中西医结合治疗及流性食管炎70例

目的观察中医疏肝健脾，和胃降逆法配合西医综合治疗反流性食管炎的临床疗效．方法反流性食管炎患者109例，随机分为两组：中西医结合治疗组70例（自拟“三白汤”主要成分为白术，白芍，白芨，半夏，旋覆花，黄连等组成，1剂／d的基础上加用西药多潘立酮片10mg，3次／d，餐前口服，雷尼替丁300mg每晚睡前30min口服．以下简称治疗组）和单纯中药治疗组39例（单独运用“三白汤”，以下简称对照组）．4wk疗程结束后，对两组患者的临床症状、体征等的改善情况进行比较分析．结果经过4wk治疗后，治疗组治愈23例，好转41例，无效6例，总有效率为91．4％；对照组治愈9例，好转21例，无效9例，总有效率76．9％．两组比较有显著的差异（P＜0．05）．结论采用中西医结合治疗反流性食管炎比单用中药治疗疗效好．

药物治疗反流性食管炎112例临床分析

目的探讨反流性食管炎的临床用药选择及疗效。方法把临床确诊的112例反流性食管炎患者随机分成两组，一组用亚沙必利和奥美拉唑，二组用多潘立酮和雷尼替丁治疗8w后观察疗效。结果两组患者总有效率分别为96．48％、77．66％。两者比较差异有统计学意义（P〉0.05），停药后观察4w，两者复发率相近，无统计学意义。结论质子泵抑制剂与胃肠动力药联合对反流性食管炎疗效显著，优于H2受体拮抗剂。

胃食管反流病中医治疗概况

胃食管反流病是临床上常见病、多发病,涉及到中医吐酸、嘈杂、噎膈、胸痛、胃脘痛等病范畴,中医认为其主要病机是胃失和降,浊气上逆。近年来,中医对其在基础理论、临床研究等方面取得了一定的成就,总结出了许多重要的经验,尤其在改善症状、抑制反流和促进受损食管粘膜修复等方面均显示了中医药的优势。

综合护理干预对反流性食管炎患者焦虑、抑郁、心理、睡眠、依从性、生活质量及相关血液指标的影响

目的探讨综合护理干预对反流性食管炎患者的疗效、心理、睡眠、依从性、生活质量及血液中胃动素、胃泌素、血管活性肠肽、炎性因子的影响。方法反流性食管炎患者179例,男93例,女86例。随机分为两组,对照组81例,观察组98例,两组一般资料比较,P>0.05。对照组给予多潘立酮和泮托拉唑钠肠溶片治疗,观察组在对照组基础上加用消炎利胆片。两组均连续行8周治疗。对照组采用常规护理,观察组采用综合护理干预。两组治疗前、治疗后60天采用焦虑自评量表、抑郁自评量表、心理量表、睡眠质量指数量表、健康状况调查问卷评分及抽晨起静脉血检测胃泌素、胃动素、血管活性肠肽、白介素-6、白介素-8、肿瘤坏死因子-α、依从性、典型反流性食管炎症状评分。所获数据采用方差分析、t检验和2检验。结果对照组干预前后焦虑、抑郁、睡眠质量、生活质量评分比较,P均<0.0005。观察组干预前后焦虑、抑郁、睡眠质量、生活质量评分比较,P均<0.0005。两组干预后焦虑、抑郁、睡眠质量、生活质量评分比较,P均<0.0005。对照组干预前后社会功能、躯体疼痛、生理功能、活力、精神状态、情感活动评分比较,P均<0.0005。观察组干预前后社会功能、躯体疼痛、生理功能、活力、精神状态、情感活动评分比较,P均<0.0005。两组干预后社会功能、躯体疼痛、生理功能、活力、精神状态、情感活动评分比较,P均<0.0005。对照组干预前后胃动素、胃泌素、血管活性肠肽水平变化比较,P均<0.0005。观察组干预前后胃动素、胃泌素、血管活性肠肽水平变化比较,P均<0.0005。两组干预后胃动素、胃泌素、血管活性肠肽水平变化比较,P均<0.0005。对照组干预前后血清白介素-6、白介素-8、肿瘤坏死因子-α水平变化比较,P均<0.0005。观察组干预前后血清白介素-6、白介素-8、肿瘤坏死因子-α水平变化比较,P均<0.0005。两组干预后血清白介素-6、白介素-8、肿瘤坏死因子-α水平变化比较,P均<0.0005。对照组干预前后恶心呕吐、胃脘胀痛、胸骨后疼痛、烧心、反酸嗳气评分比较,P均<0.0005。观察组干预前后恶心呕吐、胃脘胀痛、胸骨后疼痛、烧心、反酸嗳气评分比较,P均<0.0005。两组干预后恶心呕吐、胃脘胀痛、胸骨后疼痛、烧心、反酸嗳气评分比较,P均<0.0005。对照组干预前后完全依从、依从变化比较,P均<0.005;对照组干预前后不依从变化比较,P>0.05。观察组干预前后完全依从、依从、不依从变化比较,P均<0.005。两组干预后完全依从、不依从变化比较,P均<0.005;依从变化比较,P>0.05。结论综合护理干预对反流性食管炎从身心到分子水平均有较好的影响,治疗上加用消炎利胆片促进肠蠕动与胆汁排泄有利于疾病的恢复及根治。

