慢性胃炎患者胃内pH值相关因素分析

背景：传统观点认为胃酸分泌随年龄增加和胃黏膜萎缩而减少,但也有研究持不同观点。目的：研究慢性胃炎患者胃内pH值与性别、年龄、糖尿病、萎缩和幽门螺杆菌（H.pylori）感染之间的相关性。方法：共纳入67例慢性胃炎患者,采用pH试纸测定胃液pH值,病理切片结合快速尿素酶试验或^13C-尿素呼气试验检测H.pylori感染情况。分析不同因素与慢性胃炎患者胃内pH值的相关性。结果：67例患者中,慢性非萎缩性胃炎患者35例（52．2％）,慢性萎缩性胃炎32例（47．8％）;H.pylori阳性21例（31．3％）,H.pylori阴性46例（68．7％）。平均胃内pH值为2．86,胃内pH值随年龄增长呈升高的趋势（P=0．15）。Logistic回归分析显示胃内pH值与性别（P=0．17）、年龄（P=0．06）、糖尿病（P=0．75）、萎缩（P=0．67）和H.pylori感染（P=0．11）均无相关性。结论：性别、年龄、糖尿病、萎缩和H.pylori感染不是影响慢性胃炎患者胃内pH值的重要因素。     

Decreased Gelatin-Binding Fibronectin in Patients with Chronic Inflammatory Bowel Diseases

The plasma fibronectin concentration (PF) was measured in 48 patients with chronic inflammatory bowel disease (CIBD) and in 48 age- and sex-matched healthy controls, using electroimmunoassay and a functional (gelatin-binding) assay. Whereas no difference in immunochemically measured PF was found between the two groups, patients with CIBD had significantly lower gelatin-binding PF than healthy controls (p < 0.001). Immunochemically measured PF increased, whereas functionally measured PF tended to decrease with increasing disease activity.     

慢性萎缩性胃炎患者幽门螺杆菌根除后胃黏膜G细胞数量和血清胃泌素含量的变化

背景:幽门螺杆菌(H.pylori)感染是慢性萎缩性胃炎(CAG)最重要的致病因素,根除H.pylori能否阻止或逆转胃黏膜萎缩目前尚不清楚.目的:通过观察CAG患者H.pylori根除前后胃黏膜G细胞数量和血清胃泌素含量的变化,探讨H.pylori感染对胃黏膜G细胞数量及其分泌功能的影响.方法:60例H.pylori阳性的CAG患者进行了根除治疗,在治疗前和治疗结束3个月后分别行胃镜检查.采用免疫组织化学法和放射免疫分析法测定H.pylori根除前后胃窦黏膜G细胞数量和血清胃泌素含量.结果:31例H.pylori感染的CAG患者在根除治疗3个月后进行了复查,根除率为77.4%.G细胞数量和血清胃泌素含量随胃黏膜萎缩程度的加重而逐渐显著减少(P<0.01).轻度萎缩组H.pylori根除后G细胞数量与治疗前相比无显著差异(P<0.05),而升高的血清胃泌素含量显著降低(P<0.01);中、重度萎缩组H.pylori根除后减少的G细胞数量显著增加(P<0.05),血清胃泌素含量呈上升趋势(P<0.05).结论:CAG患者根除H.pylori后胃黏膜G细胞数量及其合成、分泌胃泌素的功能可出现恢复性变化,可能有助于阻断CAG的进一步发展.     

上海与阿姆斯特丹幽门螺杆菌感染性胃炎萎缩与肠化的对比研究

观察中国上海与荷兰阿姆斯特丹两地幽门螺杆菌（Ｈ．ｐｙｌｏｒｉ）感染性胃炎患者胃窦部粘膜萎缩与肠化的发生率及发生年龄的差异。方法：功能性消化不良伴Ｈ．ｐｙｌｏｒｉ感染的上海患者２６５例和阿姆斯特丹患者２６１例纳入研究。根据新悉尼分类法对患者治疗前胃窦粘膜标本的萎缩和肠化程度进行分级。结果：阿姆斯特丹患者的萎缩与肠化发生率（４２％和２６％）低于上海患者（５２％和３２％）,但仅萎缩的差异有统计学意义（Ｐ     

