幽门螺杆菌感染与缺铁性贫血的临床分析

目的:观察缺铁性贫血(IDA)伴幽门螺杆菌(Hp)阳性慢性胃炎患者抗Hp加铁剂治疗前后实验室检测指标的变化及疗效,探讨Hp感染与IDA形成的相关性及其临床意义。方法:将62例IDA伴Hp阳性慢性胃炎患者,分为A、B、C、D 4组。A组给予补铁及Hp根除治疗,B组仅Hp根除治疗,C组仅补铁治疗,D组中医辨证治疗胃炎;检测治疗前后其血红蛋白浓度及血清铁、总铁结合力、铁蛋白水平,并对Hp、胃蛋白酶活性、胃酸进行检测。结果:IDA伴慢性胃炎患者Hp感染率较高(82．7％,62／75),补铁联合抗Hp治疗较单纯补铁或抗Hp治疗效果显著(P<0．05)。结论:Hp感染可造成或加重机体铁营养不良,在治疗IDA的过程中应注意清除Hp感染。     

缺铁性贫血患者抗幽门螺旋杆菌治疗的价值

目的：了解幽门螺旋杆菌（HP）感染对缺铁性贫血（IDA）发病的影响及抗HP治疗对改善贫血的价值。方法：对116例IDA患者补铁治疗并检测HP感染的情况。分组：A组为给予去除缺铁原因治疗和补铁治疗可以达到IDA痊愈者,B组为无明显缺铁原因但单纯补铁效果不好的IDA患者。对B组患者给予抗HP治疗,观察抗HP治疗前后患者Hb、平均红细胞体积（MCV）、平均红细胞血红蛋白含量（MCH）、血清铁蛋白（SF）的变化。结果：116例IDA患者中,A组74例给予去除缺铁原因治疗和（或）补铁治疗可以达到IDA痊愈,其中HP感染43例,感染率58.1%;B组42例无明显缺铁原因但是单纯补铁效果不好的IDA患者中HP感染者36例,感染率85.7%,2组间HP感染率的差异有统计学意义。对B组中HP阳性者给予抗HP治疗,抗HP治疗有效者Hb、MCV、MCH、SF较治疗前有明显提高。结论：HP感染可能与IDA的发生有关,清除HP的治疗可改善IDA的疗效。     

幽门螺杆菌与中青年缺铁性贫血关系的临床研究

目的:探讨幽门螺杆菌(HP)感染与缺铁性贫血(IDA)的关系以及HP相关性IDA治疗的有效方法。方法:对132例有上消化道症状的中青年患者进行内镜下组织病理检查,胃黏膜活检标本快速尿素酶试验,同时所有患者作血常规,血清铁(SI),血清铁蛋白(SF),血清HP抗体(HP-IgG)检测。将HP感染伴慢性胃炎的IDA患者(36例)随机分成A,B2组,A组给予铁剂联合HP根治治疗,B组仅给予HP根治治疗,治疗后复查上述血液学指标。结果:HP感染的92例患者中IDA者有52例,IDA的患病率为56.5%;40例无HP感染患者中IDA者有6例,IDA的患病率为15.0%,两者相比差异有统计学意义(P<0.05)。58例IDA患者中,有52例为HP感染,HP感染率为89.7%;74例非IDA患者中,有40例为HP感染,HP感染率为54.1%,两者相比差异有统计学意义(P<0.05)。A,B2组治疗前后其血红蛋白(Hb),SI,SF均有显著性恢复,且A组比B组上述血液学指标差异有统计学意义。结论:HP感染可能为中青年IDA的病因之一,铁剂联合根治HP的治疗能显著提高中青年HP相关性IDA的治疗效果。     

