重组人生长激素治疗肝硬化低蛋白血症的影响因素及意义

目的探讨重组人生长激素对不同血清白蛋白含量肝硬化患者低蛋白血症的临床疗效及意义。方法将92例血清白蛋白含量低于35g/L的肝硬化患者根据血清白蛋白含量分为3组：轻度低水平组（30.0～35.0g/L）、中度低水平组（25.0～30.0g/L）、重度低水平组（20.0～25.0g/L）,每组随机分为两组,治疗组给予重组人生长激素4IU肌注,1次/2日;对照组给予20%人血白蛋白100ml静滴,1次/2日,两组疗程均为30d。治疗组和对照组均给予相同方案的保肝、对症治疗。分别于治疗后15d、30d、60d、90d测定相应观察指标。结果治疗后30d两组患者血清白蛋白含量均上升,治疗组于治疗后第90d后仍维持高点水平,且肝功能好转,而对照组60d后白蛋白含量开始降低;血清白蛋白浓度大于25.0g/L时,治疗组观察指标改善尤为明显。结论重组人生长激素可明显提高肝硬化低蛋白血症患者血清白蛋白水平,中远期疗效好,并可改善肝功能;肝硬化患者血清白蛋白浓度对生长激素的疗效具有显著影响。     

生长激素治疗失代偿期肝硬化34例临床观察

目的探讨重组人生长激素注射液(安苏萌)治疗肝硬化低蛋白血症的临床疗效。方法选择34例肝硬化低蛋白血症患者用重组人生长激素(r-hGH)4IU皮下注射,每天1次,20天一个疗程。疗效评估包括症状改善情况、血清白蛋白(ALB),血清前白蛋白(PALB),血清球蛋白(GLB)、血清谷丙转氨酶(ALT)。结果应用r-hGH治疗20天后,症状明显改善,血清ALB、PALB明显上升。停药4周后血清ALB仍继续升高。提示r-hGH对改善肝功能,升高血清ALB有较好疗效。结论安苏萌能促进肝细胞合成白蛋白,对低蛋白血症远期疗效好,价格便宜,值得推广。     

生长激素治疗失代偿期肝硬化34 例临床观察

目的探讨重组人生长激素注射液(安苏萌)治疗肝硬化低蛋白血症的临床疗效。方法选择34例肝硬化低蛋白血症患者用重组人生长激素(r-hGH)4IU皮下注射,每天1次,20天一个疗程。疗效评估包括症状改善情况、血清白蛋白(ALB),血清前白蛋白(PALB),血清球蛋白(GLB)、血清谷丙转氨酶(ALT)。结果应用r-hGH治疗20天后,症状明显改善,血清ALB、PALB明显上升。停药4周后血清ALB仍继续升高。提示r-hGH对改善肝功能,升高血清ALB有较好疗效。结论安苏萌能促进肝细胞合成白蛋白,对低蛋白血症远期疗效好,价格便宜,值得推广。     

生长激素治疗肝硬化低蛋白血症的临床研究

目的观察重组人生长激素(rhGH)对肝硬化低蛋白血症的治疗效果。方法60例肝硬化失代偿期患者随机分为两组,每组30例,两组均隔日输注人血白蛋白10g,治疗组每天皮下注射rhGH4IU一次,共14天。治疗前,治疗结束时及停药后1月、6月观察临床症状及肝功能、生化指标的变化。结果治疗结束时,治疗组及对照组的临床症状均有改善,血清白蛋白含量分别由27.5±3.6g/L和25.7±4.2g/L升至33.2±6.4g/L和34.1±3.2g/L(P<0.05),肝功能指标明显好转。停药1月后,对照组血清白蛋白含量开始下降,而治疗组在停药6月后血清白蛋白仍能维持较高水平(35.2±2.8g/L)。结论rhGH可以明显提高肝硬化患者血清白蛋白水平,疗效持久,远期疗效有待进一步研究。     

重组人生长激素对肝炎肝硬化患者生长激素抵抗状况改善的研究

评价重组人生长激素对不同Child -Pugh积分肝炎肝硬化患者生长激素抵抗的改善及对低蛋白血症的影响 ,根据Child -Pugh积分分为 <9组 ,2 5例 ; 9组 ,2 6例两组。再采用随机区组设计方法对上述患者分组治疗 ,治疗组 (各 16、15例 )用重组人生长激素 (0 2 5U/kg·d) ,对照组 (各 9、11例 )予人血白蛋白 (10g/d)治疗 10天。用放射免疫法测定治疗前、治疗后 2 4h及治疗结束时的血清生长激素 (GH ,μg/L)、类胰岛素生长因子 (IGF) - 1(μg/L)。肝硬化患者GH水平高于健康人 (P <0 0 5 ) ,但IGF - 1水平明显降低 (P <0 0 1)。经重组人生长激素治疗后 ,肝硬化患者生长激素抵抗均有不同程度改善 (P <0 0 1)。观察结束两治疗组比较 ,积分高组较之低组GH一直维持较高水平 (9 91± 7 6 1,4 75± 3 94 ,P <0 0 5 ) ,且IGF - 1上升幅度低 (4 8 4 3± 16 88,6 3 4 7± 2 2 19,P <0 0 5 )。两治疗组治疗后血清白蛋白 (ALB)均有明显升高。重组人生长激素可以克服肝硬化患者 ,尤其Child -Pugh积分低者的生长激素抵抗现象 ,并纠正其低蛋白血症     

