OBJECTIVE:The mortality risk among patients with diabetes is increasingly severe, yet the relationship between obesity and mortality risk in these patients remains controversial. This study evaluated the Conicity index (C-index), an indicator of abdominal obesity, to determine its value in predicting cardiovascular disease (CVD) and all-cause mortality in patients with diabetes. METHODS:This cross-sectional study utilized NHANES 1999-2018 data. Patients were grouped into quartiles based on the C-index. The relationship between the C-index and mortality risk was assessed using Cox proportional hazards regression models and restricted cubic spline (RCS) analysis. RESULTS:A total of 7694 patients with diabetes were included in the study. The obesity rate was 55.7 %, with an average follow-up duration of 88 months. During this period, 588 CVD deaths and 2094 all-cause deaths occurred. Higher C-index quartiles were associated with increased mortality risks, with hazard ratios for all-cause mortality ranging from 1.00 to 2.29 and for CVD mortality from 1.00 to 2.23. Unadjusted RCS analysis showed a linear positive correlation between the C-index and mortality risks. After adjusting for confounding factors, a non-linear positive correlation was observed between the C-index and all-cause mortality risk, particularly when the C-index exceeded 1.40. Subgroup analysis revealed that the relationship between the C-index and all-cause mortality was more significant in men and nonobese patients. CONCLUSIONS:The C-index is a valuable predictor of mortality in patients with diabetes. A C-index above 1.40, being male, and being nonobese are associated with a more significant risk of all-cause mortality.

Objective Diabetic foot ulcers (DFUs) pose significant clinical challenges, with gas therapy emerging as a promising intervention. However, the comparative efficacy of various gas therapy modalities remains unclear. This study evaluates the effectiveness of different gas therapies, particularly hyperbaric oxygen therapy (HBOT), in improving DFU outcomes. Methods We searched three major databases, PubMed, Embase, and the Cochrane Library, for randomized controlled trials (RCTs) published up to March 3, 2024, assessing the efficacy of different gas therapies in managing DFUs. Primary outcomes included ulcer healing and area reduction rates, while secondary outcomes encompassed healing time, amputation rate, and adverse events. A network meta-analysis was performed using R, with surface under the cumulative ranking curve (SUCRA) values calculated to rank therapies. Results A total of 34 RCTs involving 2,268 DFUs were included in this analysis. HBOT ranked highest for the healing rate (SUCRA = 0.8 14) and area reduction rate (SUCRA = 0.730) but also had a higher amputation rate (SUCRA = 0.621). Except for carbon dioxide therapy, HBOT demonstrated significantly greater healing rates than standard of care (SOC) (mean difference (MD) = −2.71, 95% confidence interval (CI) [−4.85 to −1.34]) and topical oxygen therapy (MD = −2.03, 95% CI [−4.50 to −0.32]), while pairwise comparisons among other gaseous therapies were non-significant (P > 0.05). For wound area reduction, HBOT was superior to SOC (MD = 0.39, 95% CI [0.11–0.67]), whereas differences among other gaseous therapies remained non-significant (P > 0.05). There was substantial heterogeneity in the area reduction rate in net work analysis (I2 = 87%). Subgroup analyses revealed greater area reduction in DFUs treated with HBOT when the treatment duration exceeded six weeks. Conclusions HBOT improves ulcer healing and area reduction rates in DFU patients; however, its association with higher amputation rates warrants cautious use, considering resource availability. Given the limited number and quality of included studies, further high-quality research is needed to validate these findings.

Objective: The combination of epithelial growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) and immune checkpoint inhibitors (ICIs) leads to an increased incidence of severe immune-related adverse events (irAEs). However, the mechanisms underlying macrophages in irAEs have not been elucidated. Methods: An osimertinib and ICI-induced irAE mouse model was constructed. Lung micro-CT scans were used to assess the degree of inflammatory infiltration. Hematoxylin-eosin staining was used to analyze the histopathologic inflammatory infiltration in mouse liver and lung tissues. Flow cytometry was used to detect the percentages of T cells, NK cells, and macrophages and the expression of EGFR. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum interleukin (IL)-6, alanine transaminase (ALT), ferritin, and tumor necrosis factor (TNF)-α levels. Total RNA extracted from mouse liver macrophages was analyzed by RNA-seq. Simple Western blot analysis was used to detect the IL-6/JAK/STAT3 pathway activation state. Results: Osimertinib combined with ICIs upregulated EGFR expression on macrophages with increased serum IL-6, ALT, and ferritin levels. RNA-seq and simple Western blot analysis of mouse liver macrophages confirmed that that the IL-6/JAK/STAT3 pathway was activated in the combination treatment group. Ruxolitinib blocked the IL-6/JAK/STAT3 pathway and significantly decreased the serum IL-6, ALT, and ferritin levels in the combination treatment group. Conclusions: An osimertinib and ICI-induced irAE mouse model was constructed that showed osimertinib combined with ICIs inhibited EGFR phosphorylation and activated the IL-6/JAK/STAT3 signaling pathway in mouse liver macrophages, which led to the release of relevant cytokines.

