消化性溃疡难治病例分析

近年来消化性溃疡的治疗已有很大进展,但临床上仍有部分病人治疗效果差,病程迁延、顽固。我们从1986年9月～1994年12月治疗的消化性溃疡患者中,筛选出难治性病例25例给予分析: 1 病例选择及临床资料 1.1 病例选择:胃镜检查诊断为活动期溃疡,经用西咪替丁、雷尼替丁、得乐冲剂或胃舒平等足量正规治疗三个月后。症状仍持续不缓解或反复发作,复查胃镜仍为活动性溃疡者,即定为难治性溃疡。     

消化性溃疡复发的治疗与预防

消化性溃疡(PU)是胃、十二指肠溃疡和复合溃疡.目前,无论西医还是中医使PU在短期内愈合已不是难事,但如何避免溃疡复发仍是临床上亟待解决的问题[1].笔者近5年来采用中西医结合的疗法,对治疗并预防消化性溃疡的复发取得满意疗效,现介绍如下:     

某院2016年-2018年消化性溃疡和胃食管反流病患者药物使用情况分析

目的:分析2016年—2018年医院消化性溃疡和胃食管反流病患者药物的实际使用情况用其趋势,为促进医院治疗消化性溃疡和胃食管反流病药物的合理使用提供参考。方法:采用回顾性调查方法,抽取2016年—2018年间消化性溃疡和胃食管反流病患者病历资料,统计和分析其药物的使用的相关因素。结果:2016年—2018年间医院抗消化性溃疡和胃食管反流病药物使用频数居首位的药物主要是质子泵抑制剂,因其抑制胃酸分泌效果佳且不良反应少等优势,受到医院临床医生的青睐;其次是使用频数较高的为胃肠动力药。结论:医院抗消化性溃疡和胃食管反流病药物的使用较为合理,但仍有待进一步的规范,需完善及加强对消化性溃疡和胃食管反流病治疗药物管理。     

儿童消化性溃疡110例临床分析

目的:探讨儿童消化性溃疡的临床特点和内镜诊断.方法:对我院住院及门诊110例1～14岁儿童消化性溃疡的内镜检查和临床资料进行回顾性分析,其中检测幽门螺杆菌72例.结果:小儿消化性溃疡男性明显多于女性,男女之比约为2∶1;十二指肠溃疡占71%,胃溃疡占24.6%,复合性溃疡占5%;幽门螺杆菌感染总阳性率80.5%;溃疡病有遗传倾向的占21.8%(24/110例),误、漏诊34例.结论:消化性溃疡是小儿上消化道出血的主要原因,幽门螺杆菌感染与小儿消化性溃疡密切相关,遗传因素在小儿消化性溃疡的发生中有一定作用.小儿内镜检查安全可靠,检出率高,误诊少;小儿消化性溃疡治疗以内科保守治疗为主.     

102例住院患者抗消化性溃疡药物使用分析

目的促进抗消化性溃疡药物的合理使用。方法采用回顾性调查方法,抽取中国人民解放军总医院2008年1月至8月102例消化性溃疡住院患者的病历资料,对用药情况、治疗天数、药物不良反应及预后等相关问题进行统计分析。结果使用频数居首位的抗消化性溃疡药物是质子泵抑制剂;用药监测仅发现5例存在不合理用药情况。结论该院抗消化性溃疡药物的使用基本合理,但仍有待进一步的规范。     

107例住院患者抗消化性溃疡药物利用分析

目的:了解南京军区福州总医院住院患者抗消化性溃疡药物利用情况。方法:回顾性调查本院消化内科2005年8月-2006年4月诊断为消化性溃疡的107例出院患者的病历,对用药频数、用药金额和药物不良反应等相关内容进行统计分析。结果:质子泵抑制剂的用药频数和用药金额在住院患者抗消化性溃疡药物应用中居首位。抗消化性溃疡药物费用占总药费的25．88％,占住院总费用的17．26％。8例患者的医嘱存在不合理用药情况,2例患者发生药物不良反应。结论:本院抗消化性溃疡药物应用基本合理,但该类药物的合理使用仍需进一步规范。     

奥美拉唑和雷尼替丁治疗消化性溃疡的系统评价

目的:评价奥美拉唑和雷尼替丁在治疗消化性溃疡方面的疗效和不良反应。方法:电子检索中文科技期刊数据库、万方数据库。采用Revan5.0软件进行Meta分析,对可合并分析资料无异质性者使用固定效应模型,有异质性者分析异质性产生原因,并使用敏感性分析或亚组分析处理,若仍无法消除异质性,采用随机效应模型合并分析。结果:奥美拉唑与雷尼替丁治疗消化性溃疡的总有效率,差异有统计学意义[P<0.05,OR=3.96,95%C(I2.57,6.11)];奥美拉唑的不良反应远低于雷尼替丁。结论:Meta结果显示,奥美拉唑治疗消化性溃疡明显优于雷尼替丁。     

