艾塞那肽治疗肥胖2型糖尿病患者的效果观察

目的 本研究旨在评估艾塞那肽对口服药物治疗效果欠佳的肥胖2型糖尿病患者的血糖、胰岛素抵抗、胰岛素B细胞功能和脂代谢的影响.方法 所选病例为2010年4月至2011年4月于解放军二五二医院内分泌科门诊及住院服用二甲双胍和(或)磺脲类促泌剂血糖控制不佳的肥胖[体质量指数(BMI)25 ～40 kg/m2]2型糖尿病(T2DM)[糖化血红蛋白(HbA1c) ＞7.0％]患者56例.随机分为对照组及艾塞那肽治疗组;两组原有降糖药物及治疗方案不变,原生活方式不变,治疗组前4周,艾塞那肽5 μg2次/d,皮下注射;后8周,艾塞那肽10 μg2次/d,皮下注射.对照组不加用其他辅助降糖药物,记录12周后患者血压、体质量、体质量指数(BMI)、空腹血糖(FPG)及餐后2h血糖(2HPG)、HbA1c、空腹胰岛素(FINS)、血甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C).结果 治疗12周后治疗组FPG、2HPG、HbA1c、FINS、BMI和胰岛素抵抗指数(HOMA-IR)与对照组比较差异均有统计学意义(t值分别为8.721、9.019、7.790、3.054、4.206、-3.102,P均＜0.05).治疗12周后血脂方面,治疗组TC及LDL-C较对照组无明显下降,差异均无统计学意义(P均＞0.05),治疗组TG、HDL-C与对照组比较,差异均有统计学意义(t值分别为3.487、-6.053,P均＜0.05).结论 艾塞那肽能降低肥胖T2DM患者体质量、改善糖代谢、改善脂代谢、改善胰岛素抵抗及胰岛细胞功能.     

二甲双胍致2型糖尿病老年患者低血糖昏迷

1例82岁男性患者,有2型糖尿病痛史15年,一直服用消渴丸5粒,3次/d治疗.3个月前开始改服二甲双胍0.25 g,2次/d治疗.近1周患者开始出现乏力,入院前5 h突然出现意识不清,四肢痉挛、抽搐,眼球上翻、牙关紧闭等症状.查体:浅昏迷,颈部及四肢肌张力增高,双侧巴彬斯基征阳性.血糖:1.70 mmol/L,头颅CT检查仪示老年性脑改变.诊断为低血糖昏迷.立即给予10%葡萄糖注射液500 ml静脉滴注,30 min后患者抽搐停止,意识逐渐恢复.停用二甲双胍,给予阿卡波糖,患者血糖波动在5.6～10.8 mmol/L,未再出现低血糖症状.     

肿胀注射法治疗直肠脱垂的临床观察(附23例报告)

目的探讨直肠外盆腔内、直肠黏膜肠壁粘连固定肿胀注射术治疗直肠脱垂的疗效。方法对23例直肠脱垂患者采用肿胀注射法治疗的临床资料作回顾性分析。结果本组患者全部临床治愈,随访3个月至2年,无复发,无并发症及后遗症。结论应用0.75%聚桂醇注射液直肠窝组织间隙、直肠和肛管黏膜下肿胀注射,形成无菌性炎症,粘连及纤维化,可有效地固定直肠肛管,配合提肛锻炼是治疗直肠脱垂安全有效的方法。     

短节段固定融合术治疗退变性腰椎侧凸合并腰椎管狭窄疗效观察

目的探讨短节段固定融合术治疗退变性腰椎侧凸(DLS)合并腰椎管狭窄的手术策略、影像学及临床疗效。方法选择性减压、短节段固定融合术治疗68例DLS合并腰椎管狭窄患者,比较患者术前及末次随访时的Cobb角、腰椎前凸角、冠状面躯干偏移及矢状面躯干偏移。以Oswestry功能障碍指数(ODI)评估患者功能改善情况。结果患者均获得随访,时间36~60个月。Cobb角术前12°~28°(15.9°±4.6°),末次随访3.6°~9.8°(5.2°±3.1°);腰椎前凸角术前1.2°~3.3°(1.9°±2.9°),末次随访-28.1°~4.6°(-23.6°±3.7°);冠状面躯干偏移术前8.2~13.7(10.8±5.2)mm,末次随访2.8~5.6(4.3±1.8)mm;矢状面躯干偏移术前10.2~15.6(12.6±3.7)mm,末次随访3.1~6(4.6±2.2)mm;ODI评分术前25.2~29.8(27.6±2.1)分,末次随访2.1~4.2(3.6±1.3)分。以上各项指标末次随访与术前比较差异均有统计学意义(P0.05)。术后早期并发症发生率为7.3%。末次随访时未发现钉棒松动或断裂等情况。结论对于冠状面Cobb角30°且躯干失平衡较小的DLS合并腰椎管狭窄患者,行选择性减压、短节段固定融合可获得良好的中期临床疗效。     

MicroRNA-491-5p调控基质金属蛋白酶9参与退变性腰椎侧凸的发病机制

BACKGROUND: MicroRNAs are widely involved in the regulation of protein expression, and play a critical role in many physiological and pathological processes in the body. But microRNA expression profile in degenerative lumbar scoliosis is rarely reported and understood. OBJECTIVE: To compare the microRNA expression profile in the normal intervertebral disc and degenerative lumbar scoliosis and to identify degenerative lumbar scoliosis-specific microRNAs, followed by functional validation. METHODS: Total RNA samples were extracted from the nucleus pulposus tissues of 57 patients with degenerative lumbar scoliosis as experimental groups and the normal nucleus pulposus tissues of 42 patients with lumbar fractures as control group. An initial screening of differentially expressed microRNAs in the nucleus pulposus tissues by microRNA microarray was performed in 10 samples from each group. Subsequently, differentially expressed microRNAs were validated using real-time quantitative RCR. The level of differentially expressed microRNAs in the degenerative nucleus pulposus tissues was investigated. Then, the functional analysis of microRNAs in regulating collagen II expression was carried out. Western blot and luciferase reporter assay were also used to detect target genes. RESULTS AND CONCLUSION: We identified 22 microRNAs that were differentially expressed (17 upregulated and 5 downregulated) in degenerative lumbar scoliosis patients compared with the controls. Following real-time quantitative RCR confirmation, miR-491-5p was significantly down-regulated in degenerative nucleus pulposus tissues in comparison with the controls. Moreover, its level was closely correlated with the pathological grading of disc degeneration. Overexpression of miR-491-5p promoted type II collagen expression in nucleus pulposus cells. Bioinformatics target prediction identified matrix metalloproteinase-9 as a putative target of miR-491-5p. Furthermore, luciferase reporter assays demonstrated that miR-491-5p directly targeted matrix metalloproteinase-9 and affected its protein expression in nucleus pulposus cells. These results show that the downregulation of miR-491-5p induces type II collagen loss by directly targeting matrix metalloproteinase-9, thereby resulting in degeneration of the intervertebral disc and degenerative lumbar scoliosis. This study also underscores the potential of miR-491-5p as a novel therapeutic target in degenerative lumbar scoliosis.