食管pH值监测观察酸相关疾病103例

目的 探讨24小时食管pH值监测在诊断上消化道疾病中（尤其胃食管反流病）的临床意义。方法 对2001年4月-2004年5月于我院进行食管pH值监测的103例临床患者，根据有无症状分为两组，无症状组20例为对照组，有症状组83例，其中反流性食管炎（RE）并慢性胃炎的患者30例，占36．1％，然后依次为十二指肠溃疡19例（22．9％）、非糜烂性食管炎13例（15．6％）、单纯反流性食管炎11例（13．3％）及胃溃疡10例（12．0％）。结果 RE并十二指肠溃疡组在各项指标中均高于其他各组（P〈0．05）。结论 RE多合并其他上消化道疾病（尤其酸相关疾病）发生．罹患十二指肠溃疡可能是RE发生和加重的原因之一。     

贲门失弛缓症合并急性尿潴留一例

贲门失弛缓症迄今病因未明。以食管下端括约肌（LES）肌间神经丛去神经病变所致的平滑肌松弛障碍、贲门狭窄、食管体部缺乏推进性蠕动为主要表现，是最早被认识和肯定的食管动力性疾病。本病占食管疾病的4％～7％。其常见并发症为食管糜烂、出血、食管癌及呼吸道感染。急性尿潴留为罕见并发症之一。     

门脉高压性胃病的研究现状及进展

肝硬化门脉高压患者首次消化道出血的原因主要为食管曲张静脉破裂（约占８０％），胃粘膜病变亦是其出血的重要原因。经内镜检查证实，门脉高压消化道出血患者中１０％～６０％存在胃粘膜病变（又称糜烂性胃炎、胃粘膜出血、充血性胃病等）。１９９２年，新意大利内镜学会...     

上消化道非静脉曲张出血的内镜下治疗

上消化道出血是指屈氏韧带以上的食管、胃、十二指肠以及胰胆管的出血。常见的出血原因包括：消化性溃疡、食管胃底静脉曲张破裂、急性胃粘膜病变、食管贲门粘膜撕裂综合征、胃癌等。世界上每年的发病率为１００／１０万。据对５１９１例上消化道出血调查分析,门脉高压引起食管胃底静脉曲张破裂出血占２５．４％,非静脉曲张破裂出血占７４．６％,其中溃疡病４８．７％,胃炎和胃肿瘤分别占４．５％和３．１％。上消化道出血的治疗包括内科保守治疗、内镜下治疗、放射介入治疗和外科手术治疗。内科药物治疗的有效率一般在７０％,并且主要…     

胃食管反流病的内镜治疗现状

胃食管反流病(gastroesophageal reflux disease．GERD)是指胃或十二指肠内容物反流入食管，引起并发症或明显地损害了病人的生活质量。主要表现为烧心、反酸或食物反流，可引起食管糜烂、溃疡、出血、狭窄等。GERD非常常见，西方国家约10％的人患有此病，老年人约1／4患有GERD。我国该病的发病率具体不详，京沪二地调查约6％的人患有GERD。GERD的     

肝硬变上消化道大出血病因的内镜诊断

肝硬变上消化道大出血患者６２例，出血后６小时～１周内行胃镜检查及硬化剂治疗。检查证实无食管胃底静脉曲张２例；胃及十二指肠球部明显糜烂１４例（２２．６％），胃和十二指肠球部溃疡６例（９．７％）。９例（１４．５％）为非静脉曲张性出血，７例（１１．３％）为双因素性出血，表明将肝硬变上消化道大出血一概推断为食管静脉曲张破裂出血是片面的。作者强调早期内镜检查和治疗的重要性。     

非糜烂性反流病的认识现状

胃食管反流病（gastroesophageal reflux disease，GERD）是临床常见病，严重影响患者的生活质量。亚太地区GERD的患病率较西方国家低，我们采用中国GERD研究协作组改良的中文版反流性疾病问卷在广东省社区人群中调查发现，社区人群中GERD的患病率为2．3％，而每周至少有一次烧心和（或）反酸症状者占6．2％。GERD包括糜烂性食管炎（erosive esophagitis，EE）、非糜烂性反流病（nonerosive reflux disease，NERD）和Barrett食管（BE），约70％的GERD表现为NERD。     