奥美拉唑三联与四联疗法治疗小儿消化性溃疡的疗效及安全性观察

目的 探讨分别选择奥美拉唑三联疗法以及四联疗法对消化性溃疡患者加以治疗后,获得的临床疗效以及治疗安全性.方法 选择我院2014年05月~2016年02月收治的消化性溃疡患儿82例作为研究对象;通过消化性溃疡患儿家属抽签展开分组研究;观察组:奥美拉唑四联疗法;对照组:奥美拉唑三联疗法;临床展开疗效评价以及不良反应评价.HT5"H结果 在疗效评价方面,观察组以及对照组消化性溃疡患儿之间凸显差异(P<0.05);在不良反应评价方面,观察组以及对照组消化性溃疡患儿之间凸显差异(P<0.05).结论 对于消化性溃疡患儿的疾病表现等加以了解,合理选择奥美拉唑四联方法进行治疗,同三联疗法进行比较,获得显著的疗效以及不良反应评价效果,值得消化性溃疡疾病治疗过程中广泛普及.     

消化性溃疡病住院患者健康教育满意度的调查分析

目的了解住院消化性溃疡患者对消化性溃疡病教育工作的满意度。方法采用问卷调查法,评估100例消化性溃疡患者对消化性溃疡病教育工作满意度状况。结果对消化性溃疡教育护士的总体工作满意度在80%以上;近20%的消化性溃疡患者提出心理健康的指导不足;消化性溃疡教育护士的业务素质有待进一步提高;个体化健康教育要更具针对性;消化性溃疡教育护士教育的技巧有待提高。结论患者对消化性溃疡工作满意度较高,但要进一步重视和加强消化性溃疡教育护士的培训,不断提高消化性溃疡教育质量。     

小剂量洛赛克预防消化性溃疡的复发

临床上洛赛克已广泛应用于消化性溃疡的治疗,并大大地促进了溃疡的愈合,但是消化性溃疡的复发在临床上却一直未得到良好的控制.我们通过对已经使用洛赛克治愈的消化性溃疡患者服用小剂量洛赛克来观察消化性溃疡的复发情况.     

135例非老年急性上消化道出血患者的病因分析

目的分析探讨非老年患者上消化道出血的原因及相关因素。方法对我院2009年²012年间收治的135例非老年上消化道出血患者的临床资料进行回顾性分析,并与同期住院86例老年患者的出血原因进行比较。结果在135例非老年上消化道出血病例中,饮酒、精神因素、不当饮食为主要相关诱发因素,老年组中以服用非甾体药物为主要诱因。而非老年组中最常见的出血病因为十二指肠溃疡占34.81%(47/135),第二位是食管胃底静脉曲张破裂占18.52%(25/135),其他常见的病因还有急性胃黏膜病变15.56%(21/135),胃溃疡11.58%(16/135),消化道肿瘤7.41%(10/135)等。其中十二指肠溃疡、食管胃底静脉曲张发病率明显高于老年组,而胃溃疡、消化道肿瘤发病率低于老年组患者(P<0.05)。结论与老年组有所不同,非老年上消化道出血诱因多与饮酒、精神因素、不当饮食有关,十二指肠溃疡、食管胃底黏膜曲张破裂是致出血的主要病因,且发病率男性多于女性。     

Elisa and western blot studies with basic fibroblast growth factor (bFGF) and platelet-derived growth factor (PDGF) in experimental duodenal ulceration and healing

Abstract

Time-dependent changes of duodenal and gastric mucosal levels of bFGF and PDGF were examined in rats after oral administration of the duodenal ulcerogen cysteamine-HCl. The animals were killed at 12 h, 24h, 48h, 7 days or 14 days after the first dose of cysteamine and the duodenal ulcers were evaluated. The gastric and duodenal mucosa was scraped and homogenized for Western blot and ELISA studies. The ulcer formation was macroscopically detectable at 12h while the largest ulcers were seen at 48h. In parallel the duodenal mucosal concentration of bFGF increased at 12 and 24h and reached its maximum at 48h, while the PDGF concentration was slightly elevated at 12 and 48h, and a more than 3-fold peak was seen at 24h. The gastric mucosal level of bFGF and PDGF did not change during the development and healing of duodenal ulcers.

