江苏省2型糖尿病患者血糖控制及治疗用药情况调查

目的了解江苏省2型糖尿病（T2DM）患者的血糖控制情况,分析治疗方法与血糖控制的关系。方法采用横断面研究方法,以调查问卷形式收集患者年龄、病程、降糖药物的使用情况等,留取血标本检测HbA1c。根据HbA1c水平将患者分为达标组（HbA1c〈6．5％）和未达标组（HbA1c≥6．5％）;根据降糖治疗情况分为胰岛素（Ins）组、胰岛素联用口服降糖药（Ins＋OA）组、口服降糖药（OA）组、生活方式干预（LS）组。结果入选T2DM患者2966例,年龄（56．4±11．2）岁,糖尿病平均病程（6．3±5．7）年,HbA1c值（7．2±1．6）％,HbA1c≥6．5％的患者占59．8％。（1）平均病程Ins组[（7．6±6．5）年]与Ins＋OA组[（8．2±6．2）年]均高于OA组C（5．3±5．0）年]（P〈0．01）。HbA1c均值及未达标比例Ins组[（7．4±1．6）％,未达标比例65．9％]与Ins＋OA组[（7．5±1．5）％,未达标比例77．9％]均高于OA组[（7．0±1．6）％,未达标比例52．4％]（P〈0．01）。（2）HbA1c达标组与未达标组病程分别为（4．8±4．9）年和（7．3±6．1）年（P〈0．01）,两组中胰岛素联合口服降糖药治疗者分别占11．5％和27．2％（P〈0．01）,单用胰岛素治疗者分别占17．0％和22．1％（P〈0．01）。结论江苏省T2DM患者血糖控制现状比3年前全国调查情况有所改善,但仍有相当比例的患者HbA1c水平没有达到IDF及《中国2型糖尿病防治指南》推荐标准。接受胰岛素治疗的患者HbA1c均值及不达标比例明显高于其他治疗组,表明由于病程延长及口服降糖药用药失效导致病情恶化后,再选择胰岛素治疗,血糖控制情况并不理想。     

口服降糖药血糖控制不佳的老年2型糖尿病患者加用甘精胰岛素的疗效观察

目的通过比较甘精胰岛素和诺和灵N对口服降糖药血糖控制不佳的老年2型糖尿病患者的治疗效果,探讨甘精胰岛素在老年2型糖尿病患者血糖达标治疗中的临床运用价值。方法44例口服降糖药治疗空腹血糖控制不佳的老年2型糖尿病患者随机分为两组：甘精胰岛素治疗组22例,诺和灵N治疗组22例,治疗12周。观察两组治疗前后的糖化血红蛋白（HbA1c）值、空腹血糖（FBG）、餐后两小时血糖（2hPG）、体重指数（BMI）和每日所需的胰岛素剂量以及两组治疗过程中低血糖发生的频率。结果治疗12周后两组HbA1c、FBG、2hPG与治疗前比较差异有统计学意义（P〈0．05）;而两组间HbA1c、2hPG、低血糖事件的发生率比较差异有统计学意义（P〈0．05）,每日胰岛素的用量、BMI、FBG比较差异无统计学意义（P〉0．05）。结论加用甘精胰岛素对口服降糖药血糖控制不佳的老年2型糖尿病患者能更有效更安全地控制血糖。     

格列奎酮联合甘精胰岛素治疗早期糖尿病肾病

将63例早期DN患者随机分为格列奎酮联合甘精胰岛素治疗组、常规胰岛素治疗组，比较12周前后的FPG达标时间、HbA1c、UAE的变化及低血糖发生率。结果：联合组血糖达标时间3．4±0．7d，HbA1c 6．5±0．8％；胰岛素组达标时间3．1±0．9d，HbA1c 6．7±1．1％比较没统计学差异。联合组UAE133±32μg／min，低血糖发生率18．2％，胰岛素组UAE167±37μg／min，低血糖发生率40．6％，有明显差异（P〈0．001）。结论：格列奎酮联合甘精胰岛素治疗早期糖尿病肾病．同样有效地控制患者血糖，可降低UAE，且低血糖发生率低。     

