陈树春医生的科普号

本报记者 周丽随着超声医学事业的不断发展，一些直径仅有几毫米的甲状腺结节无处“藏身”。由于甲状腺癌发病率的上升，不少人在体检中被诊断为“甲状腺结节”时，心中不免紧张，多数人希望通过“一刀切”的方式来降低癌变风险。对此，省人民医院内分泌一科主任陈树春教授提醒大家，其实普通甲状腺结节无需预防性切除。绝大多数甲状腺结节为良性“查出患有甲状腺结节没必要恐慌，它在人群中的发病率比较高，很常见。”陈树春对记者说，甲状腺结节是指甲状腺细胞在局部异常生长所引起的散在病变。通过触诊能检查出来的检出率为3%至7%，高分辨率超声普遍应用于临床检查后，甲状腺结节的检出率为20%至76%。从临床情况看，甲状腺结节在各个年龄段的男女人群中均可见到，但以30至50岁人群居多，女性的发病率是男性的4倍以上。“多数患者没有临床症状。”陈树春介绍，只有当结节较大压迫周围组织时，患者才会出现声音嘶哑、压气感、呼吸或吞咽困难等压迫症状。还有部分患者可能会合并甲状腺功能异常，例如患有甲亢或甲减时，才会出现相应的临床表现，因此，许多患者是在体检中才被发现的。“很多人认为甲状腺结节的高发与碘摄入过量有关，其实引起甲状腺结节的原因有很多。”陈树春分析，遗传是一个因素，现代生活节奏加快，生活压力大、精神过度紧张以及环境污染等也都可能是甲状腺结节发病率升高的原因之一。比如，甲状腺对射线非常敏感，调查显示，头颈部有照射史的人结节患病率以每年2%的速度递增。有研究显示，甲状腺结节的发病与洗涤剂、农药、食品添加剂的不当应用及摄取有关系。“如果患者被诊断为良性结节，没有必要采取‘一刀切’的方式。”陈树春说，尽管现在手术技术比较成熟，患者术中风险不大。但一味盲目切除甲状腺结节，部分患者可能会损伤甲状旁腺或造成甲状腺本身的损伤，从而造成甲旁减或甲减，患者可能需要终身服用药物，生活质量将受到一定程度的影响。绝大多数甲状腺结节为良性，癌变几率只占5%至15%。对于普通的甲状腺结节，患者只需要定期观察，每半年做一次B超检查和甲状腺功能化验，如无异常，不需要其他治疗。随着现代医疗技术的发展，即便得了甲状腺癌，患者也不必恐慌，目前甲状腺癌的治疗效果是相当不错的，如果早期采用科学规范地治疗，90%以上的患者能活30年以上。B超是筛查甲状腺癌的首选方法“判断甲状腺结节的良恶性，应重点关注患者性别、甲状腺癌家族史、头部放射性治疗史或接触史、结节大小、增长速度等因素。”陈树春介绍，患者有以下情况应引起特别关注，需要做进一步的检查。比如儿童或青春期患者有颈部放射线照射史、放射线尘埃接触史；患者有全身放射治疗史，患者有分化型甲状腺癌、甲状腺髓样癌或多发内分泌腺瘤(MEN2型)、家族性多发息肉病、某些甲状腺癌综合症的既往史或家族史；患者为男性，患者伴持续性声音嘶哑、发音困难，并可排除声带病变；患者伴有呼吸或吞咽改变，患者结节生长迅速，结节形状不规则、与周围组织粘连、固定；患者伴颈部淋巴结病理性肿大等。“超声和彩色超声技术的出现，使甲状腺疾病的诊断得到革命性的改观。”陈树春说，过去无法触摸到的1厘米以下的结节以及甲状腺周围血流改变都清晰可见。尤其是近年来采用的甲状腺高频超声技术，更能够发现2至3毫米的微小结节，同时能够准确区别甲状腺胶质潴留和实质性肿块。这表明，超声普查已在甲状腺癌原发灶诊断中起重要作用。“在B超的检查中，如果出现以下情况就需要引起患者的特别关注，需要做穿刺等进一步检查，看是否有肿瘤的可能。”陈树春说，比如结节直径超过1厘米；实性低回声结节；结节内血供丰富(TSH正常情况下)；结节形态和边缘不规则；微小钙化、针尖样弥散分布或簇状分布的钙化；低回声结节伴颈部淋巴结异常，如淋巴结呈圆形、边界不规则或模糊、内部回声不均、内部钙化、皮髓质分布不清、淋巴门结构消失、囊性变；低回声结节侵犯到甲状腺包膜外或甲状腺周围的肌肉中。“患者如果出现结节引起甲亢等情况应考虑切除结节。”陈树春说。“需要特别提醒大家的是，儿童恶性结节的比例高于成人，可高达20%，故要进一步评估。”陈树春说，儿童的恶性结节通常为多病灶，且伴淋巴结转移，甚至远处转移的几率高，故大部分需行全或近全甲状腺切除术。患儿如有甲状腺癌或MEN2型家族史建议做基因检测，突变阳性者宜行甲状腺预防性切除。“对于儿童的甲状腺结节，家长们也不必过分担心，因为儿童恶性结节即便有转移通过积极正确的治疗预后仍较好。”陈树春说。

内分泌一科 唐勇近日，我科诊治一例少见的核型为49,XXXXY的Klinefelter综合征合并糖尿病患者，体现我院在罕见内分泌疾病诊治上的水平。患者马XX，男性，19岁，主因口干、多饮、多尿1年，消瘦半年，加重伴视物模糊1月于2012-12-05入院。化验检查糖尿病诊断标准。但查体过程中发现患者智力低，语言交流能力差。我们考虑是否存在某些遗传性疾病的可能，是否存在继发糖尿病的可能，随后行垂体及性腺激素检查，发现睾酮低于正常男性，LH及FSH均高于正常男性，追问患者从未有勃起及遗精，集合查体男性器官未发育。符合高促性腺激素性功能低下的表现。继而行染色体核型检查为49, XXXXY,诊断为先天性睾丸发育不全综合征(Klinefelter综合征)。诊断为：1.Klinefelter综合征 高促性腺激素性性腺功能减退症 特殊类型糖尿病骨质疏松症2.双眼白内障。给予胰岛素降糖，补充活性维生素D、钙剂及雄激素治疗，空腹血糖控制在5～7 mmol/L，餐后血糖8-10mmol/L，病情平稳出院。 Klinefelter综合征又称先天性睾丸发育不全综合征，发病率1/500～1/700，在男性不育症中约占10%。是一种性染色体异常所致的原发性性腺功能减退症。其发病机制是生殖细胞在减数分裂或受精卵在有丝分裂时不分离所致。该病在青春期前多无明显症状，很少被发现，但随着睾丸功能的逐渐减退，青春期(后)血浆睾酮浓度明显低于正常人，最终类似无睾症。其临床特点有：(1)睾丸小而硬，生精障碍；(2)男性乳房发育，肌肉发育差，体毛、胡须及阴毛少；(3)身材过高，主要为下肢过长，骨骼比例过长；(4)低睾酮和高促性腺激素；(5)多X染色体核型，其中47XXY是最常见的核型，其他变异的核型有48XXYY、48XXXY、49XXXXY等。其中49XXXXY是核型最异常的，多同时伴有其他疾病，如糖尿病、白内障、先天畸形，智力障碍较其他核型更显著，本例患者为此类型，目前国内外文献尚未查到此类核型的Klinefelter综合征的病例报道。 本例患者以血糖升高入院，极易被诊为糖尿病而漏掉了原发疾病从而延误治疗。我科近几年来在宋光耀院长的领导下，不断拓宽思路，广泛学习，使得内分泌疾病的少见病、疑难病的诊治能力迅速提高，这方面的患者也迅速增加，同时也帮助基层医院解决了很多疑难问题，得到了同行及患者的信赖。

寒冷的冬天来了，许多疾病都会在这个气温低的时候发作，据统计，冬季70%以上的死亡高峰都出现在强冷空气影响后的三天内。糖尿病患者在冬天要保护好自己。寒冷会刺激交感神经兴奋，使体内儿茶酚胺类物质分泌增加，易使血糖升高、血小板聚集而形成血栓，会促使血糖波动、血压升高。糖尿病患者抵抗力低，严寒更易导致患者感冒，从而诱发肺感染。此外，严寒还会使外周血管收缩，增加糖尿病足的风险。预防感染特别重要在寒冷冬天人们往往门窗紧闭，这就造成空气不对流，室内聚集的烟雾、尘埃、人体呼出的二氧化碳等难以排出，室内空气污浊，特别容易诱发呼吸系统疾病。正确的做法是，在房间设置气窗或定时开窗通风。通风时，糖尿病患者注意避免身体遭受寒风袭击，以免着凉。在饮食方面，虽然冬季消化液分泌增多，人的食欲较好，但还要控制饮食，以清淡、多样、富含多种营养素的食物为主。冬天气温的降低会造成呼吸道黏膜抵抗力下降，皮肤弹性下降，皮肤感染、尿路感染等是糖尿病最常见的并发症，尤其是有慢性咽炎，鼻窦炎，支气管炎患者，很容易发生肺部感染，甚至成为危及生命的主要原因。所以，糖尿病患者预防感染特别重要。寒冬里的三个提醒增加血糖监测频率：寒冷导致肾上腺素等升糖激素增多，而糖尿病患者胰岛素分泌减少，所以血糖易波动，应增加血糖监测频率，要特别注意夜间血糖波动避免糖尿病足：寒冷可使外周末梢血管收缩，影响下肢及足部供血，加重或诱发糖尿病足的发生，所以要及时保暖。冬季出汗少、皮肤干，足部容易皲裂，所以要每天检查双足，每晚用40摄氏度左右热水泡脚15分钟，做10分钟足底按摩有助于防寒保暖及改善局部血液循环，洗完脚后可擦一些护肤霜，保持皮肤的润滑。穿宽松保暖的的鞋，避免冻伤。避免用手撕脚皮和擦脚趾止痒，以防皮肤破损招致化脓性细菌感染。预防情绪低落：糖尿病患者中有50%患有不同程度抑郁，而冬天寒冷，出门活动少，朋友很少聚会聊天，容易出现情绪波动。情绪激动能引起交感神经兴奋，可促使肝脏中的糖原释放进入血液，而使血糖水平升高，导致病情加重或降低治疗效果。所以，糖尿病患者要学会控制情绪，避免负性情绪影响，保持情绪稳定。