重组生长激素治疗肝硬化低蛋白血症的临床研究

目的：探讨重组生长激素对肝硬化低蛋白血症的治疗作用。方法：116例肝硬化患者随机分为治疗组62例和对照组54例,在相同的治疗基础上治疗组加用重组生长激素,4．5u/次,隔日1次。观察治疗前、后和治疗后1个月、3个月及6个月的血清白蛋白水平。结果：治疗组血清白蛋白水平显著改善,与对照组相比有显著性差异。结论：生长激素可有效地改善肝硬化低蛋白血症。     

生长激素治疗肝硬化低蛋白血症的

目的 探讨重组人生长激素(rhGH)治疗肝硬化低蛋白血症的疗效.方法 218例肝硬化患者随机分为治疗组116例和对照组102例,在基础护肝对症治疗上治疗组加用rhGH 4.5 IU皮下注射,每天1次,共10次为1疗程.在治疗前后动态观察临床症状体征和各项肝功能指标.结果 治疗组症状体征明显改善,血清白蛋白水平显著提高,并维持在较长时间内,与对照组相比有显著差异.结论 生长激素治疗肝硬化低蛋白血症有较好的疗效.     

生长激素治疗肝硬化低蛋白血症的临床研究

目的 探讨重组人生长激素（rhGH）治疗肝硬化低蛋白血症的疗效。方法 218例肝硬化患者随机分为治疗组116例和对照组102例，在基础护肝对症治疗上治疗组加用rhGH4．5IU皮下注射，每天1次，共10次为1疗程。在治疗前后动态观察临床症状体征和各项肝功能指标。结果 治疗组症状体征明显改善，血清白蛋白水平显著提高，并维持在较长时间内，与对照组相比有显著差异。结论 生长激素治疗肝硬化低蛋白血症有较好的疗效。     

重组人生长激素治疗肝炎肝硬化低白蛋白血症疗效观察

肝炎肝硬化失代偿期普遍存在低白蛋白血症 ,不但加重病情 ,还可引起消瘦、浮肿、腹水和各种并发症。目前 ,临床治疗低蛋白血症主要是静脉输注人血白蛋白。我们应用重组人生长激素 (思增 )治疗肝炎肝硬化低白蛋血症 ,取得较好效果 ,现报告如下。资料与方法 :本组 6 0例肝炎肝硬化患者 ,均为男性 ,年龄40～ 70岁。均符合 1995年全国肝炎会议修定的诊断标准。血清血蛋白 <35 g/ L ;消化道症状相对较轻 ,无肝功能衰竭倾向 ;无糖尿病、甲状腺机能低下等内分泌疾病 ;肝硬化程度均为 B级。将 6 0例患者随机分为观察组和对照组各 30例 (两组性别、…     

重组人生长激素治疗肝硬化低蛋白血症30例观察

目的观察重组人生长激素治疗肝硬化引起的低白蛋白血症疗效.方法选择血清白蛋白含量低于35g/L的肝硬化病人30例,男24例,女6例,年龄28～68岁,平均483±10.8岁;Child积分A级3例,B级22例,C级5例,无肿瘤和高血糖,除外其他原因引起的低蛋白血症.治疗方法为注射用重组人生长激素4IU,皮下注射,每日一次,10天为一疗程,治疗期间不得使用人血白蛋白、血浆和其他促进肝细胞生长和促进蛋白合成的药物.观察指标为食欲、腹胀、乏力和恶心等症状改善情况;血清白蛋白、球蛋白、胆红素、ALT、凝血酶原时间、血糖及血常规的变化.结果1.症状改善情况治疗后食欲增加为70%(21/30)、腹胀减轻为63.3%(19/30)、乏力减轻为83.3%(25/30)、恶心减轻为57.9%(11/19).2.血清白蛋白由治疗前的27.96±3.53g/L增加到32.33±3.3g/L(P<0.01);停药后2周血清白蛋白增加到36.41±3.69g/L(17例).Child积分减少(P<0.01),其他肝功指标无明显变化.血糖、尿素氮和肌酐亦无明显改变.结论重组人生长激素可以增加肝硬化病人的白蛋白合成,改善营养状况,无明显不良反应.长期疗效有待进一步研究.     

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。     

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.     

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.     

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。     

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。     

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。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

Study of constancy of hydrogen-consuming flora of human colon

The constancy of the hydrogen consuming flora of the human colon was studied in 15 healthy subjects via two measurements obtained 18 to 36 months apart. Hydrogen disappearance rate and the major products of H₂-consuming bacteria, methane and sulfide, were measured during incubation of fecal homogenates with excess hydrogen and sulfate. In 11/15, the hydrogen consumption rate and the predominant hydrogen-consuming pathway (methanogenesis, sulfate reduction, or neither) remained constant. However, major shifts in these pathways were observed in four subjects, with two losing and two gaining the ability to produce methane. Methanogenesis was associated with the highest hydrogen consumption rate. This study demonstrates that clinically unrecognizable, major alterations of the colonic flora occur in healthy subjects. Understanding of the factors responsible for these alterations might allow for therapeutic manipulation of the colonic flora.Supported in part by the Department of Veterans Affairs and NIDDKD RO1 DK 13309-25.