探讨慢性乙型肝炎重叠戊型肝炎病毒感染与肝炎重症化的关系

目的探究慢性乙型肝炎重叠戊型肝炎病毒(HEV)感染与肝炎重症化的关系。方法择取我院2012年7月至2015年8月收治的78例慢性乙型肝炎患者纳入本次实验研究,对所有患者均进行临床各项检测,对检测结果进行分析探讨。结果经过临床研究观察后得知,重叠HEV感染患者中,重型肝炎与中型肝炎的感染发生率较高,与轻型肝炎的感染发生率相比较数据差异显著,P<0.05。结论在肝炎重症化过程中,HEV重叠感染起着十分重要的作用,提示在今后的临床工作中更加深入研究二者之间的关联性。     

戊型肝炎

戊型肝炎既往称为肠道传播的非甲非乙型肝炎。世界上首次有记载的本病流行发生于1955～1956年新德里，共计发病97000例，其中29300例为黄疽型肝炎。1983年Balayan等首次用戊型肝炎病人的粪便提取液，经口感染一名志愿者获得成功，并从其急性期粪便中用免疫电镜技术检测到戊型肝     

戊型肝炎疫苗接种前景

戊型肝炎占发展中国家青年中急性病毒性肝炎病例的一半以上,感染的孕妇,尤其是妊娠晚期,死亡率可高达20％～30％。灭活或减毒活疫苗的研制因病毒不能在细胞培养物中有效复制而受到阻碍。利用基因重组技术研制出一种戊型肝炎疫苗,Ⅰ期临床试验表明该疫苗在人体中具有较好的安全性和免疫原性,有必要在疫区作进一步应用评估。     

慢性乙型肝炎重叠戊型肝炎感染60例临床分析

目的 观察慢性乙型肝炎患者重叠感染戊型肝炎病毒临床特点及戊型肝炎病毒对慢性乙型肝炎患者的影响.方法 对60例慢性乙型肝炎病毒重叠戊型肝炎病毒感染组患者与60例单纯慢性乙型肝炎病毒感染组的临床资料进行对照分析.结果 2组的临床生化指标,总胆红素、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、凝血酶原活动度、血白蛋白差异有统计学意...     

戊型肝炎研究进展

戊型肝炎研究进展顾秀华＊综述彭文伟审校＊＊肠道传播的非甲非乙型肝炎（ＥＴ－ＮＡＮＢＨ）病毒已定名为戊型肝炎病毒（ＨＥＶ）。近年来，由于ＨＥＶ基因组分子克隆成功及实验感染动物模型的建立〔１、４〕，为进一步阐明病毒特点，病毒血症及感染整个过程及实验室诊断...     

太原地区戊型肝炎临床研究

太原地区戊型肝炎临床研究太原市传染病医院（０３００１２）姜丽丽，韩仙梅，荀健，李彩霞山西医学院张志敏，王俊生１９８９年在日本东京召开的国际传染病学术会议上将非甲非乙型肝炎分为经血传播的丙型肝炎病毒（ＨＣＶ）和经肠道传播的戊型肝炎病毒（ＨＥＶ）两种。同...     

戊型肝炎56例报告

戊型肝炎是经粪-口途径传播的传染病,近年来国内有流行或散发流行报道,淮阴地区呈散发性流行,且老年患者有逐年增多趋势。近3年我院收治戊肝56例,现将临床分析如下: 1 临床资料 1.1 一般资料:56例均为住院病人,男性45例,女性11例,年龄4个月～79岁,平均39.8岁,其中18～45岁26例(46.2％),50岁以上25例(44.6％),本组以青壮年和老年患者为主。随机选择同期甲型肝炎46例对照,平均年龄24.7岁,以青年患者为主,两组年龄相比有显著性差异(P<0.05),戊型肝炎组中老年患者明显多于甲型肝炎组。     

戊型肝炎的研究进展

一、HE病原学研究l．HE病原学早期研究工作[1]。1982年Balayan等用免疫电镜发现肠道传播的非甲非乙型肝炎（NANBH）病人粪便中存在一种直径为27～30urn园球状病毒样颗粒。1983年Bal－ayan最先用猕猴静注10％人志愿者大便是液，在其中用免疫电镜证明有27～30urn的病毒颗粒，接种后24～36小时内ALT升高并在发病的急性期前期大便中排出27～30um的同样颗粒。BradleyDW，使用猕猴、城猴及黑猩猩，获得接种前、急性期及恢复期的血清，用来包被试剂板、免疫荧光抗体检测和进行λ－gt11cDNA库的免疫筛选研究。在接种后平均38天动物ALT升高…     