[Abstract]Objective The dysfunction of endothelial progenitor cells (EPCs) exists in obese individuals. Our objective is to study the quantity change in obese rats fed on high-fat-diet and investigate the correlation of EPCs number with visfatin---an inflammatory adipokine in rats. The impact of visfatin on EPCs quantity and function were further investigated by cell culture. Methods Male wistar rats were fed on either a standard diet (NC group) or high fat diet (HF group) for 16 weeks. Serum visfatin, Lee’s index and the protein expression of visfatin in viseral adipose tissue (VAT )were detected. Bone marrrow EPCs in 2 groups of rats were isolated, cultured and counted. EPCs primarily cultured from control male Wistar rats were treated with visfatin of different concentrations. The quantity, migration and adhesion capacity of EPCs were evaluated after visfatin treatment. Protein expression of nuclear factor κ B (NF-κB) in nuclei of EPCs was detected. Results After 16-week feeding, body weight , Lee’s index , visceral fat , visfatin, fasting blood glucose, fasting serum insulin, total cholesterol and triglyceride were significantly increased in the HF group compared with NC group (p <0.01 or p<0.05). Serum concentration of visfatin was significantly increased in HC group (P<0.01). Protein contents of visfatin in VAT in HF group were significantly higher compared with NC group (P<0.05). The quantity of EPCs primarily cultured from rats in HF group was lower than that in NC group. The quantity of EPCs was negatively correlated with serum visfatin level, visceral fat, fasting blood glucose, HOMA-IR, total cholesterol, triglyceride and body weight (p<0.01). In cultured EPCs, visfatin significantly increased the protein expression of NF-κB in EPCs nuceli (P<0.01) in a dose-dependent manner. The migration and adhesion capacity were imparied by visfatin treatment (p<0.01). Conclusions Bone-marrow-origined EPCs decrease in number and have impaired migration and adhesion function in high-fat-fed obese rats, along with increased serum visfatin and protein contents in VAT. Visfatin might have impact on the quantity and function of EPCs through NF-κB pathway.IntroductionWith the change of life style and diet structure, obesity has become increasingly prevelant all over the world. The incidence of obesity is attributable to many inter-related factors, of which high-calory intake, high-fat diet and lack of physical acitivity are important risk factors. Excess energy is stored as fat and lead to obesity. Moreover, obesity is closely associated with the development of many diseases, including hypertension, type 2 diabetes, metabolic syndrome, dyslipidemia, etc. The excessive accumulation of visceral adipose tissue, especially the accumulation of abdominal adipose tissue is the important risk factor of cardiovascular disease.Endothelial progenitor cells (EPCs) originate from bone marrow and are progenitor cells which have the capacity to migrate to the peripheralcirculation and to differenciated into mature endothelial cells. Under the circumstances of vessel impairment and tissue ischemia, the EPCs in the bone marrow can be mobilized into the blood circulation and settle in impaired and ischemic locations. EPCs are then differenciated into the mature endothelial cells and participated in the angiogenesis and re-endothelialization. Therefore, EPCs play an important role in maintaining the integrity of endothelial structures and the function of vascular endothelium. EPCs are influenced by many factors such as physical activity, smoking and age[1-3]. Many diseases can cause the decrease in the quantity of EPCs. EPCs in diabetic patients decrease significantly in quantity with an impaired