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低钠血症是指血浆(或血清)的钠浓度低于135mmol/L,常伴有血浆渗透压下降。临床上通过血钠的测定不难发现低钠血症,但单纯的限水、补钠治疗有时并不能使血钠水平完全恢复正常,应积极寻找低钠血症的病因,才能有效地纠正低钠血症。我们以2例低钠血症的诊治经过为例,探讨低钠血症的诊治策略。  相似文献   
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糖尿病是一组以糖代谢紊乱为主要表现的临床综合征.2型糖尿病主要由胰岛素抵抗和胰岛素分泌不足所致.随着肥胖、高热量饮食、体力活动不足等现象日益普遍,2型糖尿病的患病率逐年增加[1].目前,糖尿病药物治疗虽日趋成熟,却仍无法达到根治效果,很多糖尿病患者需要终生接受药物治疗,而且随着糖尿病病程的进展,胰腺β细胞进行性破坏,许多患者最终需要使用胰岛素.近年来,人们发现,减肥手术对2型糖尿病患者高血糖的控制具有显著且持久的效果,越来越多的临床研究支持这一观点.  相似文献   
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目的 本文探讨基质细胞趋化因子1α (stromal cell-derived factor-1,SDF-1α)对人肾小管上皮细胞(HK细胞)细胞外基质(Ⅳ型胶原)表达的影响.方法 不同浓度的葡萄糖培养HK细胞,分为正常葡萄糖组(NG组:含5.5 mmol/L葡萄糖)和高糖组(HG组:含25.0 mmol/L葡萄糖),分别用转化生长因子β1 (TGF-β1)和SDF-1α干预HK细胞12h,再分为空白对照组(NC组)、阴性对照组(DMSO组)、T组(TGF-β1组)、S组(SDF-1α组)、T+S组(TGF-β1和SDF-1α共同干预组),采用实时定量聚合酶链反应(RT-PCR)和Western blotting分别检测Ⅳ型胶原mRNA和蛋白的表达.两组间比较采用t检验.结果 (1)HK细胞能持续表达SDF-1α和其受体CXCR4 mRNA.高糖条件下SDF-1α和CXCR4mRNA表达呈时间梯度增加,24 h两者表达量达到高峰.24 h CXCR4 mRNA表达量是12h表达量的1.2倍(t=6.08,P<0.05),SDF-1αmRNA表达量是12h的1.58倍(t=7.52,P<0.05).(2)高糖条件下SDF-1α抑制HK细胞Ⅳ型胶原mRNA和蛋白的表达,并能降低由TGF-β1诱导的Ⅳ型胶原表达.S+T组Ⅳ型胶原mRNA表达量是T组的0.33倍(t=12.57,P<0.05),蛋白表达量是T组的0.47倍(t=14.23,P<0.05).但在正常葡萄糖条件下,SDF-1α对由TGF-β1诱导的Ⅳ型胶原表达没有影响.(3)TGF-β1促进HK细胞Ⅳ型胶原mRNA和蛋白表达,高糖条件下其促进作用更为显著.T组Ⅳ型胶原mRNA是正常对照组的6.63倍(t=19.21,P<0.05),蛋白表达量是其2.59倍(t=15.71,P<0.05).结论 高糖条件下SDF-1α能减轻TGF-β1诱导的HK细胞Ⅳ型胶原表达,可能由此改善肾脏纤维化.TGF-β1促进HK细胞Ⅳ型胶原的表达,促进肾脏纤维化的发生发展.  相似文献   
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垂体促甲状腺激素(TSH)腺瘤是临床罕见病,年发病率不足1/100万[1],占垂体瘤的0.5%~3.0%[2]。复旦大学附属华山医院2006—2011年诊断TSH腺瘤仅8例[3]。TSH腺瘤导致的甲亢症状不常见,若出现易误诊为原发性甲亢,尤其是弥漫性毒性甲状腺肿(Graves病),给予抗甲亢药物或甲状腺大部切除或放射碘治疗,不仅不能使中枢性甲亢得到控制。  相似文献   
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甲状腺激素抵抗综合征(resistance to the thyroid hormone,RTH)又称甲状腺激素不敏感综合征(thyroid hormone insensitivity syndrome,THIS),是由于甲状腺激素受体(thyroid hormone receptor,TR)基因突变,或甲状腺激素(t...  相似文献   
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The aim of this study was to assess the effects and safety of salicylates on type 2 diabetes mellitus (T2DM). We searched six databases (Cochrane Central Register of Controlled Trials, MED- LINE, EMBASE, CBM, CNKI and VIP) for all randomized controlled trials (RCTs) and self-control studies which investigated the effects of salicylates on T2DM. We included 34 RCTs and 17 self-control studies involving 13 464 patients with T2DM. It was demonstrated that salicylates had obvious effects on several parameters for patients with T2DM. (1) Any dose of salicylates could significantly reduce HbA1c level [mean difference (MD) -0.39%; 95% CI -0.47 to -0.32] in RCTs, but only high doses of salicylates (≥3000 mg/day) could effectively reduce fasting plasma glucose (FPG) level [standardized mean difference (SMD) -1.05; 95% CI -1.47 to -0.62] for patients with T2DM in both RCTs and self-control studies. Furthermore, high doses of salicylates could also