戊型肝炎疫苗接种前景

戊型肝炎占发展中国家青年中急性病毒性肝炎病例的一半以上，感染的孕妇，尤其是妊娠晚期，死亡率可高达20％－30％。灭活或减毒活疫苗的研制因病毒不能在细胞培养物中有效复制而受到阻碍。利用基因重组技术研制出一种戊型肝炎疫苗，I期临床试验表明在该疫苗在人体中具有较好的安全性和免疫原性，有必要在疫区作进一步应用评估。     

慢性乙型肝炎重叠急性戊型肝炎患者视黄醇结合蛋白检测

目的 探讨慢性乙型肝炎(慢乙肝)重叠急性戊型肝炎(戊肝)患者视黄醇结合蛋白(RBP)水平变化及临床意义.方法 慢乙肝患者81例分为单纯乙肝(A组,41例)和重叠戊肝(B组,40例)两组,同时随机选择同期健康体检者42例为对照(C组),比较各组RBP水平.结果 A、B组的RBP水平在发作期和恢复期均明显低于C组(P＜0.05或P＜0.01),B组的RBP水平在发作期和恢复期均明显低于A组(P＜0.05或P＜0.01).各组RBP与前白蛋白(PA)和白蛋白呈正相关,与ALT和AST呈负相关(P＜0.01).结论 RBP水平可以作为慢乙肝患者,尤其在重叠感染时,肝损伤的评估指标.     

Drug Discovery for Overcoming Chronic Kidney Disease (CKD): Pharmacological Effects of Mineralocorticoid-Receptor Blockers

There is increasing evidence demonstrating that the renoprotective effects of mineralocorticoid receptor (MR) blockade are independent of the effects exerted by renin-angiotensin inhibitors. MR is expressed not only in tubular cells but also in other renal cells including glomerular mesangial cells, podocytes, and renal interstitial fibroblasts. Animal experiments have shown that MR blockers prevent aldosterone-induced proteinuria, glomerular injury, and tubulointerstitial fibrosis. In vitro studies have also demonstrated that MR blockers inhibit aldosterone-induced renal cell damage. Recent clinical studies have shown that treatment with MR blockers attenuates the development of proteinuria in patients with chronic kidney disease (CKD) and hypertension, independent of changes in blood pressure. In some cases, MR blockers elicit potent renoprotective effects in conditions where aldosterone levels are not elevated. These data suggest that treatment with MR blockers may possibly present an effective therapeutic strategy for patients with CKD.     

Chronic toxicity of di(2-ethylhexyl)phthalate in rats.

Fischer 344 rats were treated with 0, 100, 500, 2500, or 12,500 ppm di(2-ethylhexyl)phthalate (DEHP) in the diet for up to 104 weeks. Blood and urine were analyzed at weeks 26, 52, 78, and 104 from 10 animals per sex per group. Survival was slightly but not statistically reduced for rats receiving 12,500 ppm DEHP. Body weights and food consumption were significantly reduced for rats receiving the highest dose level of DEHP and occasionally for the male 2500-ppm group. BUN and albumin were significantly higher and globulin lower at nearly every sampling interval for the 12,500-ppm group compared with the controls. There was an increase in the mean activities of AST and ALT at 104 weeks, but no statistically significant differences were seen. Erythrocyte count, hemoglobin, and hematocrit values for the 12,500-ppm group were significantly lower than controls at nearly every sampling interval. No other differences in hematology were seen. No toxicologically significant changes were observed in urinalysis. At termination, relative lung weights for the 2500- and 12,500-ppm male groups of rats were significantly higher than for the controls. Absolute and relative liver and kidney weights for the 2500- and 12,500-ppm male rats, and liver weights for 12,500-ppm female rats were higher compared with the controls. Absolute and relative testes weights for the 12, 500-ppm male rats were lower compared with the controls. All organs were examined for histopathology. The incidence of hepatocellular lesions has been reported separately and correlated with the induction of peroxisomal enzyme activity (David et al., 1999). A dose level of 500 ppm was the NOEL for peroxisome proliferation. Bilateral aspermatogenesis in the testes, castration cells in the pituitary gland, spongiosis hepatis, and pancreatic acinar cell adenoma were observed for 12,500-ppm male rats. Aspermatogenesis and spongiosis hepatis were observed for 2500-ppm male rats, and aspermatogenesis was seen at 500 ppm. DEHP exposure exacerbated age-, species- or strain-related lesions such as mineralization of the renal papilla and chronic progressive nephropathy in male rats. Kupffer cell pigmentation and renal tubule pigmentation were seen in male and female 12,500-ppm rats. The increased incidence of spongiosis hepatis correlated with increased palmitoyl CoA oxidase activity, but the incidence of pancreatic acinar cell adenoma was increased only at the highest dose level of 12,500 ppm. These lesions, although typical of those seen with other peroxisome proliferators, may respond differently depending on the potency of the peroxisome proliferator. A dose level of 500 ppm (28.9-36.1 mg/kg/day) was considered to be the NOAEL.     

