消化性溃疡幽门螺杆菌(Hp)清除前后血Hp抗体、PG、GAS 变化的研究

幽门螺杆菌(Helicobacter pylori,Hp)阳性消化性溃疡患者在Hp清除前后血清抗Hp-IgG,抗Hp-IgM,胃蛋白酶原(Pep-sinogen,PG)和胃泌素(Gastrin,GAS)水平如何?奥美拉唑,硫糖铝,罗红霉素治疗Hp感染的消化性溃疡的效果如何?本课题对上述问题进行了研究。1材料与方法1.1一般资料病例选     

Molecular forms of gastrin in peptic ulcer: comparison of serum and tissue concentrations of G17 and G34 in gastric and duodenal ulcer subjects

We have studied the relationships between the main molecular forms of gastrin (G17 and G34) in the serum, antral and duodenal mucosa of duodenal (DU) and gastric (GU) ulcer patients. Fasting serum G17 was similar in both DU and GU (about 6 pmol/l) and in both groups increased about three-fold with feeding. In contrast, basal serum G34 was significantly higher in GU (29 pmol/l) than in DU (12 pmol/l) and the peak post prandial increase over basal of G34 was also higher in GU (57 pmol/l) compared with DU (10 pmol/l). In sharp contrast, in the same groups of DU and GU patients mean total antral gastrin concentrations were similar (about 12 nmol/g), and in both groups 95% of antral gastrin was G17, most of the remainder being G34. In both groups total duodenal gastrin concentrations were about 20% those in antral mucosa and about 70% of duodenal gastrin was attributable to G34. The higher serum G34 in GU could therefore be explained by increased secretion of duodenal gastrin, but further work is needed to examine whether there might also be preferential secretion of antral G34 in GU, or a difference in the metabolism (or volume of distribution) of gastrin variants in GU and DU.     

Molecular forms of gastrin in peptic ulcer: comparison of serum and tissue concentrations of G17 and G34 in gastric and duodenal ulcer subjects

Abstract We have studied the relationships between the main molecular forms of gastrin (G17 and G34) in the serum, antral and duodenal mucosa of duodenal (DU) and gastric (GU) ulcer patients. Fasting serum G17 was similar in both DU and GU (about 6 pmol/1) and in both groups increased about three-fold with feeding. In contrast, basal serum G34 was significantly higher in GU (29 pmol/1) than in DU (12 pmol/1) and the peak post prandial increase over basal of G34 was also higher in GU (57 pmol/1) compared with DU (10 pmol/1). In sharp contrast, in the same groups of DU and GU patients mean total antral gastrin concentrations were similar (about 12 nmol/g), and in both groups 95% of antral gastrin was G17, most of the remainder being G34. In both groups total duodenal gastrin concentrations were about 20% those in antral mucosa and about 70% of duodenal gastrin was attributable to G34. The higher serum G34 in GU could therefore be explained by increased secretion of duodenal gastrin, but further work is needed to examine whether there might also be preferential secretion of antral G34 in GU, or a difference in the metabolism (or volume of distribution) of gastrin variants in GU and DU.     

Strategies for peptic ulcer healing after 1 week proton pump inhibitor-based triple Helicobacter pylori eradication therapy in Japanese patients: differences of gastric ulcers and duodenal ulcers

Helicobacter pylori (H. pylori) eradication therapy alone is insufficient to ensure healing of large ulcers with H. pylori-positive gastric ulcer (GU). The question of what is the optimum antiulcer treatment following H. pylori eradication therapy has not been fully elucidated. Furthermore, the ulcer healing effects of eradication therapy itself with H. pylori-positive duodenal ulcer (DU) have not been investigated. In GU study, the eradication therapy + proton pump inhibitor (PPI) group (group A) were administered eradication therapy followed by 7 weeks of a PPI, and the eradication therapy + gastroprotective drug (GP) group (group B) eradication therapy followed by 7 weeks of a GP. In DU study, the eradication therapy + PPI group (group C) were administered eradication therapy followed by 5 weeks of a PPI, and the eradication therapy only group (group D) was eradication therapy alone. In GU study, healing rates for ulcer of ≥15 mm in diameter were significant greater in the group A. In DU study, high healing rates were seen both the group C and D. In conclusion, a PPI could significantly heal GU than a GP after eradication therapy in GU. Meanwhile, the eradication alone is sufficient for DU.     