restoration capacity of vessels[4-6]. Hyperglycemia, hyperinsulinemia and hyperlipidemia can all lead to the impairment of EPCs.Overweight and obesity are closely related to the incidence and mortality of cardiovascular diseases. According to the studies, dysfunction of vascular endothelium exists in overweight and obese populations. Because endothelial damage and dysfunction is considered to be a major underlying mechanism for the cardiovascular， the prompt endothelial repair/regeneration is very meaningful in maintaining a normal endothelium function and preventing cardiovascular events[7-10]. Recent studies indicate that the function of circulating EPCs is impaired in obese individuals. However, the underlying mechanism remain unclear.Adipose tissue can secrete many different adipokines. Studies indicate that abdominal obesity can change the levels of many adipokines[11-16].Visfatin is an adiponectin discovered in 2005. The effect of visfatin on the vascular inflammation in obesity and type 2 diabetes draws more and more attentions. Visfatin possesses many biological functions. The function of visfatin is intimately correlated with glucose and lipid metabolism and can be considered a new proinflammatory factor which modulates the inflammatory processes of atherosclerosis [17-22]. Researches show that there is an increased visfatin level in diabetic and obese patients [23,24], which is related to vascular dysfunction[25].Transcriptional factor nuclear factor κ B (NF-κ B) is the key inflammatory mediators, which can modulate the expression of a series of factors in the inflammatory processes. It is found that visfatin can upregulate the expression of NF-κ B in human endothelium in umbilical veins and lead to endothelial inflammation[26,27]. Based on these findings, we hypothesized that visfatin is an upstream (上游的)如果不合适可做更改factor leading to the decrease of EPCs in obese individuals by upregulating NF-κ B in EPCs. The upregulated NF-κ B induce inflammation and apoptosis of EPCs and result in the decrease quantities of EPCs. At present, the relation of visfatin to EPCs is less investigated.In the current study, we measured the quantity of EPCs, serum visfatin and expression of visfatin in viseral adipose tissue in high-fat-fed obese rats. The correlation of the above index were analyzed. To observe the effect of visfatin on EPCs and possible underlying mechanism, cultured primary EPCs were incubated with different concentrations of visfatin. The migration and adhesion ability and the protein expression of NF-κ B in nuclei of EPCs were detected. We hope the present study can provide a potential new target for preventing and interventing the development of vascular diseases in obese individuals.Methods and materialsAnimals. Male Wistar rats weighed 200~250 grams were randomly divided into two groups: normal control group (NC, n=11) and high-fat-fed group (HF, n=11). The animals were kept in a temperature-controlled room (22 ± 1°C) on a 12-h light/dark cycle with free access to food and water. NC group were fed a standard lab diet (65.5% calories from carbohydrate, 10.3% calories from fat, and 22.4% calories from protein; 384Kcal/100g). HF group were fed a high fat diet (20% calories from carbohydrate, 60% calories from fat, and 20% calories from protein; 502 Kcal/100g; Research Diets, USA). After 16-week feeding, Lee’s Index, body weight were measured. Lee’s Index=Body weight(g)1/3×1000/body length(cm).Measurement of serum insulin and visfatin. Serum insulin and visfatin were detected by ELISA (Sensitivity：0.01 ng/ml and 1 ng/ml respectively) with microplate reader (ALISEI, Italy, SEAC).Immunoblotting Adipose tissue samples were homogenized in ice-cold lysis