慢性乙型肝炎患者擅自停用拉米夫定的原因分析及护理对策

目的 探讨慢性乙型肝炎患者擅自停用拉米夫定的原因及相应的用药指导和健康教育方法.方法 收集214例服用拉米夫定的慢性乙型肝炎病人的资料进行回顾性调查,对36例患者擅自停药后的病情转归、停药原因进行分析.结果 36例中有5例擅自停药后出现病情复发加重,其中1例因肝衰竭死亡,擅自停药的原因有5种;服用拉米夫定的慢性乙型肝炎病人擅自停药的现象发生率16.8%.结论 擅自停药的患者易导致不良后果,医护人员应做到预先告知,定期监测、随访,做好护理用药指导.     

慢性乙型肝炎拉米夫定治疗后HBeAg早期血清学转换的临床随访观察

目前拉米夫定已广泛应用于乙型肝炎的抗病毒治疗,然而治疗中及停药后可出现病情复发.本文对应用拉米夫定治疗后出现HBeAg/抗-HBe早期血清学转换(服药6个月内)的46例慢性乙型肝炎病人进行临床随访,旨在探讨病情复发的影响因素,指导合理用药.     

拉米夫定治疗慢乙肝所致YMDD变异的个体化治疗

回顾性调查48例HBV慢性感染者拉米夫定治疗中出现YMDD变异发生的时间,对其随访观察6～12个月,每1～3个月检查1次肝功和病毒学指标。结果48例患者服药10～37个月出现YMDD变异。无肝硬化者36例,其中YMDD变异后病情稳定的慢乙肝15例,继续服用拉米夫定或停药,患者预后均较好;YMDD变异后病情复发者21例,停拉米夫定者病情进一步恶化,而继续服用拉米夫定并加用保肝治疗或α-干扰素治疗者预后较好。有肝硬化者12例,3例停药后2例死亡;9例继续服用拉米夫定者3例死亡（33．3％）。认为拉米夫定治疗中出现YMDD变异后,应给予个体化治疗,以提高HBeAg的血清转换率,降低病死率。     

拉米夫定治疗慢性乙型肝炎36例临床观察

目的观察拉米夫定治疗慢性乙型肝炎的效果。方法36例患者,采取拉米夫定治疗,分别于12月和24个月时观察ALT复常率,HBV DNA转阴率及HBeAg转阴率,同时检测YMDD变异的情况。结果拉米夫定治疗1年的HBV DNA、HBeAg转阴率为别为54.5%、24.2%,HBeAg/抗HBe血清转换率12.1%,ALT复常率78.8%,YM-DD变异率5.6%。停药半年后血清HBV DNA复阳率为22.2%,YMDD变异率18.2%,ALT再次升高率33.3%,死亡1例。结论拉米夫定能够有效降低HBV DNA水平,随着用药时间的延长,YMDD变异的发生率逐渐升高,部份病例停药后出现病情反复或加重。     

e 抗原阴性慢性乙型肝炎患者核苷类停药后的临床和病毒学复发评估

目的：探讨 e 抗原阴性慢性乙型肝炎患者核苷类停药后复发的临床特点和复发情况。方法对我院自2010年5月至2013年11月治疗的80例 e 抗原阴性慢性乙型肝炎患者入院资料进行分析,医护人员分析患者临床症状、使用的药物类型、疗程、患者的停药原因、停药复发后生化及病毒、血清学等指标变化。结果49例患者服用拉米夫定（LMV）,患者用药时间为3个月～3年;14例患者服用阿德福韦酯（ADV）患者用药时间为3个月～2年;11例患者短期服用拉米夫定后再用 ADV,患者用药时间为6个月～2年;6例患者服用恩替卡韦（ETV）,患者用药时间为6个月～1年;患者复发后,有35例患者慢性中度肝炎,23例患者慢性重度肝炎,12例患者慢性重型肝炎,6例患者代偿性肝硬化,4例患者失代偿性肝硬化。结论e 抗原阴性慢性乙型肝炎患者核苷类停药后多在2年以内复发,且停药复发后肝损害更加严重。     

浅议拉米夫定停药后复发性肝炎的治疗

处于活动期的慢性乙型肝炎病情反复发作,特别是HBV-DNA阳性者病情复发更是在所难免.拉米呋啶(贺普丁)能干扰HBV DNA的合成,抑制HBV复制,而发挥治疗作用,临床应用有效率高,但短期服药停药后部分患者易复发,临床要求长期服用,并于停药后应用干扰素等抗病毒药序贯治疗以防止或减少复发率.有的患者不遵医嘱,肝功能正常后擅自停药引起复发;按疗程服用的患者,停药后少数仍有复发现象.     