老年人消化性溃疡166例胃镜分析

目的了解我院老年人消化性溃疡（Pu）发病特点。方法分析166例老年人消化性溃疡胃镜报告结果。结果老年人PU的检出率为10.78％,男女之比为4.35：1;胃溃疡（GU）占62.65％,十二指肠溃疡（DU）占30.72％,GU与Du之比为2.08：1,复合性溃疡占6.62％,多发性溃疡占24.1％。结论老年人PU的患者男性多于女性,Gu多于DU,GU的好发部位是胃窦和胃角,DU的好发部位是十二指肠球前壁;PU的幽门螺杆菌（Hp）感染率为81.93％。     

Enzyme-linked immunosorbent assays for serum pepsinogens I and II using monoclonal antibodies--with data on peptic ulcer and gastric cancer

Serum pepsinogen I and pepsinogen II levels in 369 healthy controls, 38 duodenal ulcer, 30 gastric ulcer and 46 stomach cancer including 21 early and 25 advanced gastric cancer patients were measured by enzyme-linked immunosorbent assays using pepsin moiety-reacting monoclonal antibodies to pepsinogens I and II. Serum pepsinogen I and pepsinogen II levels were higher in the duodenal and gastric ulcer groups than in the control. Although there was no significant difference in serum pepsinogen II between stomach cancer and control, serum pepsinogen I was significantly lower in the former than in the latter and also in advanced gastric cancer than in early gastric cancer. A specific negative correlation of serum pepsinogen I with patient age was observed in stomach cancer but not in peptic ulcer or control groups. Receiver operating characteristic analysis was performed and indicated that serum pepsinogen I, compared with serum pepsinogen II or the pepsinogen I/pepsinogen II ratio, is the most effective marker for stomach cancer.     

Enzyme-linked immunosorbent assay of serum pepsinogen I

A hybridoma monoclonal antibody against human pepsinogen I was used to develop an enzyme-linked immunosorbent assay for pepsinogen I in serum. In the two-step competitive procedure using antimouse immunoglobulin F(ab')2 fragment coupled to alkaline phosphatase, the measurable assay range was 8-256 micrograms/l. No cross-reactivity with rat pepsinogen 1, human pepsinogen II, gastrin I, bombesin, somatostatin and peptide YY was shown. However, there was slight cross-reactivity (0.09%) with porcine pepsinogen. The coefficients of variation within and between series were 7.6% and 13.0%. This enzyme-linked immunosorbent assay for serum pepsinogen I correlated positively with radioimmunoassay (r = 0.87, n = 92). The concentration range of serum pepsinogen I in 354 healthy controls was 15-100 micrograms/l with a lognormal distribution. Serum pepsinogen I levels were significantly higher in the subjects who developed active duodenal ulcer or active gastric ulcer, but significantly lower in those who had gastric cancer, than in control subjects.     

甘草泻心汤治疗脾胃气虚型胃溃疡患者的临床效果

目的 探讨甘草泻心汤治疗脾胃气虚型胃溃疡患者的临床效果.方法 选取2019年3月至2020年3月收治的108例脾胃气虚型胃溃疡患者,随机将其分为对照组和观察组,每组54例.对照组给予奥美拉唑胶囊治疗,观察组在对照组基础上采用甘草泻心汤治疗.比较两组的治疗效果.结果 治疗后,两组的中医症状评分均降低,且观察组低于对照组(...     

