis was to compare the long-term survival, mortality, morbidity and the operation-related events in patients with periampullary and pancreatic carcinoma undergoing pylorus-preserving pancreaticoduodenectomy (PPPD) and pylorus-resecting pancreaticoduodenectomy (PRPD). METHOD: A systematic search of literature databases (Cochrane Library, PubMed, EMBASE and Web of Science) was performed to identify studies. Outcome measures comparing PPPD versus PRPD for periampullary and pancreatic carcinoma were long-term survival, mortality, morbidity (overall morbidity, delayed gastric emptying [DGE], pancreatic fistula, wound infection, postoperative bleeding, biliary leakage, ascites and gastroenterostomy leakage) and operation related events (hospital stays, operating time, intraoperative blood loss and red blood cell transfusions). RESULTS: Eight randomized controlled trials (RCTs) including 622 patients were identified and included in the analysis. Among these patients, it revealed no difference in long-term survival between the PPPD and PRPD groups (HR = 0.23, p = 0.11). There was a lower rate of DGE (RR = 2.35, p = 0.04, 95% CI, 1.06-5.21) with PRPD. Mortality, overall morbidity, pancreatic fistula, wound infection, postoperative bleeding, biliary leakage, ascites and gastroenterostomy leakage were not significantly different between the groups. PPPDs were performed more quickly than PRPDs (WMD = 53.25 minutes, p = 0.01, 95% CI, 12.53-93.97); and there was less estimated intraoperative blood loss (WMD = 365.21 ml, p = 0.006, 95% CI, 102.71-627.71) and fewer red blood cell transfusions (WMD = 0.29 U, p = 0.003, 95% CI, 0.10-0.48) in patients undergoing PPPD. The hospital stays showed no significant difference. CONCLUSIONS: PPPD had advantages over PRPD in operating time, intraoperative blood loss and red blood cell transfusions, but had a significantly higher rate of DGE for periampullary and pancreatic carcinoma. PPPD and PRPD had comparable mortality and morbidity including pancreatic fistulas, wound infections, postoperative bleeding, biliary leakage, ascites and gastroenterostomy leakage. Our conclusions were limited by the available data. Further evaluations of high-quality RCTs are needed.

Angiogenesis inhibitor bevacizumab increases the risk of ischemic heart disease associated with chemotherapy: a meta-analysis.

Concerns have arisen regarding the risk of ischemic heart disease with the novel antiangiogenic agent bevacizumab, a recombinant humanised monoclonal antibody to the vascular endothelial growth factor that is widely used in cancer treatment. Currently, the role of bevacizumab in ischemic heart disease is controversial. This meta-analysis was therefore performed to assess the overall risk of ischemic heart disease associated with the use of bevacizumab. The databases of PubMed, EMBASE and Web of Science were searched for English language studies of randomised controlled trials comparing bevacizumab with control therapy published through October 25, 2012. Summary incidence rates, relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random-effects or fixed-effects models based on the heterogeneity of the included studies. A total of 4,617 patients from 7 randomised controlled trials were identified and included for analysis. Among those patients receiving bevacizumab, the summary incidence of ischemic heart disease was 1.0% (95% CI, 0.6%-1.4%). Patients treated with bevacizumab had a significantly increased risk of ischemic heart disease with an RR of 2.49 (95% CI, 1.37-4.52) compared with controls. In addition, both high doses and low doses of bevacizumab increased the risk of cardiac ischemia (low dose at 2.5 mg/kg per week: RR, 2.14 [95% CI, 1.09-4.19]; high dose at 5 mg/kg per week: RR, 4.81 [95% CI, 1.03-22.42]). Bevacizumab was also found to significantly increase the risk of cardiac ischemia in patients with colorectal cancer (RR, 2.13; 95% CI, 1.11-4.06) compared with controls. This meta-analysis shows the use of bevacizumab was associated with an increased risk of developing ischemic heart disease in colorectal cancer patients receiving this drug. Our conclusions are limited by the available data. Further evaluations of high-quality RCTs are needed.

Apolipoprotein a5 gene polymorphism and risk for metabolic syndrome: a meta-analysis.

BACKGROUND: Many studies have focused on the association between the apolipoprotein A5 (ApoA5) polymorphism and the risk of metabolic syndrome (MetS). However, these studies drew inconsistent conclusions. The aim of this study was to evaluate the exact association between the ApoA5 polymorphism and MetS in a large-scale meta-analysis. METHODS: The PubMed, Embase, and Science Citation Index (ISI Web of Science) databases were searched to collect all publications on the association between the ApoA5 polymorphism and MetS. Two common variants of ApoA5 (namely -1131T>C in the promoter region and c.56C>G in the coding region) with the risk of MetS were analyzed. The overall odd ratios (ORs) and 95% confidence intervals (CIs) for -1131T>C (CC+TC) versus TT genotype and c.C56G (GG+GC) versus CC were assessed between the MetS and control group. Subgroup analysis was further performed by ethnicity. The meta-analysis was performed by Stata11.0. RESULTS: Twelve studies from 10 publications were chosen in our meta-analysis. The combined results showed that C allele carriers (CC+TC) of -1131T>C had a significantly higher risk of MetS for the overall (OR=1.32; 95% CI: 1.14-1.53; p=0.000) with moderate heterogeneity (I2=54.9%, p=0.014). Subgroup analysis was further performed according to ethnicity, and the association was still significant in Asians (OR=1.42; 95% CI: 1.25-1.62; p=0.000), but not in white populations (OR=1.25; 95% CI: 0.97-1.61; p=0.087). When analyzing the association between c.C56G and MetS, the G allele carrier (GG+GC) genotype significantly increased the risk of MetS (OR=1.32; 95% CI: 1.15-1.50; p=0.000) in white populations. No significant publication bias was observed in either -1131T>C or c.C56G. CONCLUSIONS: Our study suggested that the ApoA5 -1131T>C polymorphism was significantly associated with the risk of MetS in Asians, but not in white populations. However, the c.C56G polymorphism was significantly associated with MetS in white populations.