幽门螺杆菌感染与缺铁性贫血的关系

目的：探讨幽门螺杆菌(HP)感染与缺铁性贫血(IDA)的关系，以及HP相关IDA的治疗。方法：①分别统计46例IDA伴慢性胃炎与50例非IDA慢性胃炎两组HP感染率。②将42例HP感染相关IDA随机分成两组，分别应用根除细菌加口服铁剂与单用铁剂方案治疗，检测治疗前后血液学指标、观察疗效。结果：IDA伴慢性胃炎者HP感染率高于非IDA慢性胃炎者，两者差异有统计学意义；HP感染相关IDA患者接受根除细菌加铁剂治疗前后其Hb、血清铁、铁蛋白均显著增高，而单用铁剂组治疗前后血液学指标无显著变化。结论：HP感染与IDA可能有一定相关性，当IDA患者铁剂治疗效果不显著时宜考虑是否存在HP相关IDA．根除HP感染后对IDA有一定治疗作用。     

抗幽门螺杆菌对慢性胃炎伴缺铁性贫血患者的疗效研究

目的观察治疗幽门螺杆菌（Helicobacter priori，Hp）对慢性胃炎伴缺铁性贫血（iron deficiency anemia，IDA）患者的疗效。方法对31例有长期IDA病史、病因检查只发现有Hp阳性慢性胃炎的患者，进行根除Hp治疗；同时检测患者的血红蛋白（hemoglobin，Hb）、平均红细胞体积（mean corpuscular volume，MCV）；行快速尿素酶试验、内镜下组织病理检查了解Hp感染情况。结果根除Hp治疗6个月、12个月结束时，74．2％（23／31）和90．3％（28／31）患者的贫血已得到纠正。结论根除Hp治疗可治愈以Hp阳性慢性胃炎作为唯一病因的缺铁性贫血患者的贫血。     

根除幽门螺杆菌治疗幽门螺杆菌阳性的缺铁性贫血患者的疗效观察

目的探讨根除幽门螺杆菌(Hp)治疗Hp阳性的缺铁性贫血(IDA)患者的临床疗效。方法选择2011年1月—2014年1月我科收治的Hp阳性的IDA患者84例,按随机数字表法将其分为对照组和观察组,各42例。对照组给予单独补充铁剂治疗,观察组在对照组治疗的基础上联合根除Hp治疗,两组均以14 d为1个疗程,连续补充铁剂2个疗程。观察1个疗程结束时观察组Hp转阴率,比较两组治疗前后血红蛋白(HGB)、平均红细胞体积(MCV)、血清铁蛋白(SF)、血清铁(SI)等水平。结果观察组1个疗程结束时Hp转阴率为92.9%。治疗前两组患者HGB、MCV、SF、SI水平比较,差异均无统计学意义(P0.05);治疗后观察组HGB、MCV、SF、SI水平均高于对照组(P0.05)。结论根除Hp治疗可改善Hp阳性的IDA患者的铁储备状态,提高临床疗效,对维持IDA患者HGB、MCV有重要意义。     

不同Hp感染的老年慢性胃炎患者S100蛋白表达及意义

目的 探讨不同幽门螺旋杆菌(Hp)感染情况的老年慢性胃炎患者S100蛋白表达特点及意义。方法 选取老年慢性胃炎患者92例，根据病理检查结果分为慢性非萎缩性胃炎组39例，慢性萎缩性胃炎组53例。接受碳13尿酸呼气试验，并结合快速尿素酶试验结果进行综合判断，分为Hp感染阳性(阳性组)、Hp感染阴性(阴性组)。胃镜下随机采集胃窦部黏膜组织标本，免疫组化法检测S100A8、S100A9阳性表达情况；RT-PCR检测S100A8、S100A9 mRNA表达水平；Western印迹检测S100A8、S100A9蛋白表达水平。结果 慢性萎缩性胃炎组S100A8、S100A9表达阳性率明显高于慢性非萎缩性胃炎组(P<0.01)。慢性萎缩性胃炎组S100A8、S100A9 mRNA和蛋白表达水平明显高于慢性非萎缩性胃炎组(P<0.01)。Hp感染阳性的老年慢性胃炎患者S100A8、S100A9表达阳性率明显高于Hp感染阴性的患者(P<0.01)。Hp感染阳性的老年慢性胃炎患者S100A8、S100A9 mRNA和蛋白表达水平明显高于Hp感染阴性的患者(P<0.01)。慢性萎缩性胃...     

