疣状胃炎2716例临床分析

疣状胃炎(verrucose gastritis,VG)又称豆疹状胃炎、慢性糜烂性胃炎,是胃炎的一种特殊类型,在悉尼系统中隶属隆起糜烂性胃炎类别.其病因及发病机制尚不明确.近年对本病的报道日益增多.我院2008～2009年在行胃镜检查患者中检出疣状胃炎2716例,检出率16.5%,现报道如下.     

抽动障碍患儿T淋巴细胞亚群水平变化的分析

[摘要]目的：通过比较正常儿童与抽动障碍（TD）患儿T淋巴细胞亚群的差异,探究TD患儿发病及病情严重程度与T淋巴细胞亚群之间的关系,并探索TD在细胞免疫方面可能存在的发病机制。方法：采用流式细胞仪技术测定53例TD患儿及30例健康体检儿童T淋巴细胞亚群水平,并进行比较。结果：TD组CD8+水平较对照组显著升高,CD4+及CD4+/CD8+水平均低于对照组（P均<0.05）;CD3+水平与对照组比较差异无统计学意义（P>0.05）。TD患儿的YGTSS评分、发病时间长短及病情严重程度与T淋巴细胞亚群水平均之间没有明显的对应关系。结论：TD患儿的发病与细胞免疫相关,且CD8+T淋巴细胞在其中起主导作用,但未见其与TD的病程长短及严重程度具有相关性。     

系统性红斑狼疮患儿外周血淋巴细胞亚群变化

目的：探讨系统性红斑狼疮（SLE）患儿外周血淋巴细胞亚群变化特征。方法选择24例SLE病儿和20例健康儿童为研究对象,应用流式细胞术（FCM）检测外周血的淋巴细胞亚群,对比分析两组检测结果。结果SLE患儿外周血CD4＋CD25＋T细胞、自然杀伤（NK）细胞百分率较对照组明显降低（t=2.480,3.773;P＜0.05）,CD8＋T细胞、活化T细胞和B细胞百分率明显升高（t=3.470,4.779,2.480;P＜0.05或P＜0.01）。结论SLE患儿外周血淋巴细胞亚群紊乱,调节性T细胞和NK细胞减少、B细胞增多和T细胞活化增强,在SLE发病机制中可能起重要作用。     

T淋巴细胞与川崎病免疫反应的研究进展

川崎病(KD)是幼儿期的急性发热性疾病,主要病理特征是冠状动脉受累的系统性血管炎.目前关于KD的发病机制仍未明确.但相关研究发现,T淋巴细胞的异常激活在KD免疫反应中起重要作用,且主要集中围绕在T淋巴细胞活化相关的基因、信号通路、T淋巴细胞活化后亚群分布等方面,这些研究为了解KD的发病机制、诊断及治疗提供了新思路.     

疣状胃炎病理分析

疣状胃炎是一种特殊类型的胃炎,又称隆起型糜烂性胃炎、痘疹样胃炎,其病因和发病机制尚未明确,治疗方案也不统一。本研究就2008年1月—2012年1月收集的我院门诊及住院疣状胃炎431例的临床、内镜、病理特点作回顾性分析。     

支原体肺炎和支气管肺炎儿童T淋巴细胞亚群比较

<正>T淋巴细胞亚群的分类以及判定T淋巴细胞的活动程度是机体细胞免疫功能的一项重要指标,对多种疾病的辅助诊断以及发病机制研究具有重要的价值[1]。支原体肺炎和支气管肺炎是儿童常见病和多发病,儿童患病后T淋巴细胞亚群的变化不同,疾病的转归和治疗反应也不一定相同。本研究通过检测外周血中T淋巴细胞亚群在支原体肺炎和支气管肺炎急性期儿童外周血中的表达,总结不同肺炎T淋巴细胞亚群的表达特征,探讨其临床意义。     