HbA1c达标的老年糖尿病患者HbA1c与血糖波动的关系

目的探讨糖化血红蛋白（HbA1c）达标（HbA1c〈7．5％）的老年2型糖尿病患者HbA1c与血糖波动的关系。方法选取HbA1c〈7．5％的住院老年糖尿病患者100例，采用动态血糖监测系统（CGMS）进行3d的血糖监测，分析血糖波动情况，计算平均血糖、高血糖持续时间以及平均血糖漂移幅度（MAGE），分析HbA1c与上述测定值之间的相关性。结果59．5％的患者血糖最高值超过11．1mmol/L，29．7％的患者发生低血糖（〈3．9mmol/L）；血糖超过7．8mmol/L占全天的时间百分比为33％；血糖超过11．1mmol/L占全天的时间百分比为（10．2±1．2）％；低血糖占时间百分比（5．2±1．5）％；HbA1c与CGMS平均血糖值呈显著正相关（r=0．55，P〈0．01），与高血糖持续时间相关（r=0．48，P〈0．01），与MAGE无关（r=0．12，P〉0．05）。结论HbA1c达标的老年2型糖尿病人血糖波动大；HbA1c与平均血糖以及高血糖持续时间相关。与血糖波动无关；HbA1c和血糖波动是评价血糖控制的量与质的独立指标。     

预混胰岛素血糖控制不佳的超重2型糖尿病患者联合口服亚奠利疗效观察

选择28例单用预混胰岛素治疗血糖控制不佳的超重2型糖尿病患者,即空腹血糖（FBG）〉8．0mmol／L、餐后2小时血糖（2hPBG）〉11．1mmol／L,糖化血红蛋白（HbA,c）≥7．0％,BMI≥24kg／m2者。观察组在原预混胰岛素治疗基础上加用亚莫利,观察血糖控制达标时的胰岛素剂量。治疗12周后,比较联合亚莫利前后FBG、2hPBG、糖化血红蛋白（HbA1C）、体重指数（BMI）、每天胰岛素剂量（u）等指标。结果亚莫利联合预混胰岛素治疗达标12周后,可显著降低血糖、HbA1C,而且减少预混胰岛素剂量。比较两组患者体重指数,差异没有统计学意义,但是,观察组患者调整胰岛素治疗后的体重增加较治疗组略明显。结论单用预混胰岛素治疗的超重2型糖尿病患者血糖控制不佳时,加用亚莫利后既能显著改善血糖控制,又能减少胰岛素的剂量;另外患者的体重也无明显增加。     

新诊断2型糖尿病患者综合管理6年后的达标情况及影响达标的因素分析

目的 观察新诊断T2DM患者综合管理6年后代谢指标的达标情况并分析其影响因素.方法 157例新诊断T2DM患者专人管理并定期随访,给予综合干预.结果 （1）随访6年后SBP、DBP、FPG、2 hPG、HbA1 c、TG、TC、LDL-C水平较干预前降低,HDL-C升高（P＜0.05）.随访6年后与新诊断时达标率比较,SBP：75.2％vs52.9％,DBP：66.9％vs40.8％,BP：61.8％ vs 33.1％,FPG：59.2％vs19.7％,2hPG：74.5％vs22.9％,HbA1c：52.9％vs29.9％,TC：59.2％vs37.6％,TG：58.6％vs 36.3％,HDL-C：69.4％vs43.3％,LDL-C：52.9％vs29.3％,BMI：42.7％vs38.9％.（2）糖尿病知识得分、运动和血糖监测次数与血糖不达标呈独立负相关.（3）不达标组颈动脉内膜-中层厚度（IMT）增厚发生率高于达标组;不达标组DR、糖尿病慢性肾脏疾病（CKD）发生率高于达标组.结论 长期综合管理可提高T2DM患者血糖达标率.血糖、BP、血脂和BMI不达标可增加糖尿病血管并发症的发生.     

胰岛素注射技术误区解析及国际规范推荐

我国最新的糖尿病流行病学调查显示,在20岁以上的中国人群中,糖尿病患病率高达9．7％。使人担忧的是,我国糖尿病患病率虽高,但血糖达标率却较低,两者形成极大的反差。2006年中国地区的糖尿病现状调查显示,仅26．8％的患者血糖控制理想[糖化血红蛋白（HbA1c）≤6．5％];而73．2％的患者血糖控制未能达标（HbA1c〉6．5％）,HbA1c〉8％的患者更高达28．3％;尽管有众多因素影响血糖达标,但即使在已经使用胰岛素的患者中,     

甘精胰岛素联合二甲双胍治疗老年2型糖尿病临床分析

45例血糖控制不良的老年T2DM患者（FBG〉8．0mmol／L,HbA1c〉7．5％）,随机分为A组（n=25）和B组（n=20）,两组均联台口服二甲双胍850mg,qd,以两组FPG〈60mmol／L为达标,共治疗12周,比较治疗后两组血糖达标时间、平均FPG水平、HbA1c、胰岛素用量、低血糖发生率,结果A组在血糖达标时间及低血糖发生率方面明显低于B组（P〈0．05）。结论甘精胰岛素联合二甲双胍的治疗方案,其降糖始果显著,低血糖发生率低,安全性高,适合老年糖尿病的治疗。     