胃食管反流病发病中食管内脏感觉调控的研究进展

胃食管反流病（gastroesophageal reflux disease，GERD）是指胃／十二指肠内容物反流到食管引起烧心、反酸等症状和（或）并发症的一种疾病。胃食管反流病是一种常见疾病，通过内镜检查存在食管黏膜损害者称为反流性食管炎（reflux esophagitis，RE）；根据罗马Ⅲ标准，内镜下未见明显食管黏膜损伤者且符合以下任一项者为非糜烂性反流病（non-erosive reflux disease，NERD）：（1）24h胃食管pH监测阳性者；（2）24h胃食管pH监测阴性但症状指数（symptom index）阳性者；（3）24h胃食管pH监测及症状指数均阴性；但质子泵抑制剂（PPI）诊断性治疗（PPI试验）有效者。NERD在GERD中占有较大比例。烧心是GERD的典型症状，发病率较高。群体调查研究显示，在北欧，烧心的发病率为38％，美国更高达42％。症状每月发作1次以上者超过40％，每周发作1次以上者达20％，每日均有症状者约7％。一项在日本进行的结合内镜检查的研究中，2760人参与了调查，结果显示GERD的发病率17，9％，NERD的发病率达10．9％（占GERD的60．6％）。另一项在中（国）、     

102例老年人急性上消化道出血病因分析

目的探讨老年人上消化道出血的病因。方法回顾性总结102例老年人急性上消化道出血的病因,与同期住院非老年人上消化道出血患者150例就出血病因进行对比分析。结果老年组患者胃溃疡33例,占32.4%,十二指肠球部溃疡21例,占20.5%;急性胃黏膜病变32例,占31.4%;食管癌及胃癌11例,占10.8%;食管静脉曲张2例,占2.0%;原因不明3例,占2.9%。非老年组患者胃溃疡38例,占25.3%;十二指肠球部溃疡67例,占44.6%;急性胃黏膜病变25例,占16.7%;食管静脉曲张12例,占8.0%;食管癌及胃癌5例,占3.3%;食管贲门黏膜撕裂症2例,占1.3%;胃息肉1例,占0.7%。结论老年人上消化道出血主要病因为消化性溃疡、胃黏膜糜烂、肿瘤。     

非糜烂性反流病的研究现状与进展

在西方国家，胃食管反流病（gastroesophageal reflux disease，GERD）是一种常见病，严重影响患者的生存质量。亚太地区GERD的患病率较西方国家低，但随着生活方式的改变，GERD的患病率也有上升的趋势。我们采用中国GERD研究协作组改良的中文版反流性疾病问卷，在广东省社区人群中调查发现，社区人群中GERD的患病率为2．3％，而每周至少有1次烧心及（或）反酸症状者占6．2％。GERD主要包括糜烂性食管炎（erosive esophagitis，EE）、非糜烂性反流病（non—erosive reflux disease，NERD）及Barrett食管（BE），50％～70％的GERD表现为NERD。     

Risk factors for erosive reflux esophagitis: a case-control study

OBJECTIVES: It is presently not fully understood which risk factors contribute to the occurrence of reflux esophagitis and how such factors might influence the severity of the disease. The aim of this study was to delineate the clinical epidemiology of erosive reflux esophagitis. METHODS: Outpatients from a medicine and gastroenterology clinic who underwent upper GI endoscopy were recruited into a case-control study. A total of 1,533 patients with and 3,428 patients without endoscopically diagnosed reflux esophagitis were categorized as case and control subjects, respectively. Using multivariate logistic regressions for statistical analysis, the presence of esophageal erosions, ulcers or strictures, served as three separate outcome variables. Demographic characteristics, intake of nonsteroidal anti-inflammatory drugs (NSAIDs), consumption of alcohol and cigarettes, and the presence of hiatus hernia or peptic ulcer served as predictor variables. RESULTS: Erosive reflux esophagitis tended to occur more frequently in Caucasian male patients. Hiatus hernia was associated with a strong risk for developing esophageal erosions, ulcers, and strictures. Although statistical significance was demonstrated only for esophageal erosions, in all grades of reflux esophagitis alike, gastric and duodenal ulcer exerted a protective influence. Consumption of NSAIDs increased the risk for esophageal ulcers only. Smoking and alcohol were not associated with an increased risk of developing any type of erosive reflux esophagitis. CONCLUSIONS: The results stress the critical role played by hiatus hernia in all grades of erosive reflux esophagitis. NSAIDs may act through a mechanism of topically induced esophageal injury. Our data also suggest that the presence of either gastric or duodenal ulcer exerts a protective influence against the development of reflux disease.     