小儿缺铁性贫血与幽门螺杆菌感染相关性研究

目的探讨小儿缺铁性贫血（IDA）与幽门螺杆菌（Hp）感染的相关性。方法对85例幼儿园儿童进行全血血常规、血清铁、总铁结合力及Hp检测，并将其分为IDA组和非IDA对照组，对两组Hp感染情况进行统计分析。结果41例贫血儿童中有27例感染Hp（65-85％），44例正常儿童中有12例感染Hp（27．27％），两者比较有显著差异（χ^2=12．72，P〈0．001）。结论小儿IDA与Hp感染具有相关性。     

唾液幽门螺杆菌抗原检测与慢性胃炎活动性及癌前病变关系的研究

目的评价唾液幽门螺杆菌(Helicobacterpylori,Hp)抗原与慢性胃炎活动性以及胃黏膜癌前病变肠上皮化生与不典型增生的相关性。方法应用酶联免疫吸附法(ELISA),对2004年6月至2005年6月浙江大学医学院附属第二医院消化内科246例接受胃镜检查患者的唾液标本进行幽门螺杆菌抗原检测,分别比较不同胃病患者唾液中Hp抗原的阳性检出率。结果慢性活动性胃炎组唾液中Hp抗原阳性检出率为74.29%(26/35),明显高于慢性非活动性胃炎组46.92%(99/211)(P<0.05)。慢性胃炎组患者唾液中Hp抗原的阳性检出率为45.98%(80/174),慢性胃炎伴轻度肠上皮化生(肠化)组唾液中Hp抗原阳性检出率为52.63%(20/38),慢性胃炎伴中重度肠化组唾液中Hp抗原阳性检出率为68.18%(15/22),慢性胃炎伴不典型增生组唾液中Hp抗原阳性检出率为83.33%(10/12),结果显示,慢性胃炎伴中重度肠化或不典型增生组与慢性胃炎组相比,差异有统计学意义(P<0.05)。结论唾液中存在高Hp检出率现象,口腔可能为Hp的重要寄居地,口腔内Hp感染程度与胃炎活动程度及部分胃黏膜癌前病变有关,慢性活动性胃炎或伴中重度肠化或不典型增生患者口腔内Hp检出率明显增高,口腔内Hp是否需行根除治疗,值得今后进一步研究探讨。     

幽门螺杆菌感染与冠心病患者血脂代谢的关系

目的 探讨冠心病(CHD)患者幽门螺杆菌(Hp)感染的发生状况及其与血脂代谢的关系.方法 采用酶联免疫吸附法检测78例CHD患者及30例健康对照者血清抗Hp抗体及抗Hp细胞毒素相关基因蛋白A(Hp-CagA)抗体水平,分析其阳性率与患者血脂水平的关系.结果 冠心病组血清抗Hp抗体及抗Hp-CagA抗体阳性率明显高于健康对照组(P<0.01).冠心病组中Hp抗体阳性患者血清胆固醇、甘油三酯及低密度脂蛋白包括载脂蛋白A1和载脂蛋白B水平明显高于Hp抗体阴性患者,而高密度脂蛋白却低于Hp抗体阴性患者(P<0.05).结论 Hp感染可能会通过影响机体脂质代谢,促进动脉粥样硬化(AS)的形成,进而诱发CHD.     

A hematologist's view of unexplained iron deficiency anemia in males: impact of Helicobacter pylori eradication

