AIM： To assess long-term effects of Helicobacter pylori （H pylon} eradication on antral G cell morphology and function in patients with and without duodenal ulcer （DU）.METHODS： Consecutive dyspeptic patients refe...AIM： To assess long-term effects of Helicobacter pylori （H pylon} eradication on antral G cell morphology and function in patients with and without duodenal ulcer （DU）.METHODS： Consecutive dyspeptic patients referred to the endoscopy entered the study. Out of 39 Hpylori positive patients, 8 had DU （Hpylori ＋DU） and 31 gastritis （Hpylori＋G）. Control groups consisted of 11 uninfected dyspeptic patients （CG1） and 7 healthy volunteers （CG2）. Basal plasma gastrin （PGL）, antral tissue gastrin concentrations （ATGC）, immunohistochemical and electron microscopic characteristics of G cells were determined, prior to and 6 mo after therapy.RESULTS： We-demonstrated elevated PGL in infected patients compared to uninfected controls prior to therapy.Elevated PGL were registered in all Hpylori＋patients （Hpylori＋DU： 106.78＋22.72 pg/mL, Hpylori＋G： 74.95＋15.63,CGI： 68.59＋17.97, CG2：39.24＋5.59 pg/mL, P〈0.01）.Successful eradication （e） therapy in Hpylori＋patients lead to significant decrease in PGL （Hpylori＋DU： 59.93＋9.40 and Hpylori＋Ge： 42.36＋10.28 pg/mL, P〈0.001）. ATGC at the beginning of the study were similar in infected and uninfected patients and eradication therapy lead to significant decrease in ATGC in Hpylori＋gastritis, but not in DU patients. In the Hpylori＋DU patients, the mean number of antral G cells was significantly lower in comparison with all other groups （P〈0.01）, but after successful eradication was close to normal values found in controls. By contrast, G cell number and volume density were significantly decreased （P〈0.01） in Hpylori＋Ge group after successful eradication therapy （294＋32 and 0.31＋0.02,respectively）, in comparison to values before eradication （416~40 and 0.48~0.09）. No significant change of the G cell/total endocrine cell ratio was observed during the 6 mo of follow up in any of the groups. A reversible increase in G cell secretory function was seen in all infected individuals, demonstrated by a more prominent secretory apparatus. However, differences between DU and gastritis group were identified.CONCLUSION： H py/oriinfection induces antral G cell hyperfunction resulting in increased gastrin synthesis and secretion. After eradication therapy complete morphological and functional recovery is observed in patients with gastritis. In the DU patients some other factors unrelated to the Hpyloriinfection influence antral G cell morphology and function.展开更多
In addition to regulating acid secretion, the gastric antral hormone gastrin regulates several important cellular processes in the gastric epithelium including proliferation, apoptosis, migration, invasion, tissue rem...In addition to regulating acid secretion, the gastric antral hormone gastrin regulates several important cellular processes in the gastric epithelium including proliferation, apoptosis, migration, invasion, tissue remodelling and angiogenesis. Elevated serum concentrations of this hormone are caused by many conditions, particularly hypochlorhydria (as a result of autoimmune or Helicobacter pylori (H pylori)-induced chronic atrophic gastritis or acid suppressing drugs) and gastrin producing tumors (gastrinomas). There is now accumulating evidence that altered local and plasma concentrations of gastrin may play a role during the development of various gastric tumors. In the absence of H pylori infection, marked hypergastrinemia frequently results in the development of gastric enterochromaffi n cell-like neuroendocrine tumors and surgery to remove the cause of hypergastrinemia may lead to tumor resolution in this condition. In animal models such as transgenic INS-GAS mice, hypergastrinemia has also been shown to act as a cofactor with Helicobacter infection during gastric adenocarcinoma development. However, it is currently unclear as to what extent gastrin also modulates human gastric adenocarcinoma development. Therapeutic approaches targeting hypergastrinemia,such as immunization with G17DT, have been evaluated for the treatment of gastric adenocarcinoma, with some promising results. Although the mild hypergastrinemia associated with proton pump inhibitor drug use has been shown to cause ECL-cell hyperplasia and to increase H pylori-induced gastric atrophy, there is currently no convincing evidence that this class of agents contributes towards the development of gastric neuroendocrine tumors or gastric adenocarcinomas in human subjects.展开更多
