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文摘０１胃窦幽门螺杆菌感染致十二指肠溃疡［英］／ＬａｒｓＯ…／／Ｇａｓｔｒｏｅｎｔｅｒｏｌｏｇｙ．－１９９６，１１０．－１３８６－１３９４幽门螺杆菌（ＨＰ）是十二指肠溃疡（ＤＵ）的主要发病因素，ＤＵ病人的ＨＰ感染在胃窦粘膜，ＤＵ产生的机理是ＨＰ感染的...     

胃粘膜相关淋巴组织型淋巴瘤形态学研究

目的：研究胃粘膜相关淋巴细胞（ＭＡＬＴ）型淋巴瘤及共与胃粘膜套细胞淋巴瘤和滤泡性淋巴瘤的鉴别诊断。方法：应用ＨＥ染色和免疫组化ＡＢＣ法检测胃ＭＡＬＴ型淋巴瘤，内镜作幽门螺杆菌培养基尿素试验检测ＨＰ感染。结果：３１例胃ＭＡＬＴ型淋巴瘤中低度恶性２７例，高度恶性４例。细胞类型以ＣＣＬ型最常见。免疫表型以ＩｇＭ为主，缺乏ＩｇＤ，３１例中２８例有ＨＰ感染（占９０．５２％），结论：（１）低恶ＭＡＬＴ型淋巴瘤     

三种抗原检测抗幽门螺杆菌抗体的临床意义评价

目的：寻求敏感性高、特异性强的ＨＰ抗原和简便、可靠的检测ＨＰ抗体的方法,用于诊断ＨＰ感染。方法：分别以ＨＰ尿素酶、全菌破碎物、培养上清液为抗原。采用斑点金标免疫渗滤法（ＤＩＧＦＡ）检测ＨＰ培养、病理组织学检查、尿素酶试验均阳性和均阴性的血清各５０份;胃镜检查各类胃病毒者血清２５８份,并以ＥＬＩＳＡ试剂盒做平行检测对照。结果：三种抗原的敏感性分别为１００％、９６％和７６％;５０份阴性血清的阴性符合率     

血清胃泌素测定应用于抗幽门螺杆菌疗效监？…

为探讨十二指肠溃疡患者血清试餐胃泌素（ＭＳＧ）对幽门螺杆菌（ＨＰ）感染的反应,评估抗ＨＰ治疗后ＭＳＧ的降低水平及其用于判定ＨＰ根除效果的可靠性,方法采用自身对照的方法对８４例ＨＰ阳性ＤＵ患者进行了前瞻性研究,治疗前行胃镜检查,钳聚胃窦粘膜在进行组织学检查的同时,分别进行ＨＰ培养,改良Ｇｉｅｍｓａ染色及快速尿素酶试验,并测定其血清ＭＳＧ浓度,然后给予患 抗ＨＰ三联药物治疗（德诺１２０ｍｇ、羟氨苄青霉     

幽门螺杆菌感染与慢性胃炎不同病变的相关性研究

１　材料和方法１１　病例来源　本科１９９７年诊断的７７６例慢性胃炎（ＣＧ）。１２　幽门螺杆菌（ＨＰ）检查方法　①尿素酶试验，②胃粘膜组织革兰染色，③细菌培养。以上三项检查中两项或两项以上阳性者诊断为ＨＰ阳性。１３　数据处理和分析２　结果２１　一般情况　在７７６例研究对象中，慢性浅表性胃炎（ＣＳＧ）５５９例，慢性萎缩性胃炎（ＣＡＧ）２１７例：４５８例男性，３０８例女性，年龄１４～８０岁，平均４０９６岁。２２　年龄、性别与ＨＰ感染的关系　～３０岁、～４０岁和＞４０岁组的ＨＰ感染率分别为：…     