Linear gastric erosion. A lesion associated with large diaphragmatic hernia and chronic blood loss anemia

A prospective study was undertaken to identify mucosal lesions that might cause chronic blood loss anemia in patients with large diaphragmatic hernia. Patients with one-third or more of the stomach above the diaphragm on barium x-ray were examined by a gastroscopist who was given no clinical information. A total of 109 patients were included: 55 with anemia and 54 with a large hernia but no anemia. The incidence of esophagitis and peptic ulcer did not differ significantly in the anemic and nonanemic groups. Linear gastric erosions were found on the crests of mucosal folds at or near the level of the diaphragm in 23 anemic patients and 13 without anemia (p less than 0.05). Blood on the surface of a linear erosion was found in 14 anemic patients and 4 without anemia (p less than 0.05). We suggest that these erosions are due to trauma and can cause chronic blood loss anemia in hernia patients.     

Duodenal erosions after eradication of Helicobacter pylori infection

BACKGROUND: There is interest in the development of GERD after Helicobacter pylori eradication. In contrast, the development of duodenal erosions after therapy has received scant attention. Patients were examined after eradication of H pylori infection to determine the frequency of post-therapy duodenal erosions (primary outcome) and whether there was a relation between development of duodenal and esophageal erosions. Additionally, factors were searched for that would identify patients at increased risk for duodenal erosions. METHODS: A single-center, endoscopist-blinded, observational study was conducted of 196 patients in whom H pylori was eradicated. The presence of esophageal or duodenal erosions was evaluated 4 weeks and 6 months after eradication. Serum gastrin and pepsinogen I (PG I) and II (PG II) levels were also determined for 83 patients entering the study during its final year. RESULTS: Multiple small duodenal erosions developed in 8.6% of patients after H pylori eradication and were more common in patients with pre-eradication duodenal ulcer (27.8%) compared with those with gastric ulcer (6.7%) or atrophic gastritis (1.4%) (p < 0.05). Duodenal erosions were associated with high levels of PG I before and after eradication. The frequency of duodenal erosions decreased over time (3.1% by 6 months). CONCLUSION: Duodenal erosions occur after H pylori eradication and appear to be related to duodenal ulcer and increased PG I levels, both of which are associated with increased acid secretion. Measurement of PG I may help to identify patients who have duodenal erosions develop after H pylori therapy for studies of the pathogenesis of these lesions.     

Prevalence of esophagitis in H. pylori-positive peptic ulcer disease and the impact of eradication therapy

BACKGROUND/AIMS: There have been recent reports of reflux esophagitis apparently occurring de novo after cure of H. pylori in peptic ulcer disease. The possibility that this phenomenon might be explained, at least in part, by unmasking of coexistent disease has not been assessed. The aim of this study was to assess the prevalence of esophagitis in H. pylori-positive peptic ulcer disease and examine the short-term impact of H. pylori therapy on the esophagus. METHODOLOGY: Esophagitis was systematically graded and the presence of hiatal hernia was noted in 244 peptic ulcer patients (duodenal 223; gastric 21) before and at least four weeks after triple therapy. H. pylori status was assessed using CLO test and histology, and esophagitis grade was assigned without knowledge of H. pylori status. RESULTS: Of the 244 patients, 49 (20%) had esophagitis which was grade 2 or more in over two-thirds. The prevalence of esophagitis was similar in duodenal and gastric ulcer patients. The presence of hiatal hernia was strongly associated with the finding of esophagitis (P < 0.001). Of 241 patients evaluable after therapy, 215 (89%) were H. pylori-negative and 26 remained H. pylori-positive. Esophagitis tended to improve or remain stable after H. pylori therapy and worsened in only 2 of the 49 patients (4%). Of 192 patients with a normal esophagus at baseline endoscopy, 14 (7%) showed evidence of esophagitis after therapy. The presence of hiatal hernia, but not cure of H. pylori, was significantly associated with the development of esophagitis. CONCLUSIONS: Our results indicate that esophagitis can coexist with peptic ulcer disease and persists after cure of H. pylori. Development of de novo esophagitis seems uncommon in the short-term after H. pylori therapy. Esophagitis in peptic ulcer disease is strongly associated with the presence of hiatal hernia.     