Upper gastrointestinal tract hemorrhage （UGIH） remains a common presentation requiring urgent evaluation and treatment. Accurate assessment, appropriate intervention and apt clinical skills are needed for proper man...Upper gastrointestinal tract hemorrhage （UGIH） remains a common presentation requiring urgent evaluation and treatment. Accurate assessment, appropriate intervention and apt clinical skills are needed for proper management from time of presentation to discharge. The advent of pharmacologic acid suppression, endoscopic hemostatic techniques, and recognition of Helicobacter pylori as an etiologic agent in peptic ulcer disease （PUD） has revolutionized the treatment of UGIH. Despite this, acute UGIH still carries considerable rates of morbidity and mortality. This review aims to discuss current areas of uncertainty and controversy in the management of UGIH. Neoadjuvant proton pump inhibitor （PPI） therapy has become standard empiric treatment for UGIH given that PUD is the leading cause of non variceal UGIH, and PPIs are extremely effective at promoting ulcer healing. Howeve, neoadjuvant PPI administration has not been shown to affect hard clinical outcomes such as rebleeding or mortality. The optimal timing of upper endoscopy in UGIH is often debated. Upon completion of volume resuscitation and hemodynamic stabilization, upper endoscopy should be performed within 24 h in all patientswith evidence of UGIH for both diagnostic and therapeutic purposes. With rising healthcare cost paramount in today＇s medical landscape, the ability to appropriately triage UGIH patients is of increasing value. Upper en- doscopy in conjunction with the clinical scenario allows for accurate decision making concerning early discharge home in low risk lesions or admission for further moni toring and treatment in higher risk lesions. Concomitant pharmacotherapy with non steroidal antiinflammatory drugs （NSAIDs） and antiplatelet agents, such as clopidogrel, has a major impact on the etiology, severib/, and potential treatment of UGIH. Long term PPI use in patients taking chronic NSAIDs or clopidogrel is discussed thoroughly in this review.展开更多
AIM:To study the value of serum biomarker tests to differentiate between patients with healthy or diseased stomach mucosa:i.e.those with Helicobacter pylori(H pylori)gastritis or atrophic gastritis,who have a high ris...AIM:To study the value of serum biomarker tests to differentiate between patients with healthy or diseased stomach mucosa:i.e.those with Helicobacter pylori(H pylori)gastritis or atrophic gastritis,who have a high risk of gastric cancer or peptic ulcer diseases.METHODS:Among 162 Japanese outpatients,pepsinogen-(Pg-)and(Pg)were measured using a conventional Japanese technique,and the European GastroPanel examination(Pg and Pg,gastrin-17 and H pylori antibodies).Gastroscopy with gastric biopsies was performed to classify the patients into those with healthy stomach mucosa,H pylori non-atrophic gastritis or atrophic gastritis.RESULTS:Pg-and Pg assays with the GastroPanel and the Japanese method showed a highly significant correlation.For methodological reasons,however,serum Pg-,but not Pg,was twice as high with the GastroPanel test as with the Japanese test.The biomarker assays revealed that 5%of subjects had advanced atrophic corpus gastritis which was also verified by endoscopic biopsies.GastroPanel examination revealed an additional seven patients who had either advanced atrophic gastritis limited to the antrum or antrum-predominant H pylori gastritis.When compared to the endoscopic biopsy findings,the GastroPanel examination classified the patients into groups with "healthy" or "diseased" stomach mucosa with 94% accuracy,95% sensitivity and 93% specifi city.CONCLUSION:Serum biomarker tests can be used to differentiate between subjects with healthy and diseased gastric mucosa with high accuracy.展开更多