buffer (50mM Tris PH 7.5, 150mM NaCl, 1% TritonX-100, 10mM NaP , 100 mM NaF , 2mM Na orthovanadate, 1mM EDTA, 1mM EGTA ,10% glycerol), supplemented with protease inhibitor cocktail tablets (Roche) and DL-Dithiothreitol and solubilized for 30 min at 4°C. Protein samples were then denatured in SDS sample buffer (125mmol/l Tris-HCl, pH 6.8, 50% glycerol, 2% SDS, 5%β-mercaptoethanol, and 0.01% bromophenol blue). Equal amounts of tissue lysates (60 μg protein) were resolved by SDS-PAGE and immunoblotted with appropriate antibodies against visfatin (Biovision). Immunolabeled bands were quantitated by densitometry. To determine the protein contents of NF-κ B in nuclei in EPCs, nuclear protein were extracted from cultured EPCs using a nuclear protein extraction kit (Applygen Technologies). Tissue lysates (60 μg protein) were resolved by SDS-PAGE and immunoblotted with appropriate antibodies against NF-κB (Santa Cruz). Immunolabeled bands were quantitated by densitometry. β-tubulin (Abcam)was used as an internal standard.Culture of EPCs Hollow bones of rat legs were prepared by standard surgical procedures, and whole bone marrow was harvested by flushing marrow with 500ul PBS using a syringe with a 20-gauge needle. Briefly, rat bone marrrow mononuclear cells (MNCs) were isolated from flushing liquid using by Ficoll density centrifugation.Cells were centrifuged for 30 min at room temperature (1000rpm) for 10 min. MNCs were isolated and washed with PBS. MNCs were resuspended in EGM-2MV medium (LONZA). 6-well or 24 well tissue culture plates precoated with fibronectin (Solarbio, China) were seeded with a density of 2×106/ml. and cultured in a humidified incubator. After 48h of culture, adherent cells were washed with EGM-2MV, and EGM-2MV medium was added to each well. Medium was changed daily for 7 days and then every other day until the first passage. Cells were obeseved daily under inverted microscopy.Determination of EPCs numbers and cellular characterization Immunocytochemistry was performed in cultured cells to detect the expression of CD34 and kinase insert domain receptor (KDR). CD34 and KDR termed also Flk-1 are surface markers of EPCs . Briefly, EPCs were fixed in 4% paraformaldehyde in PBS for 20 minutes, washed 3 times with PBS, and repectively stained with various EPCs specific markers: rabbit anti-rat CD34(Boster, China), mouse anti-rat KDR(Boster, China). The cells were incubated in secondary antibodies (either anti-mouse or anti-rabbit) and then in third antibody. Cells were coloured with DAB and stained with hematoxylin.Determination of EPCs under microscope.Moreover, EPCs were characterized by cellular uptake of DiI-labeled acetylated LDL (DiI -acLDL; Molecular Probes, Eugene, Oregon)and binding of fluorescein isothiocyanate–conjugated lectin from Ulex europeus agglutinin (FITC-Lectin-UEA-1; Sigma). Briefly, after 10-day culture, dil-acLDL(2.5ug/mL) were added on cells for 4 hours and washed for 3 times. After fixed in 2% paraformaldehyde for 20 min,FITC-Lectin-UEA-1(10ug/ml) were added and cultured for 1 hour. The cells were then observed under laser scanning confocal microscopy. Orange double-stained cells positive for both DiI-acLDL and FITC- Lectin-UEA-1 were identified as EPCs. EPCs were counted under laser scanning confocal microscopy.Treatment of EPCs by Visfatin incubation Bone marrow MNCs from male Wistar rats fed on standard diet were isolated and cultured as discribed. EPCs were determined from MNCs and treated with visfatin in different concentration (0 ng/mL, 50 ng/mL, 100 ng/mL, 150 ng/mL, 200ng/mL) for 48 hours.Evaluation of migration capacity of EPCs Single cell suspension were planted in 24-well plate as a density of 5×104/ml. After 24-hour