Conclusions

1. The early (24–48 h) elevation of duodenal mucosal bFGF and PDGF might be a tissue-specific response to duodenal ulceration.
2. These high endogenous levels of growth factors are not sufficient to prevent the ulcer formation and are not maintained in the spontaneous healing phase (7–14 days)
3. Thus, bFGF and PDGF may have a role in the natural history of duodenal ulcer disease.

     

胃肠功能和消化性溃疡

<正> 消化性溃疡主要指胃和十二指肠的慢性溃疡性病变,在人类的远古历史上就有记载。随着近年来消化道生理学的进展,以及临床上内窥镜技术以及各种新型制酸剂的使用,对于消化性溃疡的认识已逐步深入。50年代中期,Hollander就以胃自身何以不被胃液所消化为命题,概括了直接决定消化性溃疡能否产生的两个方面:一是胃液中盐酸和胃蛋白酶有腐蚀消化道粘膜产生溃疡的作用,二是正     

Agents with tricyclic structures for treating peptic ulcer disease

The pathogenesis, clinical signs, and conventional treatment of peptic ulcer disease (PUD) are briefly discussed, and the use of drugs with tricyclic structures in the treatment of PUD is reviewed. Peptic ulcers occur most commonly in the duodenal bulb and the stomach. Numerous factors contribute to the formation of peptic ulcers, but an imbalance between acid and pepsin secretion and mucosal resistance is considered important. Conventional drug therapy of PUD with antacids, H2-receptor antagonists, anticholinergic drugs, and sucralfate is designed to correct this imbalance by neutralizing acid, inhibiting acid secretion, preventing contact of the ulcer with acid and pepsin, and enhancing mucosal defense mechanisms. Tricyclic agents that appear to be useful in the treatment of PUD are the tricyclic antidepressants, trimipramine maleate and doxepin hydrochloride, and the selective antimuscarinic drug, pirenzepine hydrochloride. The therapeutic effects of tricyclic antidepressants may result from their anticholinergic, antidepressant, and H2-receptor blocking actions. Controlled clinical trials suggest that trimipramine 50 mg/day (as the maleate salt) and pirenzepine hydrochloride 100-150 mg/day are superior to placebo and may be as effective as cimetidine for the short-term treatment of duodenal ulcers. Limited data suggest that these drugs are also effective for treating gastric ulcers. Assessment of the apparent efficacy of doxepin in duodenal ulcer treatment requires further study. Anticholinergic side effects and sedation associated with the administration of tricyclic agents may limit their usefulness as first-line anti-ulcer agents. With further evidence of their efficacy, trimipramine, doxepin, and pirenzepine may play an important role in the treatment of patients unresponsive to conventional anti-ulcer therapy.     

Gastrointestinal mucosal gamma-glutamyl transpeptidase activity changes in different ulcer models of rat

The experiments presented gave evidence that changes in gamma-glutamyl transpeptidase activity-under experimental circumstances-seem to be in close connection with gastro-intestinal ulceration. In the pre-ulcerative period in both gastric and duodenal ulcer models, the mucosal gamma-glutamyl transpeptidase activity is higher than normal, while in the definitive ulcerative stage the gastric gamma-glutamyl transpeptidase activity is significantly decreased but in the duodenum it remained on normal level. This phenomenon may reflect to a difference in the pathomechanism of the gastric and duodenal ulceration.     

The Role of Helicobacter pylori in Peptic Ulcer Disease

The pathophysiology of peptic ulcer disease (PUD) is often described as an imbalance between aggressive factors such as acid and pepsin and alterations in the mucosal protective mechanisms. Helicobacter pylori is a gram-negative organism that has been identified as a potential causative agent in the pathogenesis of PUD. The exact mechanism by which it contributes to mucosal damage is unknown. It is thought that the organism may disrupt the protective mucous layer, allowing the underlying epithelium to be injured by gastric acid. Significant evidence indicates that H. pylori is a major etiologic factor in type B gastritis. Data confirming its etiologic role in duodenal ulcer (DU) disease is not conclusive; however, eradication of the organism is associated with a reduction in the recurrence of DU. Optimum therapy to eradicate H. pylori has not been established, although several multidrug regimens have been evaluated. Treatment of H. pylori infection should be reserved for individuals in whom conventional therapy for DU is unsuccessful and those whose ulcers relapse during maintenance therapy.     

