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| 1 | 再论术后早期炎性肠梗阻显示文摘 | 李幼生 黎介寿 | 2006 | 中国实用外科杂志2006,26,1: | 541 |
| 2 | 盆腔炎症性疾病诊治规范(草案)显示文摘盆腔炎症性疾病(pelvic inflammatory disease,PID)是由女性上生殖道炎症引起的一组疾病,包括子宫内膜炎、输卵管炎、输卵管卵巢脓肿和盆腔腹膜炎等。性传播感染(sexually transmitted infection,STI)的病原体如淋病奈瑟菌、沙眼衣原体是主要的致病原。一些需氧菌、厌氧菌、病毒和支原体等也参与PID的发病过程。多数引起PID的致病微生物是由阴道上行而来的,且多为混合感染,延误对PID的诊断和有效治疗都可能导致上生殖道感染后遗症(输卵管因素不孕和异位妊娠等)的发生。 | | 2008 | 中华妇产科杂志2008,43,7: | 83 |
| 3 | 多发性肌炎和皮肌炎诊断及治疗指南显示文摘1概述特发性炎性肌病( idiopathic inflammatory myopathies, IIM )是一组以四肢近端肌肉受累为突出表现的异质性疾病,其中以多发性肌炎(polymyositis,PM)和皮肌炎(dermatomyositis, DM )最为常见。我国PM/DM的发病率尚不十分清楚,围外报告的发病率约为(0.6~1)/万,女性多于男性.DM比PM更多见。 | | 2010 | 中华风湿病学杂志2010,14,12: | 146 |
| 4 | 盆腔炎症性疾病诊治规范(修订版)显示文摘盆腔炎症性疾病(pelvic inflammatory disease,PID)是女性上生殖道感染引起的一组疾病,包括子宫内膜炎、输卵管炎、输卵管卵巢脓肿和盆腔腹膜炎。性传播感染(sexually transmitted infection,STI)的病原体如淋病奈瑟菌、沙眼衣原体是PID主要的致病微生物。一些需氧菌、厌氧菌、病毒和支原体等也参与PID的发生。引起PID的致病微生物多数是由阴道上行而来的,且多为混合感染。延误对PID的诊断和有效治疗都可能导致PID后遗症如输卵管因素不孕和异位妊娠等。 | | 2014 | 中华妇产科杂志2014,49,6: | 271 |
| 5 | Inflammatory bowel disease:Pathogenesis显示文摘Inflammatory bowel disease(IBD),including Crohn’s disease and ulcerative colitis,is characterized by chronic relapsing intestinal inflammation.It has been a worldwide health-care problem with a continually increasing incidence.It is thought that IBD results from an aberrant and continuing immune response to the microbes in the gut,catalyzed by the genetic susceptibility of the individual.Although the etiology of IBD remains largely unknown,it involves a complex interaction between the genetic,environmental or microbial factors and the immune responses.Of the four components of IBD pathogenesis,most rapid progress has been made in the genetic study of gut inflammation.The latest internationally collaborative studies have ascertained 163susceptibility gene loci for IBD.The genes implicated in childhood-onset and adult-onset IBD overlap,suggesting similar genetic predispositions.However,the fact that genetic factors account for only a portion of overall disease variance indicates that microbial and environmental factors may interact with genetic elements in the pathogenesis of IBD.Meanwhile,the adaptive immune response has been classically considered to play a major role in the pathogenesis of IBD,as new studies in immunology and genetics have clarified that the innate immune response maintains the same importance in inducing gut inflammation.Recent progress in understanding IBD pathogenesis sheds lights on relevant disease mechanisms,including the innate and adaptive immunity,and the interactions between genetic factors and microbial and environmental cues.In this review,we provide an update on the major advances that have occurred in above areas. | Yi-Zhen Zhang Yong-Yu Li | 2014 | World Journal of Gastroenterology2014,20,1: | 103 |
| 6 | Fecal microbiota transplantation for severe enterocolonic fistulizing Crohn's disease显示文摘The concept of fecal microbiota transplantation(FMT)has been used in traditional Chinese medicine at least since the 4thcentury.Evidence from recent human studies strongly supports the link between intestinal bacteria and inflammatory bowel disease.We proposed that standardized FMT might be a promising rescue therapy for refractory inflammatory bowel disease.However,there were no reports of FMT used in patients with severe Crohn’s disease(CD).Here,we report the successful treatment of standardized FMT as a rescue therapy for a case of refractory CD complicated with fistula,residual Barium sulfate and formation of intraperitoneal large inflammatory mass.As far as we know,this is the first case of severe CD treated using FMT through mid-gut. | Fa-Ming Zhang Hong-Gang Wang Min Wang Bo-Ta Cui Zhi-Ning Fan Guo-Zhong Ji | 2013 | World Journal of Gastroenterology2013,19,41: | 78 |