胃肠相关疾病中幽门螺杆菌感染与胃黏膜白细胞介素-8含量的关系

目的　研究各种胃肠疾病幽门螺杆菌 (Hp)感染情况及其与胃黏膜白细胞介素 8(IL 8)含量的关系。 方法　采用双抗体夹心酶联免疫吸附试验检测 10 2例Hp感染与非感染患者胃黏膜匀浆上清液中的白细胞介素 8含量 ,其中胃镜下黏膜正常者 5例 ,单纯性慢性胃炎 (CG) 2 5例 ,十二指肠球部溃疡 (DU) 36例 ,胃溃疡 (GU) 15例 ,胃癌(Gca) 2 1例。结果　 10 2例中有 6 0例感染了Hp(5 8.8% ) ,其中以十二指肠球部溃疡组Hp感染率最高 (88.9% ) ,明显高于其他组 (均P <0 .0 5 ) ,Hp感染者胃黏膜IL 8含量明显高于非Hp感染者 (P <0 .0 1) ;GU、Gca、DU、CG组胃黏膜IL 8含量均明显高于黏膜正常组 (均P <0 .0 5 ) ,GU、Gca、DU组又明显高于CG组 (均P <0 .0 5 ) ,而GU、Gca、DU组间比较差异无统计学意义 (均P >0 .0 5 ) ;同时发现中度胃炎黏膜IL 8含量明显高于轻度胃炎 ,活动性胃炎又明显高于非活动性胃炎 (均P <0 .0 5 )。结论　Hp感染者与非感染者胃黏膜IL 8含量存在差异 ,疾病组胃黏膜IL 8含量明显高于正常黏膜 ,并与胃炎炎症程度和活动性有一定相关性 ,推测IL 8可能参与了Hp相关性胃炎胃黏膜损伤机制     

老年人消化性溃疡与慢性萎缩性胃炎的相关性研究

目的研究老年人消化性溃疡与慢性萎缩性胃炎的相关性。方法对十二指肠溃疡（DU）、胃溃疡（GU）和复合性溃疡（CU）的老年患者胃窦、胃窦胃体交界处和胃体黏膜以及慢性胃炎（CG）患者胃窦黏膜活检标本进行组织学检查,统计各自胃黏膜的萎缩、肠化生、慢性炎症、活动性和幽门螺杆菌（Hp）感染的发生率。结果 DU患者胃窦、胃窦胃体交界处和胃体黏膜的萎缩发生率分别为54.0%、8.0%和16.0%,肠化生发生率分别为19.0%、6.0%和4.0%。其胃窦黏膜肠化生的发生率明显低于相应的GU、CU或CG者。3种消化性溃疡和CG患者均存在胃窦部慢性炎症,且老年消化性溃疡患者胃体部炎症的发生率较高,其胃炎活动性以胃窦部为主,且均较CG者高。结论老年人消化性溃疡均可有胃窦部灶性萎缩和肠化生发生,但DU胃窦黏膜肠化发生率最低,这可能是老年DU患者罹患胃癌危险性较低的原因之一。     

Geographical Pathology of Helicobacter pylori Infection: Is There More than One Gastritis?

Helicobacter pylori is the aetiological agent of chronic gastritis and a major causative factor in duodenal and gastric peptic ulcer disease; a strong association also exists with gastric cancer and primary gastric lymphoma. The prevalence of infection in adults ranges from less than 15% in developed countries to virtually 100% in less developed areas. If H. pylori infection alone was responsible for the development of gastritis, peptic ulcer disease, gastric carcinoma and primary gastric lymphoma, one would expect the frequency of all these conditions to parallel closely the prevalence of H. pylori infection. This is clearly not the case: therefore, genetic, environmental and cultural factors must act in concert with H. pylori to induce different outcomes of the infection.

This paper outlines the geographic approach to the study of disease and discusses the possible application of this methodology to the inquiry into the relationship between H. pylori, atrophic gastritis and gastric cancer. Preliminary results of a study showing great variation in the prevalence of intestinal metaplasia in duodenal ulcer patients from different geographic origin are presented and briefly discussed.     

