糖尿病患者血清胃泌素异常及临床意义

作者对８５例糖尿病患者和３４例正常人进行了血清胃泌素测定。结果显示：糖尿病人空腹及餐后血清胃泌素值明显高于正常人，伴有植物神经病变者较无植物神经病变者亦明显升高。糖尿病人常有胃泌素分泌异常，其主要与胃植物神经功能障碍有关，可作为后者存在的标志之一。     

胃黏膜癌变过程中血清胃泌素水平的变化及其影响因素的研究

目的探讨常见因素对血清胃泌素水平的影响,揭示血清胃泌素在胃癌及其癌前疾病诊断中的价值。方法利用ELISA方法检测2002年6月至2004年7月收集的3906份血清样品的血清胃泌素水平。结果≥60岁组的血清胃泌素水平显著高于其他年龄组。患有胃窦疾病患者的血清胃泌素水平显著高于患有胃体疾病患者。HP阳性组的血清胃泌素水平显著高于HP阴性组。由正常者经浅表性胃炎至胃糜烂或溃疡,血清胃泌素水平进行性升高,由胃糜烂或溃疡至萎缩性胃炎有所下降;由萎缩性胃炎至不典型增生,血清胃泌素水平明显升高;由不典型增生至胃癌,血清胃泌素水平明显降低。胃癌的血清胃泌素水平显著低于其他胃疾病组。结论60岁以后,老年人的血清胃泌素水平已开始倾向于升高。胃部疾病的发生部位是影响血清胃泌素水平的一个重要因素。HP可使感染者的血清胃泌素水平升高。在胃癌前期,血清胃泌素水平可随疾病的发展而呈波动性递增,至胃癌形成时明显降低;血清胃泌素是鉴别胃良恶性疾病的一个较好的标志物。     

甲状腺功能亢进症的高胃泌素血症

本文测定了35例甲亢患者治疗前、后的血清胃泌素水平。甲亢患者治疗前空腹血清胃泌素为265.17±143.17pg/ml,比正常人显著升高。经治疗,甲状腺功能恢复到正常水平之后,再次测定空腹血清胃泌素为115.54±45.86pg/ml,较治疗前明显降低(P<0.01)。但仍显著较正常人高(P<0.01)。     

胃泌素与尿毒症间关系的研讨

为探讨血清胃泌素与尿毒症间的关系,本文综合文献对下述问题作了阐述:①尿毒症患者血清胃泌素水平升高是由于肾对胃泌素灭活能力减弱;胃内盐酸缺如;以及往往合并尿毒症性胃炎。②血清胃泌素升高与血清肌酐间存在负相关。③尿毒症时胃酸分泌过少可诱发胃泌素分泌增加。作者还提出通过肾移植,血液透析、口服甲氰咪胍及限制蛋白饮食等方法可改善尿毒症时的高胃泌素血症,从而减轻消化道症状。     

血清胃泌素17在慢性萎缩性胃炎患者中的表达水平及意义

目的探讨血清胃泌素17(G-17)在慢性萎缩性胃炎中的变化规律。方法根据病理诊断将198例病例分为慢性非萎缩性胃炎96例,慢性萎缩性胃炎组102例。采用酶联免疫分析(ELISA)方法检测血清G-17水平。结果慢性萎缩性胃炎组与非萎缩性胃炎组相比,G-17水平显著升高(P0.05)。胃窦萎缩组及全胃萎缩组随萎缩程度的加重血清G-17水平进行性下降(P0.01,P0.05),而胃体萎缩组血清G-17呈升高趋势(P0.01)。结论血清G-17水平可作为慢性萎缩性胃炎筛查的血清学指标,适合大规模人群普查。     

西米替丁对急性胰腺炎的影响及机制探讨

目的:探讨西米替丁治疗急性胰腺炎的利弊及其机制。方法:对156例急性水肿型胰腺炎患者进行传统疗法与传统疗法加西米替丁的治疗对照研究,并检测了50例消化性溃疡患者服用西米替丁前后的血清胃泌素及24例急性胰腺炎患者急性发病期的血清胃泌素。结果西米替丁组腹痛消失时间、血尿淀粉酶下降时间、住院时间均较对照组明显延长。另有40.16％(51/127)的患者出现病情反复。溃疡病患者服用西米替丁后血清胃泌素明显升高。急性胰腺炎发病期血清胃泌素明显高于正常,发病当日超过正常值4～10余倍。结论:急性胰腺炎的发病可能与血清胃泌素过高有关,西米替丁虽能降低胃酸,但因反馈性升高血清胃泌素而不利于急性胰腺炎的恢复。     