culture, cells were digested with 0.25% tripsin solution and counted. Culture medium were added into the lower champer of modified Boyden champer; 2×104/ml of EPCs were suspended in 150 ul of medium and added into the upper champer. After 24-hour cultrue, the unmoved cells were scratched from the filtration membrane. The migrated cells were fixed with formalin and stained with hematoxylin. Ten fields were randomly chosed to count the migrated cells under inverted microscopy (×400).Evaluation of adhesion capacity of EPCs Single cell suspension were planted in 24-well plate as a density of 5×104/ml. After 24-hour culture, cells were digested with 0.25% tripsin solution. Same numbers of cells were planted into 96-well plate and incubated for 30min at 37℃. Unattached cells were washed out. Ten fields were randomly chosed to count the attached cells under inverted microscopy (×400).Statistical Analyses. Data are presented as means ± SE. The data were tested by homogeneity test for variance. T test was used for comparison of normally distributed data with homogenous variance. The rank sum test was used for comparison of normally distributed data with heterogenous variance. One-way analysis of variance were used for comparison of normally distributed data with homogenous variance relevant groups. Linear regression was used to detect a correlation. Differences at P < 0.05 were considered to be statistically significant.ResultsComparison of baseline characteristics between NC group and HF group Lee’s index, body weight(BW), viseral adipose tissue (VAT), fasting blood glucose (FBG), fasting insulin in serum(FINS), HOMA-IR, plasma triglyceride (TG), plasma total cholesterol (TC) were all significantly higher in HF group than in NC group. (Table 1)Visfatin level in serum Serum visfatin was significantly higher in HF group than in NC group(P <0.01). (Figure 1)Protein expression of visfatin in VAT in two groups. Compared with NC group, the protein contents of visfatin in VAT in HF group were significantly higher compared with NC group(P<0.05). (Figure 2)Culture of EPCs Newly isolated bone marrow mononuclear cells were round, transparent and suspended in medium. After planted for 48 hours, part of cells attached. The adherent cells gradually enlarged and stretched. After planted for 4-7 days, adherent cells grew as colonies. Cells were round, triangle, oval or irregular. After 10 days, cell were linearly arranged.(Figure 3①)Determination of EPCs numbers and cellular characterizationEPCs were analyzed by immunohistochemical staining under microscope. CD34and KDR are surface markers of EPCs. (Figure 3②)After 10-day cultrue, by uptake of DIL-Ac-LDL and binding of FITC-Lectin-UEA-1, EPCs which were double-stained cells as yellow were observed and counted under laser scanning confocal microscopy. The numbers of EPCs were significantly lower in HF gourp compared with those in NC group(P <0.01). (Table 2，Figure 3③)Correlation analysis of different index Pearson correlation analysis indicate that the numbers of EPCs are negatively correlated with serum visfatin ( r=0-.886, P < 0.01), CRP(r=-0.849, P <0.01) , FBG( r= -0.753, P <0.01) , HOMA-IR( r=-0.775, P <0.01)、 TC( r=-0.744, P <0.01)、TG( r =- 0.821, P <0.01) , VAT (r=-0.631, P <0.01 ) and BW(r=-0.656, P <0.01).The effect of visfatin treatment on EPCs. Compared with EPCs without incubation of visfatin, the protein expression of NF--κ B in nuclei in EPCs after treated with different concentrations of visfatin was increased in a dose-dependent manner (Figure 4) （P<0.01）Compared with EPCs without incubation of visfatin, the migration and adhesion capacities of EPCs treated with visfatin were gradually decreased in a dose-depent