抗甲状腺药引起粒细胞缺乏症12例救治分析

甲状腺功能亢进症采用抗甲状腺药物 (ＡＴＤ)治疗 ,有的患者可引起白细胞减少 ,甚至出现粒细胞缺乏的严重毒副反应 ,危及病人生命。本文分析了我院 1995～ 2 0 0 0年因抗甲状腺药物引起粒细胞缺乏症而收住的 12例病人 ,现就其临床表现、抢救措施分析讨论如下。1　临床资料1 1　诊断标准　 (1)初诊时确诊甲亢 (Ｇｒａｖｅｓ病 )且有明确的抗甲状腺药物服用史。 (2 )外周血粒细胞绝对值 <0 5×10 9/Ｌ。 (3)除外其它原因所致的粒细胞缺乏症。 (4 )周围血无明显血红蛋白、血小板减少 ,且短期随访血象足以除外再生障碍性贫血。1 2　一般情况　…     

阻塞性睡眠呼吸暂停综合征和胰岛素抵抗的关系

目的 探讨阻塞性睡眠呼吸暂停综合征(OSAS)和胰岛素抵抗(IR)的关系.方法 分析对照组、肥胖的轻度OSAS组、肥胖的中重度OSAS组、非肥胖的轻度OSAS组、非肥胖的中重度OSAS组的体重指数、HOMA2-IR等.结果 ①肥胖的轻度、中重度OSAS组和非肥胖的中重度OSAS组的HOMA2-IR高于对照组(P＜0.01).肥胖的中重度OS-AS组的HOMA2-IR高于肥胖的轻度OSAS组(P＜0.01),非肥胖的中重度OSAS组的HOMA2-IR高于非肥胖的轻度OSAS组(P＜0.05).②HOMA2-IR与AHI和BMI呈显著正相关(r分别为0.427、0.546,P＜0.01),AHI与BMI呈显著正相关(r为0.428,P＜0.01).③多元逐步回归分析,得出影响HOMA2-IR的因素依次是BMI和AHI.结论 OSAS和IR存在独立的相关性,且随着OSAS程度的增加IR亦加重.     

有糖尿病家族史者2型糖尿病的临床特点

目的比较有家族史和无家族史2型糖尿病(T2DM)患者的临床特点。方法将T2DM患者按糖尿病家族史分成有DM家族史组和无家族史组。比较2组的体质指数(BMI),血糖,血压,血脂,空腹C肽,餐后2hC肽,发病年龄,大、微血管并发症等方面的差异。结果与无家族史组患者相比,有糖尿病家族史组发病年龄提前,但在BMI、糖化血红蛋白、血糖、空腹C肽、餐后2hC肽和血脂等方面差异无统计学意义。相同病程2组大、微血管病变危险性差异无统计学意义。在有家族史组中,母亲糖尿病史所占比例较父亲糖尿病史高,但两者发病年龄差异无统计学意义。多元逐步线性回归显示家族史、年龄、高BMI、高甘油三酯和舒张期血压是T2DM发病年龄提前的危险因素。结论①在T2DM遗传中存在母系优势,家族史与子女发病年龄提前相关。②遗传因素和环境因素如高BMI、高甘油三酯都与T2DM的提早发生相关。③在相同病程下,2组发生T2DM并发症的危险性无差异。     

The effect of repaglinide on blood glucose and islet β-cell function in newly diagnosed type 2 diabetic patients

Objective To explore the effect of repaglinide intensive treatment on islet β-cell function and long-term control of blood glucose in newly diagnosed type 2 diabetic patients. Methods Self-control and inter-group control prospective study was conducted in 80 newly diagnosed type 2 diabetic patients who were treated with short-term repaglinide intensive treatment and islet β-cell function was assessed by 75 g oral glucose tolerance test (OGTT) before and after repaglinide treatment. The changes of △I30/△G30 ratio, blood lipid, HOMA A and HOMA B were examined. Results After treatment, in successful group, middle group and defeat group, the fasting plasma glucose levels were decreased from 8.9±1.5, 8.6±1.6,9.0±2.0 to 5.0±1.4,6.3±0. 7,6.5±0. 9 mmol/L, 0. 5 h postprandial glucose levels were decreased from (12.6±1.6, 12.6±1.5, 12.4±1.3 to 8.4±1.0, 6.8±0. 7, 8. 6±0. 9)mmol/L,and 2 h postprandial glucose levels were decreased from (13.0±1.2, 13. 1±1.3, 13. 3±1.4 to 9.2±0.9, 6.6±0. 7, 9.2±0. 9)mmol/L,respectively (all P <0. 005). The ratio of △I30/△G30 was increased froml. 69±0. 31, 1.72±0. 33, 1.79±0. 36 to 4. 47±0. 62, 4. 42±0.46,12. 00±0.46 in the three groups, respectively (P<0.05). HOMA B was significantly improved (P<0. 05), while triglycerides and HOMA A were decreased(P<0. 05). The levels of fasting blood glucose and postprandial blood glucose in 21 patients were maintained within normal range for more than six months. There were significant differences in the ratio of △I30/△G30, age, repaglinide dosage and the time of reaching target of glucose [4.47±0.62 vs. 2. 0± 0.46; 39±8 vs. 56±9; 2.0±1.5 vs. 5.0±2.5; 32.4±8.0 vs. 53.3±7.6; all P<0.05] between successful group and defeat group. Conclusions The short-term intensive treatment with repaglinide can significantly improve the early secretion phase of insulin and the islet β-cell function, reconstruct of the physiological model of insulin secretion and relieve the disease.     

