轮状病毒的肠道外感染

近年来发现轮状病毒（ＲＶ）可发生肠道外感染,常见于中枢神经系统,呼吸系统及肠管外的其他消化器官感染,这提示ＲＶ可能在存在新的感染途径和感染机制,为其感染的预防和临床治疗提出了新的课题。     

轮状病毒肠道外感染发病机制的研究进展

轮状病毒是一种双链RNA病毒,其基因序列已经基本查明.它是引起婴幼儿严重腹泻最常见的病原体,不仅可以引起胃肠道疾病,还可导致全身各个脏器的病变,发病机制和多个因素有关.肠道外发病可能是免疫功能异常(或正常)的情况下,轮状病毒穿透胃肠道屏障通过血液播散,感染肠道外多个器官所致.     

轮状病毒的肠道外感染

近年来发现轮状病毒 (RV)可发生肠道外感染 ,常见于中枢神经系统、呼吸系统及肠管外的其他消化器官感染 ,这提示着 RV可能存在新的感染途径和感染机制 ,为其感染的预防和临床治疗提出了新的课题。     

轮状病毒肠道外感染的研究进展

近年来,不断有轮状病毒肠炎患儿在病程中出现各种肠道外脏器损伤的报道,主要见于肺、心、肝胆、肾以及神经系统的损伤,并且在部分受累器官中已找到明确的证据,提示轮状病毒可能存在新的发病机制和感染途径,但目前仍未完全清楚.     

轮状病毒肠道外损害105例临床分析

目的 了解新疆奎屯地区2005年1月～2007年1月轮状病毒(RV)感染及其肠道外损害的状况.方法 对105例RV感染患儿的各系统损害从临床表现、实验室检查等方面作临床统计.结果 单纯RV感染者20例(19%);RV感染肠道外损害85例(81%),包括呼吸系统、循环系统、中枢神经系统及其他消化系统损害.结论 RV感染致肠道外病变表现多样化,以呼吸道、心脏、神经系统受累常见,提示RV感染者有新的感染途径及靶器官.     

婴幼儿轮状病毒性肠炎168例的肠外表现分析

目的分析婴幼儿轮状病毒性肠炎的肠外表现及可能机制，为进一步认识该疾病提供帮助。方法回顾性分析我院收治的168例确诊为轮状病毒性肠炎的病例资料。结果轮状病毒肠炎合并有肠外表现的发病率依次为心肌损害、呼吸系统、肾脏损害、肝脏损害等，住院过程给予对症治疗后均预后良好。结论轮状病毒感染不仅有胃肠道症状，还可以有其他系统的损害，虽说轮状病毒性肠炎是一种自限性疾病，但也有可能引起多系统损害，甚至衰竭，临床上不容忽视。     

有肠外表现的轮状病毒肠炎93例临床分析

目的探讨轮状病毒(RV)感染肠道外脏器受损的相关因素、临床表现特点及预后。方法将2006年10月~2007年1月在本院住院的轮状病毒(RV)肠炎患儿146例,按其肠外脏器受损的有无分为观察组与对照组,比较2组的一般情况、肠道症状、肠外表现、实验室资料及预后。结果63.70%的RV肠炎合并肠外脏器受损,心肌、呼吸道、肝脏、中枢神经、血液系统受累比例分别为54.11%、26.03%、15.07%、2.74%、2.05%,有1个、2个、3个脏器受累的比例分别46.58%、15.07%、2.05%。≤6个月小儿最易有肠外表现(P<0.01),发热、脱水、酸中毒、C-反应蛋白升高亦与肠外表现相关(P<0.05)。观察组肠道症状消失时间明显延长,2组差异有非常显著性意义(P<0.01),但肠外脏器受累预后较好,心肌酶、肝酶、CRP1周内基本恢复正常,仅少数2周左右恢复。结论RV是一种能引起全身脏器损害的疾病,在诊治RV肠炎患儿时,应重视肠外脏器受损情况,予以及时有效处理。     

重视轮状病毒感染肠外表现

轮状病毒是5岁以下儿童,尤其是6月龄～3岁婴幼儿急性胃肠炎的主要病原,出现呕吐、腹泻等只是轮状病毒胃肠炎最明显和最常见的临床表现.轮状感染可通过全身性病毒血症,造成肠道外的全身系统性影响.国内有关轮状病毒感染肠外表现的相关报道并不多,许多问题尚需要进一步探讨.该文针对轮状病毒感染常见肠外损害的发病机制、临床表现、实验室...     