manner（P<0.01）. (Figure 5)DisscussionObesity has become increasingly prevelant and is the important risk factors of cardiovascular disease[28-31]. Studies indicate that obesity, the same as other risk factors including diabetes mellitus, hypertension and smoking, can impair the function of vascular endothelium [32-35] and lead to arteriosclerosis and other cardiovascular diseases[7-10]. Endothelial progenitor cells (EPCs) play an important role in maintaining the completement of endothelial structure and normal function of vascular endothelium. EPCs originate from bone marrow. The EPCs released into blood circulation after stimulation can differentiate into mature endothelial cells and specially settle in ischemic locations and participate in the reendothelialization of injured blood vessels.According to previous studies, the alterations in EPCs exist in overweight and obese individuals. Several recent studies show that the numbers of EPCs decreased in overweight and obese populations with an impaired proliferation capacity[36-41]. Heida found that the numbers of EPCs in blood circulation decreased in obese individuals and obese mice; meanwhile, the migration and adhesion capacity of EPCs were impaired[36]. MacEneaney et al also found an decrease in EPCs quantity in overweight and obese individuals with an weakened proliferation capacity[37]. However, the underlying mechanism by which the quantity and function of EPCs are impaired remain unclear.Visfatin is an adipokine which is secreted by adipose tissue. The effect of visfatin include promoting the differentiation of adipose cells and the synthesis and storage of adipose tissue, promoting inflammation of vascular endothelial cells and leading to the development of arteriosclearosis[42-47]. By far, the possible relationship of visfatin to EPCs is less investigated. We hypothesis that visfatin might be involved in the impairment of EPCs function in the situation of obesity. In the present study, we fed the rats with high fat diet for 16 weeks and induced obesity in rats along with the development of whole body insulin resistance (as shown by increased FBG, FINS and HOMA-IR). The numbers of EPCs were significantly decreased in rats in HF group, which is consistant with previous studies. Meanwhile, serum visfatin significantly increased and the protein contents of visfatin have been significantly increased by high fat feeding. Correlation analysis indicates that the quantity of EPCs are negatively correlated with visfatin levels, indicating a possible relationship of visfatin to EPCs and that visfatin is possibly an influential factor of the quantity of EPCs.A possible underlying mechanism of the influence of visfatin on EPCs quantity might be the inflammatory effect of visfatin. Previous studies found that visfatin induce the upregulation of inflammatory factors and adhesion molecules in human umbilical vein endothelial cells (HUVECs) through NF-κ B pathway[21,23,26,27]. Lee et al found the activity of NF-κ B was increased in HUVECs after incubated with visfatin, with the upregulation of IL-6, IL-8, ICAM-1, VCAM-1 and E-selectin genes[26]. From Adya’s study, the activity of NF-κ B increased in both HUVECs and epithelial tumor cells when incubated with visfatin for 24 hours; the activity of increased with the treatment of visfatin in a dose-dependent manner[27]. Futhermore, visfatin can increase the expression of NF-κ B, tumor necrosis factor-α(TNF-α), matrix metalloproteinase-9 (MMP-9), interleukin-8 (IL-8), interleukin-6 (IL-6) in monocytes by activating insulin receptor (IR) -Ras-MAPK signal pathway and insulin-independent p38 pathway[42]. Based on the knowledge, we presume that visfatin might be influence