三甲丙咪嗉对健康学生胃分泌功能和血清胃泌素浓度的作用

本文报告11例健康年轻学生作胃分泌功能检查和血清胃泌素浓度测定,研究三甲丙咪嗪(Trimipramine)对正常人胃分泌功能的影响。除测定胃基础分泌外,分别用五肽胃泌素(每45分钟逐级增加剂量为0.02,0.10,0.50,2.50mcg/kg体重/小时)、胰岛素(0.15u/kg体重静注)和试验餐作为刺激剂,每15分钟收集胃液标本一次,测定胃液分泌量和其中H~+、Cl~-、K~+、Na~+、Ca~(++)、Mg~(++)、无机磷以及内因子的浓度和排泌量,同时每45分钟观察血压、脉搏的变化,有无副作用,和采取血标本以测定血糖、血清胃泌素的浓度。6名学生使用三甲丙咪嗪25mg/小时,以五肽胃泌素或试验餐为刺激剂;另5名则予以三甲丙咪嗪15mg/小时,用胰岛素作刺激剂。     

胃炎

文內综合上海地区部分医疗单位对慢性萎缩性胃炎(C A G)的一些研究资料,发现病因与吸烟、饮食不规则、胆汁回流、饮浓茶等有关。该组患者经病理学研究、胃酸分泌功能检查、空腹及试餐后血清胃泌素测定、血清壁细胞抗体(P C A)测定等项检查,认为上海地区的CAG有以下特点:     

消化系统疾病

914061 162例上胃肠道疾病血清胃泌素测定/张宽学…//西安医科大学学报-1991,12(2).-157～158 检测健康成人30例,上胃肠道疾病162例.结果:胃溃疡11例,十二指肠球部渍疡18例,萎缩性胃炎17例,血清胃泌素浓度与正常对照组无明显差异。而胃癌有10例及浅表性胃炎96例,血清胃泌素值明显增高(P<0.01)。上述疾病血清胃泌素变化较大,在诊     

长期服药精神分裂症患者内镜成像与血清胃泌素特点

目的:探讨精神分裂症患者长期服药后内镜下成像与血清胃泌素特点方法:将自贡市第五人民医院精神科收治的60例有消化系统疾病的精神分裂患者按其服药疗程分为A组和C组各30例,自贡市第五人民医院综合科收治的长期服药的30例糖尿病或高血压患者分为B组.分别对其进行无痛胃镜检查和空腹血清胃泌素检测.结果:C组胆汁反流性胃炎、胃储留34.37%和30.21%明显高于A、B组(P0.05),差异有显著性.C组血清胃泌素明显低于A组与B组(78.43 pg/mL±10.68 pg/mL vs 88.72pg/mL±11.35 pg/mL,90.14 pg/mL±9.57 pg/mL)(P0.05),差异有显著性.结论:精神分裂症患者长期服药后易发生胆汁反流性胃炎、胃潴留,血清胃泌素降低.     

Effect of bombesin on extragastric gastrin in man

The effect of a protein test meal and a bombesin infusion on extragastric gastrin levels was studied in patients with truncal vagotomy, antrectomy, and gastroduodenostomy or gastrojejunostomy and in patients with total gastrectomy. In patients with vagotomy, antrectomy, and gastroduodenostomy and in patients with total gastrectomy the gastrin levels were raised by 33% and 35%, respectively, from basal after test meal, while during BBS infusion gastrin values decreased by 25% and 30%, respectively, from basal. In patients with vagotomy, antrectomy, and gastrojejunostomy, test meal and BBS infusion did not significantly alter basal gastrin values. It is concluded that BBS does not stimulate extragastric gastrin.     

