胃上皮化生、幽门螺杆菌与十二指肠溃疡关系的探讨

目的：研究胃上皮化生、幽门螺杆菌（HP）与十二指肠溃疡之间的关系。方法：应用特殊染色方法对60例十二指肠溃疡球部活检标本进行形态学观察及HP检测，并以50例正常十二指肠粘膜作对照。结果：胃上皮化生率球溃组（81．7％）高于对照组（26％）（P＜0．005）；球部HP检出率球溃组（50％）高于对照组（14％）（P＜0．005）；球部HP94．6％（35／37）生长在胃上皮化生区，5．4％（2／37）生长在无化生区（P＜0．050），轻度，中度，重度胃上皮化生区HP检出率分别为21．4％，64．3％，70．0％，中－重度胃上皮化生区HP检出率高于轻度化生区（P＜0．05）。结论：胃上皮化生与HP相继作用，形成十二指肠溃疡。     

幽门螺杆菌感染与十二指肠球部黏膜胃上皮化生的关系

目的 研究十二指肠球部黏膜幽门螺杆菌(Hp)感染与黏膜胃上皮化生的关系，探讨其在十二指肠球部炎症和溃疡发生中的作用。方法 2002年十二指肠球部黏膜活检的存档蜡块82例，作H-E、改良Giemsa和AB／PAS染色。内镜诊断为基本正常球部黏膜10例；十二指肠球炎47例(其中充血糜烂型16例；隆起型31例)和球部溃疡25例。结果 (1)内镜诊断基本正常的十二指肠球部黏膜，组织学60％有轻中度的炎症细胞浸润，但无胃上皮化生和Hp定植。(2)胃上皮化生是十二指肠球部黏膜最常见的病理变化(37／82，45％)。(3)Hp只有在胃上皮化生的黏膜中才能找到，检出率为76％(28／37)。十二指肠球部溃疡边缘黏膜胃上皮化生发生率(72％)明显高于球炎黏膜(40％)，差异有显著性(P=0．0078)。(4)虽然十二指肠球部溃疡边缘胃上皮化生黏膜的Hp检出率(89％，16／18)明显高于十二指肠球炎黏膜(63％，12／19)，但是两者差异无显著性(P=0．062)。不论何期溃疡Hp检出率均很高，本研究中溃疡活动期、愈合期和瘢痕期分别为15例、6例和4例，其溃疡边缘胃上皮化生中Hp检出率分别高达9／10、5／6和2／2例。结论 十二指肠球部溃疡周围黏膜高发胃上皮化生，使Hp更易于定植，推测如不根除Hp感染，可成为十二指肠球部溃疡复发的重要原因。     

十二指肠粘膜胃上皮化生的组织学及电镜观察

胃上皮化生是十二指肠球部溃疡病灶旁的一种常见病理改变,我们通过对十二指肠球部溃疡、炎症和慢性浅表性胃炎患者的十二指肠球部粘膜胃上皮化生的观察,探讨胃上皮化生在十二指肠球部溃疡发病中的作用。一、材料和方法十二指肠球部溃疡活动期（ＤＵ－Ａ）患者６１例,十二指肠球部溃疡瘢痕期（ＤＵ－Ｓ）４０例,十二指肠球炎（ＤＩ）１９例,慢性浅表性胃炎（ＣＳＧ）３０例。在常规胃镜检查时,每组病例均取胃窦和十二指肠球部粘膜标本各１块：各组胃窦粘膜标本均取自胃窦前壁２ｃｍ处,ＤＵ患者十二指肠球部粘膜标本取自溃疡旁或溃疡瘢…     

十二指肠胃化生与幽门螺杆菌感染

本调查了155例十二指肠溃疡旁粘膜的组织病理学变化，并与对照组相比较。结果显示：溃疡旁组织炎症、胃化生和Hp检出率分别为69．7％、75．5%和24．5%，显高于对照组的18．8%、10．4％和4．2％(P＜0．01)．Hp在胃化生组织中的检出率为32．8％，81例不伴胃化生的粘膜中均未检出Hp(P＜0．01)，透射电镜观察胃化生有其特征性改变。提示胃化生可能是溃疡形成的基础，Hp在化生区定植并非是产生溃疡的唯一直接因素，还可能通过其他复杂环节间接起作用。     

