熊去氧胆酸联合铝碳酸镁、莫沙必利治疗胆汁反流性胃炎的临床效果分析

目的探讨熊去氧胆酸联合铝碳酸镁、莫沙必利治疗胆汁反流性胃炎的临床效果。方法88例胆汁反流性胃炎患者,随机分为参照组和研究组,各44例。参照组患者采用莫沙必利和铝碳酸镁治疗,研究组采用氧胆酸联合铝碳酸镁、莫沙必利治疗。比较两组患者的治疗效果及治疗前后胃动素、胃泌素水平。结果治疗后,两组患者胃动素及胃泌素水平均优于治疗前,且研究组胃动素(360.12±41.18)ng/L及胃泌素(76.43±17.77)ng/L均优于参照组的(330.11±42.27)、(91.47±20.76)ng/L,差异有统计学意义(P<0.05)。参照组治疗总有效率为81.82%,研究组治疗总有效率为95.45%;研究组治疗总有效率明显高于参照组,差异有统计学意义(P<0.05)。结论在胆汁反流性胃炎患者的临床治疗中熊去氧胆酸联合铝碳酸镁、莫沙必利治疗效果理想,对患者的胃肠激素水平可以起到良好的改善作用,值得将该治疗方案进一步推广。     

Antral gastrin-producing G-cells and somatostatin-producing D-cells in peptic ulcer

Summary The number of G cells and D cells per area unit and the G cell/D cell ratio was studied in control subjects and patients with duodenal or gastric ulcer. A great inter-individual variation in the population density of both types of cells was observed in the three groups studied. G cell density was significantly decreased in both duodenal and gastric ulcer patients, when compared with controls; whereas no difference in G cell density was seen between duodenal ulcer patients and gastric ulcer patients. However, D cell density was significantly decreased in duodenal ulcer patients when compared with control subjects and gastric ulcer patients. In this latter group, D cell density was also lower than in control subjects. A significant positive linear correlation between G cell number and D cell number was found in the three groups studied. The G cell/D cell ratio was significantly increased in duodenal and gastric ulcer patients when compared with controls. This was mainly due to a decrease in D cell numbers. It is concluded that a local deficit in antral D cells in patients with peptic ulcer may favor the pathogenesis of ulcer disease.     

Morphological findings of different areas of gastric mucosa in patients with achlorhydria,extreme hypochlorhydria,Normochlorhydria and their relationship to serum gastrin level: Evidence for two different types of gastritis

Summary The morphological changes of gastric mucosa taken from different areas have been studied in patients of approximately the same age with achlorhydria, extreme hypochlorhydria and normochlorhydria. The serum gastrin level and parietal cell antibodies were determined in the achlorhydric patients. In the latter the diffuse gastritis was localized in the corpus-fundic area, while the changes in the antral region were few and occurred mostly in the superficial zone. In normochlorhydric patients however, the diffuse gastritis was localized in the antral region, with only few changes at the corpus-fundic area. In patients with extreme hypochlorhydria either the fundic or the antral region was involved. Besides the diffuse gastritis intestinal metaplasia, pseudopyloric metaplasia, and atrophy of mucosa were also observed, although much less commonly. The increase of gastrin level could not be related to a definite morphological pattern in the gastric mucosa.It can be assumed that each of the two types of gastritis has a different natural history; the antral site of gastritis cannot be transformed into the fundic site, nor can the fundic site be transformed into the antral site.Parts of this study were presented at the Fifth World Congress of Gastroenterology, Mexico, 1974     

Gastrin induces histamine release from human cutaneous mast cells

Physiologic concentrations of human gastrin I (G17) and a synthetic analog of the carboxy-terminal region of gastrin, pentagastrin, provoked a dose-related release of histamine from human cutaneous mast cells in vitro. The N-terminal tridecapeptide portion of gastrin (G1-13) neither stimulated histamine release nor blocked the action of G17. In vivo correlation studies demonstrated that low concentrations (10(-12)M to 10(-10)M) of G17 or pentagastrin administered intradermally provoked a modest but definite wheal-and-flare response in four out of six normal subjects and a more marked, dose-related response in a patient with mastocytosis. These results indicate that physiologic concentrations of gastrin can stimulate mediator release from human cutaneous mast cells. We propose that this response may be mediated through receptors recognizing the carboxy-terminal region of the gastrin molecule. The possible role of gastrin-induced human mast cell-mediator release should be considered in the assessment of allergic disorders and in experimental models investigating mast cell function.     