Serum gastrin concentrations following oral bethanechol with and without a meal

The present study was performed to test the effect of oral bethanechol (B) on endogenous gastrin release, both basally and in association with the physiologic stimulus of a protein meal. Serum gastrin levels were obtained from 10 normal subjects following: (1) an oral placebo; (2) an oral dose of 25 mg of B; (3) a 100-g protein meal plus placebo; and (4) a 100-g protein meal plus 25 mg of B. Following B or placebo there were no significant changes in basal serum gastrin levels of 98.7±29.3 (±se) pg/ml and 82.4±12.3 pg/ml, respectively. Significant increases of serum gastrin occurred after the protein meal (P<0.01) and after the protein meal combined with B. The gastrin levels thus obtained were significantly greater than basal values but not different from each other. It is proposed that LES pressure increases following B are not due to the release of endogenous gastrin as shown by the absence of increases in basal serum gastrin levels and failure to augment the gastrin release of a physiologic stimulus.This work was supported by the Department of the Navy Clinical Investigation Program Grant #5-05-530R and in part from Research Grant #AM 137111 from the National Institutes of Health.     

Opposite effects of bombesin on insulin and gastrin response to food in humans.

The effect of bombesin on insulin and gastrin response to a standard labelled meal was studied in eight healthy male volunteers. The gastric emptying of solids was simultaneously evaluated. During intravenous infusion of the peptide (5 ng/kg/min) the insulin release after eating was greatly reduced whereas food stimulated gastrin release was significantly enhanced. Both effects of bombesin are likely to be connected with the marked inhibition of gastric emptying induced by the peptide.     

Cholecystokinin in the Control of Gastric Acid Secretion and Gastrin Release in Response to a Meal at Low and High pH in Healthy Subjects and Duodenal Ulcer Patients

Objective: In healthy subjects a gastric meal at low pH inhibits gastric acid secretion, possibly by reducing gastrin release, whereas duodenal ulcer (DU) patients have been reported to show a lack of this low pH inhibition of gastric secretion.

Methods: The intragastric pH profiles were measured in seven healthy subjects and seven DU patients after meals of pH6.5 and 3.0 without or with pretreatment with loxiglumide (1.2 g orally), a selective antagonist of type-A cholecystokinin (CCK) receptors. During all tests (30min before and 30, 60, and 90min after each meal) plasma gastrin, CCK, and somatostatin were determined by specific radioimmunoassays.

Results: In healthy subjects a standard meal at pH 6.5 and 3.0 resulted in median 3-h intragastric pH of 3.8 and 2.8, respectively. In DU patients under the same conditions the pH6.5 meal resulted in median 3-h intragastric pH of 3.4, and the acidified meal in pH 2.2. After pretreatment with loxiglumide the median pH after both meals was significantly lower in healthy controls but not in DU patients. After the pH 6.5 meal, in healthy subjects the plasma gastrin rose by 57%. CCK by 177%. and somatostatin by 39%, and in DU patients by 152%, 367%, and 125%, respectively. Pretreatment with loxiglumide led to a marked increase in plasma gastrin response to the pH 6.5 meal only in healthy controls and not in DU subjects, and it was accompanied by a significant increase in plasma CCK and a decrease in plasma somatostatin. The pH 3.0 meal resulted in a significantly smaller rise in plasma gastrin and a higher increase in CCK and somatostatin in both groups; again, after treatment with loxiglurnide only healthy controls and not DU patients showed significant increase in plasma gastrin level.

Conclusions: Acidification of meals results in the reduction of plasma gastrin and increase in plasma CCK and somatostatin in both healthy subjects and DU patients. DU patients differ from healthy subjects by virtually unchanged plasma gastrin response to a meal after CCK antagonism with loxiglumide, suggesting a defect in both gastric acid and gastrin inhibition by CCK in these patients.     