解读和评述:中国慢性胃炎共识意见

中华医学会消化病学分会于2006年9月14～16日在上海召开了第二届全国慢性胃炎共识会议。自2000年全国慢性胃炎研讨会在江西召开以来，慢性胃炎的研究在以下各方面均取得了一定进展，包括萎缩性胃炎的内镜和组织病理学诊断，幽门螺杆菌（H．pylori）感染与萎缩性胃炎及其演变成胃癌的关系，根除H．pylori对胃癌的预防作用，环境因素、尤其是生物活性食物成分对萎缩性胃炎和胃癌发生、发展的预防作用等。本文对第二届全国慢性胃炎共识意见作一解读和评述。     

Smoking Habits in Patients with Inflammatory Bowel Disease

The proportion of smokers in this study was significantly lower among patients with ulcerative colitis (13%) than among patients with Crohn's disease (47%), the difference being significant for both sexes and for the age groups both below and above 40 years. The proportion of male ex-smokers among patients with ulcerative colitis (28%) was higher than among patients with Crohn's disease (8%), whereas the proportions of non-smokers differed less. Many of the patients with ulcerative colitis who had a late onset were male ex-smokers. The smoking patients with ulcerative colitis were mainly women. They smoked less than the smoking patients with Crohn's disease and less than the ex-smokers in each group. No smoking patient with ulcerative colitis smoked > 20 cigarettes/day. In the group of male ex-smokers with ulcerative colitis, there was an accumulation of onsets during the 4 years after the definitive smoking stop. The number of colectomies performed on patients with ulcerative colitis did not vary with smoking habits. In the group of ex-smokers the colectomy was performed after the smoking stop in 19 out of 20 patients.     

慢性胃炎伴良性结节状改变与幽门螺杆菌及淋巴滤泡的关系

目的研究慢性胃炎伴良性结节状改变与幽门螺杆菌（Hp）及胃黏膜淋巴滤泡的关系。方法从2004年7月1日-2005年6月30日行内镜检查患者中，筛选出胃窦黏膜有良性结节样改变者为研究对象，在患者胃窦黏膜处喷洒靛胭脂作色素内镜观察，确定有结节状形态改变，并在有明显结节处取活检组织3块，其中1块立刻作Hp快速试验，判定有无Hp感染；另外2块送病理检查，观察胃黏膜淋巴滤泡形成和淋巴细胞浸润情况，并采用亚甲蓝-硼酸染色法进一步明确诊断Hp感染情况。结果将胃黏膜良性结节状改变的慢性胃炎患者分为三组：结节性胃炎组、萎缩性胃炎组和疣状胃炎组，患者平均年龄分别为（31．OO±11．62）岁、（58．61±12．14）岁和（51．29±12．99）岁，其中结节性胃炎组患者发病年龄最小（P〈0．01）；Hp感染率分别为92．86％、82．56％和69．89％，其中结节性胃炎组的感染率明显高于其他两组（P〈0．01）；有淋巴组织增生所见依次为94．90％、27．9％、18．28％，其中结节性胃炎患者淋巴组织增生明显高于其他胃炎患者（P〈0．01）。伴有结节样改变的萎缩性胃炎患者中萎缩和肠化生百分率分别为100％和59．3％，远高于疣状胃炎组的7．53％、8．60％和结节状胃炎组的4．03％、0．00％。结论在三种常见的胃黏膜良性结节状改变的胃炎中，结节性胃炎与Hp感染及胃黏膜淋巴滤泡形成之间存在密切相关性。可以把Hp感染及淋巴组织滤泡形成和淋巴细胞浸润作为诊断结节性胃炎的病理诊断依据。     

Evaluation of gastroduodenal mucosal lesions in patients with Crohn's disease and ulcerative colitis

Background: Patients with Crohn's disease (CD) are reported to suffer from upper gastroduodenal lesions with varying frequency, although concurrent Helicobacter pylori infection is reported to be low. Methods: A prospective study was carried out on patients diagnosed with CD or ulcerative colitis (UC) in order to evaluate the degree of upper gastroduodenal tract involvement and the prevalence of Helicobacter pylori infection. Results: Gastroduodenal lesions were found in 18 (78%) of 23 CD patients, the location being the stomach in 18 (78%), the duodenal bulb in 16 (70%) and the descending duodenum in 16 (70%). Bamboo joint‐like lesions were found in four cases (17%) in gastric body and cardia. In contrast, gastroduodenal lesions were found in 10 (53%) of 19 UC patients, the location being the stomach in nine (47%), the duodenal bulb in six (32%), and the descending duodenum in three (16%). The H. pylori‐positive rate in patients with CD and UC was 0%, and 11%, respectively. Conclusion: Minute upper gastroduodenal lesions are much more common in CD than in UC patients, especially in the descending duodenum. Accordingly, upper gastrointestinal endoscopy would seem to be a useful means with which to obtain a definitive diagnosis in all suspected IBD cases.     