the function of EPCs through NF-κ B pathway.In our study, we incubated the EPCs with different concentration of visfatin to observe the effect of visfatin on the expression of NF-κ B in EPCs nuclei. The concentration of visfatin were based on the serum visfatin level we measured in the animal study. The results show the expression of NF-κ B in nuclear in EPCs were signifantly increased by visfatin treatment in a dose dependent manner, which is consistant to the previous report that visfatin possesses inflammatory effect. The effect of visfatin on NF-κ B in EPCs support our hypothesis that visfatin might have an effect on EPCs through NF-κ B pathway. Meanwhile, the migration and adhesion capacity of EPCs were impaired by visfatin treatment. The possible mechanism is the inflammation induced by visfatin causes the upregulation of a series of inflammatory factors including NF-κB and TNF-α, leading to the aging and apoptosis of EPCs and resulting in a decreased quantities and impaired functions of EPCs[48-51]. Further investigation is needed.In summary, serum visfatin and protein contents of visfatin in VAT increased in obese rats fed on high fat diet, accompanying with the decreased quantities of bone-marrow-origined EPCs. Visfatin might be involved in the development of decreased EPCs numbers and impaired functions through NF-κB pathway. The present study provide a new target for the prevention of development of cardiovasular disease in obese populations.Reference1 Ulrich L, Axel U, Nikos W, et al. 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李某，女，50岁，经常睡不够，没劲，胃口不好，身体瘦弱，10余年一直被当作胃炎间断入院治疗，病情却时常反复。今年开始间断出现抽搐，双眼上吊、牙关紧闭、四肢抽搐、口吐白沫、意识丧失，入院检查血钠105mmol/L，氯73mmol/L，查体无明显阳性体征，诊为癫痫治疗，病情仍无明显好转。患者反复辗转于各医院消化科、神经科就诊，仍有顽固低钠，间断抽搐发生。11年12月20日来到我院内分泌科，追问病史患者曾有产后大出血，产后无乳，30岁就闭经了，这些年来一直怕冷，容易疲劳，经常头晕目眩，睡不够，不能正常工作，根据其典型病史，症状及垂体激素等检查，确诊为Sheehan综合征，给予静脉激素替代治疗，3小时候患者意识恢复、精神及饮食均有好转，血钠恢复正常，后改为口服激素治疗后出院，目前患者一直坚持服用每天1片强的松，1片优甲乐治疗，身体状况良好。Sheehan综合征是由于分娩后大出血引起垂体坏死而导致垂体功能减退的疾病。本病主要临床表现为性腺、甲状腺、肾上腺功能减退，因其可引起低血压、低血糖及顽固性低血钠等情况，所以经常表现为消化系统、循环系统、神经系统症状，部分患者可出现各种精神症状。本病症状、体征差异较大，病初可有多种不同表现，易误诊误治，导致患者病情加重，甚至危及生命。该病补充相关激素后症状可迅速缓解，故尽早明确诊断并及时治疗尤为重要。所以顽固性低血钠的患者一定不要忘记检查垂体及肾上腺功能。这种疾病需要终身激素替代治疗，如果自行停药会导致激素缺乏，水电紊乱，甚至危及生命，另外如果患者突然患有其他疾病,激素就需要加量，并及时到医院治疗。

原发性醛固酮增多症(原醛)是一种具有潜在可治愈性的继发性高血压,近年来发现其患病率在高血压人群中可达5%-15%,在难治性高血压人群中高于20-30%,是最常见的内分泌性高血压。由于不同类型原醛的治疗方法及预后不同,原醛的分型诊断对患者的正确治疗及预后具有重要意义。目前，原醛症的诊断主要靠激素水平的测定、体位激发试验和影像学检查，但仍有一些诊断和分型很困难。肾上腺静脉分段取血（AVS）术是经股静脉穿刺选择性插管至肾上腺静脉及下腔静脉采样,通过检验样本中某些激素指标来判断生理病理学改变的一种介入检查方法。其在原醛的病因分型上显示出独特的诊断价值,文献报道,与手术后病理结果相比较,AVS术诊断符合率可达79%-100%,被公认为原醛分型定侧的“金标准”。 但目前国内只有北京、上海几个大医院能够开展。近期，我院内分泌科在宋光耀副院长协调下，在导管室张帆主任的大力支持下开展了此项目检查，填补了省内空白。目前已经有多例患者接受了AVS检查，结合临床试验和激素测定明确了诊断，收到了很好的效果。此项目的开展，结合临床试验、实验室激素测定和影像学检查，使我院肾上腺疾病的诊断达到了国内先进、省内领先水平。

患者男性，29岁，因眼球突出1月于２００９年１０月来诊，伴有心悸，乏力，体重减轻，曾于当地医院检查血钾偏低（具体数值不详），后一直补钾治疗。查体甲状腺不大，心率80次/分，率齐。眶CT示眼外肌肿胀，增粗，符合Graves眼病表现。 TSH：0.002U/ml（ 0.27-4.2）TT3:3.01mol/L（1.3-3.1）TT4:145.00mol/L（66-181）FT3:6.01mol/L（3.1-6.8）FT4:20.03mol/L（ 12-22）TPO-AB：69.17U/mL （≤34）TRAb 阳性血钾：3.0mmol/l肝功能正常，血常规无异常诊为亚临床甲亢。给予甲巯咪唑５ｍｇ1/日，左旋甲状腺素钠25vg 1/日口服１周复查血常规、肝功无异常继续治疗一月后复诊，眼部症状明显好转，血钾正常，停用氯化钾缓释片，继续甲巯咪唑及左旋甲状腺素钠治疗。6个月后，突眼好转，血钾正常，甲功恢复正常，继续维持用药。1年后，TRAb阴性，停药。体会：亚临床甲亢可引起低血钾，同时可伴有Graves病突眼并存，此时应积极治疗甲亢，而伴有突眼者在应用抗甲状腺药物的同时加用左旋甲状腺素钠有利于突眼的恢复。