脾氨肽治疗和预防儿童反复呼吸道感染发作的疗效及对T淋巴细胞亚群的影响

<正>反复呼吸道感染(RRI)是儿童的常见病,患儿病情常反复发作、迁延不愈,严重影响儿童的生长发育[1]。有关RRI的病因与发病机制尚不完全清楚,近年来研究认为其发病机制与儿童的细胞免疫功能低下有关,主要与T淋巴细胞亚群的失调密切相关[2]。脾氨肽是从新鲜的动物脾脏中提取的一种肽和核苷酸类的复合制剂,具有免疫调节作用,治疗儿童RRI疗     

肝癌患者血清肿瘤坏死因子β和外周血T淋巴细胞亚群变化的研究

目的 探讨肝癌患者血清肿瘤坏死因子β（TNF-β）及外周血T淋巴细胞亚群的变化.方法 应用ELISA法对肝癌患者血清TNF-β以及采用流式细胞仪（FCM）对肝癌患者外周血T淋巴细胞亚群进行检测.结果 Ⅰ、Ⅱ、Ⅲ期肝癌患者血清TNF-β水平分别为（28.46±5.14）ng/L、（24.19±4.37）ng/L、（18.23±5.27）ng/L,均显著低于健康对照组（41.35±3.19）ng/L（均P＜0.01）;而T淋巴细胞CD3＋、CD4＋、CD4＋/CD8＋均明显低于健康对照组（均P＜0.01）,而CD4＋CD25却明显高于健康对照组（P＜0.01）.结论 肝癌患者外周血T淋巴细胞亚群及血清TNF-β的水平均下降,且两者变化呈正相关,提示其与肝癌患者机体的免疫功能下降有关.     

复发性口腔溃疡大鼠动物模型的建立

目的：探讨T淋巴细胞亚群与RAU发病机制的关系。方法：用大鼠口腔黏膜抗原乳化液注射方法建立复发性口腔溃疡大鼠动物模型。大鼠眼眶采血,免疫组化染色,CD4＋、CD8＋细胞计数并计算其比值。结果：实验大鼠于最后一次抗原注射6d后开始出现口腔溃疡。溃疡大鼠CD4＋、CD4＋/CD8＋较正常大鼠降低（P＜0.05）。结论：RAU的发病与T淋巴细胞亚群的失衡有关。     

特发性血小板减少性紫癜患者外周血淋巴细胞亚群变化

目的探讨特发性血小板减少性紫癜（ITP）患者外周血T淋巴细胞亚群的变化规律及临床意义。方法用ELISA法检测42例ITP患者和30例对照者血小板相关免疫球蛋白水平,用流式细胞仪直接免疫法检测外周血T淋巴细胞亚群CD3＋、CD4＋、CD8＋、CD4＋／CD8＋,并评价其与血小板抗体水平的相关性。结果ITP患者PAIgG、PAIgA、PAIgM水平均显著高于对照者（P〈0．01）;与对照者相比,ITP患者外周血CD3＋显著降低（P〈0．01）,CD4＋减低（P〉0．05）,CD8＋明显升高（P〈0．05）,而CD4＋／CD8＋比值显著降低（P〈0．01）,同时CD4＋／CD8＋比值的降低与血小板表面抗体IgG、IgA、IgM增高有显著的相关性。结论ITP患者存在T淋巴细胞亚群功能和比例失常,存在T淋巴细胞亚群分布漂移,T淋巴细胞亚群检测对ITP的诊断有指导意义。     

