1例因血糖控制不佳的T2 DM患者,入院后停用格列齐特、加用阿卡波糖、二甲双胍,将重组甘精胰岛素等剂量转换为原研甘精胰岛素,胰岛素逐渐减量,由18U减至14U,血糖达标.结论:重组甘精胰岛素转换为原研甘精胰岛素,减量后仍实现血糖达标.

糖尿病酮症酸中毒(DKA)是糖尿病主要急性并发症之一,其诱因包括感染、饮食或治疗不当及各种应激因素导致胰岛素缺乏,主要见于1型糖尿病(T1DM)患者.高甘油三酯血症(hypertriglyceridemia, HTG)是中国人群最常见的脂质代谢异常,凡引起血浆中乳糜微粒和(或)极低密度脂蛋白(very low density lipoprotein,VLDL)升高的原因均可导致HTG.胰岛素缺乏可导致脂肪分解产生过多的脂肪酸,甘油三酯(TG)合成增加.TG水平超过11.29 mmol/L定义为重度HTG,其中部分患者合并脂蛋白脂酶(lipoprotein lipase, LPL)、载脂蛋白(apolipoprotein, APO)等基因变异.单一基因突变在个体中的表达并出现有意义的病理生理学改变在临床上并不鲜见,而同时存在LPL和APO A5基因突变却未见报道.我们在一例反复发生DKA的患者体内发现了LPL和APO A5基因同时发生了错义突变,现报道如下.

Objective In recent years,the incidence of papillary thyroid carcinoma(PTC)increased gradually and the recurrence and metastasis of PTC patients are also increasing.The aim of this study was to investigate the effect of BRAFV600E mutation on the expression of HMGB1 in PTC,to explore the mechanism of BRAF gene affecting the development and prognosis of PTC,and then guiding clinical practice of precise therapy.Methods The preoperative serum and postoperative fresh tissue were collected from 44 cases of PTC patients in our hospital from September,2015 to December,2015.According to BRAFV600E mutations divided into positive group and negative group.Western blot,immunohistochemistry and fluorescence quantitative PCR were used to detect the level of HMGB1 in cancer tissues.The level of HMGB1 in serum was tested by ELISA method.Western blot was performed using Image J software.The relative quantitative method was used to calculate the fluorescence quantitative PCR data.The concentration of HMGB1 protein in serum was calculated by ELISA Calc regression/fit calculation program.All the data were analyzed by SPSS 20.0.Western blot,fluorescence quantitative PCR and ELISA data were analyzed by Chi-square test,Mann-Whitney-Wilcoxon test and independent sample t test.The relationship between lymph node metastasis and extrathyroid infiltration and the occurrence of BRAFV600E mutation was analyzed by chi-square test.Results In PTC cancer tissues,HMGB1 was mainly located in the cytoplasm,the levels of HMGB1mRNA and protein in positive group were lower than that of the negative group(Z =2.117,P ＜0.01,x2 =19.989,P ＜ 0.05),and the change did not show in peripheral blood(t =1.135,P ＞ 0.05).The expression of HMGB1 mRNA and protein in PTC with lymph node metastasis was lower than those without lymph node metastasis(Z =-2.216,P ＜0.05;t =-2.217,P ＜ 0.05),and so as in the extrathyroid infiltration(Z =-2.267,P ＜ 0.05;t =-3.885,P ＜ 0.01).Conclusion BRAFV600E mutations may accelerate the malignant development of PTC by down regulating the expression of HMGB1.

患者男，61岁，因“口干、多饮3 a，双下肢麻木5个月余”于2014年2月25日入院。患者3 a前测空腹血糖为10．48 mmol／L，诊断为“糖尿病”，开始应用口服降糖药物（二甲双胍、格列美脲），5个月前患者无明显诱因出现双下肢麻木，呈进行性加重，逐渐出现站立、行走不稳，伴关节酸痛，于当地医院营养神经治疗后无明显减轻转到我院就诊。既往高血压病史4 a。家族史无特殊。查体：T 36．3℃， P 68次／min，R 17次／min， BP 110／70 mmHg， BMI 20．2 kg／m2，体型消瘦，皮肤黝黑，以双侧乳晕处皮肤色素沉着为著，多毛。无眼睑水肿，口唇无发绀。甲状腺Ⅰ°肿大，质韧，无压痛。左侧乳房增生。心肺未见异常。腹软，无压痛、反跳痛。肝肋下可触及，肝肾区无叩击痛，无移动性浊音。四肢末梢皮温低，痛、温、触觉减退，双侧肌力Ⅳ级、肌张力正常，双下肢无水肿，足背动脉搏动减弱。生理反射存在，病理反射未引出。血清HbA1c为6．3％。血清FT3、FT4轻度降低， TSH 正常。血清性激素水平大致正常。8 am时血清促肾上腺皮质激素（ ACTH ）水平为128．4 pg／mL，皮质醇：479．19 nmol／L；4 pm时分别为39．5 pg／mL、291 nmol／L。肿瘤标志物：癌胚抗原（CEA）0．5 ng／mL、甲胎蛋白（AFP）2．01 ng／mL、糖类抗原72-4（ CA72-4）1．60 ng／mL、糖类抗原19-9（CA19-9）1．54 U／mL、神经元特异性烯醇化酶（NSE）4．60 ng／mL，均正常。铁蛋白水平为228 ng／mL。 ALT水平为75．0 U／L，AST水平为40．2 U／L。血免疫球蛋白κ轻链水平为409 mg／dL。尿免疫球蛋白κ轻链水平为2．13 mg／dL。尿本周氏蛋白阴性。肌电图显示神经源性损害。超声检查发现脾大，颈部淋巴结肿大。腰椎间盘CT图像显示腰椎间盘突出（ L5／S1，后外侧型，向左）。骨扫描显示四肢关节退行性变。患者入院后给予降糖（伏格列波糖片、格列齐特片缓释片、阿卡波糖片）、保肝（阿托莫兰）、营养神经（甲钴铵、硫辛酸、恩经复）等对症治疗，患者下肢周围神经病变症状改善不理想，且出现双下肢轻度凹陷性水肿，并逐渐向上延伸至腰骶部。经本院多学科会诊，考虑POEMS 综合征可能性大，进一步行骨髓穿刺（图1）示：增生骨髓象，粒、红两系可，巨核数可，血小板可见；骨髓活检（图2）示：浆细胞及浆样细胞比例增高，散在及灶状分布，胞浆略丰富，核偏位，偶见双核，骨髓中约有10％左右的单克隆增生性浆细胞。遂明确诊断为POEMS综合征。与患者及家属沟通使用激素治疗，患者欲向上级医院就诊，故转院。

目的探讨痛风患者肾结石发病情况及其影响因素。方法分析400例痛风患者的肾结石发病情况及其影响因素,并与400例非痛风者进行对照。结果痛风患者的肾结石发病率22.50%,明显高于非痛风者的3.75%(P<0.01);痛风患者的不同尿酸水平及尿酸排泄分数与肾结石发病无明显关系(P>0.05)。Logistic回归分析显示,痛风患者的肾结石与其年龄、血糖及尿酸水平呈正相关(P均<0.05)。结论痛风患者易发生肾结石,且与其年龄、血糖及尿酸水平相关。