Background Abnormalities in glucose and lipid metabolism contribute to the progression and exacerbation of type 2 diabetes mellitus (T2DM). Fish oil and probiotics are dietary supplements that have the potential to improve glucose and lipid metabolism. However, their efficacy remains unclear in T2DM patients. Methods PubMed, Embase, and the Cochrane Library were retrieved to collect randomized controlled trials (RCTs) on the efficacy of fish oil or probiotic supplementation in T2DM patients from the database inception to December 13, 2023. Primary outcome indicators encompassed glycated hemoglobin (HbA1c), homeostatic model assessment for insulin resistance (HOMA-IR) and blood lipid profile (triglyceride (TG) and total cholesterol (TC). Secondary outcome indicators included inflammatory markers such as tumor necrosis factor -α (TNF-α) and adipocytokine (including leptin and adiponectin). The R software was used for statistical analysis, and GraphPad Prism was used for figure rendering. Results A total of 60 RCTs involving 3845 T2DM patients were included in the analysis. The results showed that the probiotics ( Bifidobacterium, Lactobacillus, Lactococcus, Propionibacterium, etc . ) were more effective in reducing HOMA-IR than fish oil (Surca = 0.935). Bifidobacterium demonstrated the highest efficacy in reducing HbA1c levels (Surca = 0.963). Regarding lipid metabolism, fish oil was superior to probiotics in lowering TG and TC levels (Surca values of 0.978 and 0.902, respectively). Furthermore, fish oil outperformed probiotics in reducing TNF-α (Surca = 0.839) and leptin (Surca = 0.712), and increasing adiponectin levels (Surca = 0.742). Node-splitting analysis showed good consistency (P > 0.05 for direct, indirect, and network comparison across various interventions). Conclusions In T2DM patients, fish oil was more effective than probiotics in regulating lipid metabolism. Probiotics outperformed fish oil in regulating glucose metabolism particularly; specifically, Bifidobacterium showed higher efficacy in reducing blood glucose.

The combination of epithelial growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) and immune checkpoint inhibitors (ICIs) leads to an increased incidence of severe immune-related adverse events (irAEs). Macrophages express epidermal growth factor receptor (EGFR), and play an important role in irAEs. However, the underlying mechanisms of EGFR-positive macrophages in irAEs have not been elucidated. In this study, we constructed an irAE mouse model induced by osimertinib combined with ICIs, and explore the role of EGFR-positive macrophages in irAEs. Our results found there was no significant difference in the degree of histopathological inflammatory infiltration and the percentage of macrophages in the ICIs group or the osimertinib + ICIs group, but osimertinib + ICIs increased the expression of EGFR on macrophages, accompanying with increased serum levels of interleukin (IL)-6, alanine transaminase (ALT) and ferritin. RNA-seq and Simple Western blot confirmed that IL-6/JAK/STAT3 pathway was activated in macrophages of osimertinib + ICIs group. Ruxolitinib could significantly decrease serum levels of IL-6, ALT and ferritin in oxitinib + ICIs group. Taken together, we successfully constructed an irAE mouse model induced by osimertinib combined with ICIs, and found that osimertinib increased immune checkpoint inhibitors-related severe adverse events via activating the IL-6/JAK/STAT3 pathway of EGFR-positive macrophages.