Chronic toxicity of di(2-ethylhexyl)phthalate in mice.

B6C3F1 mice were treated with 0, 100, 500, 1500, or 6000 ppm di(2-ethylhexyl)phthalate (DEHP) in the diet for up to 104 weeks. Blood and urine were analyzed at Weeks 26, 52, 78, and 104 from 10 animals per sex per group. Body weights and food consumption were measured weekly for the first 16 weeks, then monthly thereafter. Survival was reduced for mice receiving 6000 ppm DEHP. Overall weight gains were significantly lower for the 6000-ppm male group, but there was no difference among female groups. Food consumption was not affected by exposure. No biologically significant changes in clinical chemistry, hematology, or urinalysis were observed. After 104 weeks of exposure, kidney weights for the 500- and 1500-ppm male, and 6000-ppm male/female groups were significantly lower than for the controls. Significantly higher liver weight was seen for the 500-, 1500-, and 6000-ppm male groups and the 6000-ppm female group of mice. Testis weights for the 500-, 1500-, and 6000-ppm males were significantly lower than for the controls. Uterine weights for the 6000-ppm group were significantly lower than for the controls. All organs were examined for histopathology. The incidence of hepatocellular lesions has been reported separately (R. M. David et al., 1999. Toxicol. Sci. 50, 195-205). Tumors were observed at > or = 500-ppm dosages, where peroxisome proliferation was significantly increased. A NOEL for both tumors and peroxisome proliferation was 100 ppm. In the study presented here, bilateral hypospermia in the testes of male mice, hepatocyte pigmentation and cytoplasmic eosinophilia in the liver, and chronic progressive nephropathy of male and female mice were observed at 6000 ppm. Hypospermia and chronic progressive nephropathy were also observed at 1500 ppm, where peroxisome proliferation was 2.7-6.8-fold higher than controls. Many lesions observed in rats were not seen in mice. A dose level of 500 ppm (98.5-116.8 mg/kg/day) was identified as a no-observed-adverse-effect level (NOAEL) for noncarcinogenic effects.     

Drug Discovery for Overcoming Chronic Kidney Disease (CKD): The Endothelin ETB Receptor / Nitric Oxide System Functions as a Protective Factor in CKD

Accelerated cardiovascular disease (CVD) is a frequent complication of renal disease. Chronic kidney disease (CKD) develops hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. There is general agreement that endothelin-1 (ET-1), which acts through the two subtypes of receptor ET_A and ET_B, plays important physiological roles in the regulation of normal cardiovascular function and that excessive ET-1 production is linked to CVD and CKD. Although selective ET_A or nonselective ET_A/ET_B receptor antagonisms have been recognized as a potential strategy for treatment of several cardiovascular disease, it remains unclear which of the antagonisms is suitable for the individuals with CKD because upregulation of the nitric oxide (NO) system via ET_B receptor is responsible for renal function such as natriuresis, diuresis, and glomerular hemodynamics. Our findings clearly indicate that the blockade of ET receptors, in particular ET_A-receptor antagonism, not only produces a potential renoprotective effect in CKD but also reduces the risk of CVD. In contrast, pharmacological blockade or genetic deficiency of ET_B receptor seems to aggravate CKD and CVD in several experimental models of rats. Moreover, preliminary evidence in patients with CKD also suggests that both selective ET_A- and nonselective ET_A/ET_B-receptor blockade decreases blood pressure but that selective ET_A blockade has additional desirable effects on renal hemodynamics. Thus, at least in CKD, these findings support the notion that ET_B receptor– mediated actions produce a renoprotective effect and that nonselective ET_A/ET_B-receptors blockade seem to offer no advantage over selective ET_A antagonism, and if anything may potentially reduce the benefits.     