应用原位PCR技术检测阴茎癌组织中人乳头瘤病毒DNA

目的：研究人乳头瘤病毒（ＨＰＶ）与阴茎癌的关系。方法：应用原位ＰＣＲ技术对４６例阴茎癌组织中的ＨＰＶ１６和ＨＰＶ１８ＤＮＡ进行检测。结果：３３例阴茎癌中检测到了ＨＰＶＤＮＡ（７１．７％），其中２９例ＨＰＶ１６ＤＮＡ阳性（６３．０％），６例ＨＰＶ１８ＤＮＡ阳性（１３．０％），２例ＨＰＶ１６和ＨＰＶ１８ＤＮＡ均阳性，４例ＨＰＶ１８ＤＮＡ阳性而ＨＰＶ１６阴性；２例淋巴结转移癌，３例癌旁不典型增生组织和１例癌旁增生组织ＨＰＶ１６ＤＮＡ阳性。结论：阴茎癌与ＨＰＶ１６、ＨＰＶ１８感染有密切关系，原位ＰＣＲ技术是一项敏感性高、特异性强的技术。     

幽门螺杆菌相关性十二指肠溃疡患者血清、胃窦粘膜组织中胃泌素、生长抑素水平变化

目的：探讨幽门螺杆菌相关性胃窦炎症病理变化程度对血清、胃窦部粘膜组织中胃泌素水平的影响。方法：对Hp阳性的活动性DU患者30例、Hp阴性的活动性DU患者10例、Hp阴性且病理表现仅有轻度浅表性胃炎的10例正常对照患者进行内镜、胃粘膜组织学、幽门螺杆菌和血清、胃粘膜组织胃泌素水平检测，并分析其相互关系。结果：幽门螺力阳性患者血清、胃粘膜组织中胃泌素水平较幽门螺杆菌阴性患者显著升高（P＜0．01）。胃窦组织中生长抑素水平明显降低（P＜0．01）。结论：幽门螺杆菌感染后胃泌素、生长抑菌变化与DU的发生关系密切，并在疾病的发生发展中起一定作用。     

PCR鉴定HBsAg阴性肝炎HBV DNA感染的意义

ＰＣＲ鉴定ＨＢｓＡｇ阴性肝炎ＨＢＶＤＮＡ感染的意义１李伟１王学春１张金池２刁玉贞收集ＨＢｓＡｇ阴性ＨＢｃＡｂ阳性的慢性肝炎病人血清３０例及恢复期急性乙型肝炎病人血清１００例（共计１３０例），利用聚合酶链反应（ＰＣＲ）检测ＨＢＶＤＮＡ。ＰＣＲ方法及步骤...     

十二指肠溃疡病人的幽门螺杆菌感染和酸分泌异常

十二指肠溃疡病人的幽门螺杆菌感染和酸分泌异常［英］／ＥｍａｄＭ…／／Ｇａｓｔｒｏｅｎｔｅｒｏｌｏｇｙ．－１９９５；１０９：６８１～６９１幽门螺杆菌（ＨＰ）是十二指肠溃疡（ＤＵ）的主要致病因素。９５％以上ＤＵ病人有ＨＰ感染。根除ＨＰ后溃疡的复发率大大减...     

喉癌中HPV感染和p16表达的检测及临床相关性研究

目的：探讨喉鳞状细胞癌中ＨＰＶ感染和ｐ１６ 表达的情况及临床相关性。方法：用免疫组化和原位杂交的方法对５２ 例喉鳞癌组织中ＨＰＶ 感染和ｐ１６ 的表达情况进行检测。结果：ＨＰＶ感染的阳性率为６１－５４ ％（３２／５２） ，ｐ１６ 的阳性率为４４－２３ ％（２３／５２）。结论：ＨＰＶ 感染与ｐ１６ 的表达有关；ＨＰＶ 感染与临床分期、癌细胞的分化程度、肿瘤的淋巴结转移情况、临床分型无关；ｐ１６ 的表达与癌细胞的分化程度、肿瘤的颈淋巴结转移情况有关，与临床分型、分期无关。     

Helicobacter heilmannii gastritis: association with acid peptic diseases and comparison with Helicobacter pylori gastritis.