BACKGROUND AND OBJECTIVES: Helicobacter pylori infection with, or without coexisting autoimmune gastritis has been implicated in several recent studies as an important cause of IDA in patients with unexplained iron deficiency anemia (IDA). However, the role of H. pylori in the causation of IDA is still unsettled as the vast majority of reported patients were premenopausal women in whom menstrual blood loss was likely the dominant factor determining IDA. DESIGN AND METHODS: Prospective study of 44 consecutive male IDA patients referred for hematologic evaluation. Following standard endoscopic studies, all patients were screened for non-bleeding GI conditions including celiac disease, autoimmune gastritis and H. pylori gastritis. All subject with H. pylori infection were offered triple therapy for H. pylori eradication. RESULTS: Only 15 patients had a likely source of blood loss identified. The 29 males with "unexplained" IDA were distinguished by their younger age (36+/-20 vs. 57+/-17 years p<0.001), poor initial response to oral iron treatment, and high prevalence of H. pylori infection (25 of 29 vs. 5 of 15 p<0.0001) with (10) or without (15) coexistent autoimmune gastritis. Three had celiac disease. Following H. pylori eradication, all patients achieved normal hemoglobin levels with follow-up periods ranging from 4 to 69 months (38+/-15 months mean+/-1SD). This was accompanied by a significant decrease in H. pylori IgG antibodies and serum gastrin. Sixteen patients discontinued iron treatment, maintaining normal hemoglobin and ferritin and may be considered cured. Remarkably, 4 of the 16 achieved normal hemoglobin without ever having received oral iron after H. pylori eradication. INTERPRETATION AND CONCLUSIONS: The favorable long-term clinical results of H. pylori eradication offer strong evidence for a cause-and-effect relation between H. pylori and IDA. Recognition of the respective roles of H. pylori and autoimmune gastritis in the pathogenesis of iron deficiency may have a strong impact on the clinical management of unexplained and refractory iron deficiency anemia.     

Improvement of complete blood count in patients with iron deficiency anemia and Helicobacter pylori infection after the eradication of Helicobacter pylori

BACKGROUND/AIMS: Recent reports support the possible association between Hp infection and iron deficiency anemia. In the present study, the effects of the eradication therapy on iron deficiency anemia were investigated. METHODOLOGY: Fourteen women with iron deficiency anemia were enrolled (mean age: 36.4 years; range: 20-52 years old). None of the patients received iron supplementation. Several examinations including upper and lower gastrointestinal endoscopy were performed to reveal any gastrointestinal bleeding sites in all patients. Gastric biopsies during endoscopy were taken from the subjects except one whose serum anti-Hp IgG was positive. After diagnosing the Hp infection by means of microbiology, histology and Gram stain, a combination therapy consisting of lansoprosol, clarithromycin and amoxicillin was administered to each patient. Hematologic examinations and the body iron status were evaluated periodically, following the eradication therapy. RESULTS: Endoscopic findings were as follows: Seven patients with antral gastritis, two patients with pangastritis, whereas five patients were found to be endoscopically normal. None of the subjects were found to have gastrointestinal bleeding of any type. Serum hemoglobin, iron and transferrin saturations of the patients were found to be increased at 20-24 weeks of follow-up after the eradication therapy. Serum ferritin levels were not found to be increased. CONCLUSIONS: Hp infection may be involved in cases of iron deficiency anemia of unknown origin, and the eradication of the infection may improve blood parameters other than serum ferritin levels.     

Effects of H pylori therapy on erythrocytic and iron parameters in iron deficiency anemia patients with H pylori-positive chronic gastristis

AIM： To elucidate the influences of Hpylori infection on oral iron treatment for iron deficiency anemia （IDA）.
METHODS： A total of 86 patients were divided into two groups： group A, receiving ferrous succinate combined with triple therapy for H pylori eradication, and group B （control）, treated with ferrous succinate only. During treatment of IDA, dynamic changes in hemoglobin （Hb） level, mean corpuscular volume （MCV）, mean corpuscular hemoglobin （MCH）, serum iron （SI）, and serum ferritin （SF） were compared between the groups.
RESULTS： Hb was slightly higher in group A at d 14 alter the start of triple therapy for H pylori eradication （P 〉 0.05）. After the therapy, the increase of Hb in group A became significantly faster than that in group B （P 〈 0.05）. At d 56, the mean Hb in group A returned to the normal level, however, in group B, it was lower than that in group A （P 〈 0.05） although it had also increased compared with that before oral iron treatment. The MCV and MCH in group A recovered to the normal level, and were much higher than those in group B （P 〈 0.05） at d 21. In Group B, the MCV and MCH remained at lower than normal levels until d 42 alter the start of therapy. And then, they reached a plateau in both groups and the differences disappeared （P 〉 0.05）. The SF in group A was higher than that in group B （P 〈 0.05） 28 d alter the treatment and its improvement was quicker in group A （P 〈 0.05）, and the difference between the two groups was even more significant （P 〈 0.01） at d 56. The SI in group A was higher than that in group B （P 〈 0.05） at d 14 and this persisted until d 56 when the follow-up of this research was finished.
CONCLUSION： Treatment of H pylori can enhance the efficacy of ferrous succinate therapy in IDA patients with Hpylori-positive chronic gastritis.     