放射性食管炎的临床研究进展

放射性食管炎是肿瘤放疗的剂量限制性毒性之一,常发生于行放疗的肺及纵隔等胸部恶性肿瘤患者。临床表现为放疗期间或放疗后一段时间吞咽困难、吞咽疼痛伴有烧灼感。食管内镜下改变(如红斑和溃疡)是非特异性的,没有诊断意义。受累区域的活检显示多种炎性改变以及射线相关的内皮细胞和基质细胞异形。急性食管炎可以非常严重,可能需要住院行鼻饲营养和持续的支持性治疗。食管晚期损伤可在放疗结束后继续发展,出现狭窄、溃疡甚至穿孔等并发症。本文从放射性食管炎的临床特征、内镜表现、组织病理学检查、并发症、鉴别诊断、治疗与预后方面分别进行阐述,以期为放射性食管炎的临床诊治提供参考。

胃底折叠囊状瓣成形术预防反流性食管炎

目的观察食管胃肠吻合附加胃底折叠囊状成形术预防反流性食管炎临床疗效．方法经左第6，7肋间进胸、常规切除食管肿瘤、保留胃底、关闭胃腔，把胃底向胃腔内折叠6cm～8cm，基底部用4号线间断缝合线距0．8cm，约6～8针．使胃内翻入胃腔的胃底形成一巨大的瓣膜，于左侧胃壁距基底部5cm平行切开胃壁，切口与食管外径相应，常规行食管胃两层吻合法，吻合口保证无张力，固定胃底折叠基底部子纵隔床，要求基底部高于吻合口2cm，瓣膜成型及食管胃吻合完毕.结果本组32例病例，平均术后15d出院，无死亡病例及并发症．术后3mo～6mo通过食管反流液pH值测定：术后领餐检查；术后内镜观察及病理检查，27例未见反流，pH5～7，3例少量反流，2例反流较多pH7～8，28例患者可观察到的吻合口随吞咽钡剂的开闭情况，未见反流及潴留，4例有少量反流，内镜检查24例，吻合口呈闭缩状，无胃液反流及食管粘膜炎性改变的有19例，3例轻度反流性食管炎，2例见食管粘膜及吻合口炎，术后随访1a～3a，5例死于肿瘤复发．2例有胃液反流症状，余病例生活质量明显提高.结论胃底折叠囊状瓣成形术，是贲门切除后胸腔内胃食管吻合抗反流的一种较理想的术式．

中药辨证治疗反流性食管炎疗效的Meta分析

[目的]：系统评价中药辨证治疗反流性食管炎的疗效。[方法]以中药、反流性食管炎、reflux esophagitis（RE）和traditional Chinese medicine（TCM）为关键词在PubMed、CBM、CNKI、维普、万方数据库检索中药辨证治疗反流性食管炎临床研究,采用Rev-man 5.2软件分析。[结果]共纳入6篇文献,统计分析显示中药辨证治疗反流性食管炎疗效对比西药组有效（OR：3.03;95%CI：1.91~4.80）。[结论]依据数据,中药辨证治疗反流性食管炎有较好的疗效。

反流性食管炎186例内镜诊断和治疗分析

目的探讨内镜检查结合临床表现对反流性食管炎(RE)的诊断以及临床治疗方法。方法回顾性分析贵州省息烽县人民医院2008-08-2010-06 186例经消化内镜诊断为反流性食管炎患者的临床资料。结果内镜下RE表现为A级78例,B级87例,C级16例,D级5例。所有患者经综合治疗后治愈33例,有效72例,显效61例,无效20例,总有效率达89.2%。结论内镜结合临床表现可提高RE的诊断准确性,抗酸剂、抑酸剂、胃动力药、黏膜保护剂联合用药是治疗反流性食管炎的有效方法。