幽门螺杆菌感染诱导髓源抑制细胞在胃癌发生中的作用

目的探讨幽门螺杆菌(Hp)感染与外周血髓源抑制细胞(MDSC)水平的关联及Hp感染或非感染人群体内免疫功能的变化。方法 129例受试者分为健康组(32例)、慢性胃炎组(48例)、胃上皮内瘤变组(27例)和胃癌组(22例),快速尿素酶检测Hp。应用流式细胞术检测外周血MDSC、T细胞亚群的比例。结果 Hp感染能显著增加外周血MDSC的比例(P<0.01),而T细胞亚群的比例变化与Hp感染无关(P>0.05)。三组外周血MDSC、T细胞亚群的比例差异有统计学意义(P<0.01)。外周血MDSC比例与CD4+/CD8+比值呈显著负相关(r=-0.768),与胃癌TNM分期呈显著正相关(r=0.856)。结论 Hp感染可导致外周血MDSC比例的升高,并引起人体免疫功能紊乱,在慢性胃炎演变至胃癌的肿瘤逃逸过程中起重要作用。     

Lymphocyte subpopulations in gastric disease; effect of histamine and cimetidine on immunoregulatory T cell subsets

The numbers of T lymphocytes, helper and suppressor T lymphocytes, were measured in peripheral blood of 10 patients, 13 patients with gastric cancer and 20 normal controls. T lymphocyte subpopulations were enumerated by the use of monoclonal antibodies OKT3 (pan-T lymphocytes), OKT4 (helper/inducer lymphocytes) and OKT8 (cytotoxic/suppressor lymphocytes) in an indirect immunofluorescence technique. Furthermore, the possible pharmacological modulation of 10(-4) histamine and 10(-4), 10(-6) M cimetidine of T lymphocyte subsets was investigated. Lymphocyte subpopulations were found to range in normal values in patients with ulcer and chronic gastritis. A marked decrease of OKT3 and OKT8 positive lymphocytes was noted in patients with gastric cancer, whereas OKT4 lymphocytes from the three groups of patients to histamine and cimetidine resulted in no significant changes of lymphocyte subsets.     

干燥综合征患者外周血中T淋巴细胞亚群的分析与临床意义

目的探讨干燥综合征(SS)患者外周血T淋巴细胞亚群的变化及其临床意义。方法用流式细胞仪检测并比较SS患者与正常对照者外周血T淋巴细胞亚群有无差异。以红细胞沉降率及血清IgG来判断SS病情活动度,分析SS患者中T淋巴细胞亚群与病情活动的关系。结果与正常对照组相比,SS患者外周血中CD8+T淋巴细胞、CD8+CD28+T淋巴细胞构成比及CD8+/CD4+比值均显著降低;而CD4+T淋巴细胞、CD4+CD45RA+T淋巴细胞及CD4+CD28+T淋巴细胞在两组中则差异无统计学意义。与病情非活动者相比,病情活动的SS患者的CD8+T淋巴细胞构成比及CD8+/CD4+比值均显著降低。结论SS患者外周血T淋巴细胞亚群存在异常,并与SS的病情活动有关,可能在SS发病中具有重要作用。     

直肠癌术前短程快速放疗前后外周血T细胞亚群变化的临床价值

对中低位可切除性直肠癌的治疗目前仍然是以手术治疗为主,但单纯手术治疗的术后局部复发率可达15%~50%[1],因此对可切除性直肠癌多采取术前新辅助治疗,以减少术后的局部复发率。短程术前放疗目前已成为可切除性直肠癌术前的标准治疗方案[2],但部分学者仍然担心术前放疗会使本来就存在免疫低下的患者的免疫功能进一步紊乱,促进肿瘤的播散和妨碍或延迟患者术后的恢复。本文就直肠癌术前放疗前后的T细胞亚群的变化进行研究,为术前放疗的选择提供理论依据。资料和方法直肠癌患者102例均为我院2002年6月至2004年8月收治的病例。术前放疗组50例,…     

Helicobacter pylori and the risk and management of associated diseases: gastritis, ulcer disease, atrophic gastritis and gastric cancer