患者男性，15岁，汉族，学生。发现个子矮小4年于2010-4-26 入院。缘于4年前发现个子较同龄人矮小，每年生长不足3cm，不喜运动，思睡，畏寒、纳差、乏力，无发热、头晕、头痛，无视物模糊，无腹痛、便秘、腹泻，无明显颜面及双下肢水肿，无毛发脱失，学习成绩尚可。3月前曾就诊于邢台某医院，垂体MRI：垂体瘤，为进一步治疗而来我院。入院查体：T36.1℃ P62次/分 R18次/分 BP98/65mmHg身材较矮小（身高135cm），营养中等，自动体位，表情自然，神清语利，查体合作。皮肤粗糙，，颜面及眼睑水肿，结膜无充血及苍白，甲状腺不大。双肺呼吸音清，未闻及干湿罗音。心率62次/分，律整，心音稍低钝，各瓣膜听诊区未闻及杂音。腹平坦，未见胃肠型及蠕动波。腹软，无压痛、反跳痛，肝脾未触及。辅助检查：1. 垂体激素ACTH(pg/mL)TSH(uIU/ml)GH(ng/mL)FSH(IU/L)LH(IU/L)PRL(ng/mL)14.3＞150↑0.294.535.9718.52.生化全项：碱性磷酸酶 189IU/L，肌酸激酶1034mmol/l，甘油三酯2.83mmol/L，极低密度脂蛋白 1.29mmol/L3.甲功TT3﹤0.3nmol/l（1.3-3.1），TT4 ﹤5.4nmol/l（66-181），TSH ﹥150uIU/ml（0.27-4.2）4.甲状腺彩超：甲状腺弥漫性病变，多发稍强回声结节；诊断：原发性甲状腺功能减退症，垂体腺瘤样增生。治疗：左旋甲状腺素钠50vg 1/日。1月后：TT3 ：0.6nmol/l（1.3-3.1），TT4 :51nmol/l（66-181），TSH ：100uIU/ml（0.27-4.2），左旋甲状腺素钠加量至75vg 1/日。肌酸激酶360mmol/l2月后：TT3 ：1.2nmol/l（1.3-3.1），TT4 :60nmol/l（66-181），TSH ：96uIU/ml（0.27-4.2），左旋甲状腺素钠加量至100vg 1/日。肌酸激酶240mmol/l以后根据甲功调整左旋甲状腺素钠剂量。6个月后：TT3 ：1.6nmol/l（1.3-3.1），TT4 :78nmol/l（66-181），TSH ：4.0uIU/ml（0.27-4.2）。肌酸激酶200 mmol/l。此时甲状腺素钠150vg 1/日。垂体MRI显示，垂体腺瘤样增生已消失。体会：原发性甲减引起甲状腺激素减低，反馈性刺激垂体TSH过度分泌，久而久之可引起垂体增生，这这时用左旋甲状腺素钠治疗可使垂体恢复正常。所以如果患者首先以垂体瘤就诊，一定要查垂体激素，如果TSH水平升高，一定要进一步查甲功，明确诊断，采取正确的治疗措施，患者可治愈，切不可见到垂体瘤就盲目外科切除，这样会导致患者终身痛苦。

花样年华的“甜蜜烦恼”（该文已发表于《名医杂志》第9期）近日，美国北卡罗来纳大学和中国疾控中心联合进行的一项研究表明，在我国7～17岁的青少年中，糖尿病的发病率是美国同龄青少年的4倍，糖尿病前期率更高达14.9%。这与最近几十年来国人生活方式和营养结构发生巨大变化、体重超标的青少年数量不断增加息息相关。那么，如何及早发现孩子患有糖尿病？青少年糖尿病患者应该注意什么问题？青少年糖尿病主要包括1型和2型糖尿病。1型糖尿病是一种自身免疫性疾病，表现为患者体内胰岛素绝对缺乏，需要终身使用外源性胰岛素来控制血糖。2型糖尿病表现为环境与遗传因素共同导致的胰岛素抵抗及胰岛素分泌缺陷，糖尿病家族史与肥胖是2型糖尿病发病的重要原因。部分2型糖尿病患者通过饮食及运动治疗使血糖控制在理想范围，饮食及运动不能良好控制血糖的可以应用胰岛素及口服药物治疗。 过去，在青少年发病的糖尿病主要为1型糖尿病，但近30年来，全球青少年2型糖尿病患者增加了2~3倍，高脂饮食、体力活动减少、营养过剩、肥胖等多种因素，都可能青少年2型糖尿病的发病率升高 肥胖儿：易发病，难治疗家长要想早期发现孩子是否患有糖尿病，必须了解糖尿病的特点。典型的1型糖尿病具有以下特征：发病年龄较轻、急性起病、“三多一少”（多饮、多食、多尿、体重减轻）症状明显、一些患者以酮症酸中毒起病，另一些患者可由感染等应激情况造成严重高血糖或酮症酸中毒，部分患者同时伴有甲状腺机能减退。而2型糖尿病包括以下几个重要的临床特点：肥胖和超重；大多在青春期发病，以女性居多；常伴有2型糖尿病家族史；存在胰岛素抵抗相关疾病，如多囊卵巢综合征；出生时为低体重儿或巨大儿。“所以，当孩子出现以上情况时，家长应该定期带他们查空腹血糖、餐后血糖及糖化血红蛋白，必要时做糖耐量试验，以便早期发现孩子是否是糖尿病或处于糖尿病前期阶段，及时进行干预。”青少年2型糖尿病患者，85%以上伴有肥胖或超重。国外研究结果显示，青少年糖尿病患者体重越重，其血糖越难控制，在临床工作中我们也有同感。这类青少年患者的血糖控制难度之所以比较大，原因在于，体重越重，胰岛素抵抗越严重，血糖也就越难以控制。因此，对于肥胖的青少年患者，医生都会结合孩子的年龄、身高、体重、血糖，更加严格而且更个体化地控制其饮食及运动，在减重的同时增加胰岛素敏感性，从而使其血糖更易于控制。一味严格控制饮食，或影响发育在临床治疗中，陈树春发现，不少家长存在一个认识误区，即一味通过严格控制饮食来降低孩子血糖，却没有意识到，这种做法会影响孩子的生长发育。其实，“青少年糖尿病的治疗不同于成人糖尿病。青少年需要足够的营养来满足生长发育的需要，所以，在饮食治疗方面，应该根据每一位患者的不同情况制定饮食计划，尽可能达到既能控制血糖，又能满足生长发育的需要。”而且，青少年患者的血糖并非控制得越低越好，一味追求把血糖控制在低水平，可能使患儿出现低血糖。要知道，低血糖对身体造成的危害并不比高血糖小。一旦患儿出现低血糖反应，轻则肢体颤抖、面色苍白、心慌眼黑，重则意识不清甚至昏迷，还可能出现生命危险。青少年糖尿病患者，特别是青春期的孩子的血糖波动较大，血糖难以控制，而又易发低血糖，增加了治疗难度，需要根据患者的不同情况设立个体化的血糖控制目标，进行密切的血糖监测，并实施及时的调整治疗措施。家长应选择操作简单、方便、结果准确的血糖仪，尽量关注孩子的血糖监测，并督促其进行监测，不能认为按照医生给的药物治疗了就不用监测血糖了，或者血糖控制良好后自行停药，中断治疗。除了注意不能一味严格控制饮食外，家长还要注意不能让患儿盲目增加运动量，应综合考虑患者的身体状况，并根据患者的进食时间及胰岛素注射时间选择运动时间，当患儿出现糖尿病并发症时适当减少运动量。并发症危害不容忽视对青少年1型糖尿病患者而言，由于其胰岛素绝对缺乏，较成人2型糖尿病患者更易发生酮症酸中毒。而慢性并发症如视网膜病变、糖尿病肾病一般在糖尿病发病3～5年以后出现。为了避免或延缓这些并发症的出现，应注意一下问题：1.确诊糖尿病同时应测定血脂水平，如果血脂不正常，应每年监测血脂。如LDL胆固醇<2.6 mmol/L，每5年复查血脂谱。2.一旦儿童达到10岁，且糖尿病病程业已5年，应该每年筛查微量白蛋白尿，取随机时间点的尿样，计算白蛋白与肌苷的比值（ACR），如2次非同日尿样本，ACR均升高，应该考虑治疗。3.及时监测血压，如持续高于同年龄、性别、身高组的第95百分位数或持续>130/80 mmHg，应降压治疗。4.儿童≥10岁且患糖尿病病程3～5年，应该进行眼科检查，并每年检查一次。最后，提醒大家，在治疗的过程中，“由于青少年的心理、情绪变化较大，极易出现对疾病的恐惧感从而产生消极情绪，不能配合治疗，所以，医生和家长还需要更加关注孩子的心理反应，多与孩子沟通，一方面要充分了解疾病的危害，还要帮其排除心理障碍，树立战胜疾病的信心，从而更好的配合治疗。”胰岛素泵——应对患儿“黎明现象”对于青少年糖尿病患者来说，如何注射准确剂量的胰岛素一直是难题。胰岛素泵治疗是采用人工智能控制的胰岛素输入装置，通过持续皮下输注胰岛素的方式，模拟胰岛素的生理性分泌模式从而控制高血糖的一种胰岛素治疗方法。它可以避免不同部位、不同手法及不同注射装置造成的注射剂量的差异，使得血糖更易于控制。青少年糖尿病患者由于生长激素及类固醇激素的分泌特点，极易出现黎明现象（指糖尿病患者在夜间血糖控制尚可且平稳，即无低血糖的情况下，于黎明时分，即清晨3～9时由各种激素间不平衡分泌所引起的一种清晨高血糖状态），应用胰岛素泵较皮下注射胰岛素能更灵活、更有效地调整血糖。近年来，越来越多的青少年糖尿病患者开始应用胰岛素泵治疗，但由于价格较高，需长期佩戴等问题，仍没有广泛应用。

患者男性，51岁，因多饮、多尿、多食、消瘦就诊于多家医院，检查血糖明显升高，诊断2型糖尿病，给予多种降糖药及胰岛素治疗，血糖控制不理想，导致患者丧失信心。后经人介绍来我院内分泌科就诊，检查空腹血糖25mmol/L，早餐后2小时血糖32mmol/L，尿中检查有酮体2+，以“糖尿病酮症”收入院。入院查体时发现患者面容特殊，口唇肥厚、舌鼻肥大、鼻翼增厚，追问病史得知近4年来患者手足增大，鞋码增加2号，伴有声音低沉、打鼾、性功能减退等情况，考虑存在肢端肥大症，检查垂体MRI提示垂体瘤，诊断垂体瘤 肢端肥大症 继发性糖尿病 糖尿病酮症，在我科血糖控制平稳后转入我院神经外科手术治疗，术后患者血糖明显下降，症状消失，患者很快康复出院。继发性糖尿病是糖尿病的特殊类型，可以由多种原因引起，如垂体、肾上腺、肝脏、肾脏、甲状腺及胰腺等疾病均可引起，该病例就是由垂体瘤分泌过多生长激素导致糖代谢紊乱，血糖升高，临床上非常容易被误诊，导致疗效不佳，该患者就是这样的典型病例。正是因为我院内分泌科细致的查体，仔细的追问病史避免了本例患者的继续误诊，使患者得到了正确的治疗。在内分泌实验室、神经外科、伽马刀治疗中心的共同努力下，我院垂体疾病的检查、治疗手段在全省最全。另外，我院以内分泌科牵头成立了垂体疾病诊治协作组，规范了诊治流程，使我院垂体疾病的诊断和治疗水平达到了国内先进、省内领先的水平，邯郸、邢台、衡水和保定等地的很多患者慕名而来，使我科垂体疾病的病人住院数较前明显增加。