幽门螺杆菌阳性的消化性溃疡患者中胃、十二指肠上皮细胞及幽门螺杆菌的超微结构特点

目的研究幽门螺杆菌（Helicobacter pylori,H．pylori）阳性的消化性溃疡患者胃、十二指肠上皮细胞及H．pylori的超微结构特点。方法经尿素酶实验和^14C-尿素呼气实验证实为H．pylori阳性的消化性溃疡30例（胃溃疡和十二指肠球部溃疡各15例）作为观察组,以无H．pylori感染的健康成年人的胃和十二指肠黏膜组织作为对照,通过透射电镜技术观察上皮细胞及H.pylori的超微结构变化。结果透射电镜观察结果显示,H．pylori阳性的胃黏膜上皮细胞多数肿大,排列紊乱,部分发生肠腺化生,肠腺化生标本中发现上皮内瘤细胞。细胞内线粒体肿胀,粗面内质网扩张。H.pylori感染引起胃上皮内淋巴细胞浸润。H．pylori阳性的十二指肠黏膜上皮细胞明显肿胀,出现空泡变性,细胞游离面微绒毛减少或消失,排列稀疏。部分细胞间连接复合体消失,间隙加大。局部浆细胞增生,毛细血管结构不完整,血浆及红细胞渗出。胃、十二指肠黏膜组织中H．pylori呈杆状或球状,黏附于细胞表面或进入细胞内。结论H．pylori以不同形态、不同的寄生及黏附方式感染黏膜,引起消化性溃疡患者胃、十二指肠上皮细胞及细胞内结构发生多种炎性改变,甚至引起胃上皮细胞内瘤细胞形成。     

胃十二指肠疾病患者中cagA阳性幽门螺杆菌的普遍易感性

明确cagA阳性幽门螺杆菌（H.pyloril)胃十二指肠疾病患者中的感染情况。方法：用聚合酶链反应（PCR）方法扩增从30例十二指肠球部溃疡、30例慢性胃炎和6例胃癌虱活检组织中分离培养出的H.pylori菌株的cagA基因片段,用酶联免疫吸附测定（ELISA）方法检测血清抗H.pylori抗体,用免疫印迹（Western blot)方法检测血清抗cagA抗体。结果：用PCR方法测得的cagA基因阳性率为：十二指肠球部溃疡70％（21／30）,慢性胃炎73％（22／30）,胃癌83％（5／6）。66份血清标本抗H.phlori抗体均为阳性。用Western blot方法测得的抗cagA抗体阳性率为：十二指肠球部溃疡83％（25／30）,慢性胃炎77％（23／30）,胃癌83％（5／6）。结论：在我国人群中,cagA基因不能作为消化性溃疡的标志物,cagA阳性H.pylori在消化性溃疡和慢性胃炎患者中存在普遍易感性。     

十二指肠球部多发隆起病变与幽门螺杆菌和胃上皮化生的关系

目的探讨内镜下十二指肠球部多发隆起病变与幽门螺杆菌（Hp）感染和胃上皮化生等组织学异常关系.方法连续调查86例经胃镜检查证实十二指肠球部多发隆起病变患者,并以40例球部基本正常患者作为对照.病变组Hp阳性患者接受三联根除治疗（奥美拉唑20mg、克拉霉素250mg、甲硝唑400mg,每天2次）,疗程7 d,停药后随访6个月后复查胃镜;病变组Hp阴性者接受奥美拉唑20 mg,每天1次治疗,疗程4～6个月,停药后2周复查胃镜.比较2次胃镜检查结果,包括胃镜下隆起病变程度及球部黏膜胃上皮化生等组织学异常,分析Hp感染与上述胃镜下表现及组织学异常关系.结果对照组患者组织学仅部分发现轻度慢性炎症,未发现球部Hp感染.病变组患者Hp检出率为58.1%,胃上皮化生检出率为57.0%.Hp阳性与Hp阴性患者胃镜下隆起病变程度差异无统计学意义（P＞0.05）,但胃上皮化生检出率更高,程度更严重（P＜0.05）.76例患者复查胃镜,根除Hp或奥美拉唑治疗对Hp阳性或阴性患者球部多发隆起病变无明显作用,但根除Hp后6个月,53.6%（15/28）患者胃上皮化生消失,61.0%（25/41）患者绒毛萎缩恢复正常,所有患者淋巴滤泡完全消失（26/26）,杯状细胞减少完全恢复（25/25）,同时炎症和活动性显著减轻（P值均＜0.01）.奥美拉唑疗效不显著.结论十二指肠球部多发隆起病变患者半数以上有Hp感染.Hp感染与隆起病变伴随组织学炎症密切相关,而与其内镜下表现及严重程度无关.根除Hp可使炎症显著减轻,胃上皮化生范围缩小或消退.     