We analyzed 2 antral and 1 corpus full-thickness random endoscopic gastric mucosal samples obtained from 946 patients with duodenal ulcers (6077 biopsies) and from 281 patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (1794 biopsies). We stained tissue sections with hematoxylin and eosin and Warthin-Starry silver stain and immunostained them with polyclonal antibodies against Helicobacter pylori. Hematoxylin- and eosin-stained sections from 6 patients with Helicobacter heilmannii (18 biopsies) and 23 randomly selected patients with H. pylori (68 biopsies) were evaluated and semiquantitated for the presence of acute inflammation, chronic inflammation, glandular atrophy, intestinal metaplasia, H. pylori, H. heilmannii, lymphoid follicles, or vasodilatation. Additional specimens were obtained for H. pylori culture, a CLO test, and serologic examination. H. heilmannii was detected in 6 (0.49%) of 1227 patients (14 [0.18%] of 7871 biopsies). Of these, 4 (0.42%) of 946 were patients with duodenal ulcers (9 [0.15%] of 6077 biopsies), and 2 (0.71%) of 281 were patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (5 [0.28%] of 1794 biopsies). We found H. heilmannii with hematoxylin and eosin stain, Warthin-Starry stain, and immunoperoxidase stain for H. pylori. Culture for H. pylori was negative in the four patients with duodenal ulcers. The CLO and serologic tests were positive in three of five and five of five patients, respectively. Our results indicate that H. heilmannii, like H. pylori, is associated with peptic ulcer disease (both active and inactive gastritis) and that it preferentially colonizes the gastric antrum. The severity of the H. heilmannii-associated gastritis is less intense and lymphoid aggregates are less common than in H. pylori-associated gastritis. Morphologic detection seems to be the method of choice for detecting H. heilmanni. Immunoperoxidase stain specific for H. pylori also stains H. heilmannii, indicating cross-reacting antigenic epitopes between H. heilmannii and H. pylori.     

Reflux esophagitis or Helicobacter infection? – Diagnostic value of the inflammatory pattern in metaplastic mucosa at the squamocolumnar junction

OBJECTIVES: Metaplastic glandular mucosa with goblet cells at the squamocolumnar junction is induced either by reflux or by Helicobacter infection. We investigated whether the accompanying inflammation may give information about the etiology of these metaplastic changes and whether there are further criteria which are helpful in differentiating Helicobacter-induced vs. reflux-caused metaplasia. METHODS: One hundred and nine patients with intestinal metaplasia diagnosed in biopsies obtained immediately below the Z-line were evaluated. Further biopsies were taken from the gastric body and antrum. Patients were diagnosed as having a normal Z-line, or as showing short tongues or segments of Barrett's esophagus endoscopically. Inflammation was graded according to the updated Sydney-system. Metaplasia was typed using Gomori's-aldehyde-fuchsin-Alcianblue staining. RESULTS: Compared to patients with Barrett's esophagus, the active (p=0.0002) and chronic inflammation (p=0.0004) at the squamocolumnar junction was higher in patients with a normal Z-line and frequently accompanied by lymphoid aggregates (p<0.0001) and regular cardia- (p=0.0044) and/or corpus-type glands (p=0.0004). Pseudogoblet cells were more frequent in Barrett's esophagus (p=0.0159). CONCLUSIONS: The endoscopic aspect of the Z-line, the inflammatory pattern, and the type of glands in biopsies from the squamocolumnar junction, as well as the presence of pseudogoblet cells are helpful tools in distinguishing Barrett's mucosa from Helicobacter-associated intestinal metaplasia.     

Helicobacter pylori associated gastric diseases and lymphoid tissue hyperplasia in gastric antral mucosa