胰岛素泵强化治疗2型糖尿病的疗效观察及长期随访研究

观察、随访、对照性分析64例2型糖尿病患者经胰岛素泵强化治疗2周后血糖控制情况、血糖达标（空腹血糖4．0～7．0mmol／L,餐后2小时血糖4．4～9．0mmol／L）所需时间等。结果：胰岛素泵治疗组胰岛素用量、血糖达标时间、低血糖发生率及血糖达标后6个月、1年、2年一直到第五年糖化血红蛋白（HbA1c）明显优于皮下每日2次注射预混胰岛素30R组。结论：胰岛素泵可迅速有效使2型糖尿病患者血糖达标,消除高血糖的毒性作用,使受糖毒性损伤的残存胰岛8细胞功能得到一定程度恢复,可延缓胰岛B细胞功能的衰退。     

甘精胰岛素联合二甲双胍治疗老年2型糖尿病的疗效观察

54例OAD但血糖控制不良的老年T2DM患者（HbA1c〉7．5％）,随机分为甘精组（n=28）和预混组（n=26）,分别采用每晚9点注射甘精加二甲双胍和预混素（诺和灵30R）早晚餐前皮下注射治3个月。结果治疗后两组空腹血糖（FBG）、餐后2小时血糖（2hPBG）和糖化血红蛋白（HbA1c）无明显差异（P〉0．05）。但甘精组低血糖发生率明显少于预混组P〈（0．05）。结论甘精联合二甲双胍可使更多的老年T2DM患者的血糖达标,减少低血糖事件发生。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

CagA-Hp抗体IgG与胃炎的组织学分析

研究幽门螺杆菌(Hp)感染与胃炎的关系。方法对204例慢性胃炎患者胃粘膜进行观察分析,并测定其中137例Hp阳性患者血清CagA-Hp抗体IgG水平,与组织学对照。结果慢性萎缩性胃炎伴肠上皮化生患者血清CagA抗体IgG明显高于对照组(P＜0.01);其他类型胃炎患者血清CagA抗体IgG水平无明显增高(P＞0.05)。结论CagA-Hp可能是导致慢性萎缩性胃炎伴肠上皮化生的因素之一,对这类患者应密切随访观察。     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

慢阻肺急性加重期患者预后的影响因素分析

目的探讨慢性阻塞性肺病急性加重期(AECOPD)患者预后的相关危险因素。方法回顾性调查、收集58例AECOPD患者可能影响其预后的相关因素,并对其分别进行单因素分析。并进行Logistic多元逐步回归进行多因素分析,筛选影响AECOPD患者预后的独立危险因素。结果单因素分析后将结果 P0.1的因素纳入多因素Logistic回归,分析发现是否合并呼吸衰竭、气促程度、白细胞计数、APACHEⅡ、应用抗氧化剂、慢阻肺治疗依从性为影响AECOPD患者预后不佳的独立因素(P0.05)。结论根据AECOPD患者预后的独立危险因素,及早判断,选择合适的后续治疗方案,对提高其生存率及生存质量具有重要意义。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Results of treatment of fistula-in-ano

To evaluate the application of Parks' classification in the management of patients with fistula-in-ano, a study was undertaken to assess the outcome of surgery, especially with respect to the recurrence rate and alteration of continence. A retrospective analysis of 160 consecutive patients who were classified at the time of operation was conducted. The distribution of fistulas was as follows: intersphincteric, 41.9 percent, transsphincteric, 52.1 percent, suprasphincteric, 1.3 percent, extrasphincteric, 0. A horseshoe extension occurred in 8.8 percent of the fistulas and 3.8 percent did not exactly conform to the classification as they were either complex or combinations of more than one type of fistula. The sole immediate postoperative complication was bleeding, which occurred one week postoperatively and ceased spontaneously (0.7 percent). Alteration in continence occurred in 6 percent of patients with 2.6 percent experiencing temporary incontinence to flatus, 1.3 percent to liquid stool, and 0.7 percent to solid stool. Permanent loss of control for flatus occurred in one patient (0.7 percent) and for liquid stool in one patient (0.7 percent). No patients suffered loss of control for solid stool. Recurrence developed in 6.3 percent of patients, all between five and 25 months postoperatively. Classifcation was found to be a useful guide in the operative management of patients with fistula-in-ano. Read at the joint meeting of the American Society of Colon and Rectal Surgeons with the Section of Colo-Proctology, Royal Society of Medicine, and the Section of Colonic and Rectal Surgery, Royal Australasian College of Surgeons, New Orleans, Louisiana, May 6 to 11, 1984.