Potentialities of a serological method in diagnosis of atrophic gastritis

AIM: To analyse diagnostic potential of "serological gastrobiopsy" in patients with various gastroduodenal diseases. MATERIAL AND METHODS: A total of 244 patients with gastroduodenal pathology have been examined. The diagnoses made morphologically were compared with those made by the serological method. The diagnosis of duodenal ulcer, gastric ulcer, atrophic gastritis, nonatrophic gastritis was made in 155, 31, 43 and 15 patients, respectively. The type of chronic gastritis was diagnosed by the levels of gastrin-17, pepsinogen I, pepsinogen II and antibodies to Helicobacter pylori in blood serum. The diagnoses made serologically were compared with those made morphologically. RESULTS: The highest accuracy of a serological diagnosis of mucosal atrophy of the antral stomach was observed in gastric ulcer (80.6%) and duodenal ulcer (71.6%) in high sensitivity and low specificity. The accuracy of the diagnosis of gastric body mucosa atrophy in atrophic gastritis was 60.5%, in gastric ulcer--51.6%, in duodenal ulcer 58.7% in high specificity and low sensitivity. Serological diagnosis of gastric atrophy was accurate in 71.7%. In weak morphological picture of gastric body atrophy false negative serological diagnosis is possible. No false positive results occurred in diagnosis of gastric body mucosal atrophy (specificity 100%). A negative correlation was found between the severity of gastric body atrophy and pepsinogen I serum level (r = -0.380), pepsinogen I to pepsinogen II in blood serum (r = -0.392). No differences were revealed in gastrin-17 levels in the serum in different atrophy severity in the antral mucosa. CONCLUSION: "Serological gastrobiopsy"provides satisfactory accuracy of atrophic gastritis diagnosis in gastroduodenal diseases.     

Serum gastrin concentration and changes in G and D cell densities in gastric antrum in children with chronic gastritis

Background: Elevated gastrin concentration leading to gastritis is explained as the effect of change in the density of D and G cells. The aim of the study was to determine and compare fasting serum gastrin concentrations, G and D cell densities in gastric antrum mucosa in children with chronic gastritis and in children with no gastritis or Helicobacter pylori infection. Material and Methods: A total of 184 patients aged 6–18 years, with chronic abdominal pain underwent endoscopic examination. We created three groups: I – patients with chronic gastritis and H. pylori infection; II – patients with chronic gastritis but no H. pylori infection; III – patients with neither gastric mucosal abnormalities nor H. pylori infection. G and D cell densities were determined in the biopsy specimens (using Rbα H Gastrin & Somatostatin antibodies). Fasting serum gastrin concentrations were measured using a Beckmann gamma‐counter and a GASK‐PR kit. Results: The mean serum gastrin concentration in group I was higher when compared with group II (p = 0.04) and group III (p = 0.019). No statistically significant differences were found between groups II and III (p = 0.91). There were no statistically significant differences in G and D cell densities between groups. Conclusion: The mean G/D cell ratios in groups I and III were almost identical. The mean fasting serum gastrin concentration was higher in children with both chronic gastritis and H. pylori infection compared with patients without infection or without antral inflammation. No difference in the G cell density or D cell density in children was found, regardless of the presence or absence of gastritis or H. pylori infection.     

Pepsinogens, pepsins, and peptic ulcer

The role of pepsin in the pathogenesis of peptic ulcer has been the subject of intense study and debate for many years. Two difficulties inherent in distinguishing between the role of acid alone vs acid and pepsin are that a) acid-containing gastric juice always contains pepsin, and, b) that hydrogen ion concentration (pH) is a major determinant of the activity of pepsin. However, studies in animal models of peptic ulcer indicate clearly that pepsin, in combination with acid, produces much more severe and more extensive mucosal damage than acid alone. Recent interest in pepsin and its precursor, pepsinogen, has stemmed from the finding that each is remarkably heterogeneous, and that the heterogeneity has a genetic basis. Results of studies using radioimmunoassays specific for the 2 major forms of pepsinogen, pepsinogen I and pepsinogen II, have shown that serum levels of pepsinogen I and pepsinogen II, and the ratio of pepsinogen I to pepsinogen II, can be used as noninvasive probes of gastric mucosal structure and function, indicators of the genetics and heterogeneity of duodenal ulcer, and as markers of increased risk for duodenal ulcer and gastric ulcer.     

