Association of MetS status and number of metabolic components with incident gastric cancer.

Subgroup analyses of the association between metabolic syndrome and gastric cancer risk.

Sensitivity analyses of the association between metabolic syndrome and gastric cancer risk.

Restricted cubic spline analyses of individual metabolic components and gastric cancer risk.

Flow diagram of the participant's enrollments

Risk of gastric cancer according to individual metabolic component categories.

Association between metabolic syndrome defined using IDF criteria and gastric cancer risk by anatomical subsite.

Association between MetS and gastric cancer risk by anatomic subsite.

Risk of gastric cancer per 1-SD increase in individual metabolic components.

Baseline characteristics according to MetS category.

Association of metabolic syndrome defined using IDF criteria and number of metabolic components with incident gastric cancer.

OBJECTIVE:There is an urgent need for novel biomarkers that are inexpensive, effective and easily accessible to complement the early diagnosis of hepatocellular carcinoma. This study aimed to analyze the relationship between serum gamma-glutamate-transpeptidase to platelet ratio, alkaline phosphatase-to-platelet ratio index, fibrosis index based on four factors and the risk of hepatocellular carcinoma, and to determine the optimal cut-offs for predicting hepatocellular carcinoma.METHODS:Based on a prospective cohort study, 44 215 participants who were cancer-free at baseline (2011-13) were included in the study. Cox proportional hazard models and receiver operating characteristics curves were used to analyze the diagnostic value and optimal cut-off value of gamma-glutamyl-transpeptidase to platelet ratio, alkaline phosphatase-to-platelet ratio index and fibrosis index based on four factors in predicting hepatocellular carcinoma patients.RESULTS:Gamma-glutamyl-transpeptidase to platelet ratio, alkaline phosphatase-to-platelet ratio index and fibrosis index based on four factors can be used as early independent predictors of hepatocellular carcinoma risk. The risk of hepatocellular carcinoma in the fourth quantile of gamma-glutamyl-transpeptidase to platelet ratio and alkaline phosphatase-to-platelet ratio index was 4.04 times (hazard ratio = 4.04, 95% confidence interval: 2.09, 7.80) and 2.59 times (hazard ratio = 2.59, 95% confidence interval: 1.45, 4.61), respectively, compared with the first quantile. With fibrosis index based on four factors first quantile as a reference, fibrosis index based on four factors fourth quantile had the highest risk (hazard ratio = 18.58, 95% confidence interval: 7.55, 45.72). Receiver operating characteristic results showed that fibrosis index based on four factors had a stronger ability to predict the risk of hepatocellular carcinoma (area under curve = 0.81, 95% confidence interval: 0.80, 0.81), and similar results were shown for gender stratification. In the total population, the optimal cut-off values of gamma-glutamyl-transpeptidase to platelet ratio, alkaline phosphatase-to-platelet ratio index and fibrosis index based on four factors were 0.208, 0.629 and 1.942, respectively.CONCLUSIONS:Gamma-glutamyl-transpeptidase to platelet ratio, alkaline phosphatase-to-platelet ratio index and fibrosis index based on four factors were independent predictors of hepatocellular carcinoma risk. Amongst them, fibrosis index based on four factors shows a stronger predictive ability for hepatocellular carcinoma risk, and gamma-glutamyl-transpeptidase to platelet ratio and alkaline phosphatase-to-platelet ratio index can be used as complementary indicators.

