幽门螺杆菌感染治疗现状与展望

随着时间的变迁,幽门螺杆菌(Helicobacter pylori,H.pylori)对常用抗生素的耐药率逐渐增加,其根除率逐渐下降。四联疗法已成为当前治疗H.pylori的主要一线方案,另外欧州MaastrichtIV共识意见中还推荐了序贯疗法和伴同疗法。在H.pylori对常用抗生素耐药的情况下,对于如何提高H.pylori根除率,我国H.pylori学者正在进行H.pylori治疗新路径探索:(1)三联(或四联)联合中药治疗;(2)三联(或四联)联合益生菌治疗;(3)探索口腔H.pylori对H.pylori根除治疗的影响;(4)强调个体化治疗。今天的新思路也许会成为明天治疗H.pylori的新手段。     

标准三联、新四联及10天序贯疗法对幽门螺杆菌感染的疗效观察

目的观察标准三联、新四联及10天序贯疗法对幽门螺杆菌(H.pylori)感染的疗效。方法 215例H.pylori阳性的患者随机分为3组。A组72例,用新四联疗法(雷贝拉唑+可乐必妥+阿莫西林+果胶铋治疗7天);B组72例,用10天序贯疗法(奥美拉唑+阿莫西林治疗5天,继之以奥美拉唑+克拉霉素+替硝唑再治疗5天);C组71例,用标准三联疗法(奥美拉唑+阿莫西林+克拉霉素治疗7天)。治疗后,3组均继续服用3周奥美拉唑。停药4周后复查胃镜、快速尿素酶实验与14C尿素呼气试验,评估H.pylori根除率及溃疡愈合率。结果 215例均完成抗H.pylori治疗周期及随访。A、B、C三组的H.pylori根除率分别为83.33%、88.89%和81.69%;溃疡愈合率分别为86.44%、90.16%和84.91%。B组H.pylori根除率及溃疡愈合率比A、C组稍高,H.pylori根除率与A、C组比较差异亦有统计学意义(P0.05),但A、C组间H.pylori根除率比较差异无统计学意义(P0.05);三组溃疡愈合率比较差异无统计学意义(P0.05),不良反应发生率组间比较差异无统计学意义(P0.05),普遍均能耐受。结论标准三联、新四联及10天序贯疗法均能有效根除H.pylori感染,无明显不良反应,但10天序贯疗法更为理想。     

双联每日4次口服疗法和铋剂四联疗法治疗幽门螺杆菌感染疗效Meta分析

目的 比较质子泵抑制剂(proton pump inhibitor, PPI)+阿莫西林4次/d口服双联疗法和铋剂四联疗法(bismuth quadruple therapy, BQT)治疗幽门螺杆菌(Helicobacter pylori,H.pylori)的有效性及安全性。方法 用计算机检索3个中文数据库(知网、维普、中国生物医学文献服务系统)和3个英文数据库(PubMed、EmBase、Cochrane library)搜索比较PPI+阿莫西林4次/d口服双联疗法与BQT疗法治疗H.pylori的研究，根据纳入及排除标准筛选文献，采用RevMan 5.4.1统计软件进行Meta分析。观察指标：意向治疗(intention-to-treat analysis, ITT)分析和符合方案(per-protocol, PP)分析的H.pylori根除率、不良反应、依从性。结果 本研究共纳入6篇文献，共2 550例H.pylori感染者。ITT分析显示：两种疗法的合并根除率比较，差异无统计学意义(84.5%vs 82.7%,RR=1.02,95%CI:0.99～1.06,P=0.21);P...     

提高幽门螺杆菌根除率的当代观点

幽门螺杆菌(H.pylori)对克拉霉素和甲硝唑耐药率进行性上升降低了标准三联疗法的疗效,目前我国多数地区标准三联疗法根除率已降低到不可接受的水平[按意向治疗(ITT)分析H.pylori根除率80%]。本文讨论了有可能达到可接受根除率的初次治疗的当代方案,包括含铋剂四联疗法、序贯疗法、质子泵抑制剂(PPI)加3种抗生素(不含铋剂四联疗法)和高剂量PPI方案,对治疗失败后补救治疗问题也提出了讨论和建议。     

幽门螺杆菌治疗研究现状

MaastrichtⅣ共识意见和我国第四次全国幽门螺杆菌感染共识报告中均推荐含铋剂四联疗法作为根除H.pylori一线根除治疗方案,共识意见还指出:对铋剂有禁忌或证实H.pylori耐药率仍较低的地区也可选用三联疗法。但是目前各国各地区尚缺乏H.pylori对抗生素的耐药谱,传统的三联疗法是否还适用于临床仍然未知。为进一步了解这一领域的治疗和研究现状,近年来,国内外学者采取不同的治疗方案,如含铋剂四联疗法、序贯疗法、伴同疗法、混合疗法、在标准三联疗法中加入益生菌、中药或加口腔洁治等方法对H.pylori根除率进行研究。     