幽门螺杆菌感染与十二指肠胃上皮化生及胃泌素之间关系的研究

目的　通过对幽门螺杆菌 (Hp)感染与十二指肠胃上皮化生 (DGM )及胃泌素 (GAS)关系的研究 ,探讨Hp导致十二指肠溃疡 (DU)的发病机制。 方法　检测了 12 1例患者内镜、病理、Hp感染及DGM情况。同时测定了其中 6 6例患者的血清GAS浓度。结果　球部有溃疡者 ,胃及球部Hp检出率均显著高于球部无溃疡者 (P <0 .0 0 1) ;但球部Hp检出率在DU与CU、GU与CG之间无差别 (P >0 .0 5 ) ;球部有溃疡者DGM的检出率显著高于球部无溃疡者 (P <0 .0 0 1) ,且前者的DGM程度更重 (P <0 .0 0 1) ,但在DU与CU、GU与CG之间无差别 (P >0 .0 5 ) ;胃部Hp阳性者DGM的发生率 (73.0 % )显著高于胃部Hp阴性者 (37.5 % ,P <0 .0 0 1) ,DGM( )及以上者在Hp阳性组发生率 (47.2 % )也高于Hp阴性组 (2 1.9% ,P <0 .0 5 ) ;Hp阳性者血清GAS浓度显著高于Hp阴性者 (P <0 .0 1) ,但血清GAS浓度在Hp阳性的DU、CU、GU与CG之间无差别(P >0 .0 5 ) ;有DGM者血清GAS浓度也显著高于无DGM者 (P <0 .0 1) ,且随着DGM程度的加重 ,血清GAS浓度早递增趋势 ,两者呈正相关 (rs=0 .4 2 ,P <0 .0 1)。结论　Hp感染特别是十二指肠Hp定植及DGM是影响DU发生、发展的两大危险因素。Hp可影响DGM的发生与发展 ,其中部分可能通过增加血清GAS分泌的作用。     

Genotyping of Helicobacter pylori strains from gastric biopsies by multiplex polymerase chain reaction. How advantageous is it?

Recent application of multiplex polymerase chain reaction (PCR) for genotyping Helicobacter pylori direct from biopsies revealed variable results (detection of amplicons from DNA extracted by boiling biopsies, variable size amplicons and deletions, uniform intensity of amplicon bands). We aimed to look at how applicable the technique is for determining cagA and vacA genotypes and to correlate the results with the severity of the disease. H. pylori strains from 52 patients (35 duodenal ulcers [DUs], 7 gastric ulcers [GUs], 10 gastritis) were included. Three antral biopsies were obtained for Campylobacter-like organism (CLO) and PCR. Primers for cagA, vacA s1s2, and m1m2 alleles were used. No PCR amplicons were detected from boiling biopsies; thus, DNA was extracted by QIAamp kit. H. pylori was positive in 84.6% of the patients (85.7% DU, 100% GU, and 70% gastritis). The cagA gene was detected in 86.6% DU, 71.4% GU, and 57.0% gastritis patients. The vacA allelic distribution among cagA-positive strains was 80.7% s1m1 in DU and 60.0% in GU patients, whereas 75.0% of gastritis had s1m2. No variability in the amplicon sizes was found, and the intensity of the amplicon bands was not uniform. A deleted band of approximately 420 bp below the m1 band was detected in strains from 2 DU and 1 GU patients. Although the multiplex PCR is a rapid and an effective tool for detecting several genes in a single-step system, one has to adjust for optimization of the technique when genotyping H. pylori direct from biopsies. A significant association was found between the cagA-positive vacA-s1m1 genotype and peptic ulcers.     

Are tryptase and cathepsin D related toHelicobacter pylori infection and mucosal gastrin in peptic ulcer?