轮状病毒肠道外感染与血清甘露聚糖结合蛋白水平的关系研究

目的 探讨轮状病毒肠道外感染患儿血清甘露聚糖结合蛋白(MBP)水平的变化及其与轮状病毒肠道外感染的关系.方法 采用双抗体夹心酶联免疫吸附法(ELISA)测定76例轮状病毒肠道外感染患儿和63例单纯轮状病毒肠炎患儿不同病程中的血清MBP水平以及50例健康对照组小儿血清MBP水平.结果 轮状病毒肠道外感染患儿急性期血清MBP为(176.35±113.12)μg/L,明显低于单纯轮状病毒肠炎急性期水平(392.27±128.96)μg/L以及健康对照组小儿MBP血清水平(676.25±248.63)μg/L,差异有显著性(P＜0.001);轮状病毒肠道外感染患儿恢复期血清MBP水平为(358.63±106.54)μg/L,低于单纯轮状病毒肠炎恢复期水平[(558.49±173.24)μg/L]以及健康对照组小儿血清MBP水平,差异有显著性(P＜0.001);轮状病毒肠道外感染导致的肺炎、肝损害、心肌损害以及中枢神经系统损害急性期患儿血清MBP水平分别为(198.24±126.47)μg/L、(169.34±124.38)μg/L、(184.62±123.64)μg/L、(180.74±126.86)μg/L,差异无显著性(P＞0.05).结论 轮状病毒肠道外感染患儿急性期及恢复期血清MBP水平明显低于单纯轮状病毒肠炎急性期及恢复期血清MBP水平,但轮状病毒肠道外感染导致的不同肠道外脏器损害患儿急性期血清MBP水平无显著差异;轮状病毒肠道外感染的发生与血清MBP水平低下密切相关.     

轮状病毒肠道外感染与血清甘露聚糖结合蛋白水平的关系研究

Objective To explore the relationship between extraintestinal rotavirus infections and serum MBP levels. Methods Serum MBP levels were measured by double-antibody sandwich enzyme-linked immunosorbent assays (ELISA) in children including extraintestinal rotavirus infections (n = 76) and common rotavirus enteritis ( n = 63 ) during the acute and convalescence phases. A group of healthy children ( n =50) were recruited as control. Results MBP levels were significantly lower in patients with extraintestinal rotavirus infections( 176.35 ± 113.12 ) μg/L in acute phases than those in patients with common rotavirus enteritis (392. 27 ± 128.96) μg/L and healthy control group(676. 25 ± 248. 63) μg/L, and the difference was significant (P ＜0. 001 ). The serum MBP levels in convalescence phases in the group of extraintestinal rotavirus infections( 358.63 ± 106. 54 ) μg/L was lower than those in the group of common rotavirus enteritis (558. 49 ± 173. 24 ) μg/L and the healthy controls, and their difference was significant ( P ＜ 0. 001 ). The MBP levels in the acute phases among pneumonia group, hepatic lesion group, cardiac damage group and central nervous system damage group caused by rotavirus infection were ( 198.24 ± 126.47) μg/L, ( 169.34 ±124. 38) μg/L,( 184. 62 ± 123.64) μg/L, ( 180. 74 ± 126. 86) μg/L, respectively. The difference among those groups was not significant ( P ＞ 0. 05 ). Conclusion Patients with extraintestinal rotavirus infections showed significantly lower MBP levels during acute and convalescence phases than patients with common rotavirus enteritis. But MBP levels showed no significant differences among those groups of patients with different extraintestinal organ damage caused by rotavirus infection. Lower MBP levels may be associated with the increased susceptibility to extraintestinal rotavirus infections.     

Viral enteritis

Rotavirus has emerged as the major enteric pathogen causing acute diarrhea in young children throughout the world. Other viral pathogens have been recognized and additional candidate agents are suspected but none approaches rotavirus in its global impact. A strong appropriate emphasis has been placed on preventive therapy. Although vaccines are not yet available, it is clear that improved hygienic practices, particularly in pediatric institutions, and breast feeding can do much to prevent serious illness during the early months when babies are so vulnerable. During the past decade, from clinical studies and animal models, much has been learned about the pathogenesis of rotavirus diarrhea. These findings provide a sound basis for the use of rational oral fluid therapy, early feeding, and avoidance of drugs during active management. Among the many challenges that remain are the elucidation of the full spectrum of enteric viral pathogens, their impact on man, and their prevention and active therapy.     

Extraintestinal rotavirus infections in children with immunodeficiency.

Some rotavirus strains, including vaccine candidates, have been demonstrated to cause hepatitis in immunodeficient and malnourished mice and to grow in human liver cells. To determine whether rotavirus spreads outside the intestine in naturally infected children, we examined tissues from four immunodeficient children affected with severe combined immunodeficiency disease, acquired immunodeficiency disease syndrome, or DiGeorge syndrome. Chronic rotavirus-related diarrhea, which persisted until death, had also developed in each child. Using indirect immunoperoxidase techniques, we identified rotavirus antigen in the liver and kidney with a hyperimmune guinea pig antiserum prepared to double-shelled rotavirus particles. Similar immunostaining with an antiserum to a rotavirus nonstructural protein (NS26) provided evidence of active virus replication. The observed reactivity was eliminated specifically when serial sections were immunostained with the same antiserum that had been absorbed with either double-shelled rotavirus particles or NS26. Immunostaining was not observed in the liver of children with other diseases (alpha 1-antitrypsin deficiency, inspissated bile syndrome, and acute rejection of a transplanted liver). These findings demonstrate that rotavirus infections in children can extend beyond the intestinal tract. Further studies are warranted to determine whether extraintestinal rotavirus replication occurs in children without severe immunodeficiency, such as malnourished children.     

Appendicitis in enteritis

We are confronted with the fact that in a considerable number of cases appendicitis occurring during enteritis is diagnosed late and is often only operated on in the state of perforation. Among our own cases of 519 appendectomies in the last five-years-period this applied to 13 children (2.4%). The problems of these cases and methods to a correct and immediate diagnosis are shown.