Significance of an exaggerated meal-stimulated gastrin response in pathogenesis of Helicobacter pylori-negative duodenal ulcer

The aim of this study was to clarify the pathogenesis of Helicobacter pylori-negative duodenal ulcer (DU) by investigating the meal-stimulated serum gastrin (SG) response. The subjects were 9 patients with H. pylori-negative DU, 28 H. pylori-positive DU, 11 H. pylori-positive volunteers, and 30 H. pylori-negative volunteers. Blood samples were taken before and after consumption of a test meal. The integrated 1-hr gastrin response (IGR) was taken to be the area under the SG time curve, calculated by the trapezoid method. H. pylori infection status was determined by histology, serology, and the [¹³C] urea breath test. The mean basal SG concentration was lower in the H. pylori-negative DU patients than in the H. pylori-positive DU patients, but an exaggerated IGR was observed in three patients (33.3%) with H. pylori-negative DU. In conclusion, our findings indicate that an exaggerated meal-stimulated gastrin response may contribute to the pathogenesis of H. pylori-negative DU.     

Cholecystokinin in the control of gastric acid secretion in man.

This study was designed to determine the role of cholecystokinin in the control gastric acid secretion in men using loxiglumide, a specific cholecystokinin receptor blocker. Three groups of healthy subjects (A, B, and C) were used; group A--for studies with postprandial gastric secretion, group B--for studies with exogenous gastric secretagogues and group C--for 12 hour intragastric pH-metry. Cephalic phase stimulated by modified sham feeding in group A subjects increased gastric acid secretion to about 50% of pentagastrin maximum and the treatment with loxiglumide in a standard dose (20 mumol/kg iv loading dose plus infusion of 20 mumol/kg/h afterwards) failed to affect this secretion. Gastric acid response to a 5% peptone meal instilled intragastrically greatly enhanced gastric acid secretion and plasma gastrin concentration but the addition of loxiglumide in the standard dose resulted in further increase in both gastric acid and plasma gastrin responses to peptone meal. Infusion of caerulein in gradually increasing doses (15-120 pmol/kg/h) and gastrin releasing peptide (25-200 pmol/kg/h) resulted in a dose dependent stimulation of gastric acid secretion reaching about 35% and 25% of maximum attained with pentagastrin. When loxiglumide was added in a standard dose, the acid responses to caerulein and gastrin releasing peptide were further increased two to three fold attaining the peak reaching, respectively, about 100% and 50% of pentagastrin maximum. In group C subjects, 12 hour pH-metry revealed the usual increase in gastric pH after each meal in tests with placebo. Loxiglumide (1200 mg tablets tid, po) resulted in significantly lower pH after each meal and this was accompanied by significantly higher gastrin responses than in placebo tests. We conclude that cholecystokinin released by peptone meal, ordinary meals or gastrin releasing peptide exerts a potent inhibitory influence on gastric acid secretion and gastrin release in men and this inhibition involves subtype A cholecystokinin receptors.     

Effect of gastric alkalinization on serum gastrin concentrations in humans

Previous studies have shown that alkalinizing the stomach with sodium bicarbonate for periods up to 3 h does not cause an increase in serum gastrin concentration. We evaluated the effect of a 5-h period of continuous intragastric alkalinization on serum gastrin concentration in 12 healthy humans and 12 asymptomatic duodenal ulcer patients. On the first day, intragastric pH was maintained between 6.0 and 7.0 for 5 h by infusing 0.3 N sodium bicarbonate into the stomach. On the second day, an identical amount of sodium bicarbonate was infused intravenously while intragastric pH was permitted to remain at its natural level for 5 h. Serum gastrin concentration was also measured in each subject and patient after infusion of a homogenized steak meal. In both healthy subjects and duodenal ulcer patients, mean serum gastrin concentrations were significantly (p less than 0.05) higher after 5 h of intragastric bicarbonate infusion than after 5 h of intravenous bicarbonate infusion during which intragastric pH remained at its natural level. Increases in serum gastrin concentration with alkalinization averaged 23% and 30% of the increases in serum gastrin after a homogenized steak meal in the same subjects and patients, respectively. We conclude that continuous gastric alkalinization for 5 h increases serum gastrin concentrations in humans.     

Is antral gastrin important in the resistance of duodenal ulcers to H2 receptor antagonists or in recurrent ulceration after highly selective vagotomy?