Drug Discovery for Overcoming Chronic Kidney Disease (CKD): Development of Drugs on Endothelial Cell Protection for Overcoming CKD

Chronic kidney disease (CKD) is becoming a major public health problem worldwide. It is important to protect endothelial function in CKD treatment because injury of the endothelium is a critical event for the generation and progression of CKD. Recently, clinical studies showed that nifedipine, an antihypertensive drug, acts as a protective agent of endothelial cells (ECs). Nifedipine is reported to partially decompose to a nitrosonifedipine that has high reactivity against lipid-derived radicals in vitro. However, it is still unclear whether nitrosonifedipine is a biologically active agent against endothelial injury. We observed that nitrosonifedipine was converted to radical form by reaction with cultured ECs. The cumene hydroperoxide mediated cytotoxity was reduced by nitrosonifedipine in cultured human glomerular ECs (HGECs). Also nitrosonifedipine suppressed the expression of TNF-α–induced intercellular cell adhesion molecule-1 in HGECs. Chronic administration of N^ω-nitro-L-arginine methyl ester (L-NAME) caused systemic arterial hypertension, endotherial injury, and renal dysfunction. In L-NAME– induced hypertensive rats, nitrosonifedipine treatment improved not only the acetylcholine-induced vasodilation of the aortic rings, but also renal dysfunction such as increasing the levels of serum creatinine and urinary protein excretion. Our preliminary data suggest that nitrosonifedipine is a new and useful drug for the treatment of CKD involving ameliorating effects on EC disorder.     

吸入糖皮质激素治疗稳定期慢性阻塞性肺病的临床研究进展和评价

目的:探讨糖皮质激素对稳定期慢性阻塞性肺病的治疗情况,以期为临床应用提供参考。方法:收集近年来有关糖皮质激素对稳定期慢性阻塞性肺病的临床研究结果作一回顾性分析。结果及结论:目前,糖皮质激素在治疗稳定期慢性阻塞性肺病方面的应用正在增多,但是其疗效是否确切还有待进一步的研究证实,而治疗费用、不良反应等相关因素都有待广泛观察。     

头孢吡肟治疗慢性阻塞性肺疾病急性加重期并呼吸衰竭的疗效观察

目的:观察国产头孢吡肟治疗慢性阻塞性肺疾病急性加重期(AECOPD)并呼吸衰竭的疗效及安全性。方法:96例AE-COPD并呼吸衰竭患者随机分成A组(n=48)与B组(n=48),分别给予头孢吡肟、头孢哌酮钠/他唑巴坦钠治疗。2组给药剂量均为2.0g,静脉滴注,bid,疗程7～14d。结果:A组与B组总有效率分别为82%、62%(P<0.01);A组与B组痰菌清除率分别为79.1%、45.8%(P<0.05);A组与B组不良反应发生率分别为8.3%、10.4%(P>0.05)。结论:头孢吡肟治疗AECOPD并呼吸衰竭疗效优于头孢哌酮钠/他唑巴坦钠,两者均有较好的安全性。     

哈乐在慢性前列腺炎治疗中的应用

目的以慢性前列腺炎症状积分指数（NIH-CPSI）和最大尿流率（Qmax）检查为评价指标,探讨哈乐在慢性前列腺炎（CP）中的治疗作用。方法108例慢性前列腺炎患者按最大尿流率（Qmax）〈20m l/s和≥20m l/s,分为两组,每组再分哈乐治疗组和抗生素（左氧氟沙星）治疗组。治疗前后进行前列腺液（EPS）常规检查和细菌培养、慢性前列腺炎症状积分指数（NIH-CPSI）和最大尿流率（Qmax）测定。结果各治疗组治愈率间差异无显著性（P〉0.05）。各组治疗前后CPSI评分差别均有显著性（P〈0.01）,低尿流率组中哈乐治疗组治疗前后最大尿流率明显改善（P〈0.01）,而其他各组最大尿流率无明显改善（P〉0.05）。结论哈乐和抗生素对慢性前列腺炎都有治疗作用,且哈乐对尿流率降低者尚有提高最大尿流率的作用。最大尿流率（Qmax）对慢性前列腺炎的临床治疗药物的选择有一定的指导意义,并为疗效评价提供客观指标。     

复方甘草酸苷治疗慢性乙型肝炎的成本-效果分析

目的:评价复方甘草酸苷治疗慢性乙型肝炎的成本-效果比.方法:选取在我院住院的慢性乙型肝炎患者112例,随机分为治疗组和对照组,分别给予复方甘草酸苷、甘利欣等治疗,观察各组疗效并运用药物经济学方法成本-效果分析方法进行比较.结果:治疗组有效率为92.59%,对照组为77.59%,两种方案单位效果所需成本为61.50元、59.04元,在对照组的基础上,增加单位效果所需成本为74.22元.结论:药物经济学分析结果为复方甘草酸苷优于甘利欣等.