AIM: To investigate the relation between Helicobacter pylori associated gastroduodenal diseases and lymphoid tissue hyperplasia in the antral mucosa and to pursue its evolution after eradication of H pylori. METHODS: Gastric antral biopsy specimens were obtained from 438 patients with H pylori positive gastroduodenal diseases (185 chronic gastritis, 69 gastric ulcer, and 184 duodenal ulcer) and 50 H pylori negative healthy controls. Lymphoid follicles and aggregates were counted and other pathological features were scored according to the updated Sydney system for classification of chronic gastritis. After a course of anti-H pylori treatment, biopsy specimens were obtained at four to six weeks, 12 months, and 24 months in the chronic gastritis patient group. RESULTS: The total prevalence of lymphoid follicles and aggregates in the biopsies was 79.9% (350 of 438; 95% confidence intervals (CI), 0.76 to 0.84). The prevalence and density of lymphoid follicles and aggregates were significantly different in the various gastroduodenal diseases. The highest prevalence (89.9%; 95% CI, 0.83 to 0.97) and density (0.82) of lymphoid follicles and aggregates occurred in patients with gastric ulcers. The lowest prevalence of lymphoid follicles and aggregates was found in patients with chronic gastritis (74.6%; 95% CI, 0.68 to 0.81), and the lowest density of lymphoid follicles and aggregates (0.56) was seen in patients with duodenal ulcers. The prevalence and density of lymphoid follicles and aggregates correlated strongly with the activity and severity of gastric antral mucosal inflammation. The eradication of H pylori resulted in a decrease in the prevalence and density of lymphoid follicles and aggregates. CONCLUSION: The prevalence and density of lymphoid follicles and aggregates in gastric antral mucosal biopsies correlated closely with H pylori infection.     

Chronic urticaria and Helicobacter pylori

Background: Helicobacter pylori (HP) have recently emerged as a novel eliciting factor for chronic urticaria (CU). The possible association between HP and CU has enormous potential, as eradicating HP could cure CU. Aims and Objectives: We conducted a study to assess the prevalence of HP infection and effect of bacterium eradication on skin lesions in patients of chronic idiopathic urticaria (CIU). Settings and Design: Four hundred sixty patients of CU attending the allergy clinic, SMS hospital, Jaipur during the period February 6, 2004, to February 6, 2006, were screened for possible eliciting factors. Patients with CIU were enrolled and others were excluded. Materials and Methods: Sixty-eight patients of CIU and similar number of age and sex matched controls, attending the allergy clinic, SMS Hospital, Jaipur were enrolled in the study. All patients underwent endoscopy with antral biopsy for urease and histopathology to identify HP-associated gastritis. Infected patients were given HP eradication therapy. Eradication of bacterium was confirmed by fecal antigen assay. Subjective response to treatment was judged using chronic urticaria quality-of-life questionnaire (CU-Q 2 oL) while objective response to treatment was judged by need for 'rescue medication' (antihistaminics). Statistical Analysis: Data were analyzed using Chi square and paired't' test for their level of significance. Results: HP associated gastritis was present in 48 (70.58%) patients, out of which 39 (81.25%) patients responded to eradication therapy. Ten (50.00%) patients without HP associated gastritis showed response to symptomatic therapy. Overall 49 (72.05%) patients responded and 19 (27.94%) showed no response. The value of chi2 was 28.571 (P = 0.003), which showed significant association between presence of HP and response to eradication regimen. Conclusion: The response of HP eradication therapy in infected patients of CIU is significant. HP should be included in diagnostic workup of patients with CIU.     

Duodenal bulb biopsy findings for patients with non-ulcer dyspepsia with or without Campylobacter pylori gastritis

Duodenal bulb biopsy specimens from 85 patients with non-ulcer dyspepsia (30 of whom had normal stomachs and 52 of whom had Campylobacter pylori gastritis) were examined for the presence and amount of gastric surface epithelial metaplasia (using both the hematoxylin and eosin stain and the Alcian blue-periodic acid-Schiff method), acute inflammation, and C. pylori (using the Giemsa stain). Gastric metaplasia occurred in the duodenal bulb in 61% of patients with gastric C. pylori and in an identical percentage for those who lacked C. pylori gastritis. For patients with gastric metaplasia, foci of metaplastic cells were seen in 70% of their bulb biopsy fragments. The Alcian blue-periodic acid-Schiff stain was superior to the hematoxylin and eosin stain for detecting gastric metaplasia. Only one of 33 patients without gastric C. pylori had gastritis and duodenitis. Fourteen of 52 (27%) patients with C. pylori gastritis had duodenitis; C. pylori was seen in the duodenal biopsy specimens from 13 of these patients. The organisms were often few, requiring oil immersion microscopy for detection. Each patient with duodenitis had gastric metaplasia, but some of these metaplastic foci were not inflamed. When present in the duodenum of patients with C. pylori gastritis, gastric metaplasia, acute inflammation, and C. pylori are typically patchy. Hence, several biopsy fragments of the duodenal bulb would be required for studies designed to determine the effectiveness of compounds used to treat C. pylori duodenitis.     