[目的]探索常规循环肝功能标志物与结直肠癌发病风险的关系.[方法]采用巢式病例对照研究,剔除基线慢性结肠炎、肠息肉和恶性肿瘤患者及基本资料不全者,以金昌队列3次随访期间新发结直肠癌患者145例为病例组,以随访未发生结直肠癌的人群作为对照来源,根据同期随访、基线年龄±2岁和同性别进行1∶4个体匹配,获得对照组580名,最终纳入725名研究对象.通过条件Lo-gistic 回归分析探究常规循环肝功能标志物与结直肠癌发病风险的关系,计算比值比(odds ratio,OR)及其95％置信区间(confidence interval,CI),采用限制性立方样条分析相关因素与结直肠癌发病的剂量-反应关系.[结果]研究对象平均年龄为61.24岁,男性占比71.72％.多因素条件Logistic回归分析结果显示,在调整混杂因素后,发现总胆红素第2四分位数组研究对象发生结直肠癌的风险是第1四分位数组的0.490倍(OR=0.490,95％CI:0.273～0.879),处于白蛋白第2、3、4四分位数组的研究对象发生结直肠癌的风险分别较处于第1四分位数组的研究对象降低41.6％(OR=0.584,95％CI:0.342～0.996)、42.9％(OR=0.571,95％CI:0.337～0.970)和 42.7％(OR=0.573,95％CI:0.330～0.996).对结直肠癌发病部位进行分区,以白蛋白第1四分位数组为对照,第3、4四分位数组的个体发生结肠癌的风险分别降低 66.6％(OR=0.334,95％CI:0.139～0.804)和 80.7％(OR=0.193,95％CI:0.066～0.566).未发现白蛋白与直肠癌发病风险之间具有统计学意义.白蛋白与结直肠癌发病风险之间存在明显的负向线性剂量-反应关系(P总趋势＜0.050,P非线性=0.191),结直肠癌发病风险随白蛋白的升高而降低.[结论]白蛋白和总胆红素水平的升高与结直肠癌发病风险降低相关,且白蛋白与结直肠癌的发病风险存在剂量-反应关系.白蛋白与结肠癌发病风险存在较强的负相关性,而与直肠癌不存在关联.

Objective To evaluate the correlation between metabolic syndrome (MetS) and its components on the incidence of colorectal cancer (CRC) based on data from Jinchang Cohort. Methods This is a large prospective cohort study. Between 2011 and 2020, a total of 43 516 individuals from Jinchang Cohort were included for this study. Hazard ratios (HRs) with 95% confidence intervals (CIs) for CRC according to MetS were calculated with the Cox proportional hazard models. The restricted cubic spine models with four knots were conducted to fit the dose-response relationships. Results MetS was associated with increased risk of CRC (n = 141; HR: 1.64, 95% CI: 1.15–2.33) after adjusting for confounding factors (age, sex, education level, family history of CRC, smoking index and alcohol index). Participants with hyperglycemia had a significantly higher risk of developing incident CRC (HR: 1.70; 95% CI: 1.19–2.43). The positive association between MetS and CRC was observed in males (HR: 1.76; 95% CI: 1.17–2.63), but not in females (HR: 1.24; 95% CI: 0.59–2.64). Furthermore, linear dose-response relationship was found between fasting plasma glucose (FPG) and CRC risk in males ( P overall < 0.05, P non-linear = 0.35). When stratified by smoke and drink, MetS was found to increase the incidence of CRC only in the smoke (HR: 2.07, 95% CI: 1.35–3.18) and drink (HR: 2.93, 95% CI: 1.51–5.69) groups. Conclusion MetS was associated with a higher risk of CRC incidence. Hyperglycemia lended strong support to the role of MetS in new-onset CRC, especially in males. Other components of MetS were not found to be associated with increased risk of CRC.

目的 基于队列入群研究心源性猝死(sudden cardiac death,SCD)的影响因素,为SCD的预防和病因学研究提供科学依据.方法 采用巢式病例对照研究的方法,以金昌队列2011-2019年三次随访新发52例SCD者为病例组,按照年龄(±2岁)及同性别1∶4个体匹配的方法,以同期随访未发生SCD者的208例为对照组.用条件logistic回归分析模型分析金昌队列人群发生SCD的影响因素,并通过限制性立方样条(restricted cubic spline,RCS)模型拟合SCD发病风险的剂量-反应关系曲线.结果 多因素条件logistic回归分析模型分析结果显示:三酰甘油(triglycerides,TG)(OR=2.94,95％CI:1.15～7.51)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)(OR=2.70,95％CI:1.18～6.22)、糖尿病(OR=5.59,95％CI:1.79～17.46)和心电图异常(OR=5.54,95％CI:2.11～14.56)是SCD的危险因素;文化程度在高中及以上(OR=0.33,95％CI:0.12～0.88)是SCD的保护因素.RCS结果显示:空腹血糖(fasting plasma glucose,FPG)、TG与SCD发病风险间呈正向线性剂量-反应关系(P总趋势＜0.05,P非线性＞0.05).结论 TG、LDL-C、糖尿病、心电图异常和文化程度与SCD的发生有关且FPG、TG与SCD的发生风险间存在线性剂量-反应关系.