生物反馈电刺激疗法联合盆底肌训练治疗高龄产妇产后盆底功能障碍的临床效果

目的 观察生物反馈电刺激疗法联合盆底肌训练治疗高龄产妇产后盆底功能障碍的临床效果.方法 收集120例阴道分娩高龄产妇盆底功能障碍患者,随机分为试验组和对照组.对照组仅给予盆底肌训练,试验组给予盆底肌训练联合生物反馈电刺激治疗.比较两组治疗前(Q)、治疗1个月(H1)、治疗3个月(H3)的Ⅰ类和Ⅱ类盆底肌纤维肌电压变化情...     

序贯疗法补救根除幽门螺杆菌感染的疗效观察

目的比较序贯疗法与传统四联疗法对幽门螺杆菌(H.pylori)根除失败后补救治疗的临床疗效。方法选取胃镜下H.pylori快速尿素酶试验或14C尿素呼气试验阳性的患者,经我国标准H.pylori一线三联根除方案治疗7天,停药4周后检测H.pylori,结果仍为阳性者判定为H.pylori根治失败,即进行H.pylori的补救根除治疗,共68例患者入选。随机分为两组:治疗组予以序贯疗法:前5天口服埃索美拉唑20mg和阿莫西林1000mg,2次/d,后5天口服埃索美拉唑20mg、克拉霉素500mg和甲硝唑400mg,2次/d;对照组予以传统四联疗法:口服埃索美拉唑20mg、阿莫西林1000mg、呋喃唑酮100mg和胶体果胶铋100mg,2次/d,疗程7天。疗程结束后4周行14C尿素呼气试验检测H.pylori。结果疗程结束后4周,治疗组H.pylori根除率为93.9%,对照组H.pylori根除率为73.3%,两组H.pylori根除率比较有显著性差异(P0.05)。结论序贯疗法对H.pylori的根除率高于传统四联疗法,可作为有效的H.pylori补救根除治疗方案。     

10d序贯疗法对根除幽门螺杆菌疗效的随访研究

背景:幽门螺杆菌(H.pylori)与慢性胃炎、消化性溃疡、胃癌和胃黏膜相关淋巴组织(MALT)淋巴瘤密切相关,但标准三联疗法的根除率逐年下降。目的:比较10 d序贯疗法和三联疗法根除H.pylori的疗效。方法:将经快速尿素酶试验(RUT)和~(14)C-尿素呼气试验(UBT)证实为H.pylori阳性的106例消化性溃疡、慢性糜烂性胃炎和萎缩性胃炎患者随机分为以雷贝拉唑为基础的10 d序贯疗法组(n=56)和三联疗法组(n=50)。治疗结束4周后复查RUT和,~(14)C-UBT,评估H.pylori根除情况;随访1年后再复查~(14)C-UBT评估H.pylori复发情况。结果:共93例患者按方案完成治疗。10 d序贯疗法组H.pylori根除率按意向治疗(ITT)和按方案(PP)分析均显著高于三联疗法组(ITF:89.3%对62.0%,P0.01;PP:94.3%对77.5%,P0.05);10 d序贯疗法组不良反应发生率(7.1%对30.0%,P0.01)和随访1年后的H.pylori复发率(6.0%对25.8%,P0.01)均显著低于三联疗法组。结论:以雷贝拉唑为基础的10 d序贯疗法可明显提高H.pylori根除率,提高患者的依从性,减少不良反应的发生。     

中药体外抑杀幽门螺杆菌的实验研究

幽门螺杆菌(H elicobacter pylori,H P)是一种定植于人胃黏膜的革兰阴性细菌,可以引起多种胃十二指肠疾病[1]。1983年自W arren和M arshall成功分离幽门螺杆菌,人们发现H P是慢性胃炎和消化性溃疡的重要致病因子,是胃黏膜相关淋巴组织(M A LT)淋巴瘤的重要致病因素,且与胃癌的发生有很大的关联[2]。目前根除H P的药物主要分为两大类:一类为含铋制剂;另一类为含质子泵抑制剂(PPI)或H2受体阻断剂(H2R A)。根据药物组合又可分为二联疗法,三联疗法和四联疗法[3],均具有肯定的抗H P作用。但目前这些药物治疗的根除方案中仍存在着很多问…     