The effect of repaglinide on blood glucose and islet β-cell function in newly diagnosed type 2 diabetic patients

Objective To explore the effect of repaglinide intensive treatment on islet β-cell function and long-term control of blood glucose in newly diagnosed type 2 diabetic patients. Methods Self-control and inter-group control prospective study was conducted in 80 newly diagnosed type 2 diabetic patients who were treated with short-term repaglinide intensive treatment and islet β-cell function was assessed by 75 g oral glucose tolerance test (OGTT) before and after repaglinide treatment. The changes of △I30/△G30 ratio, blood lipid, HOMA A and HOMA B were examined. Results After treatment, in successful group, middle group and defeat group, the fasting plasma glucose levels were decreased from 8.9±1.5, 8.6±1.6,9.0±2.0 to 5.0±1.4,6.3±0. 7,6.5±0. 9 mmol/L, 0. 5 h postprandial glucose levels were decreased from (12.6±1.6, 12.6±1.5, 12.4±1.3 to 8.4±1.0, 6.8±0. 7, 8. 6±0. 9)mmol/L,and 2 h postprandial glucose levels were decreased from (13.0±1.2, 13. 1±1.3, 13. 3±1.4 to 9.2±0.9, 6.6±0. 7, 9.2±0. 9)mmol/L,respectively (all P <0. 005). The ratio of △I30/△G30 was increased froml. 69±0. 31, 1.72±0. 33, 1.79±0. 36 to 4. 47±0. 62, 4. 42±0.46,12. 00±0.46 in the three groups, respectively (P<0.05). HOMA B was significantly improved (P<0. 05), while triglycerides and HOMA A were decreased(P<0. 05). The levels of fasting blood glucose and postprandial blood glucose in 21 patients were maintained within normal range for more than six months. There were significant differences in the ratio of △I30/△G30, age, repaglinide dosage and the time of reaching target of glucose [4.47±0.62 vs. 2. 0± 0.46; 39±8 vs. 56±9; 2.0±1.5 vs. 5.0±2.5; 32.4±8.0 vs. 53.3±7.6; all P<0.05] between successful group and defeat group. Conclusions The short-term intensive treatment with repaglinide can significantly improve the early secretion phase of insulin and the islet β-cell function, reconstruct of the physiological model of insulin secretion and relieve the disease.     

成人隐匿性自身免疫性糖尿病研究进展

成人隐匿性自身免疫性糖尿病(LADA)属于1型糖尿病的一种亚型,临床上与2型糖尿病不易区分.目前对LADA的研究进展主要集中在流行病学、胰岛自身抗体、遗传学及治疗学等方面,其中对胰岛自身抗体的研究为当前热点.本文就近几年来国内外对LADA的发病机制、遗传学、自身抗体及治疗方面的新进展作一综述.     

肾上腺嗜铬细胞瘤致异位ACTH综合征的临诊应对

肾上腺嗜铬细胞瘤引起的异位ACTH综合征非常罕见.本文详细介绍1例肾上腺嗜铬细胞瘤引起异位ACTH综合征临床特点并结合国内外研究进展,讨论其诊治.提出正确的诊断应结合临床、生化、激素分泌、影像学、病理学、肿瘤免疫组化染色进行最终的综合判断.     

2型糖尿病患者餐后血脂影响因素研究

目的探讨2型DM患者餐后脂代谢异常的影响因素。方法30例2型DM患者正常饮食下测定早餐前后及中餐前后血脂、血糖、C-肽，对可能影响2型DM患者餐后脂代谢异常的因素进行分析。结果早、中餐后TG、C-肽水平均较餐前明显升高（P〈0．001），HDL—C水平较餐前有所降低（P〈0．001）；早餐前后PC升高水平明显大于中餐前后PG变化（P〈0．05），TG水平升高则略低于中餐前后（P〈0．001），HDL—C变化不大，但早餐后TC、LDL—C较餐前降低，而中餐后TC、LDL—C较餐前升高，两者差异有显著性（P〈0．001）。结论2型DM患者存在明显的餐后脂代谢紊乱，饮食中脂肪、碳水化合物比例不同会导致餐后血糖、血脂及C-肽水平的不同变化。     

糖尿病合并乳酸性酸中毒二例

糖尿病合并乳酸酸中毒国内较少报道,现报告二例。 [例1]女,74岁,患高血压二年,发现糖尿病一年半。多食、多饮、多尿,但无明显消瘦。曾在我院门诊检查空腹血糖12.6mmol/L,尿糖( ),确诊为Ⅱ型糖尿病。在门诊经饮食控制、优降糖及降糖片治疗,血糖基本控制在8.32mmol/L左右。入院前四天,外院予以降糖