This review addresses the role of H. pylori and the effect of H. pylori eradication on gastritis, peptic ulcer disease, atrophic gastritis and gastric cancer. Specific emphasis is given to various factors that influence the clinical course of this infection. H. pylori induces chronic gastritis in virtually all infected subjects. This inflammation can lead to peptic ulceration and atrophic gastritis in a considerable number of infected subjects. A minority eventually develops gastric cancer. The risk of such complications depends upon the severity of gastritis, which is determined by various host- and bacteria-related factors. Among bacterial factors, most of the evidence addresses the cagA pathogenicity island, the presence of which has been associated with more severe gastritis, peptic ulceration, atrophic gastritis and gastric cancer. Among host factors, most of the evidence focuses on acid production in response to H. pylori infection. An increase in acid secretion limits H. pylori gastritis to the antrum at the risk of duodenal ulcer disease; a reduction allows more proximal inflammation at the risk of atrophic gastritis, gastric ulcer disease, and gastric cancer. Gastritis and atrophy negatively influence acid secretion. H. pylori eradication is required in peptic ulcer disease and may be advocated in patients on profound acid suppressive therapy; it has been shown to cure gastritis and prevent ulcer recurrence. Further study is required to determine the efficacy of H. pylori eradication in the primary and secondary prevention of atrophic gastritis and gastric cancer.     

Is Helicobacter pylori status relevant in the management of GORD?

There is growing interest in the relationship between H. pylori infection and gastro-oesophageal reflux disease (GORD). However, this relationship is complex, as yet not fully elucidated, and probably based on a multiplicity of factors. The prevalence of H. pylori infection in patients with GORD is similar, more often lower than in matched controls. There is a negative correlation between H. pylori infection and the severity of GORD. There are many hypothetical mechanisms by which H. pylori infection may protect from the development of GORD. Conversely, there are many possible mechanisms by which H. pylori infection could theoretically foster the GORD. Patients after H. pylori eradication may develop GORD, and this seems to suggest a protective role of H. pylori infection, but other possible explanations include weight gain after H. pylori eradication, changes in dietary habits and smoking, and pre-existing GORD. H. pylori infected patients treated by various acid-inhibiting therapies such as proton pump inhibitors (PPIs), H2-receptors antagonists (H2-RA) or vagotomy, have an increase of their corpus gastritis severity, both in the activity of inflammation and in the density of organisms. Long-term therapy of GORD in H. pylori infected may lead to rapid progression of atrophic gastritis intestinal metaplasia and dysplasia, and increase the risk of developing gastric cancer. More recently it has been shown that H. pylori infection may interfere with the acid suppressive therapies used for treating GORD. In our opinion the progression of gastritis depends on the threshold of acid output at which H. pylori can 'flourish'. Recently interest is growing on gastric transitional zones and Helicobacter ecology. Any decrease of acid secretion changes the behaviour of H. pylori: the activity of gastritis improves in the antrum, but it deteriorates in the body. During proton pump inhibitor treatment, H. pylori redistribution occurs within the stomach, from an antral to a corpus or fundus prevalent pattern; corpus-fundus gastritis, exacerbated by PPI therapy, may result both in a diminished acid secretion and gastro-oesophageal reflux. The interest in Barrett's oesophagus is growing due to the associated risk of adenocarcinoma. The literature seems to demonstrate that the prevalence of H. pylori infection of the stomach in Barrett's oesophagus patients is not different from that exhibited by controls, roughly one-third of the subjects. Intestinal metaplasia of the gastric cardia seems to be equally frequent in patients with and without GORD. Finally, it appears unlikely that a causal relationship exists between H. pylori infection and Barrett's-associated adenocarcinoma.     

灯盏细辛注射液对慢性肾功能不全患者T细胞亚群的影响

目的：观察灯盏细辛注射液对慢性肾功能不全患者T细胞亚群的影响。方法：应用T淋巴细胞（OKT）系列单克隆抗体检测人体外周T细胞亚群。结果：治疗组治疗前与对照组比较,T细胞亚群显著下降（P〈0.05）。治疗组用药前后比较,T细胞亚群明显上升（P〈0.05）。结论：灯盏细辛注射液可改善慢性肾功能不全患者T细胞亚群功能,从而提高患者机体免疫。     

Proton Pump Inhibitors and Helicobacter pylori Gastritis: Friends or Foes?