Comparison of endoscopic brush cytology with biopsy for detection of Helicobacter pylori in patients with gastroduodenal diseases

Upper GI endoscopy was performed in 50 adult patients attending the gastroenterology OPD with gastroduodenal diseases. Gastric antral mucosal brushings were taken for cytological evaluation and urea broth test followed by antral biopsy. The slides prepared were stained with Wright Giemsa (WG), Hema toxylin & Eosin (H&E) and Papanicolaou (Pap). Brush Cytology Smears were compared with biopsy sections for detection of Helicobacter pylori and the staining techniques were evaluated to see which stain was easiest to perform and interpret on routine basis. H&E stained sections were examined for histomorphological parameters associated with H. pylori infection. Brush cytology was rapid and simple with observed sensitivity of 90% and specificity of 100%. On evaluating the various stains, M.B. and W.G. were found to the rapid and easy to perform and the bacteria stood out very well against the background. Of the histomorphological parameters studied, presence of actively and lymphoid aggregates and absence of intestinal metaplasia correlated positively with the presence of the bacteria. Cytological brushing urea broth test was not very sensitive (55.2%) and specific (51%) for detection of the bacteria.     

Reliability of rectal biopsy in distinguishing between chronic inflammatory bowel disease and acute self-limiting colitis

Aims : In order to assess the validity of previously proposed criteria for the differentiation of chronic inflammatory bowel disease (CIBD) from acute self-limiting colitis (ASLC) all rectal biopsies were reported by a single histopathologist with a long-term gastrointestinal interest over a 4.5-year period. Methods and results : The presence or absence of distorted crypt architecture, increased lymphocytes and plasma cells, villous mucosal architecture, granulomata, basal lymphoid aggregates, basal giant cells and Paneth cell metaplasia was noted for each biopsy. The definite presence of any of the above features, with the exception of intramucosal granulomata, was regarded as indicative of CIBD. Eighteen months later all available case notes were examined and the presenting clinical symptoms and working clinical diagnosis extracted. The final diagnosis, histopathological diagnosis and the presence or absence of any of the above histopathological features were correlated and the positive predictive value of each histopathological feature was calculated. A correct diagnosis of either CIBD or ASLC was made in 80 of 84 and 29 of 31 cases, respectively. Conclusions : Villous mucosal architecture and Paneth cell metaplasia were found to be specific features of CIBD. Distorted crypt architecture, basal lymphoid aggregates and plasma cell infiltration of the lamina propria were also useful features but strict definition of these features is required and discussed. Intramucosal epithelioid granulomas were identified in eight cases of CIBD and four cases of ASLC. In association with ruptured crypts intramucosal granulomas are not specific features of Crohn's colitis.     

Helicobacter pylori in areas of gastric metaplasia in the gallbladder and isolation of H. pylori DNA from gallstones