目的:探讨幽门螺杆菌(Helicobacter pylori,H.pylori)感染与糖尿病性脂肪肝的关系,为临床诊治提供依据.方法:131例2型糖尿病患者行胃黏膜组织切片染色确定H.pylori感染,分为H.pylori阳性组62例,H.pylori阴性组69例,行腹部彩超检查和血...目的:探讨幽门螺杆菌(Helicobacter pylori,H.pylori)感染与糖尿病性脂肪肝的关系,为临床诊治提供依据.方法:131例2型糖尿病患者行胃黏膜组织切片染色确定H.pylori感染,分为H.pylori阳性组62例,H.pylori阴性组69例,行腹部彩超检查和血脂、血清C肽、空腹血糖、空腹胰岛素,并计算胰岛素抵抗指数(homeostasis model assessment for insulin resistance,HOMR-IR)及体质量指数(body mass index,BMI).结果:H.pylori阳性组的糖尿病性脂肪肝发生率71.0%(44/62),H.pylori阴性组糖尿病性脂肪肝发生率50.7%(35/69),差异有统计学意义(P<0.05);H.pylori阳性组甘油三酯、HOMR-IR均明显高于H.pylori阴性组,血清C肽低于H.pylori阴性组,差异均有统计学意义(P<0.05),而胆固醇及低密度脂蛋白(lowdensity lipoprotein,LDL)、高密度脂蛋白(high-density lipoprotein,HDL)、BMI在两组间均无统计学差异(P>0.05).结论:糖尿病性脂肪肝患者中H.pylori感染率高,高H.pylori感染加重糖尿病性糖脂代谢紊乱及胰岛素抵抗,加重脂肪肝进展,或许积极抗H.pylori治疗,有利于缓解或减少糖尿病性脂肪肝的发生、发展.展开更多
Giant duodenal ulcers （GDUs） are a subset of duodenal ulcers that have historically resulted in greater morbidity than usual duodenal ulcers. Until recently, few cases had been successfully treated with medical ther...Giant duodenal ulcers （GDUs） are a subset of duodenal ulcers that have historically resulted in greater morbidity than usual duodenal ulcers. Until recently, few cases had been successfully treated with medical therapy. However, the widespread use of endoscopy, the introduction of H-2 receptor blockers and proton p^Jmp inhibitors, and the improvement in surgical techniques all have revolutionized the diagnosis, treatment and outcome of this condition. Nevertheless, GDUs are still associated with high rates of morbidity, mortality and complications. Thus, surgical evaluation of a patient with a GDU should remain an integral part of patient care. These giant variants, while usually benign, can frequently harbor malignancy. A careful review of the literature highlights the important differences when comparing GDUs to classical peptic ulcers and why they must be thought of differently than their more common counterpart.展开更多
基金Supported by a Grant From Serbian Ministry for Science, Technology and Development, No. 1752
文摘AIM： To assess long-term effects of Helicobacter pylori （H pylon} eradication on antral G cell morphology and function in patients with and without duodenal ulcer （DU）.METHODS： Consecutive dyspeptic patients referred to the endoscopy entered the study. Out of 39 Hpylori positive patients, 8 had DU （Hpylori ＋DU） and 31 gastritis （Hpylori＋G）. Control groups consisted of 11 uninfected dyspeptic patients （CG1） and 7 healthy volunteers （CG2）. Basal plasma gastrin （PGL）, antral tissue gastrin concentrations （ATGC）, immunohistochemical and electron microscopic characteristics of G cells were determined, prior to and 6 mo after therapy.RESULTS： We-demonstrated elevated PGL in infected patients compared to uninfected controls prior to therapy.Elevated PGL were registered in all Hpylori＋patients （Hpylori＋DU： 106.78＋22.72 pg/mL, Hpylori＋G： 74.95＋15.63,CGI： 68.59＋17.97, CG2：39.24＋5.59 pg/mL, P〈0.01）.Successful eradication （e） therapy in Hpylori＋patients lead to significant decrease in PGL （Hpylori＋DU： 59.93＋9.40 and Hpylori＋Ge： 42.36＋10.28 pg/mL, P〈0.001）. ATGC at the beginning of the study were similar in infected and uninfected patients and eradication therapy lead to significant decrease in ATGC in Hpylori＋gastritis, but not in DU patients. In the Hpylori＋DU patients, the mean number of antral G cells was significantly lower in comparison with all other groups （P〈0.01）, but after successful eradication was close to normal values found in controls. By contrast, G cell number and volume density were significantly decreased （P〈0.01） in Hpylori＋Ge group after successful eradication therapy （294＋32 and 0.31＋0.02,respectively）, in comparison to values before eradication （416~40 and 0.48~0.09）. No significant change of the G cell/total endocrine cell ratio was observed during the 6 mo of follow up in any of the groups. A reversible increase in G cell secretory function was seen in all infected individuals, demonstrated by a more prominent secretory apparatus. However, differences between DU and gastritis group were identified.CONCLUSION： H py/oriinfection induces antral G cell hyperfunction resulting in increased gastrin synthesis and secretion. After eradication therapy complete morphological and functional recovery is observed in patients with gastritis. In the DU patients some other factors unrelated to the Hpyloriinfection influence antral G cell morphology and function.