复方嗜酸乳杆菌片在幽门螺杆菌根除失败补救方案中作用的研究

幽门螺杆菌(Hp)感染与慢性胃炎、消化性溃疡、胃黏膜相关淋巴样组织淋巴瘤和胃癌等疾病的发生有关。有研究显示,联合使用嗜酸乳杆菌能提高Hp根除率,并降低治疗过程中的不良反应。目的:探讨复方嗜酸乳杆菌片联合含铋剂四联疗法对首次根除失败的Hp感染的疗效。方法:将180例经标准三联疗法首次根除失败的Hp阳性的消化性溃疡患者随机分为试验组和对照组,试验组患者给予复方嗜酸乳杆菌片1 g tid,餐后服用,疗程14 d,然后给予雷贝拉唑10 mg bid+阿莫西林1 000 mg bid+呋喃唑酮100 mg bid+枸橼酸铋钾300 mg qid,疗程10 d。对照组患者给予雷贝拉唑10 mg bid+阿莫西林1 000 mg bid+呋喃唑酮100 mg bid+枸橼酸铋钾300 mg qid,疗程10 d。治疗结束至少4周后行~(13)C-尿素呼气试验,评估Hp根除率和不良反应。结果:试验组PP根除率和ITT根除率与对照组相比均无明显差异(PP:81.2%对78.2%,χ~2=0.241,P=0.623;ITT:76.7%对75.6%,χ~2=0.031,P=0.861)。试验组恶心呕吐(2.4%对11.5%)、腹泻(0对9.2%)的发生率明显低于对照组(P0.05)。结论:复方嗜酸乳杆菌片联合含铋剂四联疗法对首次标准三联疗法根除失败的Hp患者疗效较好,同时可有效减少不良反应。     

老年幽门螺杆菌相关性胃炎患者抗幽门螺杆菌根除治疗前后的病理学研究

目的分析老年幽门螺杆菌（Hp）相关性胃炎患者抗Hp根除治疗前后胃黏膜病理炎症变化程度,探讨老年Hp相关性胃炎患者行抗Hp根除治疗的重要性。方法收集1989年4月至2011年6月经内镜活检病理、13C-尿素呼气试验、粪便Hp抗原检测,有长期随访资料的老年Hp相关性胃炎患者共239例,观察抗Hp根除治疗前后胃黏膜病理炎症改变程度。结果Hp彻底根除的199次治疗中,179次镜下组织学慢性炎症程度明显好转,治疗前64次有活动性炎症,治疗后27次有活动性炎症;Hp未彻底根除的66次治疗中,42次镜下组织学慢性炎症程度明显好转,治疗前39次有活动性炎症,治疗后22次有活动性炎症。Hp达根除标准的老年患者较Hp未能根除者镜下组织学慢性炎症及活动性炎症程度均明显好转（P〈0．05）。结论对老年Hp相关性胃炎患者进行抗Hp根除治疗,可明显改善患者的胃黏膜组织学慢性炎症及活动性炎症程度,有效地减少慢性胃炎的发病及减轻病变程度。     