P-物质、血管活性肠肽、胃泌素和5-羟色胺与胃肠功能的研究进展

P-物质、血管活性肽和胃泌素属于胃肠激素;5-羟色胺(5-HT)属于神经递质.P-物质和血管活性肽是广泛存在肠黏膜中的神经肽,在肠道运动和分泌方面发挥着重要作用.胃泌素是第一个被阐明结构的胃肠激素,可以促进胃肠运动,破坏自发和胃动素所致的移行性运动复合波,使空腹样胃肠运动转变为餐后样运动.5-HT是血管活性胺类物质,通过5-HT受体调控血管壁的通透性.该文从P-物质、血管活性肠肽、胃泌素和5-HT的来源、分布及在胃肠功能中的研究进展作一综述.     

Development of XPA067.06, a potent high affinity human anti-gastrin monoclonal antibody

The peptide hormone gastrin is a key factor in regulation of gastric acid secretion. It has also been implicated in the development or maintenance of various types of cancer, such as pancreatic and stomach carcinoma. Inhibition of gastrin activity has potential for therapeutic use as a suppressor of acid secretion as well as an inhibitor of gastrin-responsive tumors. XPA067.06 is an affinity matured, 30 pM fully human anti-gastrin monoclonal antibody that was generated. The antibody was tested in a mouse gastric pH model to determine its effect on acid secretion. In this model, animals were treated with human gastrin, XPA067.06, and H2R or M1 receptor antagonists. Gastric fluid was collected and acid output was measured as a function of pH. XPA067.06 was shown to significantly inhibit gastrin-17-stimulated acid output for at least 48h. These results demonstrate that XPA067.06 effectively binds and neutralizes human gastrin-17 in vivo with rapid onset and prolonged duration of efficacy.     

清肝宁胃汤联合熊去氧胆酸对原发性胆汁反流性胃炎患者疗效分析

目的:探讨给予原发性胆汁反流性胃炎(PBRG)患者熊去氧胆酸、清肝宁胃汤联合治疗的临床价值。方法:选取2017年4月至2018年4月新疆维吾尔自治区中医医院收治的PBRG患者86例作为研究对象,按照随机数字表法分为对照组和观察组,每组43例。对照组采用常规西药治疗,观察组采用清肝宁胃汤+熊去氧胆酸治疗,观察患者中医证候积分、血清胆囊收缩素(Gastrin)及胃泌素(CCK)水平等改善情况。结果:经治疗,观察组患者胃脘痞满、嗳气、恶心呕吐、胃痛或痛窜两胁等症状中医证候积分均显著低于对照组(P 0. 05);观察组治疗后血清Gastrin为(50. 18±10. 46) ng/L,显著低于对照组的(76. 36±10. 36) ng/L,CCK为(139. 64±8. 39) ng/L,显著高于对照组的(120. 24±8. 35) ng/L(t=11. 660、10. 747,P 0. 05);观察组治疗后Ig A、Ig M、Ig G及补体C3改善程度均显著优于对照组(P 0. 05); 2组腹痛、腹泻、心悸等不良反应总发生率为9. 30%,相比对照组的32. 56%显著更低(P 0. 05),2组均为患者出现血尿常规异常。结论:给予PBRG患者清肝宁胃汤联合熊去氧胆酸治疗,可促进患者临床症状及血清Gastrin、CCK水平获得更大程度改善,可使患者机体免疫功能获得有效调节。     

Study on content of serum epidermal growth factor,gastric acid secretion and serum gastrin in duodenitis