消化道疾病

一、返流性食管炎返流性食管炎是由于食管下部括约肌(LES)压力降低,胃内容物返流入食管,损伤食道粘膜所致。目前主要使用抗酸剂、H_2受体阻断剂中和胃酸、抑制酸排泄和分泌,但最近市售的作用于局部胃粘膜壁细胞的H^+/K^+-ATP 酶阻断剂奥美拉唑(omeprazol)的划时代药效颇引人注目。随着生活方式的欧美化,本病正在增多,必须进行强有力的抑酸治疗,故该药可成为特效药。许多研究报道,奥美拉唑20mg/日,二周症状消失,四周治愈率达75%。

Have patients with esophagitis got an increased risk of adenocarcinoma? Results from a population-based study

AIM: To examine an increased risk of esophageal adenocarcinoma is restricted to patients who develop Barrett's esophagus or whether esophagitis per se is a risk factor for adenocarcinoma.METHODS: A population-based cohort of patients with histological evidence of esophagitis without Barrett's esophagus was constructed using electronic pathology reports relating to all esophageal biopsies in Northern Ireland between 1993 and 1996. Person-years of followup and incident cases of esophageal cancer were calculated by linking the cohort to death files and the Northern Ireland Cancer Registry records. Standardized incidence ratios (SIR) were calculated for esophageal cancers (adenocarcinoma, squamous cell carcinoma (SCC), and histologically unspecified cancers).RESULTS: A total of 2 013 patients in the cohort provided 13 559 patient-years of follow-up (mean follow-up 6.7 years). None of the patients developed adenocarcinoma. Three patients developed SCC, and six developed histologically unspecified cancers. The SIR for all esophageal cancers and for SCC were 2.73 (95%CI 1.25-5.19) and 2.93 (95%CI 0.61-8.59), respectively. In a sensitivity analysis in which all unspecified esophageal cancers were treated as adenocarcinomas, the SIR for adenocarcinoma was 2.64 (0.97-5.75).CONCLUSION: The risk of adenocarcinoma is not elevated in patients with histological evidence of esophagitis without Barrett's esophagus; however, these patients may have a moderately increased risk of SCC.Further studies are required to confirm these findings,which suggest that Barrett's esophagus, not esophagitis,is the key precursor lesion in the development of adenocarcinoma.

Esophageal cell proliferation in gastroesophageal reflux disease: Clinical-morphological data before and after pantoprazole

AIM: To evaluate esophageal mucosal defense mechanisms at an epithelial level to establish if pantoprazole treatment can induce ultrastructural healing and improvement in the proliferation activity of the esophageal epithelium in gastroesophageal reflux disease (GERD). METHODS: This was a single-blinded study for pHmonitoring, and histological, ultrastructural and MIB1 immunostaining evaluation. Fifty eight patients with GERD were enrolled and underwent 24 h pH-monitoring and endoscopy. Patients were treated for 12 and 24 mo with pantoprazole. Esophageal specimens were taken for histological and ultrastructural evaluation, before and after the treatment. RESULTS: With transmission electron microscopy, all patients with GERD showed ultrastructural signs of damage with dilation of intercellular spaces (DIS). After 3 mo of therapy the mean DIS values showed asignificant reduction and the mean MIB1-LI values of GERD showed an increase in cell proliferation. A further 3 mo of therapy significantly increased cell proliferation only in the erosive esophagitis (ERD) group. CONCLUSION: Three months of pantoprazole therapy induced ultrastructural healing of mucosal damage in 89% and 93% of ERD and non-erosion patients, respectively. Moreover, long-term pantoprazole treatment may be helpful in increasing the capability for esophageal cell proliferation in GERD, particularly in ERD patients.

Prevalence of Barrett's esophagus in patients with moderate to severe erosive esophagitis

AIM: To investigate the proportion of patients with moderate-severe erosive esophagitis (EE) who will have Barrett's esophagus (BE) after healing of inflammation. METHODS: Patients with EE of Los Angeles (LA) class B, C and D who underwent follow-up endoscopy documenting complete mucosal healing. RESULTS: A total of 86/169 patients were suspected of having BE (38 before healing and 48 after healing of EE) and, 46/86 eventually had the histological confirmation. At index esophago-gastro-duodenoscopy (EGD), BE was suspected in 38/169 (22%), and ultimately, histologically confirmed in 20 of these. In 11 patients where biopsies were performed in the presence of inflammation, BE was detected in 2 and missed in 5 (including 2 dysplasias). In 131/169 patients (77.5%), BE was not suspected at index EGD. After healing of EE though, 48 patients had suspicion of BE who underwent biopsies, and in 26 of these histology was positive for BE. The length of inflammation had a linear correlation with the length of BE (P = 0.01). Out of multiple variables to predict BE, only the suspicion at index endoscopy was statistically significant (P = 0.01). CONCLUSION: BE was seen in 46/169 (27%) patients with EE of LA class B, C and D. The length of EE can predict the length of underlying BE segment.Even when suspected, BE and associated dysplasia can be missed in the presence of inflammation; therefore, repeat evaluation should be considered after complete healing of esophagitis.