increase plasma fasting insulin level (MD 12.20 mU/L; 95% CI 3.33 to 21.07); (2) In both RCTs and self-control studies, high doses of salicylates could significantly reduce plasma triglycerides concentration. The results for RCTs were MD -0.44 mmol/L, 95% CI -0.71 to -0.18, and those for self-control studies were 227±29 mg/dL (pre-treatment) and 117±8 mg/dL (post-treatment) (P=0.009); (3) All trials which reported cardiovascu- lar events were RCTs using low doses (<1000 mg/day) of salicylates, and it was revealed that aspirin could significantly reduce the risk of myocardial infarction (OR 0.73; 95% CI 0.57 to 0.92); (4) Two RCTs and two self-control studies with ≥3000 mg/day salicylates reported adverse effects, and the over- all effects were mild, and tinnitus occurred most frequently. No evidence of gastrointestinal bleeding was found in all these studies. In conclusion, from our systematic review, the anti-diabetic effect of salicylates is in a dose-dependent manner. High doses of salicylates may have beneficial effects on re- ducing FPG, HbA1c level and increasing fasting insulin concentration, and may also have some positive effects on lipidemia and inflammation-associated parameters for patients with T2DM, without serious adverse effects.  相似文献   
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正垂体促甲状腺激素(TSH)腺瘤是临床罕见病,年发病率不足1/100万~([1]),占垂体瘤的0.5%~3.0%~([2])。复旦大学附属华山医院2006—2011年诊断TSH腺瘤仅8例~([3])。TSH腺瘤导致的甲亢症状不常见,若出现易误诊为原发性甲亢,尤其是弥漫性毒性甲状腺肿(Graves病),给予抗甲亢药物或甲状腺大部切除或放射碘治疗,不仅不能使中枢性甲亢得到控制,反而导  相似文献   
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 目的:2型糖尿病(type 2 diabetes, T2D)时大脑出现胰岛素水平下降及胰岛素信号通路下调,使大脑海马tau蛋白出现过度磷酸化的阿尔茨海默病(Alzheimer disease,AD)样改变。本研究选取2型糖尿病大鼠,皮下注射及鼻腔滴入胰岛素,观察大脑AD样病变的改变,并探讨其机制。方法:高糖、高脂、高蛋白喂饲3个月后链脲佐菌素腹腔注射制备T2D大鼠模型。运用2种方法干预:鼻腔滴入胰岛素(T2D+I-I)及皮下注射胰岛素(T2D+S-I)。检测血浆葡萄糖、血浆胰岛素和脑脊液胰岛素水平,免疫印记方法检测大脑海马总tau蛋白和tau蛋白部分位点磷酸化状态、胰岛素信号转导途径中关键酶磷脂酰肌醇3-激酶(phosphatidylinositol 3-kinase, PI3K)/Akt及糖原合成激酶3β(glycogen synthase kinase 3β, GSK-3β)活性。结果:T2D组大鼠血浆葡萄糖及胰岛素水平显著升高,脑脊液胰岛素水平显著降低,大脑海马组织中tau蛋白呈过度磷酸化状态,PI3K/Akt活性下降, GSK-3β磷酸化水平升高; T2D+I-I组大鼠血浆胰岛素及葡萄糖水平无显著改变,但大脑海马tau蛋白过度磷酸化状态显著好转,PI3K/Akt活性显著升高,GSK-3β活性显著下降; T2D+S-I组大鼠血糖显著下降,但血浆及脑脊液胰岛素水平无显著改变,大脑海马tau蛋白磷酸化水平有轻度改善,但变化不显著。结论:运用鼻腔滴入胰岛素可减轻T2D时大脑海马组织的AD样病变;外周皮下胰岛素注射对T2D时AD样病变无明显作用。  相似文献   
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目的:本研究检测2型糖尿病患者外周白细胞中端粒长度及端粒酶活性,并运用降糖药磷酸西格列汀干预2个月,分析其与年龄、病程、胰岛素抵抗、血糖控制水平的相关性,探讨磷酸西格列汀对初发糖尿病患者B细胞保护的可能机制。方法:以41例正常对照组(control,CTL)和32例初发糖尿病患者组(type 2diabetes,T2D)为研究对象,葡萄糖氧化酶法检测空腹静脉血糖(fasting plasma glucose,FPG),电化学发光法检测空腹静脉胰岛素水平(fasting insulin,FIN),测量体重指数(bodymass index,BMI),根据FPG及FIN评估胰岛素抵抗程度(HOMA-IR)。提取研究对象外周白细胞,southernblots法检测细胞内端粒长度,TRAP-ELISA检测端粒酶活性。结果:2组研究对象年龄、性别、BMI具可比性。T2D组端粒长度较CTL组明显减短,端粒酶活性变化不显著。T2D组中相关分析结果显示,端粒长度与年龄显著相关。经2个月的磷酸西格列汀干预后,端粒长度逐渐增加,而端粒酶活性仍无显著改变。结论:初发糖尿病中,磷酸西格列汀可能是通过改善减短的端粒长度来保护B细胞。  相似文献   
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