What the gastroenterologist does all day. A survey of a state society's practice.

Members of a state society of gastroenterologist collected information about their pattern of practice. Twenty-two of the 41 members voluntarily kept a list of 25 sequential new patients seen during the spring of 1973. Five hundred and fory-nine diagnoses were accumulated; 369 (67%) of these diagnoses were gastroenterological. The five most common gastroenterological diagnoses were: functional disorder, duodenal ulcer, hiatus hernia, biliary tract disease, and esophagitis. The five most common over-all diagnostic areas were: functional disorder, cardiovascular disease, "other" nongastroenterological diagnoses (including obesity), duodenal ulcer, and endocrine malfunction. Geographically dispersed gastroenterologists in Virginia make more than one-half of their primary diagnoses in the area of their subspecialty interest. The primary gastroenterological problems seen are "upper gut" lesions and biliary tract disease. These observations may be of value in planning education, training, or research activities, especially if verified by a broader sample of gastroenterological practitioners.     

Barrett's esophagus: prevalence and size of hiatal hernia

OBJECTIVE: Barrett's esophagus is caused by gastroesophageal reflux and predisposes to adenocarcinoma. Hiatal hernia may cause reflux. The prevalence and size of hernias in patients with Barrett's esophagus was investigated. METHODS: Axial hernia length and the width of the diaphragmatic hiatus were measured prospectively at endoscopy. RESULTS: A 2-cm or longer hernia was found in 96% of 46 patients with Barrett's esophagus, in 42% of 103 controls (p < 0.001), and in 72% of 18 patients with short segment Barrett's esophagus (p < 0.05 vs controls). A hernia was found in 71% of 31 controls with esophagitis and in 29% of 72 controls without esophagitis (p < 0.001). Of 54 controls with neither esophagitis or reflux symptoms, 20% had a hernia. Mean hernia length was 3.95 cm in Barrett's esophagus, and 2.81 cm in controls (p < 0.005). Mean hiatus width was 3.52 cm in patients with Barrett's esophagus and hernia, and 2.24 cm in controls with hernia. Hernia length was similar in patients with and without esophagitis, and in short segment Barrett's esophagus. CONCLUSIONS: Most patients with Barrett's esophagus have hiatal hernia; their hernias are longer and the hiatal openings wider than in controls with or without esophagitis. Hiatal hernia likely contributes to the development of Barrett's esophagus.     

Adrenocorticosteroid therapy and gastroduodenal lesions

Gastroduodenoscopy was performed in 25 patients with various disorders, such as liver cirrhosis, nephrotic syndrome, and ulcerative colitis, to assess the effects of corticosteroids on the stomach and duodenum. The main criterion for entry into the trial was the absence of open ulcer, healed ulcer, erosion, or bleeding from the stomach or duodenum on pretreatment endoscopy performed within 48 hours before administration of corticosteroids. Endoscopy repeated at 2 to 4 weeks disclosed gastroduodenal lesions in 11 cases (44%)and no lesion in 14 cases (56%). The gastroduodenal lesions observed in 11 cases are as follows: one gastric ulcer (4.0%), six gastric erosions (24.0%), two gastroduodenal erosions (8.0%), and two duodenal erosions (8.0%). A lack of correlation between the patients' subjective complaints and endoscopic findings indicates the unreliability of patients' complaints and the importance of endoscopy in assessing gastroduodenal lesions. There were no differences in the total and average daily doses of corticosteroid between a group with gastric and/ or duodenal lesions and a group without such lesions. Corticosteroids may produce gastroduodenal lesions, regardless of the dose.     

Gastric Acid Secretion and Pattern of Gastroesophageal Reflux in Patients with Esophagitis and Concomitant Duodenal Ulcer: A Multivariate Analysis of Pathogenetic Factors

This study was designed to assess the relationship between gastric acid output (GAO) and both pattern of gastroesophageal reflux (GER) and severity of esophageal lesions. Gastric acid secretory testing and 24-h intraesophageal pH-monitoring were performed in 31 patients with esophagitis and concomitant duodenal ulcer (E + DU) and compared with those of 72 patients with esophagitis (E). The second aim of this study was to evaluate the role of GAO and other potential pathogenetic factors in the development of esophagitis. The results of the study showed that GAO in patients with E + DU was significantly higher than in patients with E (p < 0.05). There was no significant difference between the two groups of patients with regard to endoscopic findings or GER variables (p > 0.05). Multiple regression analysis with stepwise deletion showed that the presence of hiatal hernia, GER in the upright position and age appear to correlate significantly with the presence of esophagitis. We conclude that no parallel relationship exists between GAO and severity of GER or esophageal lesions in patients with E + DU and that GAO is not a major pathogenetic factor in GER disease.     