Background Our previous studies have confirmed that Honokiol exerts protective effect on cardiomyocytes and cardiac tissue against ATO-induced cardiotoxicity, which is attributed to inhibiting cardiomyocyte apoptosis via reduced oxidative stress.Objectives This research aimed to explore the entire mechanism by which Honokiol provides protection against arsenic trioxide-induced cardiotoxicity.Materials and methods 129S1/SvImJ male wild type (WT) mice and SIRT3-knockout (SIRT3−/−) mice with 129S1 background were applied to verify the pathway of Honokiol on myocardial toxicity of arsenic trioxide; MitoSox, carboxy-DCFDA and Amplex Red were used to detect oxidative stress; ferroptosis-associated markers (MDA, GSH, tissue iron, GPX4 and 4-HNE expression) were tested by test kit or immunohistochemistry; autophagic flux was analyzed by western blot.Results SIRT3 knockout abolishes protective effects of HKL in ATO-induced myocardial injury and hypertrophy; Honokiol protects myocardium from ATO-induced oxidative stress through SIRT3/SOD2 pathway; Honokiol inhibited ATO-induced ferroptosis via the SIRT3 pathway in myocardial tissues; Honokiol improve autophagic flux in cardiomyocytes exposed to ATO treatment. Autophagic flux plays a critical role in protective effect of Honokiol on ATO-induced ferroptosis. The present study confirmed that Honokiol inhibits oxidative stress injury and ferroptosis in cardiomyocytes by promoting the autophagic flux in cardiomyocytes through the activation of SIRT3.

BackgroundWith the increasing incidence of diabetes, diabetic foot ulcer(DFU) has become one of the most common and serious complications in people with diabetes. DFU is associated with significant morbidity and mortality, and can also result in significant economic, social and public health burdens. Due to peripheral neuropathy, peripheral vascular disease, hyperglycemic environment, inflammatory disorders and other factors, the healing of DFU is impaired or delayed, resulting in the formation of diabetic chronic refractory ulcer. Because of these pathological abnormalities in DFU, it may be difficult to promote wound healing with conventional therapies or antibiotics, whereas platelet-rich plasma(PRP) can promote wound healing by releasing various bioactive molecules stored in platelets, making it more promising than traditional antibiotics. Therefore, the purpose of this systematic review is to summarize and analyze the efficacy of PRP in the treatment of DFU.MethodsA literature search was undertaken in PubMed, CNKI, EMB-ASE, the Cochrane Library, the WanFang Database and the WeiPu Database by computer. Included controlled studies evaluating the efficacy of PRP in the treatment of diabetic foot ulcers. The data extraction and assessment are on the basis of PRISMA.ResultsTwenty studies were evaluated, and nineteen measures for the evaluation of the efficacy of PRP in DFU treatment were introduced by eliminating relevant duplicate measures. The efficacy measures that were repeated in various studies mainly included the rate of complete ulcer healing, the percentage of ulcer area reduction, the time required for ulcer healing, wound complications (including infection rate, amputation rate, and degree of amputation), the rate of ulcer recurrence, and the cost and duration of hospitalization for DFU, as well as subsequent survival and quality of life scores. One of the most important indicators were healing rate, ulcer area reduction and healing time. The meta-analysis found that PRP was significantly improve the healing rate(OR = 4.37, 95% CI 3.02-6.33, P < 0.001) and shorten the healing time(MD = -3.21, 95% CI -3.83 to -2.59,P < 0.001)of patients with DFU when compared to the conventional treatment, but there was no significant difference in reducing the of ulcer area(MD = 5.67, 95% CI -0.77 to 12.11,P =0.08>0.05 ).ConclusionThe application of PRP to DFU can improve ulcer healing rate and shorten ulcer healing time, but more clinical data are needed to clarify some efficacy measures. At the same time, a standardized preparation process for PRP is essential.