| 7 | 中国结直肠癌预防共识意见(2016年,上海)显示文摘无论是遗传性(约占5%)还是散发性结直肠癌(colorectal cancer),环境因素均是影响其发生和进展的重要因素。因散发性结直肠癌(或称大肠癌)的发生途径大致分为腺瘤-腺癌途径(含锯齿状腺瘤引起的锯齿状途径)、炎-癌途径、de novo途径,结直肠癌的主要癌前疾病为结直腺瘤(colorectal adenoma,占全部结直肠癌癌前疾病的85%~90%,甚至更高)和溃疡性结肠炎(ulcerative colitis,UC)等炎症性肠病(inflammatory bowel disease,IBD)。尽管结直肠可发生间质瘤和神经内分泌肿瘤等,但临床上通常将结直肠癌和腺瘤统称为结直肠肿瘤。多数结直肠癌确诊时已届中晚期,疗效不佳,故结直肠癌的早期发现和及早预防至关重要。有鉴于此,应重视结直肠癌的预防。结直肠癌的预防包括对上述癌前疾病的预防和治疗。结直肠腺瘤的一级预防即预防结直肠腺瘤的发生,结直肠腺瘤的二级预防即结直肠腺瘤摘除后预防再发(recurrence,或称复发,包括原处复发和他处再发)或恶变。上述两者应归属于结直肠癌的一级预防。结直肠癌的二级预防包括早期结直肠癌的内镜下处理和内镜随访以防止复发。70%的散发性结直肠癌与生活习惯有关,且66%~78%的结直肠癌可通过健康的生活习惯而避免。 | 无 房静远 时永全 陈萦晅 李景南 盛剑秋 | 2016 | 胃肠病学2016,21,11: | 74 |
| 8 | Inflammatory mediators and microcirculatory disturbance in acute pancreatitis显示文摘BACKGROUND:Inflammatory mediators are not only initiation factors of acute pancreatitis(AP)but also key factors causing pancreatic hemorrhage and necrosis,which damage important organs such as the heart,brain,liver, kidney and lung.Microcirculatory disturbance in AP has attracted widespread attention.In order to provide a theoretical basis for clinical therapy of AP,it is very important to explore the effect of inflammatory mediators on microcirculatory disturbance in this disease. DATA SOURCES:In this review,the impact of inflammatory mediators on microcirculatory disturbance in AP was reviewed according to the literature,especially the articles indexed in PubMed and books published in China and reports from websites. RESULTS:At present,inflammatory mediation and micro- circulatory disturbance are the two major hypotheses to explain the development of AP.Although experimental studies have shown that inflammatory mediators induce or aggravate microcirculatory disturbance,the clinical application of these findings is still difficult because the inflammatory mediators are diverse and their research is not comprehensive and thorough. CONCLUSION:It is very important to explore the influence of inflammatory mediators on microcirculatory disturbance in AP. | Zhang, Xi-Ping Li, Zhi-Jun Zhang, Jie | 2009 | Hepatobiliary & Pancreatic Diseases International2009,8,4: | 60 |
| 9 | Effects of different resuscitation fluid on severe acute pancreatitis显示文摘AIM: To compare effects of different resuscitation fluid on microcirculation, inflammation, intestinal barrier and clinical results in severe acute pancreatitis (SAP). METHODS: One hundred and twenty patients with SAP were enrolled at the Pancreatic Disease Institute between January 2007 and March 2010. The patients were randomly treated with normal saline (NS group), combination of normal saline and hydroxyethyl starch (HES) (SH group), combination of normal saline, hydroxyethyl starch and glutamine (SHG group) in resuscitation. The ratio of normal saline to HES in the SH and SHG groups was 3:1. The glutamine (20% glutamine dipeptide, 100 mL/d) was supplemented into the resuscitation liquid in the SHG group. Complications and outcomes including respiratory and abdominal infection, sepsis, abdominal hemorrhage, intra-abdominal hypertension, abdominal compartment syndrome (ACS), renal failure, acute respiratory distress syndrome (ARDS), multiple organ dysfunction syndrome (MODS), operation intervention, length of intensive care unit stay, length of hospital stay, and mortality at 60 d were compared. Moreover, blood oxygen saturation (SpO 2 ), gastric intramucosal pH value (pHi), intra-abdominal pressure (IAP), inflammation cytokines, urine lactulose/mannitol (L/M) ratio, and serum endotoxin were investigated to evaluate the inflammatory reaction and gut barrier. RESULTS: Compared to the NS group, patients in the SH and SHG groups accessed the endpoint more quickly (3.9 ± 0.23 d and 4.1 ± 0.21 d vs 5.8 ± 0.25 d, P < 0.05) with less fluid volume (67.26 ± 28.53 mL/kg/d, 61.79 ± 27.61 mL/kg per day vs 85.23 ± 21.27 mL/kg per day, P < 0.05). Compared to the NS group, incidence of renal dysfunction, ARDS, MODS and ACS in the SH and SHG groups was obviously lower. Furthermore, incidence of respiratory and abdominal infection was significantly decreased in the SH and SHG groups, while no significant difference in sepsis was seen. Moreover, less operation time was needed in the SH and SHG group than the NS group, but the difference was not significant. The mortality did not differ significantly among these groups. Blood SpO 2 and gastric mucosal pHi in the SH and SHG groups increased more quickly than in the NS group, while IAP was significantly decreased in the SH and SHG group. Moreover, the serum tumor necrosis factor-α, interleukin-8 and C-reactive protein levels in the SH and SHG groups were obviously lower than in the NS group at each time point. Furthermore, urine L/M ratio and serum endotoxin were significantly lower in the SH group and further decreased in the SHG group.CONCLUSION: Results indicated that combination of normal saline, HES and glutamine are more efficient in resuscitation of SAP by relieving inflammation and sustaining the intestinal barrier. | Gang Zhao Jun-Gang Zhang He-Shui Wu Jin Tao Qi Qin Shi-Chang Deng Yang Liu Lin Liu Bo Wang Kui Tian Xiang Li Shuai Zhu Chun-You Wang | 2013 | World Journal of Gastroenterology2013,19,13: | 56 |
| 10 | 中国慢性炎性脱髓鞘性多发性神经根神经病诊疗指南显示文摘慢性炎性脱髓鞘性多发性神经根神经病(chronic inflammatory demyelinating potyradiculoneuropathy,CIDP)是一类由免疫介导的运动感觉周围神经病,其病程呈慢性进展或缓解复发,多伴有脑脊液蛋白一细胞分离,电生理表现为周围神经传导速度减慢、传导阻滞及异常波形离散;病理显示有髓纤维多灶性脱髓鞘、神经内膜水肿、炎细胞浸润等特点。CIDP属于慢性获得性脱髓鞘性多发性神经病(chronic acquired demyelinating polyneuropathy,CADP),是CADP中最常见的一种类型.大部分患者对免疫治疗反应良好。 | 无 | 2010 | 中华神经科杂志2010,43,8: | 54 |
| 11 | 盆腔炎性疾病发病机制的现代研究显示文摘盆腔炎性疾病(pelvic inflammatory disease,PID)是妇科常见病,是指女性上生殖道感染引起的一组疾病〔2006美国疾病预防控制中心(CDC)定义〕,主要包括子宫内膜炎(endometritis)、输卵管炎(salpingitis)、输卵管卵巢脓肿(tubo-ovarian abscess,TOA)和盆腔腹膜炎(peritonitis)。 | 李世蓉 张三元 | 2011 | 中国妇幼保健2011,26,27: | 54 |
| 12 | 降钙素原:指导重症细菌感染诊疗的可靠指标显示文摘全身炎症反应综合征(systemic inflammatory responses yndrome,SIRS)、脓毒症、严重脓毒症和感染性休克(septicshock)是同一病理过程的不同阶段,该定义1992年由美国胸科医师协会/危重病医学会(ACCP/SCCM)联席大会提出, | 叶枫 钟南山 | 2012 | 中华结核和呼吸杂志2012,35,11: | 51 |
| 13 | 护理干预对慢性盆腔炎患者生存质量的影响显示文摘慢性盆腔炎(chronic pelvic inflammatory disease,CPID)为育龄妇女最常见的生殖器官炎症,近年来其发病率居高不下,严重影响妇女健康。长期慢性盆腔疼痛或腰部疼痛,影响妇女健康,增加家庭与社会的经济负担, | 李利军 | 2010 | 当代医学2010,16,10: | 43 |
| 14 | 术后早期炎性肠梗阻显示文摘术后早期炎性肠梗阻(early postoperative inflammatory small bowel obstruction,EPISBO)是由于剖腹手术后,由于创伤、炎症等各种因素导致的肠壁水肿、渗出而形成的一种机械性、动力性同时存在的肠梗阻;约占腹部手术后肠梗阻的20.0%,是术后较常见的并发症,也是延长住院时间的原因。 | 张群 于健春 康维明 | 2011 | 中华普通外科杂志2011,26,2: | 44 |
| 15 | Fecal microbiota transplantation as novel therapy in gastroenterology:A systematic review显示文摘AIM:To study the clinical efficacy and safety of Fecal microbiota transplantation(FMT).We systematically reviewed FMT used as clinical therapy.METHODS:We searched MEDLINE,EMBASE,the Cochrane Library and Conference proceedings from inception to July,2013.Treatment effect of FMT was calculated as the percentage of patients who achieved clinical improvement per patient category,on an intention-to-treat basis.RESULTS:We included 45 studies;34 on Clostridium