Upper GI mucosal effects of parecoxib sodium in healthy elderly subjects

OBJECTIVE: The aim of this study was to compare the upper GI mucosal effects of i.v. parecoxib sodium with i.v. ketorolac tromethamine and placebo in healthy elderly subjects. METHODS: This was a two-center, double-blind, randomized, placebo-controlled study. Healthy subjects aged 65-75 yr who were shown at baseline endoscopy to have no gastric or duodenal lesions received either parecoxib sodium 40 mg b.i.d. for 7 days, ketorolac 15 mg q.i.d. for 5 days, or placebo for 7 days. Endoscopy was repeated at the end of dosing. Measures of upper GI effects were: 1) ulceration, 2) incidence of an ulcer and/or any erosions, and 3) incidence of an ulcer and/or > or = 11 erosions in the stomach, duodenum, or both. RESULTS: No gastric or duodenal ulcers occurred in any subjects receiving parecoxib sodium (n = 29) or placebo (n = 32). In contrast, seven (23%) of the 31 ketorolac subjects had at least one ulcer; five (16%) had gastric ulcers, and two (6%) had duodenal ulcers (p < 0.05 vs parecoxib sodium and placebo for gastroduodenal ulcers and for gastric ulcers). A total of 28 (90%) ketorolac subjects had an ulcer or at least one erosion in the stomach, compared with incidences of four (14%) and two (6%) for parecoxib sodium and placebo, respectively. Incidences of duodenal ulcers/erosions were 45% (n = 14) for ketorolac, 10% (n = 3) for parecoxib sodium, and none for placebo. The differences between ketorolac and both other treatment groups were statistically significant for both stomach and duodenum. No parecoxib sodium or placebo subjects had an ulcer or > or = 11 erosions in the stomach, compared with eight (26%) ketorolac subjects (p < 0.05 vs both parecoxib sodium and placebo). No subject in any group had > or = 11 duodenal erosions. CONCLUSIONS: These results indicate that multiple dose administration of parecoxib sodium is safe and well tolerated in healthy elderly subjects, with a decreased risk of gastroduodenal mucosal injury compared with ketorolac.     

Proton Pump Inhibitors: Effective First-Line Treatment for Management of Dyspepsia

The aim of this study was to evaluate the reasons for trial exclusion among dyspeptic patients and estimate the proportion that may have benefited from proton pump inhibitor (PPI) therapy. Stringent inclusion criteria for enrollment in two multicenter functional dyspepsia trials included dyspepsia (predominant persistent/recurrent upper abdominal discomfort [UAD] during the prior 3 months) of at least moderate intensity during ≥30% of days during the prior 2 to 3 weeks. Exclusion criteria were mild/infrequent UAD; heartburn and UAD of equal frequency; predominant heartburn with UAD; endoscopic evidence of erosive esophagitis or Barrett’s or gastric and/or duodenal erosions (>5) or ulcers; irritable bowel syndrome (IBS); other gastrointestinal diagnoses; or other “non-categorized” disorders. Of 2,588 screened patients, 1,667 were excluded. Excluded patients by category had mild/infrequent UAD (12.5%, n=324), heartburn and UAD of equal frequency (1.1%, n=29), predominant heartburn with UAD (11.6%, n=300), endoscopic evidence of erosive esophagitis or Barrett's (6.2%, n=160), gastric and/or duodenal erosions (1.4%, n=36), gastric and/or duodenal ulcers (2.0%, n=53), IBS (7%, n=180), “other” gastrointestinal diagnoses (2.8%, n=73), or other “non-categorized” disorders (19.8%, n=512). Fifty-four percent of patients (902/1,667) had symptoms/diagnoses that would be expected to improve with PPI therapy. Individuals with IBS, “other,” or “non-categorized” disorders were considered to have symptoms unlikely to respond to PPI treatment. Empiric PPI treatment would be expected to provide symptom relief to the majority of dyspepsia sufferer who present in clinical practice. PPIs represent the best currently available therapy for acid-related disorders and should be considered the first-line management approach in patients with uninvestigated dyspepsia.