贲门失弛缓症发病机制的初步探讨

目的 应用氯苄烷铵(BAC)建立猫贲门失弛缓症模型,探讨贲门失弛缓症发病机制。方法 24只猫随机分为两组,模型组胃镜下LES处环形注射BAC,对照组注射生理盐水,8周后检测食管动力学变化,并取组织进行HE染色、乙酰胆碱酯酶(AChE)免疫组化染色检查和AChE活力测定。结果 模型组下食管括约肌压力较对照组明显升高(P<0.01),两组食管收缩幅度无显著性差异;组织学检查显示模型组环肌层和纵肌层之间可见炎细胞浸润,对照组正常;对照组可见AChE染色阳性神经节,环肌层和纵肌层可见AChE染色阳性产物,模型组AChE染色阳性产物明显减少(P<0.01);模型组乙酰胆碱酯酶活力与对照组比较明显降低(P<0.01)。结论 肌间神经丛的炎性反应和乙酰胆碱酯酶活力降低是贲门失弛缓症的重要发病原因。     

贲门失弛缓症治疗研究进展

贲门失弛缓症是一种食管功能性疾病。传统疗法为药物、气囊扩张术和开放手术,其中药物疗效有限;扩张术疗效不如手术且易发生穿孔;常规开放手术创伤大,术后恢复慢,易发生反流。近年来,微创手术和食管下括约肌内肉毒毒素(BT)注射治疗研究得以发展,但远期疗效需进一步随访。     

机械扩张治疗贲门失弛缓症

采用纤维型金属贲门扩张器治疗贲门失弛缓症27例,男10例,女17例,年龄16～54岁。病史5个月～12年。贲门狭窄段横径0.1～0.4cm,平均0.2mm。扩张横径2.8～3.2cm,平均3.0cm。扩张后饮食改善26例(96.3％),无效1例(3.7％),与本院手术治疗组比较,无显著性差异(P>0.01)。本文阐述了纤维型金属贲门扩张器的结构特征,扩张方法,扩张前准备,扩张中与扩张后可能出现的问题及预防处理措施等,认为贲门失弛缓症如无食管溃疡等合并症,以先行扩张治疗为宜。     

贲门失弛缓症治疗进展

贲门失弛缓症的传统治疗以开放式外科手术为主。近年随着内镜技术的发展,内镜下球囊扩张治疗逐渐成为贲门失弛缓症的首选治疗方法。此外,内镜下肉毒素注射治疗及微创手术治疗也已应用于临床,并取得肯定的疗效。本文就近年来贲门失弛缓症的治疗进展作一综述。     

贲门失弛缓症的治疗进展

贲门失弛缓症是一种少见的食管运动障碍性疾病, 其病因及发病机制至今仍未确定. 目前本症的治疗多以缓解症状为主, 主要的治疗方法包括: 药物治疗、内镜下治疗及外科手术治疗. 本文就近年来贲门失弛缓症的治疗进展作一综述.     

贲门失弛缓症诊治的新进展

贲门失弛缓症是一种病因不明的原发性食管运动障碍性疾病,其难治性、易复发、长病程的特点严重影响患者的生活质量。近年来的诊断技术如定时食管吞钡检查、食管高分辨率测压引起了研究者的重视。临床治疗以降低食管下端括约肌压力、缓解梗阻症状为目的,治疗方法处于不断探索和更新中,此文主要就腔镜下改良Heller术及经口内镜下肌切开术进行综述。     

贲门失弛缓症的治疗进展

贲门失弛缓症是一种病因不明的食管功能性疾病,目前对其治疗主要是缓解临床症状,本文比较四种治疗贲门失弛缓症的方法即药物治疗、肉毒毒素治疗、球囊扩张以及肌切开术的疗效,用于选择治疗贲门失弛缓症的最佳方案。     

贲门失弛缓症的内镜及手术治疗

贲门失弛缓症是一种原因不明的以下食管括约肌(LES)松弛障碍和食管体部无蠕动为主要特征的原发性食管动力紊乱性疾病。临床常见症状为:吞咽困难、食物反流以及下段胸骨后不适或疼痛,可伴有体重减轻甚至营养不良,严重影响患者的生活质量。目前贲门失弛缓症的治疗策略主要集中在降低LES压力,以利于排空食管内容物,从而降低相关症状。主要的治疗选择包括口服药物治疗、内镜治疗、外科手术治疗。失弛缓症以外科手术尤其是腹腔镜治疗为主,开放式Heller肌切开治疗失弛缓症有效率可达80%。本文结合近期的一些文献,就贲门失驰缓症的内镜及手术治疗方法作一综述。     

肉毒毒素治疗贲门失弛缓症

贲门失弛缓症(achalasia,AC)的病因和发病机制尚未完全阐明,有学者认为下食管括约肌(LES)不能松弛的机制是肠肌丛内抑制性神经元的选择性丧失,导致乙酰胆碱引起肌缩神经的无对抗性兴奋[1].LES持续性收缩,引起咽下困难、食物反流和胸骨后疼痛等症状.曾有人[2]将本病分为典型(classic)型和高动力(vigorous)型,前者食管明显扩张且缺乏蠕动,后者食管扩张较轻,有高振幅的同步收缩,胸痛症状较突出.但后来Goldenbarg et al[3]证实两者并无明显差别,认为以食管的收缩振幅作为AC分类的标准是不可靠的.我院曾收治1例17岁的男性患者,病程12+mo,1 a前因急性上呼吸道感染,在输液抗炎治疗的过程中出现咽下困难等AC的症状,推测本病的发生是否与病毒感染或某些药物有关,尚待进一步探讨.     