拉米夫定与阿德福韦先后治疗慢性乙型肝炎的近期疗效观察

目的探讨拉米夫定停药后乙型肝炎复发的治疗方法。方法对76例慢性乙型肝炎患者经拉米夫定治疗48周达到停药条件而停用后病情复发者,患者自愿继续服用阿德福韦者37例,给予阿德福韦酯片10mg口服,每日一次,连用6个月。另外39例停用拉米夫定后未接受任何治疗者为对照组。结果两组治疗后临床症状、体征、血生化指标、HBeAg转阴及HBeAg/抗-HBe血清转换无明显差异(P>0.05),而治疗组HBVDNA转阳者与对照组比,差异非常显著(P<0.01)。结论阿德福韦应用于拉米夫定治疗后复发的慢性乙型肝炎,对HBVDNA持续阴转疗效较好,表明阿德福韦有较好地抑制乙型肝炎病毒的作用。     

拉米夫定治疗活动性肝炎肝硬化的疗效观察

目的 观察活动性肝炎肝硬化患者拉米夫定长程治疗的疗效及对停药后肝功能异常的对策探讨。 方法口服拉米夫定100 mg,每日一次,连服18个月治疗活动性肝炎肝硬化患者58例。观察治疗前后的临床症状体征、生化指标、病毒学改变情况、停药后情况及对策探讨。 结果 (1)35例(74.5％)患者治疗后病情缓解稳定,生活质量改善,child-pugh积分下降;肝功恢复正常或好转。(2)HBV DNA下降>10~3拷贝/ml;HBeAg阴转率达33.3％(13/39)。(3)10例停药后,在3-6个月随访期间肝炎复发再次住院。停药后肝功能异常的治疗:2例用干扰素治疗1个月后出现黄疸、肝损害加重,立即停药保肝处理后缓解;8例患者未加任何抗病毒药物,经加强保肝、调节免疫等治疗后,肝功能得到改善。 结论 乙型肝炎后肝硬化患者伴有活动性病毒复制及肝炎时,长程拉米夫定治疗可改善肝功能,阻止病情进展,提高生活质量;停拉米夫定后肝炎活动不宜应用干扰素治疗。     

拉米夫定治疗后乙型肝炎e抗原血清转换患者的长期随访

目的观察托米夫定治疗发生乙型肝炎e抗原(ⅡBeAg)／抗-HBe血清转换的慢性乙型肝炎患者的转归。方法对发生ⅡBeAg／抗HBe血清转换时间≥6个月、拉米夫定治疗疗程≥18个月的68例患者进行24个月以上的随访观察。结果拉米夫定治疗后HBeAg／抗-HBe血清转换率为25．19％，YMDD变异率为20．59％，HBeAg／抗HBe血清转换后随访期内复发率为27．94％，停药后复发者再服拉米夫定有效。复发与年龄、治疗前丙氨酸氨基转移酶水平有关，与治疗前HBVDNA水平、疗程及有无YMDD变异无关。结论拉米夫定治疗慢性乙型肝炎即使HBeAg／抗HBe血清转换≥6个月仍有较高的复发率，对长期接受拉米夫定治疗的患者应加强随访观察。     

胸腺肽α1联合苦参素防治拉米夫定治疗慢性乙肝停药复发的疗效观察

拉米夫定治疗慢性乙型肝炎近期疗效较好,但需长期服用,且随用药时间的延长,HBV耐药变异率逐步增加,拉米夫定耐药变异后需换用或加用抗病毒药物治疗,导致医疗费用大幅度增加,患者不能承受而停止用药,引起病情复发或加重。为避免和减少长期用拉米夫定引起病毒耐药变异或停药造成慢性乙肝病情复发,我们在拉米夫定治疗慢性乙型肝炎取得完全应答后,停用拉米夫定,用胸腺肽α1联合苦参素继续治疗防治复发取得较好效果,报告如下：     

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.