慢性胃炎的临床与病理学诊断进展

慢性胃炎在中国相当普遍,其中绝大多数源自胃幽门螺杆菌(Hp)感染,如不及时治疗,将导致胃黏膜肠上皮化生、萎缩、异型增生和癌变。近来大量临床和病理学研究结果提示,不完全性肠上皮化生和多灶性胃上皮萎缩具有较高致癌潜能。这些癌前病变多始于胃角和胃窦,沿胃小弯发展至全胃窦,然后扩展至胃体和贲门,伴功能性胃泌酸细胞萎缩、血清胃蛋白酶原Ⅰ水平下降、胃泌素-17水平上升。随着广泛胃上皮萎缩的发生,胃上皮细胞发生异型增生,直至癌变。及时阻断这些癌前病变环节,能从源头遏制、防止胃癌的发生。因此,应对所有行胃镜检查的患者作系统性活检和详尽的组织病理学分析,以得出准确的诊断和分期,这是成功治疗慢性胃炎,防止胃癌发展的有效措施之一。     

Frequency of Helicobacter pylori and Gastritis in Healthy Subjects without Gastrointestinal Symptoms

To investigate the frequency of Helicobacter pylori and gastritis in asymptomatic adults, 30 healthy volunteers underwent upper endoscopy. Biopsy specimens were obtained from the corporeal and antral mucosa of the stomach. The specimens were examined by light microscopy for gastritis and the occurrence of H. pylori. In 12 subjects signs of gastritis were noted at endoscopy, but only in 7 of them was this diagnosis confirmed histologically. No other abnormalities were observed by the endoscopist. Histologic examination was normal in 17 subjects, but in 13 subjects (43%) inflammation was found in the gastric specimens. Ten had inflammation both in the corpus and in the prepyloric specimens, and in six of these subjects H. pylori was discovered. H. pylori was only found in subjects with inflammation in both the corpus and the antrum. Subjects with gastritis were slightly older than subjects with normal gastric mucosa (median age, 47 versus 37 years; not significant). In the group of subjects with gastritis, persons with H. pylori were older than those without (median age, 53.5 versus 36 years; p = 0.05). The results of our study indicate that gastritis is present before colonization with H. pylori occurs. This could imply that H. pylori is not the cause of gastritis but that the presence of gastritis is a prerequisite for colonization of the bacterium in the stomach.     

Smoking Habits in Patients with Inflammatory Bowel Disease: A Case-Control Study

In a case-control study there were significantly fewer smokers among patients with ulcerative colitis both at disease onset and at interview, the relative risk compared with non-smokers being 0.33 and 0.12, respectively. Among female patients with Crohn's disease there were significantly more smokers, the relative risk being 2.70 and 2.33, respectively. Of the ex-smokers with ulcerative colitis, two-thirds became ill after they stopped smoking, and most of these during the first years after stopping. Neither in ulcerative colitis nor in Crohn's disease could any relation be found between the localization of disease and smoking habits at the time of diagnosis. The findings in the present study support the hypothesis that smoking may influence the course of inflammatory bowel disease.     