OBJECTIVETo compare the benefits and harms of drug treatments for adults with type 2 diabetes, adding non-steroidal mineralocorticoid receptor antagonists (including finerenone) and tirzepatide (a dual glucose dependent insulinotropic polypeptide (GIP)/glucagon-like peptide-1 (GLP-1) receptor agonist) to previously existing treatment options.DESIGNSystematic review and network meta-analysis.DATA SOURCESOvid Medline, Embase, and Cochrane Central up to 14 October 2022. ELIGIBILITY CRITERIA FOR SELECTING STUDIESEligible randomised controlled trials compared drugs of interest in adults with type 2 diabetes. Eligible trials had a follow-up of 24 weeks or longer. Trials systematically comparing combinations of more than one drug treatment class with no drug, subgroup analyses of randomised controlled trials, and non-English language studies were deemed ineligible. Certainty of evidence was assessed following the GRADE (grading of recommendations, assessment, development and evaluation) approach.RESULTSThe analysis identified 816 trials with 471 038 patients, together evaluating 13 different drug classes; all subsequent estimates refer to the comparison with standard treatments. Sodium glucose cotransporter-2 (SGLT-2) inhibitors (odds ratio 0.88, 95% confidence interval 0.83 to 0.94; high certainty) and GLP-1 receptor agonists (0.88, 0.82 to 0.93; high certainty) reduce all cause death; non-steroidal mineralocorticoid receptor antagonists, so far tested only with finerenone in patients with chronic kidney disease, probably reduce mortality (0.89, 0.79 to 1.00; moderate certainty); other drugs may not. The study confirmed the benefits of SGLT-2 inhibitors and GLP-1 receptor agonists in reducing cardiovascular death, non-fatal myocardial infarction, admission to hospital for heart failure, and end stage kidney disease. Finerenone probably reduces admissions to hospital for heart failure and end stage kidney disease, and possibly cardiovascular death. Only GLP-1 receptor agonists reduce non-fatal stroke; SGLT-2 inhibitors are superior to other drugs in reducing end stage kidney disease. GLP-1 receptor agonists and probably SGLT-2 inhibitors and tirzepatide improve quality of life. Reported harms were largely specific to drug class (eg, genital infections with SGLT-2 inhibitors, severe gastrointestinal adverse events with tirzepatide and GLP-1 receptor agonists, hyperkalaemia leading to admission to hospital with finerenone). Tirzepatide probably results in the largest reduction in body weight (mean difference -8.57 kg; moderate certainty). Basal insulin (mean difference 2.15 kg; moderate certainty) and thiazolidinediones (mean difference 2.81 kg; moderate certainty) probably result in the largest increases in body weight. Absolute benefits of SGLT-2 inhibitors, GLP-1 receptor agonists, and finerenone vary in people with type 2 diabetes, depending on baseline risks for cardiovascular and kidney outcomes (https://matchit. magicevidence.org/230125dist-diabetes/#!/).CONCLUSIONSThis network meta-analysis extends knowledge beyond confirming the substantial benefits with the use of SGLT-2 inhibitors and GLP-1 receptor agonists in reducing adverse cardiovascular and kidney outcomes and death by adding information on finerenone and tirzepatide. These findings highlight the need for continuous assessment of scientific progress to introduce cutting edge updates in clinical practice guidelines for people with type 2 diabetes. SYSTEMATIC REVIEW REGISTRATIONPROSPERO CRD42022325948.

Background: Hepatic ischemia-reperfusion (IR) injury is the primary reason for complications following hepatectomy and liver transplantation (LT). Insulin-induced gene 2 (Insig2) is one of several proteins that anchor the reticulum in the cytoplasm and is essential for metabolism and inflammatory responses. However, its function in IR injury remains ambiguous.Methods: Insig2 global knock-out (KO) mice and mice with adeno-associated-virus8 (AAV8)-delivered Insig2 hepatocyte-specific overexpression were subjected to a 70% hepatic IR model. Liver injury was assessed by monitoring hepatic histology, inflammatory responses, and apoptosis. Hypoxia/reoxygenation stimulation (H/R) of primary hepatocytes and hypoxia model induced by cobalt chloride (CoCl2) were used for in vitro experiments. Multi-omics analysis of transcriptomics, proteomics, and metabolomics was used to investigate the molecular mechanisms underlying Insig2.Results: Hepatic Insig2 expression was significantly reduced in clinical samples undergoing LT and the mouse IR model. Our findings showed that Insig2 depletion significantly aggravated IR-induced hepatic inflammation, cell death and injury, whereas Insig2 overexpression caused the opposite phenotypes. The results of in vitro H/R experiments were consistent with those in vivo. Mechanistically, multi-omics analysis revealed that Insig2 is associated with increased antioxidant pentose phosphate pathway (PPP) activity. The inhibition of glucose-6-phosphate-dehydrogenase (G6PD), a rate-limiting enzyme of PPP, rescued the protective effect of Insig2 overexpression, exacerbating liver injury. Finally, our findings indicated that mouse IR injury could be attenuated by developing a nanoparticle delivery system that enables liver-targeted delivery of substrate of PPP (glucose 6-phosphate).Conclusions: Insig2 has a protective function in liver IR by upregulating the PPP activity and remodeling glucose metabolism. The supplementary glucose 6-phosphate (G6P) salt may serve as a viable therapeutic target for alleviating hepatic IR.