Basal serum gastrin, integrated gastrin response to a meal, and integrated gastrin response to insulin induced hypoglycaemia were measured in 60 patients with duodenal ulcer before and after elective highly selective vagotomy to determine whether antral gastrin has a role in resistance to H2 receptor antagonist treatment which the patients had received before surgery or in the development of recurrent ulceration after vagotomy. The basal gastrin, integrated gastrin response to a meal, and the integrated gastrin response to insulin were similar in patients whose ulcers healed after H2 receptor agonist treatment or were refractory to at least three months of this treatment. The same parameters measured before or after highly selective vagotomy were similar in patients who eventually developed recurrent ulceration compared with those who did not. As expected the basal and meal stimulated (but not insulin stimulated) serum gastrin values increased after highly selective vagotomy. Ulcer patients with particularly high gastrin values (whether basal or stimulated) were not more resistant to H2 receptor antagonist treatment or prone to develop ulcer recurrence after highly selective vagotomy. This study suggests that antral gastrin is not important in 'resistance' of duodenal ulceration either to H2 receptor antagonist treatment or to highly selective vagotomy.     

Prospective study of the standard meal provocative test in Zollinger-Ellison syndrome

PURPOSE: The purpose of this work was to evaluate the proposed usefulness of a standard meal-stimulated gastrin provocative test in: (1) distinguishing Zollinger-Ellison syndrome (ZES) from antral syndromes; (2) localizing duodenal gastrinomas; or (3) suggesting that patients with multiple endocrine neoplasia type I (MEN-I) may have an increased incidence of antral syndromes. PATIENTS AND METHODS: Seventy-four consecutive patients with ZES referred to the National Institutes of Health were studied prospectively. The extent and location of gastrinomas, acid secretory studies, and the presence or absence of MEN-I were determined and correlated with the results of the gastrin response to standard meal provocative testing. RESULTS: For patients with fasting serum gastrin levels less than 1,000 pg/mL (n = 43), only 44% had a less than 50% increase over the pre-meal value, which is reported to be the typical response in ZES, and 40% had a 50% to 99% increase. Furthermore 16% had a 100% or greater increase, 9% a 150% or greater increase, and 5% a 200% or greater increase, which overlaps with values reported to be characteristic of 98%, 92%, and 46% of patients with antral syndromes. Results did not differ for patients with or without MEN-I, depend on the extent of the gastrinoma (duodenal versus pancreatic gastrinomas), the presence of previous gastric surgery or type of gastric surgery, or for patients with fasting serum gastrin concentrations greater than or equal to 1,000 pg/mL or less than 1,000 pg/mL. studies of four patients before and after resection of the gastrinoma, who prior to surgery had a greater than 100% increase in gastrin secretion after the meal, demonstrated that all patients had a less than 100% increase postoperatively even though no gastric resection was done. CONCLUSIONS: Approximately half of the patients with ZES have a greater than 50% increase in serum gastrin concentration following a standard test meal and one fifth have a 100% or greater increase. Therefore, they cannot be distinguished on this basis from patients with antral syndromes. The increased serum gastrin level after the meal in these patients with ZES appears to be due to the gastrinoma. Furthermore, the current study provides no evidence for the proposals that antral syndromes are more common in patients with MEN-I, that gastric surgery affects the meal response in patients with gastrinomas, or that the meal test is useful in localizing duodenal gastrinomas.     

Gastroesophageal Sphincter Pressure and Serum Gastrin: Reaction to Food Stimulation in Normal Subjects and in Patients with Gastric or Duodenal Ulcer

Gastroesophageal sphincter pressure and serum gastrin concentration were determined in the fasting state and after the intake of a protein food in 6 normal subjects, 6 patients with gastric ulcer, and in 6 patients with duodenal ulcer. No significant differences in the fasting state were found. After the food intake, gastroesophageal sphincter pressure increased significantly over basal values in normals and in patients with duodenal ulcer, but in patients with gastric ulcer a decrease in pressure was noted. Serum gastrin rose in all subjects studied after the food stimulation, but it was significant only in the gastric and duodenal ulcer group. In two normals and two patients with duodenal ulcer the ingestion of a potato meal of similar weight to that of the protein meal showed no change either in serum gastrin or in sphincter pressure. In one additional normal subject and one duodenal ulcer patient the constant intravenous infusion of Aminosol for 2 h produced no change in serum gastrin or sphincter pressure. These results indicate that the effect of protein food on sphincter pressure is different for gastric or duodenal ulcers, and, furthermore, that this effect is mediated by proteins in the gastrointestinal tract.