H. pylori gastritis and gastric acid closely interact. In H. pylori-positive patients, profound acid suppressive therapy induces a corpus-predominant pangastritis, which is associated with accelerated corpus gland loss and development of atrophic gastritis. Both corpus-predominant and atrophic gastritis have been associated with an increased risk of development of gastric cancer. H. pylori eradication leads to resolution of gastritis and may induce partial regression of pre-existent gland loss. H. pylori eradication does not aggravate GERD nor does it impair the efficacy of proton pump inhibitor maintenance therapy for this condition. This is the background of the advise within the European guidelines for the management of H. pylori infection to offer an H. pylori test and treat policy to patients who require proton pump inhibitor maintenance therapy for GERD. As such a policy fully reverses H. pylori pangastritis even in patients who have been treated for years with proton pump inhibitors, there is no need to eradicate H. pylori before the start of proton pump inhibitors. In fact, the somewhat slower initial response of H. pylori-negative GERD patients to proton pump inhibitor therapy and the fact that many GERD patients will only require short-term therapy suggests to first start the proton pump inhibitor, and only test and treat when maintenance therapy needs to be prescribed. Such considerations prevent the persistent presence of active corpus-predominant gastritis in proton pump inhibitor-treated reflux patients without impairing the clinical efficacy of treatment.     

Intragastric distribution of Helicobacter pylori during short-term omeprazole therapy: study using Carnoy's fixation and immunohistochemistry for detection of bacteria

BACKGROUND: There is controversy about the effect of acid-suppressive therapy on Helicobacter pylori density and the severity of histological gastritis in the corpus. AIM: To evaluate the precise distribution of H. pylori, both on the surface mucus cells and in the surface mucus gel layer, by using Carnoy's fixation and immunostaining for the detection of bacteria. METHODS: A total of 19 peptic ulcer patients with H. pylori infection were studied. All patients received a 6-week course of treatment with omeprazole (20 mg/day). Before and after the therapy, H. pylori density in Carnoy-fixed tissue sections was examined immunohistochemically. The effect of omeprazole therapy on the severity of gastritis was also evaluated. RESULTS: H. pylori density and the grade of gastritis significantly decreased in the antrum after omeprazole therapy. In the corpus, however, there were no significant changes in H. pylori density or the severity of gastritis after omeprazole therapy. CONCLUSION: Carnoy's fixation and immunostaining was found to be useful for the detection of H. pylori in the surface mucus gel layer as well as on the surface mucus cells in biopsy tissue sections. By using this method, H. pylori density decreased in the antrum, but remained unchanged in the corpus after a 6-week course of omeprazole therapy.     

Helicobacter pylori associated chronic gastritis and peptic ulceration in patients taking non-steroidal anti-inflammatory drugs

Helicobacter pylori is now recognized as a frequent cause of histological chronic gastritis, and this has radically changed our understanding of this common condition. In the light of these developments, the traditional view that non-steroidal anti-inflammatory drugs are one of the common 'environmental' causes of chronic gastritis has been re-examined. Gastric mucosal biopsies have been studied from 430 patients undergoing routine upper gastrointestinal endoscopy, 99 of whom had recently been taking non-steroidal anti-inflammatory drugs. No significant association was found between the use of these drugs and either the presence of chronic gastritis or the frequency of colonization with H. pylori, although there was a strong association (P less than 0.0001) between H. pylori and gastritis. Non-steroidal anti-inflammatory drugs appear, however, to modify the inflammatory process in the gastric body, leading to a lower frequency of atrophic gastritis (P less than 0.05). The majority of peptic ulcers were associated with H. pylori irrespective of non-steroidal anti-inflammatory drug use, but there was a higher frequency of H. pylori negative ulceration in the patients who had used these agents (P less than 0.04). Peptic ulceration was uncommon in the absence of either H. pylori or recent non-steroidal anti-inflammatory drug use.