difficile-infection(CDI),7 on inflammatory bowel disease,1 on metabolic syndrome,1 on constipation,1 on pouchitis and 1 on irritable bowel syndrome(IBS).In CDI 90% resolution of diarrhea in 33 case series(n = 867) was reported,and 94% resolution of diarrhea after repeated FMT in a randomized controlled trial(RCT)(n = 16).In ulcerative colitis(UC) remission rates of 0% to 68% were found(n = 106).In Crohn's disease(CD)(n = 6),no benefit was observed.In IBS,70% improvement of symptoms was found(n = 13).100% Reversal of symptoms was observed in constipation(n = 3).In pouchitis,none of the patients(n = 8) achieved remission.One RCT showed significant improvement of insulin sensitivity in metabolic syndrome(n = 10).Serious adverse events were rare.CONCLUSION:FMT is highly effective in CDI,and holds promise in UC.As for CD,chronic constipation,pouchitis and IBS data are too limited to draw conclusions.FMT increases insulin sensitivity in metabolic syndrome. | Noortje G Rossen John K Mac Donald Elisabeth M de Vries Geert R D'Haens Willem M de Vos Erwin G Zoetendal Cyriel Y Ponsioen | 2015 | World Journal of Gastroenterology2015,21,17: | 41 |
| 16 | 上尿路结石患者围手术期抗菌药物应用的专家意见显示文摘感染性并发症是上尿路结石微创手术最常见的并发症,正确的围手术期抗菌药物应用可减少此类手术感染性并发症的发生.但上尿路结石合并泌尿系感染的表现千差万别,从无症状尿路感染至危及生命的脓毒症.目前,国内学界在上尿路结石与感染相互关系和治疗原则上还存在一些问题和错误需要厘清、纠正:如结石合并感染甚至出现全身炎症反应综合征(systemic inflammatory response syndrome,SIRS)时外科干预时机的掌握不当,不积极引流或者激进地采用微创方式取石导致患者感染加重、脓毒性休克甚至死亡;具有感染高危因素或尿培养阳性者术前未进行相应的抗菌药物治疗,增加了术后出现感染性并发症的概率;对简单的经尿道输尿管镜取石术盲目地术前、术后长时间应用抗菌药物,不仅增加医疗支出,还会增加细菌耐药性的产生. | 乔庐东 陈山 马小军 郑波 吴文起 高小峰 陈明 孔祥波 杨嗣星 孙则禹 叶章群 | 2017 | 中华泌尿外科杂志2017,38,9: | 41 |
| 17 | Moxibustion treatment modulates the gut microbiota and immune function in a dextran sulphate sodium-induced colitis rat model显示文摘AIM To investigate the effect and mechanism of moxibustion in rats with ulcerative colitis.METHODS A rat colitis model was established by administering 4% dextran sulphate sodium solution. Seventy male rats were randomly divided into seven groups: Healthy controls(HC), ulcerative colitis model group(UC), UC with 7 d of moxibustion(UC-7), UC with 14 d of moxibustion(UC-14), UC with mesalazine gavage(UC-W), HC with 7 d of moxibustion(HC-7), HC with 14 d of moxibustion(HC-14). Moxibustion was applied to the bilateral Tianshu(ST25). Gut microbiome profiling was conducted by 16 S r RNA amplicon sequencing, and PCR and ELISA determined the expression of inflammatory cytokines in colon mucosa and serum, respectively. RESULTS Moxibustion treatment restored the colonic mucosa and decreased submucosal inflammatory cell infiltration in colitis rats. Rats treated with moxibustion and mesalazine had significantly lower levels of the dominant phyla Proteobacteria and the genera Saccharibacteria, Sphingomonas and Barnesiella than colitis rats, and they could restore the microbiome to levels similar to those observed in healthy rats. UC rats had reduced alpha diversity, which could be alleviated by moxibustion therapy, and UC-7 had a higher alpha diversity than UC-14. This finding suggests that short-term(7 d) but no longer term(14 d) moxibustion treatment may significantly affect the gut microbiome. The potential bacterial functions affected by moxibustion may be ascorbate and aldarate metabolism, and amino acid metabolism. Compared with HC group, the levels of the cytokines interleukin-12(IL-12)(P < 0.05) and IL-6, IL-17, IL-23, interferon-γ, lipopolysaccharide, Ig A, tumour necrosis factor-α and its receptors 1(TNFR1) and TNFR2(P < 0.01) were all increased, whereas anti-inflammatory cytokine IL-2 and IL-10(P < 0.01) and transforming growth factor-β(P < 0.05) were decreased in UC rats. These changes were reversed by moxibustion.CONCLUSION Our findings suggest that moxibustion exerts its therapeutic effect by repairing mucosal tissue damage and modulating the gut microbiome and intestinal mucosal immunity. | Qin Qi Ya-Nan Liu Xiao-Ming Jin Lin-Shuang Zhang Cun Wang Chun-Hui Bao Hui-Rong Liu Huan-Gan Wu Xiao-Mei Wang | 2018 | World Journal of Gastroenterology2018,24,28: | 42 |