序贯疗法在幽门螺杆菌感染性浅表型胃炎患者中的临床效果观察

目的研究序贯疗法对于幽门螺杆菌(Helicobacter pylori,H.pylori)感染的浅表型胃炎患者的治疗效果。方法将2013年2月至2014年2月我院收治的80例H.pylori(+)浅表性胃炎患者纳入本次研究,根据治疗方式的不同分为对照组与研究组,对照组给予传统的三联疗法治疗,研究组给予序贯疗法治疗,比较两组的治疗效果以及H.pylori根除情况。结果研究组患者H.pylori根除率、症状改善总有效率、不良反应总发生率明显优于对照组(P0.05),差异具有统计学意义;两组患者除对照组1例因不良反应严重退出试验,其余停药后不良反应自行缓解,依从性良好。结论序贯疗法对于H.pylori(+)浅表性胃炎患者的治疗效果确切,能有效改善患者的症状,且药物不良反应少,患者适应性良好。     

von Willebrand因子与蛛网膜下腔出血后脑血管痉挛

脑血管痉挛是蛛网膜下腔出血后的并发症之一,也是蛛网膜下腔出血患者残疾和死亡的重要原因,其发病机制至今尚不明确,目前有关血管内皮细胞功能的研究较多.von Willebrand因子(vWF)是反映血管内皮细胞功能的特异标志物,文章就vWF在脑血管痉挛中的作用做了综述.     

蛛网膜下腔出血后脑脊液细胞因子水平与脑血管痉挛的关系

脑血管痉挛是蛛网膜下腔出血(SAH)的一种常见并发症。目前,脑血管痉挛的确切发生机制还不完全清楚,也缺乏有效控制脑血管痉挛发生和发展的方法。近年来,一些学者发现,SAH后脑脊液和血清某些细胞因子水平可能发生改变,细胞因子所引起的炎症反应可能与脑血管痉挛有一定关联。因此,检测脑脊液和血清细胞因子水平对预测SAH的严重程度、转归和及早治疗均有重要意义。     

改良Fisher分级与破裂动脉瘤患者症状性脑血管痉挛的关系

目的分析破裂出血动脉瘤患者改良Fisher分级与术后症状性脑血管痉挛发生的关系。方法按改良Fisher分级评价动脉瘤破裂出血患者216例。症状性血管痉挛的诊断根据迟发性神经功能损害并经颅多普勒检查证实。结果 216例患者中共发生症状性血管痉挛79例(36.6%),按照改良Fisher分级评价,术前不同级别的患者术后症状性脑血管痉挛发生率比较,差异有统计学意义。结论症状性脑血管痉挛的发生率与蛛网膜下腔出血量有显著的相关关系。     

Gene therapy for stroke: 2006 overview

Gene therapy is a promising approach for treatment of stroke and other cerebrovascular diseases, although it may take many years to realize. Gene therapy could occur prior to a stroke (eg, to stabilize atherosclerotic plaques) and/or following a stroke (eg, to prevent vasospasm after subarachnoid hemorrhage [SAH] or reduce injury to neurons by ischemic insult). We have transferred the gene coding for vasoactive calcitonin gene-related peptide via cerebrospinal fluid, and demonstrated attenuation of vasospasm after SAH. Transfer of neuroprotective genes or small interfering RNA for neurotoxic genes has good potential for ischemic stroke. In this brief report, we review recent developments in experimental gene therapy for stroke. Fundamental advances, including development of safer, more specific gene transfer vectors, are discussed.     

自由基清除剂防治蛛网膜下腔出血后脑血管痉挛

脑血管痉挛是蛛网膜下腔出血后的常见并发症,其病理生理学机制未完全明确.越来越多的研究表明,自由基在诱发脑血管痉挛中起着十分重要的作用.近年来,有关自由基清除剂防治蛛网膜下腔出血后脑血管痉挛的研究不断增多.文章对多类自由基清除剂在蛛网膜下腔出血后脑血管痉挛防治中的作用进行了综述.     

脑脊液置换术治疗蛛网膜下腔出血临床研究

目的探讨脑脊液置换术治疗蛛网膜下腔出血的临床效果。方法将80例蛛网膜下腔出血患者随机分治疗组及对照组,各40例,治疗组在常规治疗的基础上进行脑脊液置换术治疗,对照组使用单纯的常规治疗。结果治疗组治疗的有效例数与对照组比较差异有统计学意义。治疗组中有头痛颈强者21例,持续时间6～12.5d,对照组头痛颈强持续时间14～21d,两组比较差异有统计学意义。治疗组中表现不同意识障碍者6例,经置换2～3次最短在4d内意识恢复正常,对照组意识障碍11例,意识障碍恢复时间6～14d,两组比较有显著差异。蛛网膜下腔出血3大并发症脑血管痉挛、脑积水、脑梗死,治疗组与对照组比较,均有显著差异。结论脑脊液置换术治疗蛛网膜下腔出血,能减少脑血管痉挛、脑积水、脑梗死等并发症,有利于患者恢复,操作简单易行、安全,疗效显著,值得临床推广应用。     