目的 探索女性人群乳腺癌发病的影响因素,为乳腺癌的防治提供科学依据.方法 基于金昌队列,以2014-2020年中3次随访新发乳腺癌者96例为病例组,按照年龄(±2岁)1∶2个体匹配的方法,以同期随访未发生癌症的192例为对照组.采用条件Logistic回归模型、限制性立方样条模型及相乘和相加交互模型探讨乳腺癌发病的影响因素及因素间的交互作用.结果 多因素条件Logistic回归模型结果显示体重指数(BMI)≥24kg.m-2、血清低密度脂蛋白胆固醇(LDL-C)水平异常的人群乳腺癌发病风险增加,分别是BMI＜24kg·m-2组、LDL-C水平正常组的1.87倍(OR=1.87,95％CI:[1.05,3.34])、2.66倍(OR=2.66,95％CI:[1.39,5.08]),且LDL-C及BMI水平与乳腺癌发病风险间存在正向线性剂量-反应关系(LDL-C:总趋势P=0.001,非线性P=0.413;BMI:总趋势P＜0.001,非线性P=0.376),但未发现两者的交互作用.结论 超重/肥胖和LDL-C异常是乳腺癌发病的危险因素,且BMI、LDL-C和乳腺癌的发病风险间存在正向线性剂量-反应关系.

Background: The risk of hepatocellular carcinoma (HCC) is associated with a variety of factors. However, the possible association between the abnormal metabolism of fasting plasma glucose (FPG) and alanine aminotransferase (ALT) and the risk of HCC has not been widely studied. We examined this relationship based on a prospective cohort study.Methods: 162 first-attack HCC cases during three follow-up periods (2014-2020) were selected as the case group. A control group of 648 participants was obtained by 1:4 matching of age (+/- 2 years) and sex with noncancer participants in the same period. Conditional logistic regression models, restricted cubic spline models, additive interaction models, and generalized additive models were used to explore the effects of FPG and ALT on the risk of HCC.Results: After correction for confounding factors, we found that abnormal FPG and elevated ALT increased the risk of HCC, respectively. Compared with the normal FPG group, the risk of HCC was significantly increased in the impaired fasting glucose (IFG) (OR = 1.91, 95 %CI: 1.04, 3.50) and diabetes groups (OR = 2.12, 95 %CI: 1.24, 3.63). Compared with the lowest quartile of ALT, subjects in the fourth quartile had an 84 % increased risk of HCC (OR = 1.84, 95 %CI: 1.05-3.21). Moreover, there was an interaction between FPG and ALT on the risk of HCC, and 74 % of the HCC risk could be attributed to their synergistic effect (AP = 0.74, 95 %CI: 0.56-0.92).Conclusion: Abnormal FPG and elevated ALT are independent risk factors for HCC, and they have a synergistic effect on the risk of HCC. Therefore, serum FPG and ALT levels should be monitored to prevent the development of HCC.