Background Increased arterial stiffness is common in patients with diabetes, and inflammation is one of the main causes of increased arterial stiffness. Platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), and monocyte-to-lymphocyte ratio (MLR) are novel inflammatory markers that are reproducible, widely available, and easy to measure, and are associated with low costs. This study sought to investigate the predictive value of these novel inflammatory markers in patients with diabetes having arterial stiffness. Methods We retrospectively included inpatients with diabetes mellitus from the Endocrinology Department of the Chengdu Fifth People’s Hospital from June 2021 to May 2022 and collected data on their general information, biochemical indicators, and brachial-ankle pulse wave velocity (baPWV). After propensity matching, the risk relationship between PLR, NLR, and MLR and arterial stiffness was assessed in the recruited patients. Results A total of 882 hospitalized patients with diabetes were included in this study and categorized into the low baPWV (507 cases) or high baPWV group (375 cases) based on the baPWV. After propensity matching, there were 180 patients in all in the high and low baPWV groups. Univariate and multivariate logistic regression analyses revealed that high PLR, NLR, and MLR were independently associated with an increased risk of arterial stiffness in patients with diabetes. In the receiver operating characteristic curve analysis, the NLR area under the curve (AUC) was 0.7194 (sensitivity = 84.4%, specificity = 51.1%) when distinguishing low baPWV and high baPWV in patients with diabetes, which was higher than that for PLR AUC (0.6477) and MLR AUC (0.6479), and the combined diagnosis for AUC. Conclusions NLR was superior to PLR, and MLR and combined diagnosis have certain predictive values that indicate the increase in arterial stiffness in patients with diabetes. These predictive values can help with the early identification of increased arterial stiffness in patients with diabetes.

Glucose and lipid metabolism disorders caused by insulin resistance (IR) can lead to metabolic disorders such as diabetes, obesity, and the metabolic syndrome. Early and targeted intervention of IR is beneficial for the treatment of various metabolic disorders. Although significant progress has been made in the development of IR drug therapies, the state of the condition has not improved significantly. There is a critical need to identify novel therapeutic targets. Mitophagy is a type of selective autophagy quality control system that is activated to clear damaged and dysfunctional mitochondria. Mitophagy is highly regulated by various signaling pathways, such as the AMPK/mTOR pathway which is involved in the initiation of mitophagy, and the PINK1/Parkin, BNIP3/Nix, and FUNDC1 pathways, which are involved in mitophagosome formation. Mitophagy is involved in numerous human diseases such as neurological disorders, cardiovascular diseases, cancer, and aging. However, recently, there has been an increasing interest in the role of mitophagy in metabolic disorders. There is emerging evidence that normal mitophagy can improve IR. Unfortunately, few studies have investigated the relationship between mitophagy and IR. Therefore, we set out to review the role of mitophagy in IR and explore whether mitophagy may be a potential new target for IR therapy. We hope that this effort serves to stimulate further research in this area.

Introduction: As a severe and specific neurovascular complication of type 2 diabetes mellitus (T2DM), diabetic retinopathy (DR) remains the leading cause of vision loss and preventable blindness in adults aged 20 to 74. The pathogenesis of DR is not completely understood, however, studies indicate that chronic inflammation plays a significant role. Emerging evidence suggests that the neutrophil-to-lymphocyte ratio (NLR), the platelet-to-lymphocyte ratio (PLR), and the monocyte-to-lymphocyte ratio (MLR) are novel potential inflammatory response markers. The purpose of this study was to investigate the relationships between the NLR, PLR, MLR, and DR. Patients and Methods: 290 patients who had been diagnosed with T2DM participated in the study. Patients were categorized into three groups: 142 control subjects with T2DM, 124 subjects with nonproliferative diabetic retinopathy (NPDR), and 24 patients with proliferative diabetic retinopathy (PDR). Characteristics, laboratory data, as well as NLR, PLR and MLR levels of the study groups were compared. Results: In patients with DR, the median NLR, PLR, and MLR were significantly higher than in patients without DR (p = 0.012, p < 0.001, and p = 0.043, respectively). In the post hoc analysis, there was no correlation between the severity of retinopathy and the increase in NLR or PLR. Multiple logistic regression revealed that the PLR was an independent risk factor for DR (odds ratio [OR]: 1.020, 95% confidence interval [CI]: 1.010-1.029 p = 0.026). Based on the receiver operating characteristic (ROC) curve, the cutoff value of PLR as an indicator for diagnosing DR was estimated to be 129.65, with a sensitivity and specificity of 53.4% and 76.1%, respectively, and an area under the curve of 0.668 (95% CI: 0.605-0.730, p < 0.001). Conclusion: Our findings suggest that PLR may be an independent risk factor for evaluating DR in type 2 diabetes patients.