Oral Cavity as a Potential Source of Gastric Reinfection by Helicobacter pylori

Helicobacter pylori (Hp) is a common pathogen colonizing the a gastric mucosa, but some reports indicated that it may also be found in the oral cavity, which could serve as a reservoir of the bacteria and a source of gastric reinfection. Accordingly, we aimed to study whether the oral cavity, particularly gingival pockets, are colonized by Hp and whether it could be the source of gastric reinfection. We studied 329 patients with dyspeptic symptoms (257 with chronic gastritis, 15 with gastric ulcer, and 57 with duodenal ulcer). The [¹³C]urea breath test (UBT), gastroscopy, and Hp culture from gastric biopsies were carried out, and material was collected from the oral cavity (gingival pocket) for bacteriological culture and genomic DNA studies. The serum was obtained for anti-Hp IgG and anti-CagA assays and saliva for anti-Hp IgA determination using the ELISA technique. Bacteria in material from gingival pockets and biopsies from the corpus and antrum of stomach of 30 DU patients before and after Hp eradication were also examined by PCR technique, using primers specific for 16S rRNA. All Hp-positive patients (276) were subjected to one week of triple therapy (omeprazole 2 × 20 mg twice a day, clarithromycin 2 × 500 mg twice a day, and metronidazole 2 × 500 mg twice a day). The measurements described above were then repeated at four weeks and six months. Bacteriological culture showed the presence of Hp in the material from oral cavity in about 50% of patients, whereas UBT, used as a gold standard, revealed gastric Hp infection in about 84% of these patients. The eradication was successful in the majority of patients (87%), but about 13% of them were still Hp positive after four weeks and about 21% after six months. Four weeks after Hp therapy, Hp was found in culture from oral samples in 23% (P < 0.05 vs initial) and after six months in 35.1%. The IgA levels recorded in saliva were in a close agreement with UBT results. Hp DNA assessed by PCR in 30 DUs before eradication of Hp was detected in 95% of antral mucosa, 90% in corpus mucosa, and in 35% of gingival pocket material, and after eradication therapy Hp DNA values fell to 25%, 20%, and 10%, respectively. In conclusion, Hp is commonly detected in the oral cavity of patients with dyspeptic symptoms, but the gastric reinfection does not appear to occur in the patients despite oral Hp colonization.     

Gastropathic sideropenia

There has been an increasing awareness recently of subtle, non-bleeding gastrointestinal conditions that may result in abnormal iron absorption leading to iron-deficiency anaemia (IDA) in the absence of gastrointestinal symptoms. Thus, the importance of coeliac disease as a possible cause of IDA refractory to oral iron treatment, without other manifestations of malabsorption syndrome, is increasingly being recognized. In addition, Helicobacter pylori has been implicated in several recent studies as a cause of IDA refractory to oral iron treatment, and the anaemia responds favourably to H. pylori eradication. Likewise, achlorhydric gastric atrophy or atrophic body gastritis (ABG), a condition associated with chronic idiopathic iron deficiency, has been shown to be responsible for refractory IDA in over 20% of patients with no evidence of gastrointestinal blood loss. It has also been suggested that H. pylori gastritis may represent an early phase of ABG in which infection may trigger an autoimmune process directed against gastric parietal cells by means of antigenic mimicry. In this review we examine in a critical manner the role of H. pylori gastritis in the causation of IDA, the role of ABG in the pathogenesis of iron malabsorption, the evidence supporting a possible cause-and-effect relationship between H. pylori gastritis and ABG, and the implications of these findings for the diagnostic work-up and management of IDA.     

Healing of lymphocytic gastritis by eradication of Helicobacter pylori

BACKGROUND: It is not yet clear whether lymphocytic gastritis might not be a sequela of Helicobacter pylori (Hp) infection. The aim of the present pilot study was, therefore, to investigate whether lymphocytic gastritis can be cured by Hp eradication, which, if affirmed, would provide indirect evidence for an etiopathogenic relationship. PATIENTS AND METHODS: 98 of 220 patients with lymphocytic gastritis diagnosed between 1988 and 1998 were investigated at least twice, with 61 of them undergoing Hp eradication treatment. In 29 of these patients, the pretreatment histological work-up using the Warthin-Starry silver stain revealed Hp colonisation, while in the remaining 32 patients the biopsies from the antrum and corpus were negative for Hp. The other 37 patients received no treatment, and served as a control group. RESULTS: Both in the group with Hp-positive, and in the group with Hp-negative histology prior to treatment, eradication treatment led to healing of the gastritis, i.e. to regression of the gastritis parameters including normalisation of the intra-epithelial lymphocyte count, in 93.1% and 84.3% of the cases, respectively. In the control group the histological findings did not change. CONCLUSIONS: The results of our retrospective study support the notion that most cases of lymphocytic gastritis might be a consequence of Hp infection. This, however, needs to be clarified definitively by a prospective, randomized, double-blind study.