Analysis of Pancreatic Elastase-1 Concentrations in Duodenal Aspirates from Healthy Subjects and Patients with Chronic Pancreatitis

Fecal pancreatic elastase 1 (PE-1) has been advocated as a noninvasive marker of pancreatic function and allows detection of moderate and severe exocrine insufficiency. Few studies have evaluated the utility of measuring PE-1 in duodenal fluid for the diagnosis of pancreatic insufficiency. Our purpose was (1) to determine the feasibility of measuring PE-1 concentrations in duodenal aspirates obtained through our endoscopic pancreatic function test (ePFT) in healthy subjects and patients with chronic pancreatitis (CP) and (2) to determine correlations between duodenal PE-1 concentrations and bicarbonate and lipase concentrations in duodenal fluid. Healthy subjects (HS) and CP patients underwent an ePFT with CCK or secretin. CP was defined as endoscopic retrograde pancreatography (ERP) Cambridge class III-IV, endoscopic ultrasound (EUS) score >5, or presence of pancreatic calcifications on CT scan. Duodenal fluid PE-1, lipase, and bicarbonate concentrations were measured in each study group. Duodenal lipase and bicarbonate concentrations were measured using an autoanalyzer (Roche Diagnostics, Indianapolis, IN). PE-1 was measured using an ELISA (Genova Diagnostics, Asheville, NC). Ten HS and 10 CP patients were studied. In the CCK test the median peak lipase for HS and CP was 1605 and 113 IU/L, respectively (P < 0.008). In the secretin test the median peak bicarbonate for HS and CP was 102 and 40 mEq/L, respectively (p < 0.008). Median PE-1 concentrations for HS and CP were 317 and 63 microg/ml, respectively, after CCK stimulation (p = 0.046) and 87 and 17 microg/ml, respectively, after secretin stimulation (p = 0.033). Statistically significant correlations were found between [PE-1] and peak [lipase] (r = 0.83, P < 0.001), as well as [PE-1] and peak [HCO3(3)-] (r = 0.65, P = 0.037). Conclusions are as follows: (1) PE-1 concentrations can be measured from duodenal fluid obtained by endoscopic aspiration. (2) Duodenal fluid PE-1 concentrations are decreased in CP compared to HS. (3) Duodenal fluid [PE-1] has an excellent correlation with [lipase] and therefore is a marker of acinar cell function. (4) Secretin-stimulated endoscopic function testing with measurement of bicarbonate and PE-1 may provide a simultaneous assessment of both ductal cell and acinar cell function.     

根除幽门螺杆菌对消化性溃疡合并胃炎及胃泌素的影响

目的 :评估胃舒散联合呋喃唑酮、阿莫西林对消化性溃疡 (PU)患者Hp根除的效果及其对溃疡合并胃炎、血清胃泌素(Gas)的影响。方法 :77例Hp阳性十二指肠溃疡组 (DU ,52例 )和胃溃疡组 (GU ,2 5例 )患者 ,均服用胃舒散 2 .0g(含铋 0 .1 2g) ,呋喃唑酮0 .1g,阿莫西林 0 .5g ,各 3次 /d ,2周后再继服胃舒散 4周。治疗前及疗程结束 1月后进行内镜检查并对胃窦、胃体胃炎予以内镜下评分。采用放射免疫法于治疗前及结束 1月、6月后检测胃泌素水平。结果 :DU组与GU组溃疡愈合率分别为 1 0 0 %和 92 % ,Hp根除率分别为 90 .3 %和 84.0 % ,二组比较差异均无显著性 (P >0 .0 5)。将根除Hp的 47例DU和 2 1例GU患者分为 2组 ,治疗前 2组胃窦胃炎的评分差异无显著性 (P >0 .0 5) ;GU组胃体胃炎的评分显著高于DU组 (P <0 .0 0 1 ) ;血浆中胃泌素含量 (DU组 39.4± 1 3 .6pg/ml;GU组38.4± 1 2 .3pg/ml)均显著高于正常对照值 (2 8.5± 1 0 .6pg/ml,P <0 .0 5)。Hp根除 1月后 ,2组患者胃窦胃炎与胃体胃炎的评分均显著下降 ,与治疗前自身比较 ,差异有统计学意义 (均P <0 .0 0 1 )。DU组Hp根除治疗 1月后 ,胃泌素水平显著下降到 32 .7± 1 0 .5pg/ml (P <0 .0 5)。GU组Hp根除 1月后 ,胃泌素水平有所下降 ,但与治疗前相比 ,差     