目的:评价社区运用亚洲人骨质疏松自我筛查工具(OSTA)、国际骨质疏松基金会(IOF)骨质疏松风险一分钟测试题筛查骨质疏松症的效果.方法:选取2020年5-8月400例成都某社区绝经后妇女和年龄大于50岁的男性为研究对象.设计问卷调查表,收集受试者基本人口学资料、病史资料、骨质疏松症相关危险因素,并对400例受试者进行OSTA评分、IOF骨质疏松风险一分钟测试题及双能X线骨密度(DEX)测定.比较单独或联合运用亚洲人骨质疏松自我筛查工具(OSTA)、IOF骨质疏松风险一分钟测试题筛查骨质疏松症的诊断价值.结果:单独运用OSTA、IOF骨质疏松风险一分钟测试题作为筛查标准时ROC曲线下面积分别是0.742、0.676,切点值分别是:-2.7、6.5,其敏感度分别为64.50％、62.30％,特异度分别为68.60％、62.50％,具有一定的诊断价值.多因素回归分析方程为:Y=-0.278OSTA+0.360IOF-2.746.OSTA联合IOF骨质疏松风险一分钟测试题作为筛查标准时,ROC曲线下面积是0.779,Y=-6.1748,此时敏感度为73.10％,特异度为70.20％.当OSTA≤-2.7或IOF骨质疏松风险一分钟测试题评分≤6.5满足其中之一即可诊断为骨质疏松症,其敏感度为77.84％,特异度为62.05％;当OSTA≤-2.7和IOF骨质疏松风险一分钟测试题评分≤6.5同时满足时即诊断为骨质疏松症,其敏感度为26.14％,特异度为96.43％.结论:单独或联合运用亚洲人骨质疏松自我筛查工具、IOF骨质疏松风险一分钟测试题筛查骨质疏松症具有一定的诊断价值.

目的 以双能X线骨密度(DEX)测定为诊断骨质疏松症的金标准,评价IOF骨质疏松风险一分钟测试题(IOF)、定量超声骨密度(QUS-T)诊断骨质疏松症(OP)的切点值及单独或联合运用筛查骨质疏松症的诊断价值,以期找到更为行之有效的骨质疏松症筛查工具,为该人群骨质疏松症的早期诊断提供参考和依据.方法 选取400名成都社区绝经后妇女和年龄大于50岁的男性为研究对象,设计问卷调查表,收集受试者基本人口学资料、病史资料、骨质疏松症相关危险因素,并对400名受试者进行IOF骨质疏松风险一分钟测试题、定量超声骨密度测定及双能X线骨密度(DEX)测定.结果 单独运用IOF、QUS-T作为筛查标准时ROC曲线下面积分别是0.676、0.832,切点值分别是:6.5、-2.75,其约登指数分别是0.278、0.527,具有一定的诊断价值;IOF联合QUS-T作为筛查标准时,ROC曲线下面积是0.834,以Y=23.196,此时灵敏度为64.8％,特异性为91.1％,约登指数为0.559;QUS-T与IOF并联时即满足IOF≥6.5或QUS-T≤-2.75其中之一即可诊断为骨质疏松症,其灵敏度为77.84％,特异性为76.79％,约登指数为0.546;串联即同时满足IOF≥6.5和QUS-T≤-2.75即诊断为骨质疏松症,其灵敏度为29.55％,特异性为96.43％,约登指数为0.260,具有较高的诊断价值.结论 单独或联合运用IOF骨质疏松风险一分钟测试题、定量超声骨密度筛查骨质疏松症具有一定的诊断价值,但仍有待进一步验证.