结节型十二指肠炎的内镜表现及其临床病理学特征

目的 探讨结节型十二指肠炎内镜下表现与其组织学特征的关系及其发病机制。方法 观察内镜下136例结节型十二指肠炎的表现，对其活检标本均行H-E染色，观察病理改变，Giemsa染色及快速尿素酶试验诊断幽门螺杆菌感染，十二指肠黏膜兼作AB／PAS染色，观察十二指肠胃上皮化生。结果 136例结节型十二指肠炎内镜下表现为直径0．2～1．0cm大小不等的结节，伴有不同程度的充血、水肿，其中伴糜烂21例，出血点及（或）瘀斑30例。检出率占同期15820例内镜检查的0．9％，十二指肠炎的3．8％。病理诊断为十二指肠炎107例，其中慢性十二指肠炎53例，表现为间质内可见慢性炎性细胞浸润，肠绒毛缩短或萎缩、变平．肠腺不同程度减少；活动性十二指肠炎54例，除慢性炎性细胞外，黏膜层及固有层内还有不同程度的中性粒细胞浸润，伴Brunner腺增生51例，胃型上皮化生59例。136例中检出胃黏膜异位增生7例以及血吸虫虫卵所致的炎性病变4例，107例结节型十二指肠炎中，幽门螺杆阳性（Hp^＋）者为45．8％（49／107）。其中，53例慢性十二指肠炎患者中HP^＋者为32．1％（17／53），54例活动性十二指肠炎中Hp^＋检出率为59．3％（32／54），后者的Hp^＋检出率显著高于前者（P〈0．01）。结论 结节型十二指肠炎是一类特殊的非特异性十二指肠炎，内镜下表现与组织学改变存在不一致性。其发生可能与Hp感染及胃上皮化生、Brunner腺增生有关。     

幽门弯曲菌与十二指肠溃疡的发生

十二指肠溃疡的复发是由于溃疡愈合后幽门弯曲菌(Campylobacter pylori,CP)感染的持续存在,Coghlan 等认为这一事实有力地证明了 CP 在溃疡发生中的作用。CP 不能移生于小肠上皮,那么胃中的 CP 感染是怎样引起十二指肠溃疡的呢?答案很可能就足在十二指肠中出现了胃上皮化生。胃上皮化生为小肠上皮对损伤的一种反应。在人和实验动物中,十二指肠球部的胃上皮化生都与胃酸增高有关,这意味着胃上皮化生是十二指肠对其内容     

十二指肠胃反流和幽门螺杆菌感染关系研究

目的：探讨消化性溃疡患者中的十二指肠胃反流对幽门螺杆菌（Hp)感染的影响。方法：70例消化性溃疡患者，用核素^99MTC-EHIDA测定十二指肠胃反流，胃黏膜Giemsa染色后检测Hp和双抗体夹心ELISA法测定血清Hp-IgG水平。结果：在42例十二指肠胃反流阴性组中，Hp感染率为83．3％（35／42）；28例十二指肠胃反流阳性组中，Hp感染率为39．3％（11／28），两组间Hp感染率差异有显著性（P＜0．05）。而Hp阳性组46例患者中，十二指肠胃反流阳性率为30．4％（14／46）；Hp阴性组24例中，十二指肠胃反流率为58．3％（14／24），两组间十二指肠胃反流率差异也有显著性（P＜0．05）。结论：在消化性溃疡中，十二指肠胃反流对胃内Hp感染可能有抑制作用。     