返流性食管炎患者睡眠障碍63例的护理干预

目的探讨对返流性食管炎患者睡眠障碍护理干预的重要性。方法对我院2010-01-2010-10收治的63例睡眠障碍返流性食管炎患者给予改善生活方式,心理护理并结合药物治疗。结果本组63例中有60例返流性食管炎患者睡眠障碍有不同程度的改善。结论对返流性食管炎患者睡眠障碍进行护理干预可提高治疗效果,减少复发。

大黄的应用与药理

目的总结与探讨大黄在整个消化系统炎症性疾病的应用与药理．方法以单味大黄或简方复方，运用散剂，胶囊，沸水冲浸，水煎等不同剂型，采用口服鼻饲、灌肠等相应方法治疗口腔溃疡，食管炎，胃十二指肠溃疡，上消化道出血，肝炎，胆囊炎，胆道蛔虫，胰脉炎，阑尾炎，菌痢，结肠炎．肛门疾患等200余例，部分较重病例辅以西药常规治疗，大黄用量最多达300／d～500g／d，在炎症控制、退热、疼痛缓解等方面与单纯西药进行统计单对照分析．结果94％的患者优于单纯西药组，尤其在急性肝炎、胆囊炎。胆道蛔虫、胰腺炎、上消化道出血等疾病的临床控制方面疗效尤佳，平均时间缩短1／3，部分早期就诊者甚至收到立杆见影之效，取得较好的疗效需把握好“辨证准确，配方合理，用法得当，剂量适宜”四要点，本人也通过实验室药敏及其他实验证实，大黄有高效的抗生活性，强大的利胆、写下作用及改善微循环，激发细胞免疫功能．结论大黄对整个消化道炎症性疾患肯定有较高的疗效，其剂形的科学化，规范化尚需改进．

Eosinophilic esophagitis: A newly established cause of dysphagia

Eosinophilic esophagitis has rapidly become a recognized entity causing dysphagia in young adults. This review summarizes the current knowledge of eosinophilic esophagitis including the epidemiology, clinical presentation, diagnostic criteria, pathophysiology, treatment, and prognosis. An extensive search of PubMed/Medline （1966-December 2005） for available English literature in humans for eosinophilic esophagitis was completed. Appropriate articles listed in the bibliographies were also attained. The estimated incidence is 43/10s in children and 2.5/10s in adults. Clinically, patients have a long history of intermittent solid food dysphagia or food impaction. Some have a history of atopy. Subtle endoscopic features may be easily overlooked, including a ＂feline＂ or corrugated esophagus with fine rings, a diffusely narrowed esophagus that may have proximal strictures, the presence of linear furrows, adherent white plaques, or a friable （crepe paper） mucosa, prone to tearing with minimal contact. Although no pathologic consensus has been established, a histologic diagnosis is critical. The accepted criteria are a dense eosinophilic infiltrate （〉20/high power field） within the superficial esophageal mucosa. In contrast, the esophagitis associated with acid reflux disease can also possess eosinophils but they are fewer in number. Once the diagnosis is established, treatment options may include specific food avoidance, topical corticosteroids, systemic corticosteroids, leukotriene inhibitors, or biologic treatment. The long-term prognosis of EE is uncertain; however available data suggests a benign, albeit inconvenient, course. With increasing recognition, this entity is taking its place as an established cause of solid food dysphagia.

Mediastinal tuberculous lymphadenitis presenting as an esophageal intramural tumor: A very rare but important cause for dysphagia

Dysphagia associated with esophageal mechanical obstruction is usually related to malignant esophageal diseases. Benign lesions are rarely a cause for this type of dysphagia, and usually occur either as an intramural tumor or as an extrinsic compression. Mediastinal tuberculous lymphadenitis is rare in adults, and even more rarely causes dysphagia. We report two cases of dysphagia in adult patients caused by mediastinal tuberculous lymphadenitis, presenting radiologicaUy and endoscopically as an esophageal submucosal tumor. Based on the clinical and imaging diagnosis, the patients underwent a right thoracotomy, and excision of the mass attached to and compressing the esophagus. Pathological examination of the specimens showed a chronic granulomatous inflammation with caseous necrosis, which was consistent with tuberculous lymphadenitis.