| 18 | Update on ischemia-reperfusion injury in kidney transplantation: Pathogenesis and treatment显示文摘Ischemia/reperfusion injury is an unavoidable relevant consequence after kidney transplantation and influences short term as well as long-term graft outcome. Clinically ischemia/reperfusion injury is associated with delayed graft function, graft rejection, chronic rejection and chronic graft dysfunction. Ischemia/reperfusion affects many regulatory systems at the cellular level as well as in the renal tissue that result in a distinct inflammatory reaction of the kidney graft. Underlying factors of ischemia reperfusion include energy metabolism, cellular changes of the mitochondria and cellular membranes, initiation of different forms of cell death-like apoptosis and necrosis together with a recently discovered mixed form termed necroptosis. Chemokines and cytokines together with other factors promote the inflammatory response leading to activation of the innate immune system as well as the adaptive immune system. If the inflammatory reaction continues within the graft tissue, a progressive interstitial fibrosis develops that impacts long-term graft outcome. It is of particular importance in kidney transplantation to understand the underlying mechanisms and effects of ischemia/reperfusion on the graft as this knowledge also opens strategies to prevent or treat ischemia/reperfusion injury after transplantation in order to improve graft outcome. | Maurizio Salvadori Giuseppina Rosso Elisabetta Bertoni | 2015 | World Journal of Transplantation2015,5,2: | 43 |
| 19 | Immunopathology of inflammatory bowel disease显示文摘Inflammatory bowel disease(IBD)results from a complex series of interactions between susceptibility genes,the environment,and the immune system.The host microbiome,as well as viruses and fungi,play important roles in the development of IBD either by causing inflammation directly or indirectly through an altered immune system.New technologies have allowed researchers to be able to quantify the various components of the microbiome,which will allow for future developments in the etiology of IBD.Various components of the mucosal immune system are implicated in the pathogenesis of IBD and include intestinal epithelial cells,innate lymphoid cells,cells of the innate(macrophages/monocytes,neutrophils,and dendritic cells)and adaptive(T-cells and B-cells)immune system,and their secreted mediators(cytokines and chemokines).Either a mucosal susceptibility or defect in sampling of gut luminal antigen,possibly through the process of autophagy,leads to activation of innate immune response that may be mediated by enhanced toll-like receptor activity.The antigen presenting cells then mediate the differentiation of na?ve T-cells into effector T helper(Th)cells,including Th1,Th2,and Th17,which alter gut homeostasis and lead to IBD.In this review,the effects of these components in the immunopathogenesis of IBD will be discussed. | Kori L Wallace Li-Bo Zheng Yoshitake Kanazawa David Q Shih | 2014 | World Journal of Gastroenterology2014,20,1: | 45 |
| 20 | 术后早期炎性肠梗阻的诊疗进展显示文摘 | 马留学 邹忠东 姚和祥 王瑜 | 2009 | 中国临床医学2009,16,6: | 40 |