早期胃癌和进展期胃癌患者幽门螺杆菌感染与胃黏膜组织学特点的关系

背景幽门螺杆菌(H.pylori)感染已被确认为慢性胃炎的主要病因,由慢性非萎缩性胃炎、慢性萎缩性胃炎至肠化生,经过数十年最终可能导致胃癌发生。目的评价H.pylori感染与胃镜检查正常者、慢性胃炎、早期胃癌和进展期胃癌患者胃黏膜组织学特点的关系。方法在受检者胃窦大弯侧、胃体大弯侧和胃角处各取一块黏膜活检标本,以Giemsa染色和免疫组化染色检测H.pylori感染情况;以HE染色评价胃黏膜炎症、活动性、萎缩和肠化生情况。结果慢性胃炎、早期胃癌和进展期胃癌患者的总体H.pylori感染率均显著高于胃镜检查正常者(52.4%、52.4%和81.2%对44.9%,P<0.05),慢性胃炎与早期胃癌患者的感染率无显著差异,但均显著低于进展期胃癌患者(P<0.05)。胃镜检查正常和慢性胃炎组H.pylori感染者的胃黏膜炎症、活动性、萎缩和肠化生检出率均显著高于无感染者(P<0.05);早期胃癌和进展期胃癌组H.pylori感染者的炎症活动性检出率显著高于无感染者(P<0.05),而炎症、萎缩和肠化生检出率与无感染者无显著差异。结论由H.pylori感染引起的胃黏膜慢性炎症、萎缩和肠化生可能在胃癌的发生、发展过程中起直接或间接作用。     

Prevalence of Barrett's Epithelium Shown by Endoscopic Observations with Linked Color Imaging in Subjects with Different H. pylori Infection Statuses

Objective This study was conducted to clarify the prevalence of short segment Barrett''s esophagus (SSBE) using endoscopic observations with linked color imaging (LCI). In addition, the relationship between the presence of Barrett''s epithelium (BE) and the status of H. pylori infection was investigated. Methods The study subjects were 3,353 individuals (2,186 men, 1,167 women; mean age 55.2±9.4 years old) whose status of H. pylori infection had been determined. An endoscopic observation using LCI was performed to examine the distal margin of palisade vessels and confirm the area of BE. The prevalence of BE ≥5 mm in length was investigated. Results BE was diagnosed in 1,884 (56.2%) subjects, with lengths of <10, 10-19, 20-29, and ≥30 mm found in 1,005, 851, 27, and 1, respectively. Its prevalence in H. pylori-negative, H. pylori-positive, and post-eradicated subjects was 41.7%, 64.4%, and 69.9%, respectively (p<0.001). The duration since successful eradication of H. pylori did not affect the prevalence of BE. The degree of gastric mucosal atrophy was higher in cases with BE (p<0.001), although negativity for H. pylori infection and mild gastric mucosal atrophy were significant factors for the development of longer BE. Conclusion A high prevalence of SSBE was noted when LCI was used to determine the area of BE, as the distal end of the palisade vessels was easily visualized. Negativity for H. pylori infection and mild gastric mucosal atrophy were not correlated with SSBE prevalence.     

Helicobacter Pylori, Active Chronic Antral Gastritis, and Gastrointestinal Symptoms in Alcoholics

The frequency of Helicobacter pylori (Hp.) infection and active chronic antral gastritis among people with excessive alcohol consumption is not known. A high alcohol intake regularly causes acute gastroduodenitis. In this study, the prevalence of Hp. Infection and active chronic antral gastritis in alcoholics compared with nonalcoholic controls was studied. Further, the frequency of gastrointestinal symptoms was registered. Diagnostic methods for Hp. were compared.
Twenty-four alcoholics admitted to the hospital for detoxification underwent upper gastrointestinal endoscopy regardless of symptoms. Twelve individuals admitted to upper endoscopy mainly for dyspepsia, with low alcohol consumption and without gross pathology by upper endoscopy, were chosen as controls. Three diagnostic methods for Hp. were used: culture, direct microscopy, and histology.
Hp. infection was found in 7 of the 24 alcoholics (29%) according to culture. In controls, 4 of 12 (33%) had a positive Hp. culture. In the alcoholic group, culture was more sensitive than histology. There was a good correlation between the different diagnostic methods in the control group. Histologically active chronic antral gastritis was found in 6 of the alcoholics (25%) and in 5 of the controls (42%). Five of the 7 Hp.-positive alcoholics and all of the Hp.-positive controls had an active chronic antral gastritis.
Hp. infection is not more frequent in alcoholics than in controls. In both groups, there was a good correlation between Hp. infection and histologically, active chronic antral gastritis.     

