Zhao Jinlong, Liang Guihong, Luo Miaohui, Yang Weiyi, Xu Nanjun, Luo Minghui, Pan Jianke, Liu Jun, Zeng Lingfeng
The Second Clinical Medical College of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou 510120, China.
Heliyon. 2022 Oct 8;8(10):e11001. doi: 10.1016/j.heliyon.2022.e11001. eCollection 2022 Oct.
Diabetic microangiopathy is a type of vascular dysfunction. The effect of type 2 diabetes microangiopathy (DMA) on bone mineral density (BMD) and bone metabolism is still unclear.
A meta-analysis was performed to investigate the effects of microangiopathy on BMD and bone metabolism in type 2 diabetic patients.
We searched the PubMed, Embase, Cochrane Library and CNKI databases to identify observational studies investigating the effects of type 2 diabetes microangiopathy on BMD or bone metabolism. The time limit for the literature retrieval was from the establishment of the database to September 25, 2021. The Newcastle-Ottawa scale (NOS) and the Agency for Healthcare Research and Quality (AHRQ) scale were used to evaluate the quality of the studies. RevMan 5.3 software was used for the data analysis. Stata 14.0 was used to quantitatively evaluate the publication bias of the outcome indicators.
In total, 12 observational studies were included, including 7 cohort studies, 4 case-control studies and 1 cross-sectional study. In total, 2,500 patients with type 2 diabetes were included. Among them, 1,249 patients had microangiopathy (DMA group), and 1,251 patients did not have microangiopathy (control group). The results of the meta-analysis showed that the BMDs of the femoral neck (SMD = -1.34, 95% CI = -2.22 to -0.45, P = 0.003), lumbar spine (SMD = -0.69, 95% CI = -1.31 to -0.08, P = 0.03) and Ward's triangle (SMD = -2.84, 95% CI = -4.84 to -0.83, P = 0.006) in the DMA group were lower than those in the control group. In the comparison of the bone metabolism indexes, the contents of N-terminal propeptide of type I procollagen (P1NP) (SMD = 0.18, 95% CI = 0.03 to 0.32, P = 0.02), osteocalcin (SMD = 6.97, 95% CI = 3.46 to 10.48, P < 0. 0001), parathyroid hormone (PTH) (SMD = 0.38, 95% CI = 0.03 to 0.73, P = 0.03) and C-telopeptide of type 1 collagen (CTX) (SMD = 0.39, 95% CI = 0.03 to 0.75, P = 0.03) in serum from the DMA group were higher than those in serum from the control group. The serum content of 25-hydroxyvitamin D (25(OH)D) (SMD = -0.63, 95% CI = -1.19 to -0.07, P = 0.03) in the DMA group was lower than that in the control group. There was no significant difference in serum alkaline phosphatase (ALP), calcium or phosphorus between the two groups (P > 0.05).
Type 2 diabetes microangiopathy can reduce the lumbar spine, femoral neck and Ward's triangle BMD and has a higher risk of osteoporosis or osteoporosis fractures. The levels of P1NP, PTH, CTX and OC in the serum of patients with type 2 diabetes microangiopathy are higher, and the lower 25(OH)D content may be a mechanism by which DMA destroys bone metabolism balance.
糖尿病微血管病变是一种血管功能障碍。2型糖尿病微血管病变（DMA）对骨密度（BMD）和骨代谢的影响仍不清楚。
进行一项荟萃分析，以研究微血管病变对2型糖尿病患者BMD和骨代谢的影响。
我们检索了PubMed、Embase、Cochrane图书馆和中国知网数据库，以识别调查2型糖尿病微血管病变对BMD或骨代谢影响的观察性研究。文献检索的时间限制为从数据库建立到2021年9月25日。使用纽卡斯尔-渥太华量表（NOS）和医疗保健研究与质量局（AHRQ）量表来评估研究质量。使用RevMan 5.3软件进行数据分析。使用Stata 14.0对结果指标的发表偏倚进行定量评估。
总共纳入了12项观察性研究，包括7项队列研究、4项病例对照研究和1项横断面研究。总共纳入了2500例2型糖尿病患者。其中，1249例患者患有微血管病变（DMA组），1251例患者没有微血管病变（对照组）。荟萃分析结果显示，DMA组的股骨颈骨密度（标准化均数差[SMD]=-1.34，95%置信区间[CI]=-2.22至-0.45，P=0.003）、腰椎骨密度（SMD=-0.69，95%CI=-1.31至-0.08，P=0.03）和沃德三角区骨密度（SMD=-2.84，95%CI=-4.84至-0.83，P=0.006）低于对照组。在骨代谢指标比较中，DMA组血清中I型前胶原N端前肽（P1NP）（SMD=0.18，95%CI=0.03至0.32，P=0.02）、骨钙素（SMD=6.97，95%CI=3.46至10.48，P<0.0001）、甲状旁腺激素（PTH）（SMD=0.38，95%CI=0.03至0.73，P=0.03）和I型胶原C端肽（CTX）（SMD=0.39，95%CI=0.03至0.75，P=0.03）的含量高于对照组。DMA组血清25-羟维生素D（25(OH)D）含量（SMD=-0.63，95%CI=-1.19至-0.07，P=0.03）低于对照组。两组血清碱性磷酸酶（ALP）、钙或磷水平无显著差异（P>0.05）。
2型糖尿病微血管病变可降低腰椎、股骨颈和沃德三角区的骨密度，骨质疏松或骨质疏松性骨折风险较高。2型糖尿病微血管病变患者血清中P1NP、PTH、CTX和OC水平较高，较低的25(OH)D含量可能是DMA破坏骨代谢平衡的一种机制。