Investigation of the extent of gastric metaplasia in the duodenal bulb by using methylene blue staining

BACKGROUND AND AIMS: The existence of gastric metaplasia (GM) of the duodenal mucosa has been considered to be highly related to the recurrence of duodenal ulcers (DU). The aims of this study are to evaluate the usefulness of methylene blue staining in the detection of GM, and to clarify the relationship between GM and the deformity of the duodenal bulb. METHODS: Fifteen patients with healed DU and four patients with symptoms of dyspepsia without evidence of ulcers were enrolled into this endoscopic study. During each endoscopy, methylene blue was sprayed evenly on the duodenal bulb, and biopsies were taken from blue-stained and unstained areas. The existence and extent of GM were assessed histologically and grossly. The correlation between duodenal bulb deformity and the extent of GM was also studied. RESULTS: The mean score of methylene blue non-staining (MBNS) was 0, 1.30 +/- 0.15, and 3.00 +/- 0.00 in group A (non-ulcer patients), group B (patients with healed DU and with normal-shaped bulb) and C (patients with healed DU and with deformed duodenal bulb), respectively; showing significant differences among the groups (P < 0.05 in each). Both the existence and the grading of GM were higher in unstained specimens than in blue-stained specimens (100 vs 16.6%, P < 0.0001 and 3.62 +/- 0.09 vs 0.19 +/- 0.06, P < 0.001, respectively). CONCLUSIONS: Methylene blue non-staining can be applied to investigate the existence and extent of GM in the duodenal bulb accurately. The incidence of GM in the duodenal bulb was higher in patients with healed ulcers than in non-ulcer patients. Patients with deformed duodenal bulbs have a higher extent of GM than those without deformed duodenal bulbs.     

Accuracy of magnifying endoscopy with methylene blue in the diagnosis of specialized intestinal metaplasia and short-segment Barrett's esophagus in Japanese patients without Helicobacter pylori infection

BACKGROUND: The use of methylene blue chromoendoscopy in the diagnosis of specialized intestinal metaplasia in short-segment Barrett's esophagus is controversial. This study evaluated the use of magnifying endoscopy with methylene blue for this purpose. METHODS: A total of 30 patients (21 men, 9 women; median age 61 years, range 32-79 years) with short lengths of columnar-lined esophagus were enrolled in a prospective trial of magnifying endoscopy with methylene blue in which the appearance after methylene blue staining was used to target biopsy specimens. Patients were screened for Helicobacter pylori infection, and only those without infection were enrolled (because many Japanese patients have pan-gastritis caused by H pylori infection, and intestinal metaplasia distal to the squamocolumnar junction may be secondary to H pylori-induced gastritis). All biopsy specimens were stained with H and E; MUC2 immunostaining was used to identify specialized intestinal metaplasia. RESULTS: Thirty patients with short-segment columnar-lined esophagus underwent magnifying endoscopy with methylene blue. Ninety-three biopsy specimens were obtained, 33 from methylene blue-stained areas and 60 from unstained areas, each about 7 mm from the marginal edge of stained areas. Specialized intestinal metaplasia was confirmed in biopsy specimens from 28 of the 33 stained areas (sensitivity 84.8%); in biopsy specimens from 55 of the 60 unstained areas, specialized intestinal metaplasia was not found (specificity 91.7%). In magnified views of methylene blue-positive areas, a tubular, cavernous, or elliptical pattern was seen. Sixteen of 21 men (76.2%) and 3 of 9 women had specialized intestinal metaplasia, and short-segment Barrett's esophagus was diagnosed in these patients. Even in patients with less than 1 cm of columnar-lined esophagus, 8 of 10 stained areas contained specialized intestinal metaplasia (sensitivity 80%) and 23 of 24 unstained areas did not (specificity 95.8%). Six of 12 patients (50%) with less than 1 cm of columnar-lined esophagus had specialized intestinal metaplasia. In total, 19 of 30 patients had specialized intestinal metaplasia. CONCLUSIONS: Magnifying endoscopy with methylene blue selectively detects specialized intestinal metaplasia within short-segment columnar-lined esophagus.     