贲门失弛缓症内镜扩张治疗再探

1992-04／1998－02诊治10例贲门失弛缓症（Achalasi）患者，在内镜检查同时即行内镜直接扩张治疗，现报告如下：1对象和方法1．1对象本组Achalasa10例，男6例，女4例，职业：农民8例，教师1例，职员1例；年龄20岁～71岁，平均41．62岁；病程：9mo～3a.按Achalasia诊断标准[1]，本组均有吞咽困难，反流和胸骨下疼痛，6例（4男2女）体质明显消瘦，均属病程1a以上者．临床分型[2]，Ⅰ型8例（5男3女），Ⅱ型2例，按Stooler分级法[3]：1级2例，2级6例，3级2例．1例（女）因喝冷水后即出现吞咽困难，并食后即吐6 mo直至就诊．1．2方法术前准备同…     

电针与氢化麦角碱对血管性痴呆大鼠脑乙酰胆碱酯酶的作用

目的　探讨电针对血管性痴呆(VD)大鼠的学习记忆行为及乙酰胆碱酯酶(AChE)的影响。方法　将制成肾性高血压(RHR)后再造脑反复缺血拟VD的大鼠30只,随机分为模型组、电针组和药物组(用氢化麦角碱,DHET)各10只,共治疗28d。治疗后均以水迷宫检测学习记忆行为情况,并检测脑AchE含量。结果　电针组、药物组水迷宫潜伏期明显短于模型组(P＜0.05～P＜0.005),电针组短于药物组(P＜0.05～P＜0.005)。在海马、纹状体,电针组和药物组的AchE含量显著高于模型组,而电针组又高于药物组(P＜0.05)。结论　电针能改善VD大鼠学习记忆能力,提高脑AchE含量并使之重新分布,其作用优于DHET。     

Family case of achalasia cardia: Case report and review of literature

Achalasia cardia is an idiopathic disease that occurs as a result of inflammation and degeneration of myenteric plexi leading to the loss of postganglionic inhibitory neurons required for relaxation of the lower esophageal sphincter and peristalsis of the esophagus.The main symptoms of achalasia are dysphagia,regurgitation,chest pain and weight loss.At present,there are three main hypotheses regarding etiology of achalasia cardia which are under consideration,these are genetic,infectious and autoimmune.Genetic theory is one of the most widely discussed.Case report given below represents an inheritable case of achalasia cardia which was not diagnosed for a long time in an 81-year-old woman and her 58-year-old daughter.     

Patients' perceptions of self-help groups in achalasia

The possible role of a self-help group was investigated among 126 patients with achalasia. Forty-one patients initially expressed an interest, but only 19 were willing to complete a questionnaire about their role in such a group. Only 14 patients were willing to be identified by other sufferers, and only 8 were ready to take an active part in organising meetings. Although patients with achalasia want more information about their disease, few wish to join a self-help group.     

Non-surgical treatment of esophageal achalasia

INTRODUCTION Esophageal achalasia is a rare neuromuscular disorder characterized by degenerative changes of myenteric plexus leading to a selective loss of inhibitory nerve endings. The consequences of this damage are the irreversible loss of peristaltic …     

食管测压在贲门失弛缓症诊治中的应用及评价

目的　研究贲门失弛缓症患者的食管压力变化。方法　对 35例贲门失弛缓症患者与 30位正常对照的食管测压数据进行对比分析。结果　贲门失弛缓症组食管体部均为同步蠕动波 ,91 4 % (32 / 35 )为低幅同步收缩波 ;食管下括约肌松弛率 (LESRR)为 (6 9 1± 16 3) % ,明显低于正常对照的 (96 0± 0 1) % (P <0 0 1) ;食管下括约肌压增加 ;食管上括约肌各项指标与正常对照组比较无明显差别。结论　贲门失弛缓症的食管压力以低幅同步收缩波和LESRR增高为特征性表现。     

贲门失弛缓症的诊断与治疗研究进展

贲门失弛缓症(AC)作为原发性食管动力障碍性疾病的一种,以食管下段括约肌松弛功能受损、食管蠕动减弱或消失为主要特征,年发病率为1/100 000~3/100 000,临床表现以吞咽困难最为常见。食管测压法为其诊断金标准,另外还有内镜检查、食管钡餐造影检查等诊断方法。目前发病机制尚未明确,临床上可通过药物治疗、肉毒杆菌毒素注射、气囊扩张术、食管支架植入术、腹腔镜下Heller肌切开术、经口内镜下肌切开术等进行治疗。     

Symptoms of achalasia in young women mistaken as indicating primary anorexia nervosa

The case of a young women with dysphagia, regurgitation, and weight loss, who was diagnosed as having anorexia nervosa but in whom reevaluation showed that achalasia was causing the symptoms, is presented together with related observations. Misinterpretation of esophageal symptoms may occur not only as a consequence of inadequate history taking and of being biased by a patient's emaciation, age, and gender, which leads to view certain aspects of the patient's history and behavior as suggesting a pathologic attitude towards eating and body weight, but also as a consequence of a misinterpretation of the symptoms as indicative of an eating disorder by the patients themselves. In some cases a disordered attitude toward eating and body weight may develop together or coexist with achalasia. The clinical evaluation of patients with symptoms suggestive of anorexia nervosa but also of bulimia nervosa should include the taking of a thorough history regarding swallowing and vomiting in order to recognize a possible esophageal motor disorder.