The pathogenesis of peptic ulcer is a complex phenomenon and several factors are thought to be involved in this process. Among others,Helicobacter pylori infection, hypergastrinaemia and some proteases seem to play an essential role in inducing peptic ulceration. We investigated whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (a lysosomal hydrolase which seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked toHelicobacter pylori infection and mucosal content of gastrin. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer and 11 with duodenitis. Tryptase and cathepsin D were measured in mucosal biopsy specimens (body and antrum of the stomach and duodenum) using IRMA methods. Gastrin was assayed in the antral mucosa by means of a RIA method.Helicobacter pylori infection was histologically evaluated (Giemsa). Tryptase and cathepsin D levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. The mucosal content of cathepsin D, but not that of tryptase, was associated withHelicobacter pylori infection. Tryptase, on the other hand, was related to gastrin content. No correlation was found between the two enzymes. It is concluded that tryptase and cathepsin D probably reflect different pathophysiological modifications in ulcer disease. Cathepsin D seems to be mainly related to the phlogistic reaction of the mucosa toHelicobacter pylori infection; tryptase may reflect and indirect link between the action of gastrin and the function of mast cells.     

HP根治前后胃粘膜Gas、SS、SP变化及G、D、EC_1细胞图像定量研究

该研究旨在探讨HP感染的慢性胃炎和消化性溃疡患者HP根治前后胃粘膜中胃肠激素Gas、SS、SP及G、D、EC1细胞变化和其相关性。方法 :1997年 3月～ 1999年 12月对 10 2例HP感染的病人 ,HP根治前后分别用放射免疫法及免疫组化染色图像定量分析Gas、SS、SP含量和G、D、EC1细胞密度、灰度。结果 :HP阳性的三组病人经药物治疗根治后胃粘膜Gas含量均较治疗前明显降低 (P <0 .0 1) ,SS、SP含量较治疗前升高 (P<0 .0 1,P <0 .0 5 )。图像定量分析示HP根治前后胃粘膜G、D、EC1细胞密度显著降低 (P <0 .0 5 ) ,D、EC1细胞灰度增加 (P <0 .0 5 )。结论 :三组病人HP根除后胃粘膜Gas减少 ,G细胞灰度降低 ,SS、SP升高 ,D、EC1细胞灰度增加 ,细胞分泌颗粒变化与粘膜相应激素变化呈正相关。提示HP感染干扰了这些激素分泌释放的调控 ,可能是HP相关性胃炎和消化性溃疡的发病机制之一。根除HP后SS、SP升高 ,Gas降低纠正HP感染所致的这些激素分泌释放紊乱 ,可能是HP根除后溃疡复发率降低的原因之一。在HP根除前SP ,EC1细胞灰度降低 ,根除后升高 ,提示SP抑制胃泌素分泌释放 ,而对生长抑素无抑制作用 ,具有胃粘膜保护功能。     

Time course changes in morphological and functional characteristics of gastric mucosa after eradication of Helicobacter pylori in duodenal ulcers

AIM: To study trends in morphological changes of gastric mucosa (GM) and its functional characteristics (serum gastrin-17, pepsinogens I and II) in eradication of Helicobacter pylori (HP) in patients with duodenal ulcer (DU). MATERIAL AND METHODS: HP infection was detected with a rapid urease test, morphological study of gastrobiopsies and polymerase chain reaction in 59 patients with DU. The results of HP eradication were assessed two months after the treatment. Morphological study of gastrobiopsies, assays for gastrin-17, pepsinogens I and II in blood serum were made before the treatment and one year after HP eradication. RESULTS: By the results of eradication two groups were formed: with effective eradication and uneffective eradication of H. pylori. Examination of GM one year after successful H. pylori eradication in DU patients GM inflammation relieved: reduction in polymorphonuclear (by 42.6%), mononuclear (by 29.3%) infiltration and number of lymphocytic follicules (16.8-fold). GM atrophy decreased by 47.8%. In patients with uneffective eradication the above positive changes were not registered. After H. pylori eradication, serum gastrin-17 lowered by 46. 7%, pepsinogen I--by 30.5%, pepsinogen II--by 36.9%. In uneffective eradication this decrease did not occur. CONCLUSION: H. pylori eradication leads to positive changes in morphological and functional indices reflecting GM condition.