Expression of trefoil peptides pS2 and human spasmolytic polypeptide in gastric metaplasia at the margin of duodenal ulcers.

Duodenal ulcers are associated with gastric metaplasia in the duodenum, both at the ulcer margin and at more distant sites in the duodenal bulb. pS2 and human spasmolytic polypeptide (hSP) are secretory peptides expressed in gastric epithelial cells and in gastric metaplasia. As these peptides may be important in ulcer healing, this study investigated the possibility that the expression of pS2 and hSP is increased in gastric metaplasia at the margin of duodenal ulcers. Duodenal bulb biopsy specimens from 12 duodenal ulcer patients were assessed. Sections were immunostained with monoclonal antibodies for pS2 and hSP. Cytoplasmic stain intensities were measured by an image analysis system and expressed as integrated optical density (IOD) units, In situ hybridisation for pS2 and hSP mRNA was carried out on parallel sections. Duodenal sections were also stained with diatase periodic acid Schiff/alcian blue to localise areas of gastric metaplasia. pS2 antigen staining in the duodenum was restricted to surface epithelial cells, and hSP to acinar and ductular components of Brunner's gland. mRNA localisation corresponded to immunostaining cells. In gastric metaplasia, pS2 expression was greater at the ulcer margin than away from the ulcer, as judged by the intensity of antibody staining (mean IOD units (SEM), 20.6 (3.3) v 9.5 (3.0); p < 0.001). There was a trend towards greater hSP staining at the ulcer margin but this did not achieve statistical significance. These findings support the putative role of pS2 and possible hSP in mucosal healing and providy further evidence for an autocrine 'ulcer-gastric metaplasia-repair' loop involving these trefoil peptides.     

Gastric metaplasia and duodenal ulcer disease in children infected by Helicobacter pylori.

BACKGROUND--Helicobacter pylori infection of the gastric mucosa is vital in the pathogenesis of duodenal ulcer disease. H pylori will only colonise gastric epithelium and its association with duodenal disease is therefore not easily explained. AIMS--To determine if gastric metaplasia in the duodenum increases the risk of duodenal ulcer disease in children infected with H pylori. PATIENTS--All children undergoing upper endoscopy over a 20 month period in a children's hospital in Ireland. METHODS--Two biopsy specimens were obtained from the antral mucosa and two from the first part of the duodenum. One antral biopsy specimen was used in a rapid urease test (Clo Test). Biopsy sections were stained with haematoxylin and eosin and also with cresyl violet for identification of H pylori. Periodic acid Schiff (PAS) stain was performed to identify areas of gastric metaplasia. RESULTS--Gastric and duodenal biopsy specimens were obtained from 148 patients (M:F 1:2:1). Twenty five children (17%) had H pylori positive gastritis. Thirty four children (23%) had gastric metaplasia in the duodenum. Nine per cent of children under the age of 8 years had gastric metaplasia compared with 38% in those 12 years of age or over (p < 0.005). Seven children had duodenal ulcer disease. Gastric metaplasia was present in six of seven (86%) children with duodenal ulcer disease compared with 28 of 141 (20%) without ulceration (p < 0.001). While both H pylori and gastric metaplasia were each significant risk factors for duodenal ulcer disease, the combined presence of both factors was associated with a pronounced increase in duodenal ulcer disease. Duodenal ulcer disease occurred in over 50% of children with both H pylori infection and gastric metaplasia. In contrast duodenal disease did not occur in children (0 of 100) when both were absent. CONCLUSION--The presence of gastric metaplasia in the duodenum is the major risk factor for duodenal ulcer disease in patients colonised by H pylori.     

Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum.

BACKGROUND: The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors. AIMS: To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia. PATIENTS: Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study. METHODS: Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959). RESULTS: Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed. CONCLUSION: The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.     

Campylobacter pylori, duodenal ulcer, and gastric metaplasia: possible role of functional heterotopic tissue in ulcerogenesis.