Severe Pancreatitis after Parathyroidectomy

Cope showed in 1957 that pancreatitis may be the presenting symptom in hyperparathyroidism. Since then, the literature has reported a coincidence of primary hyperparathyroidism and pancreatitis between 1% and 19%, but the true relationship has not been fully established. When severe pancreatitis follows parathyroidectomy, a condition familiar to parathyroid surgeons, reports are mostly anecdotal and by many authors considered to be coincidental. We present the case history of a 58-year-old man with a longstanding history of untreated primary hyperparathyroidism who developed severe pancreatitis immediately after removal of a 400-mg parathyroid adenoma. He was the first in a series of 108 operated patients to develop this complication. His preoperative levels of parathormone and serum calcium were the highest in our material. We believe that pancreatitis after parathyroidectomy is a real but rare complication that might be predicted by preoperative high values of serum calcium and parathormone.     

影响慢性胃炎患者幽门螺杆菌根除的临床因素分析

背景:幽门螺杆菌(H.pylori)感染与慢性胃炎和消化性溃疡密切相关,然而,目前临床普遍采用的三联疗法对相当一部分患者的H.pylori根除无效。目的:探讨影响慢性胃炎患者H.Pylori根除的主要临床因素。方法:取128例H.pylori阳性的慢性胃炎患者的内镜活检标本行H.pylori培养和药敏试验,以奥美拉唑+克拉霉素+甲硝唑的7 d三联疗法行H.pylori根除治疗,以PCR-RFLP法检测CYP2C19基因型。分析不同因素对H.pylori根除率的影响。结果:共123例完成治疗,H.pylori根除率按ITT和按PP分析分别为66.4%和69.1%。H.pylori对甲硝唑和克拉霉素的耐药率分别为48.4%和14.1%。有吸烟史者的H.pylori根除率显著低于无吸烟史者(37.0%对88.3%,P0.01)。甲硝唑敏感菌株和克拉霉素敏感菌株的根除率均显著高于相应的耐药菌株(90.5%对46.7%,P0.01;76.6%对18.8%,P0.01)。CYP2C19强代谢型的根除率显著低于弱代谢型(63.4%对 86.7%,P0.05)。不同性别、年龄以及是否饮酒的患者之间H.pylori根除率差异均无统计学意义(P0.05)。结论:H.pylori对抗生素耐药和宿主CYP2C19强代谢型是导致H.pylori根除失败的主要原因,吸烟史对根除失败亦具有一定的意义。     

Expression of cell membrane complement regulatory glycoproteins along the normal and diseased human gastrointestinal tract

Background/Aims—Uncontrolled complementactivation may be of immunopathological importance in inflammatorydiseases of the gastrointestinal tract. Expression of membrane boundfactors that regulate complement activation was therefore studied in situ.
Methods—Frozen tissue specimens were obtained frompatients with Helicobacter pylori gastritis, coeliacdisease, Crohn's disease, or ulcerative colitis, and fromhistologically normal controls. Sections were examined byimmunofluorescence with monoclonal antibodies to protectin (CD59),decay accelerating factor (DAF), and membrane cofactor protein (MCP).
Results—Protectin and MCP were widely expressed innormal and diseased mucosae. MCP was generally observed basolaterallyon all epithelial cells, whereas apical protectin expression was moreintense on the epithelium of normal colonic mucosa than in the normalduodenum (p = 0.001). Epithelial DAF and to some extent protectin wereupregulated in gastritis, coeliac disease, and inflammatory boweldisease. Areas of the stomach with intestinal metaplasia expressed DAF,unlike the adjacent gastric epithelium. Parietal cells of the gastricbody expressed neither protectin nor DAF.
Conclusion—Epithelial complement inhibitorymolecules were expressed differently at various normal gastrointestinalsites and also in association with mucosal disease, suggesting variable protective potential. Such molecules could play a role in the development of gastric atrophy by protecting areas of intestinal metaplasia. Conversely, parietal cells appeared to be potentially vulnerable targets for complement attack.

Keywords:Helicobacter pylori; coeliac disease; Crohn's disease; ulcerative colitis; immunofluorescence; complementregulatory proteins