AIM: To study whether there is EGF secreting abnormality in duodenitis and its relationship with gastric acid output and serum gastrin, so as to further explore the pathogenesis of duodenitis. METHODS: Twenty-five duodenitis patients were confirmed by electrogastroscopy and biopsy, with an average age of 35.9 ± 7.0 years (range, 24-52 years). The control group consisted of 20 healthy volunteers (10 females, 10 males), with an average age of 34.4 ± 7.6 years (range, 23-48 years). Twenty duodenal ulcer patients (10 females, 10 males), with an average age of 35.0 ± 7.6 years (range, 24-52 years), were also included. Serum EGF and gastrin were measured using radioimmunoassay. Intragastric acidity was determined by pentagastrin method. Statistical analysis was performed using Student’s t-test. RESULTS: In comparison with those in the control group, the contents of serum EGF and serum gastrin in duodenitis patients were all significantly increased. In comparison with those in the duodenal ulcer group, serum EGF was significantly increased, basal acid output and peak acid output were decreased, and serum gastrin was increased significantly in duodenitis patients. Serum EGF was negatively correlated with gastric acid output and positively correlated with serum gastrin. CONCLUSION: In duodenitis, serum EGF concentration was increased, which was positively correlated with serum gastrin content, but was negatively correlated with gastric acid output. This indicates that EGF plays a protective role in the pathogenesis of duodenitis, which provides a new clue to pathogenesis study of duodenitis.     

应激性胃粘膜出血与血浆血栓素、前列环素和胃泌素水平的关系

目的　探讨应激性胃粘膜出血与血浆TXA2 、PGI2 和胃泌素 (G)水平的关系。方法　 2 0只SD大鼠随机分成实验组和对照组 ,每组 10只 ,禁食 2 4小时后 ,实验组放在 2℃冰水中应激 4小时 ,对照组不给刺激。应激结束后麻醉大鼠 ,分别取血 2ml分离血浆 ,放免法测定TXB2 (TXA2 的稳定代谢物 )、6 酮 PGF1a(PGI2 的衍生物 )和G水平 ;另取大鼠胃沿小弯剪开 ,肉眼观察胃粘膜有无出血灶 ,用pH值试纸测定胃液酸碱度。结果　 8只实验鼠胃粘膜见片状出血灶 ,对照组鼠胃粘膜无出血性改变 ;两组鼠胃液pH值测定无明显差异。实验组血浆TXB2 、6 酮 PGF1a和G水平分别为 15 45 11±14 2 89、16 2 80± 42 13和 112 75± 2 3 6 8,对照组分别为 96 6 5 0± 5 18 48、3 5 6 0 0± 91 0 6和 2 47 14± 5 3 6 0 ,两组分别比较均具有显著意义 (P <0 0 1)。结论　大鼠应激性胃粘膜出血与血浆TXA2 水平升高和PGI2 水平降低有关 ;而与胃酸分泌无关。     

Hp相关性胃窦炎对十二指肠溃疡患者血清胃泌素浓度的影响

目的探讨幽门螺杆菌相关性胃窦炎对十二指肠溃疡（ＤＵ）血清试餐胃泌素（ＭＳＧ）浓度的影响。方法对１００例ＤＵ患者进行内镜、胃粘膜组织学、幽门螺杆菌（Ｈｐ）和血清ＭＳＧ检查,并分析其相互关系。结果ＤＵ患者血清ＭＳＧ浓度（１２９．９±８７．２ｐｇ／ｍｌ）较对照组（８６．１±５１．２ｐｇ／ｍｌ）显著升高（Ｐ＜０．０１）,但其升高水平在伴发的不同胃窦炎中有显著差异（Ｐ＜０．０１）,即胃窦炎越重,血清ＭＳＧ越高。胃窦炎的轻重与Ｈｐ感染有关,ＤＵ患者中Ｈｐ感染率高（７５．０％）,与Ｈｐ相关的胃窦炎较重,其血清ＭＳＧ升高也较明显（１３７．０±１０７．５ｐｇ／ｍｌ）,但在Ｈｐ阴性的胃窦炎中,血清ＭＳＧ也随炎症的加重而升高。结论ＤＵ患者血清ＭＳＧ浓度升高可能受伴发胃窦炎的影响,Ｈｐ感染引起血清ＭＳＧ升高,可能也是通过促发或加重胃窦炎所致。