Multiple pinch biopsies were taken from the duodenum and antrum of 137 subjects (46 active duodenal ulceration; 44 healed ulcers; 47 'normal'), and examined for the presence and grade of gastritis, gastric metaplasia, and Campylobacter pylori. These factors, as well as age, sex, cigarette, and anti-inflammatory agent intake were evaluated as possible risk factors for duodenal ulceration. Pentagastrin induced Congo Red staining of the duodenal bulb was performed in an additional 43 cases, to determine the presence of functioning parietal cells in the duodenum. Ninety eight per cent of patients with duodenal infection with C pylori had active or healed duodenal ulcers. Bacteria were confined to areas of gastric metaplasia which was always infiltrated with inflammatory cells. The metaplastic tissue was usually superficial in type, although patients had C pylori associated with heterotopic tissue: this has not been previously described. Congo Red staining of the duodenal bulb showed that functioning endogenous acid producing tissue could be found most often at the edges of duodenal ulcers, but also in non-ulcer subjects. Cigarette smoking, age, sex, and ingestion of non-steroidal anti-inflammatory agents were not to be found to be significant risk factors for duodenal ulceration. In contrast, the presence of duodenal infection with C pylori proved to be a strong risk factor for duodenal ulceration (RR = 51), together with gastric metaplasia (RR = 6.2), and antral C pylori infection (RR = 7.6). These data identify duodenal infection with C pylori as the strongest risk factor for development of duodenal ulceration. Our finding of endogenous acid production around the edges of duodenal ulcers suggests an active role for parietal cells in the duodenum. We postulate a synergistic role for duodenal C pylori and endogenous acid production in the development of duodenal ulceration.     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients.

BACKGROUND: Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients. AIMS: To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status. PATIENTS AND METHODS: A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination. RESULTS: There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum. CONCLUSION: Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

Long-term follow-up of intestinal metaplasia of the gastric cardia

OBJECTIVE: Recent studies have found a relatively high prevalence of gastric cardia intestinal metaplasia in individuals presenting for elective upper endoscopy. It has been hypothesized that this lesion may be a precursor of gastric cardia cancer. Our objective was to identify the incidence of dysplasia in patients with gastric cardia intestinal metaplasia. METHODS: Twenty-eight patients who had previously been identified with cardia intestinal metaplasia had follow-up examinations performed. None of the patients had dysplasia at the time of diagnosis. All had an examination at 1 yr, and 20 patients had an examination at 3 yr after diagnosis. During follow-up examinations all patients underwent vital staining with methylene blue to help identify areas of intestinal metaplasia in the cardia. Two to four biopsies were taken from blue-stained mucosa. Histological specimens were stained using a combination of hematoxylin and eosin with Alcian blue at pH 2.5. RESULTS: There were 27 men and one woman with a mean age of 69.8 yr (range, 48-83 yr). The mean length of follow-up was 2.5 yr (range, 12-46 months). Only one patient was diagnosed with dysplasia (low-grade) during the study, for an incidence of 1.4% per yr. CONCLUSIONS: The prevalence (0%) and incidence (1.4%/yr) of dysplasia in cardia intestinal metaplasia are low. Although further studies are needed, screening and surveillance for gastric cardia intestinal metaplasia is unlikely to be clinically useful for the prevention of gastric cardia cancer.     

A study of incidence and relationship of intestinal metaplasia of gastric antrum and gastric metaplasia of duodenum in patients with nonulcer dyspepsia

The incidence and relationship of intestinal metaplasia of the gastric antrum and gastric metaplasia of the first part of the duodenum were studied in endoscopic biopsies from 120 patients with nonulcer dyspepsia. Intestinal metaplasia was present in 29% of antral biopsies and gastric metaplasia in 39% of duodenal biopsies, with 9% of patients having both. Intestinal metaplasia was not related to alcohol consumption, but was significantly higher in patients who smoked 10 cigarettes or more daily. (P<0.002). Gastric metaplasia was associated with duodenitis. Its incidence was significantly higher in males (P<0.001) and in patients with a history of high/moderate alcohol intake (P<0.02); these findings are reminiscent of the presence of a similar relationship between these factors and duodenal ulcers and support the suggestion that duodenitis and duodenal ulcers probably represent different parts of a single disease spectrum. The presence of both types of metaplasia in 9% of the patients suggest that factors other than gastric acidity may influence the development of metaplasia.Dr. S. Khan is supported by the Cancer Research Campaign.