AIMS: To assess if the areas of gastric metaplasia in the gallbladder are colonised by Helicobacter pylori and to conduct a molecular study of gallstones for presence of H. pylori DNA. METHODS: Sections from 111 gallbladders with evidence of gastric metaplasia on H&E and Alcian blue-periodic acid-Schiff (pH 2.5) stain were stained with Loeffler's methylene blue and Warthin Starry stain for demonstration of H. pylori. Presence of H. pylori was confirmed by immunohistochemistry. Formalin fixed mucosal tissues and gallstones from 11 cases showing heavy colonisation were subjected to molecular analysis. RESULTS: Helicobacter pylori was present in 50 of 111 (45%) sections with gastric metaplasia. Areas adjacent to gastric metaplasia in gallbladder showed acute inflammation (6%) and lymphoid follicle formation in 58% of cases with H. pylori that were significantly higher than those seen in sections without H. pylori. In molecular study, 8 of 11 gallstones showed 16S rDNA. Amplification of material from one stone showed positivity for atpA, efp, mutY, ppa, trpC, UreI and vacA genes. Phylogenetic affiliation study of the isolates indicated that H. pylori sequence from the gallstones clustered with Indian strains of H. pylori. No considerable difference was observed in phylogenetic affiliations of eight stones studied. CONCLUSION: H. pylori colonises areas of gastric metaplasia in gallbladder producing histological changes similar to those seen in gastric mucosa. Isolation of H. pylori DNA from gallstones further support its presence in the gallbladder.     

Laboratory signs of acute or recent cytomegalovirus infection are common in cirrhosis of the liver

Human cytomegalovirus (CMV) is an ubiquitous pathogen that can cause severe and often fatal infections in immunocompromised patients. Patients with cirrhosis often show various degrees of impaired cellular immunity that could lead to acute CMV reactivation. The aim of the present study was to determine whether laboratory findings of active CMV infections are common in patients with cirrhosis. Fifty-five patients with cirrhosis were studied for acute CMV infection by virological (antigenemia and quantitative polymerase chain reaction in polymorphonuclear leukocytes) and serological (detection of anti-CMV IgM by immunoblot) methods. The same tests were carried out on 50 blood donors and on 20 chronic hepatitis patients, considered as control populations. Acute or recent CMV infection had occurred in 31 (56%) of 55 patients with cirrhosis, whereas only 1 out of 20 (5%) patients with chronic non-cirrhotic liver disease and none of the 50 blood donors had laboratory signs of active CMV infection. The difference between patients with cirrhosis and the control groups was significant (P < 0.001, chi(2) test). CMV in patients with cirrhosis was not related to age, gender, hepatitis C virus infection or hepatocellular carcinoma. There was no significant correlation between impairment of liver function and the presence of active CMV infection. Patients with cirrhosis should be considered at risk for CMV infection, that seems to be mild and asymptomatic.     

Lymphoid aggregates in gastric biopsies: relationship to other mucosal lesions

The purpose of this study is to estimate the prevalence of lymphocyte aggregates (precursor of MALT lymphomas) in gastric mucosal biopsies and to associate gastric lymphoid tissue with the age of patients, Helicobacter-associated gastritis and other gastric mucosal pathology. A consecutive series of gastric mucosal samples from 150 children and 256 adults were assessed for the presence of lymphoid aggregates as well as morphological characteristics, Helicobacter pylori status, signs of gastritis, mucosal atrophy and lymphoepithelial lesions. Fifteen selected samples with prominent lymphoid aggregates and 10 controls were examined immunohistochemically for the immunoglobulins A, G, M, lymphocytes B and T, clonality of B cell population, atypical lymphocytes and Epstein-Barr virus (EBV) antigen. There was an increase of H. pylori infection and mucosal lymphoid aggregates (MALT) rates in parallel with the increasing age of patients noted in the histological assessment of the mucosal samples. A close association of lymphoid aggregates with H. pylori infection and prominent active gastritis was found, but in adults with chronic non-active, particularly atrophic gastritis this association became weaker. No morphological and immunohistochemical signs of MALT lymphoma were present. Lymphoid aggregates in children were larger, with follicles, but less numerous and tended to be located in the intermediate and deeper parts of the gastric mucosa. Immunohistochemical studies showed an increase of IgA, IgM and lymphocytes T in the deeper part of the lamina propria in H. pylori-associated gastritis and lymphocyte T accumulation in the periphery of the lymphoid follicles. No evidence of monoclonality, CD31 positive lymphocytes or EBV antigen was detected. Lymphoid aggregates are related, but not exclusively, to H. pylori infection. Their detection rates achieve a peak in young adults with H. pylori infection. Lymphocytic aggregates are also present in chronic atrophic gastritis without H. pylori infection and may relate to autoimmune inflammatory response to other factors.