Aims To quantify the trajectories from normoglycaemia to pre-diabetes, subsequently to type 2 diabetes mellitus (T2DM), cardiovascular diseases (CVD), and cardiovascular death, and the effects of risk factors on the rates of transition. Methods and results We used data from the Jinchang Cohort of 42 585 adults aged 20-88 free of coronary heart disease (CHD) and stroke at baseline. A multistate model was applied for analysing the progression of CVD and its relation to various risk factors. During a median follow-up of 7 years, 7498 participants developed pre-diabetes, 2307 developed T2DM, 2499 developed CVD, and 324 died from CVD. Among 15 postulated transitions, transition from comorbid CHD and stroke to cardiovascular death had the highest rate (157.21/1000 person-years), followed by transition from stroke alone to cardiovascular death (69.31/1000 person-years) and transition from pre-diabetes to normoglycaemia (46.51/1000 person-years). Pre-diabetes had a sojourn time of 6.77 years, and controlling weight, blood lipids, blood pressure, and uric acid within normal limits may promote reversion to normoglycaemia. Among transitions to CHD alone and stroke alone, transition from T2DM had the highest rate (12.21/1000 and 12.16/1000 person-years), followed by transition from pre-diabetes (6.81/1000 and 4.93/1000 person-years) and normoglycaemia (3.28/1000 and 2.39/1000 person-years). Age and hypertension were associated with an accelerated rate for most transitions. Overweight/obesity, smoking, dyslipidaemia, and hyperuricaemia played crucial but different roles in transitions. Conclusion Pre-diabetes was the optimal intervention stage in the disease trajectory. The derived transition rates, sojourn time, and influence factors could provide scientific support for the primary prevention of both T2DM and CVD. Lay summary Former single-outcome studies on the relationship between glycaemia and cardiovascular disease (CVD) may ignore the complexity and multi-transformations across the multiple stages from normoglycaemia to CVD in real-world setting. We aimed to quantify the trajectories from normoglycaemia to pre-diabetes, subsequently to type 2 diabetes, CVD, and cardiovascular death.Pre-diabetes was the optimal intervention stage in the disease trajectory.Transitions from CVD to death had much higher rates than other transitions.Age and hypertension were associated with an accelerated rate for most transitions. Overweight/obesity, smoking, dyslipidaemia, and hyperuricaemia played crucial but different roles in transitions.

Background and aims: Studies have shown that elevated serum uric acid (SUA) may increase the risk of coronary heart disease (CHD). However, it is still disputable how mediate ef-fects between metabolic diseases and hyperuricemia affect the incidence of CHD. This study aimed to explore whether metabolic diseases may mediate the connection from hyperuricemia at baseline to the elevated incidence risk of CHD during follow-ups. Methods and Results: Based on the Jinchang cohort, 48 001 subjects were followed for 9 years be-tween June 2011 and December 2019. Multivariate-adjusted Cox regression models were applied to estimate hazard ratios (HRs) of CHD with 95% confidence intervals (CIs). Significantly increased risks of CHD were observed in hyperuricemia (HR:1.46, 95%CI:1.2 8, 1.67) when compared with normouricemia population. The mediating effect model further demonstrated that metabolic diseases could mediate the association between hyperuricemia and CHD patho-genesis, partially for the combined metabolic diseases with mediation effects of 45.12%, 25.24% for hypertension, 28.58% for overweight or obese status, 29.05% for hypertriglyceridemia, 6.70% for hypercholesterolemia, 3.52% for low high density lipoprotein cholesterol (HDL-C), and 6.51% for high low density lipoprotein cholesterol (LDL-C), respectively. Conclusions: Hyperuricemia significantly increased the risk of incident CHD, and this association was partly mediated by metabolic diseases. & COPY; 2022 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Ital-ian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.

目的 了解金昌队列随访人群2011-2020年循环系统疾病死亡率及早死概率的变化趋势,为制定循环系统疾病的防控策略提供依据.方法 收集金昌队列随访人群2011年1月1日-2020年12月31日死于循环系统疾病的相关数据,通过计算粗死亡率(CDR)、年龄标化死亡率(ASMR)、早死概率等指标分析该人群循环系统疾病的10年死亡率和早死概率的变化趋势.结果 金昌队列随访人群2011-2020年因循环系统疾病死亡1 387例,CDR 为 283.22/10 万,ASMR 为 161.80/10 万,循环系统疾病 10 年 CDR 呈上升趋势(APC=10.02％,t=5.80,P＜0.01).金昌队列随访人群2011-2020年循环系统疾病核心病种为脑卒中和冠心病,CDR分别为128.44/10万和84.33/10万,ASMR分别为73.02/10万和47.88/10万,此2种疾病死亡数占循环系统疾病死亡数的75.13％,其中冠心病10年CDR呈上升趋势(APC=17.90％,t=5.83,P＜0.01).金昌队列随访人群2011-2020年循环系统疾病的早死概率为1.46％,其中脑卒中为1.21％,冠心病为1.03％.结论 金昌队列随访人群2011-2020年循环系统疾病死亡率有所上升,核心病种为脑卒中和冠心病,其中冠心病的死亡率及早死概率上升明显.