Review article: gastroduodenal bicarbonate secretion

The gastroduodenal epithelium is covered by an adherent mucus layer into which bicarbonate is secreted by surface epithelial cells. This mucus-bicarbonate barrier is an important first line of defence against damage by gastric acid and pepsin, and has been demonstrated in all species including human. Similar to gastric acid secretion, regulation of gastric and duodenal bicarbonate secretion can be divided into three phases: cephalic, gastric and duodenal. In humans, sham-feeding increases bicarbonate secretion in both the stomach and duodenum which is mediated by cholinergic vagal fibres in the stomach, but seems to be noncholinergic in the duodenum. Gastric distention and luminal acidification increases gastric bicarbonate production. Whereas there are no data relating to the gastric phase of human duodenal bicarbonate secretion, in animals, food and acid in the stomach independently stimulate duodenal bicarbonate output. To date, the duodenal phase of human gastric bicarbonate secretion has not been studied, but data from animals reveal that duodenal acidification augments bicarbonate secretion in the stomach. In all species tested, direct acidification of the duodenum is a potent stimulant of local bicarbonate production. In humans, the pH threshold for bicarbonate secretion is pH 3.0. Mediation of gastroduodenal bicarbonate secretion is provided by a variety of agonists and antagonists, tested mainly in animals, but some have been evaluated in humans. Prostaglandins of the E class and VIP are major factors that control bicarbonate secretion. Bicarbonate secretion, and the mucus-bicarbonate layer in general, is adversely effected by ulcerogenic factors such as aspirin, NSAIDs, bile salts, and cigarette smoking. Furthermore, duodenal ulcer patients have an impairment in bicarbonate production within the duodenal bulb, at rest and in response to stimulation. These findings indicate that the mucus-bicarbonate barrier is an important first line of defence in the pathogenesis of peptic ulcer disease.     

Anti-ulcer actions of phytosphingosine hydrochloride in different experimental rat ulcer models

The gastroprotective activity of phytosphingosine hydrochloride (PS-HCl, CAS 554-62-1) was assessed in four different rat models of experimentally induced gastric ulcer. Various doses (2.5-10 mg/kg) of PS-HCI were orally administered to rats 30 min before the treatment with HCl/ethanol, indometacin, cysteamine, or to rats with ligated pylorus. Oral administration of PS-HCl (2.5-10 mg/kg) to rats prevented the acute ulcer formation in 4 different types of ulcer in a dose-dependent manner as follows: (1) HCl/ethanol-induced gastric mucosal membrane lesions (20.1-47.8% inhibition), (2) indometacin-induced gastric mucosal membrane lesions (4.6-31.9% inhibition), (3) duodenal ulcer induced by cysteamine (10-20% inhibition), (4) gastric secretion and ulceration following pylorus ligation (33.3-61.9% inhibition). These results indicate that PS-HCI may be useful for the prevention of gastric ulcer.     

非甾体抗炎药致上消化道出血的临床特征分析

目的分析非甾体抗炎药致上消化道出血的临床特征。方法选取天津市第一中心医院2012年10月—2015年6月消化道出血的住院患者110例,对其临床资料进行分析统计。按照出血前10 d内是否服用过非甾体抗炎药为标准对患者进行分组,比较两组的临床特征。结果两组患者在急性胃黏膜病变、胃底和胃窦胃溃疡、心血管病史以及前壁和后壁十二指肠溃疡方面存在显著差异,两组比较具有统计学意义(P0.05)。其中用药组的急性胃黏膜病变、胃底和胃窦胃溃疡、心血管病史所占比例大于非用药组,而用药组的前壁和后壁十二指肠溃疡所占比例小于非用药组。结论在临床治疗过程中,需要采取适当的措施有效地降低非甾体抗炎药所致的上消化道出血等不良反应。     

Effects of FRG-8813, a new-type histamine H2-receptor antagonist, on the healing of gastric and duodenal ulcer in rats and spontaneously ulcerative mice]

We examined the anti-ulcer effects of FRG-8813, a new-type histamine H2-receptor antagonist, in chronic ulcer models of rats and mice (W/WV). FRG-8813, given orally twice a day for 7 days, accelerated the healing of gastric or duodenal ulcer induced by acetic acid injection or application at the non-antisecretory doses (0.3 approximately 3 mg/kg). Administration of FRG-8813 to rats with ulcers increased the amounts of mucus in the gastric mucosa. These actions of FRG-8813 were more potent than those of famotidine or cimetidine. In W/WV mice, several ulcers spontaneously developed on gastric mucosa during the 8 weeks after the birth. The ulcers were aggravated by several unknown factors after the ulcer generation in W/WV mice. The aggravation of ulcers was inhibited by the 4-week administration of FRG-8813 with diet at the dose of 1 or 10 mg/kg/day, but was not inhibited by cimetidine at the dose of 100 mg/kg/day. From these results, we suggest that FRG-8813 is able to accelerate the healing of ulcers by antisecretory plus increasing actions on the integrity of the gastric mucosal defense mechanisms; therefore FRG-8813 is expected to be a useful drug for the treatment of gastric or duodenal ulcers in humans.