Management of post-subarachnoid hemorrhage vasospasm

Permanent neurologic injury and death remain common outcomes following aneurysmal subarachnoid hemorrhage. Although many sophisticated techniques are evolving for securing intracranial aneurysms to prevent rebleeding, progress is lagging in the management of posthemorrhagic complications, particularly cerebral vasospasm. Vasospasm can be defined either angiographically, by visible reduction in arterial lumen diameters, or clinically, with signs of focal or regional cerebral ischemia. The relationship between angiographic and clinical vasospasm is not straightforward. The most important known risk factors for developing posthemorrhagic vasospasm include volume and distribution of subarachnoid blood, and no preventive measures have proven effective. Established treatment strategies for vasospasm include hyperdynamic therapy, angioplasty, and selective intra-arterial injection of vasodilators. The vasodilatory approach has been called into question by recent data suggesting that reduction of arterial luminal diameters may be due largely to a proliferative arteriopathy. Novel treatment strategies have focused on protecting the cerebrum, targeting components of the inflammatory cascade, and identifying genetic factors predisposing toward vasospasm, all of which may soon yield new treatment modalities.     

蛛网膜下腔出血后迟发性血管痉挛的炎症机制

迟发性血管痉挛是蛛网膜下腔出血的重要并发症 ,是致死和致残的主要原因 ,但其发病机制尚不完全清楚 ,治疗效果尚不满意。文章综述了迟发性血管痉挛的炎症机制 ,介绍了通过抗炎治疗缓解迟发性血管痉挛的新进展。     

A case of coronary spasm induced by 5-fluorouracil

Cardiotoxicity is an uncommon adverse effect of 5-fluorouracil (5-FU). Coronary artery spasm has been postulated to be involved in the mechanism of this incident Patients may present with angina, myocardial infarction, arrhythmias and/or even sudden death.When the drug is readministered, there is a high risk of relapse.The underlying mechanisms of cardiotoxicity are not yet fully understood, although coronary vasospasm may be responsible. We report one woman receiving 5-fluorouracil therapy with typical chest pain and electrocardiographic changes consistent with acute coronary syndrome. A resolving pain and normalisation of ECG changes with nitrate therapy and normal coronary arteries indicate that this incident was about a coronary spasm caused by 5-FU.     

Ventricular Fibrillation Cardiac Arrest due to 5-Fluorouracil Cardiotoxicity

The antimetabolite chemotherapeutic agent 5-fluorouracil is used to treat a variety of cancers. Although 5-fluorouracil is generally well tolerated, its toxicity profile includes potential cardiac ischemia, vasospasm, arrhythmia, and direct myocardial injury. These actual or potential toxicities are thought to resolve upon cessation of the medication; however, information about the long-term cardiovascular effects of therapy is not sufficient. We present the case of a 58-year-old man who had 2 ventricular fibrillation cardiac arrests, with evidence of coronary vasospasm and myocarditis, on his 4th day of continuous infusion with 5-fluorouracil. External defibrillation and cessation of the 5-fluorouracil therapy resolved the patient''s electrocardiographic abnormalities. In addition to reporting the clinical manifestations of 5-fluorouracil–associated cardiotoxicity in our patient, we discuss management challenges in patients who develop severe 5-fluorouracil–induced ventricular arrhythmias.Key words: Arrhythmias, cardiac/chemically induced; coronary vasospasm/chemically induced; fluorouracil/adverse effects; heart/drug effects; heart diseases/drug therapy; myocarditis/chemically induced; treatment outcomeChemotherapeutic agents have greatly improved the overall prognosis of patients with various cancers. Nevertheless, these drugs can have severe and sometimes life-threatening side effects. The cardiovascular complications can be particularly dramatic. One such agent, 5-fluorouracil (5-FU), interferes with DNA synthesis in cancer cells, leading to cell death. It is used to treat a variety of malignancies, including gastrointestinal, esophageal, bladder, and head and neck cancers.¹ Its severe cardiotoxic effects include vasospasm, ischemia, arrhythmias, and myopathic processes. We report the case of a patient who survived ventricular fibrillation (VF) cardiac arrest attributed to 5-FU–induced vasospasm and myocarditis. This case suggests that the multiple cardiotoxic effects of 5-FU can occur simultaneously and might be interrelated. In addition, we discuss management challenges in this patient population.