基金Supported by Wellcome Trust Clinical Research Training Fellowship to MDB
文摘In addition to regulating acid secretion, the gastric antral hormone gastrin regulates several important cellular processes in the gastric epithelium including proliferation, apoptosis, migration, invasion, tissue remodelling and angiogenesis. Elevated serum concentrations of this hormone are caused by many conditions, particularly hypochlorhydria (as a result of autoimmune or Helicobacter pylori (H pylori)-induced chronic atrophic gastritis or acid suppressing drugs) and gastrin producing tumors (gastrinomas). There is now accumulating evidence that altered local and plasma concentrations of gastrin may play a role during the development of various gastric tumors. In the absence of H pylori infection, marked hypergastrinemia frequently results in the development of gastric enterochromaffi n cell-like neuroendocrine tumors and surgery to remove the cause of hypergastrinemia may lead to tumor resolution in this condition. In animal models such as transgenic INS-GAS mice, hypergastrinemia has also been shown to act as a cofactor with Helicobacter infection during gastric adenocarcinoma development. However, it is currently unclear as to what extent gastrin also modulates human gastric adenocarcinoma development. Therapeutic approaches targeting hypergastrinemia,such as immunization with G17DT, have been evaluated for the treatment of gastric adenocarcinoma, with some promising results. Although the mild hypergastrinemia associated with proton pump inhibitor drug use has been shown to cause ECL-cell hyperplasia and to increase H pylori-induced gastric atrophy, there is currently no convincing evidence that this class of agents contributes towards the development of gastric neuroendocrine tumors or gastric adenocarcinomas in human subjects.
文摘Upper gastrointestinal tract hemorrhage （UGIH） remains a common presentation requiring urgent evaluation and treatment. Accurate assessment, appropriate intervention and apt clinical skills are needed for proper management from time of presentation to discharge. The advent of pharmacologic acid suppression, endoscopic hemostatic techniques, and recognition of Helicobacter pylori as an etiologic agent in peptic ulcer disease （PUD） has revolutionized the treatment of UGIH. Despite this, acute UGIH still carries considerable rates of morbidity and mortality. This review aims to discuss current areas of uncertainty and controversy in the management of UGIH. Neoadjuvant proton pump inhibitor （PPI） therapy has become standard empiric treatment for UGIH given that PUD is the leading cause of non variceal UGIH, and PPIs are extremely effective at promoting ulcer healing. Howeve, neoadjuvant PPI administration has not been shown to affect hard clinical outcomes such as rebleeding or mortality. The optimal timing of upper endoscopy in UGIH is often debated. Upon completion of volume resuscitation and hemodynamic stabilization, upper endoscopy should be performed within 24 h in all patientswith evidence of UGIH for both diagnostic and therapeutic purposes. With rising healthcare cost paramount in today＇s medical landscape, the ability to appropriately triage UGIH patients is of increasing value. Upper en- doscopy in conjunction with the clinical scenario allows for accurate decision making concerning early discharge home in low risk lesions or admission for further moni toring and treatment in higher risk lesions. Concomitant pharmacotherapy with non steroidal antiinflammatory drugs （NSAIDs） and antiplatelet agents, such as clopidogrel, has a major impact on the etiology, severib/, and potential treatment of UGIH. Long term PPI use in patients taking chronic NSAIDs or clopidogrel is discussed thoroughly in this review.
文摘AIM:To study the value of serum biomarker tests to differentiate between patients with healthy or diseased stomach mucosa:i.e.those with Helicobacter pylori(H pylori)gastritis or atrophic gastritis,who have a high risk of gastric cancer or peptic ulcer diseases.METHODS:Among 162 Japanese outpatients,pepsinogen-(Pg-)and(Pg)were measured using a conventional Japanese technique,and the European GastroPanel examination(Pg and Pg,gastrin-17 and H pylori antibodies).Gastroscopy with gastric biopsies was performed to classify the patients into those with healthy stomach mucosa,H pylori non-atrophic gastritis or atrophic gastritis.RESULTS:Pg-and Pg assays with the GastroPanel and the Japanese method showed a highly significant correlation.For methodological reasons,however,serum Pg-,but not Pg,was twice as high with the GastroPanel test as with the Japanese test.The biomarker assays revealed that 5%of subjects had advanced atrophic corpus gastritis which was also verified by endoscopic biopsies.GastroPanel examination revealed an additional seven patients who had either advanced atrophic gastritis limited to the antrum or antrum-predominant H pylori gastritis.When compared to the endoscopic biopsy findings,the GastroPanel examination classified the patients into groups with "healthy" or "diseased" stomach mucosa with 94% accuracy,95% sensitivity and 93% specifi city.CONCLUSION:Serum biomarker tests can be used to differentiate between subjects with healthy and diseased gastric mucosa with high accuracy.
文摘目的:探讨幽门螺杆菌(Helicobacter pylori,H.pylori)感染与糖尿病性脂肪肝的关系,为临床诊治提供依据.方法:131例2型糖尿病患者行胃黏膜组织切片染色确定H.pylori感染,分为H.pylori阳性组62例,H.pylori阴性组69例,行腹部彩超检查和血脂、血清C肽、空腹血糖、空腹胰岛素,并计算胰岛素抵抗指数(homeostasis model assessment for insulin resistance,HOMR-IR)及体质量指数(body mass index,BMI).结果:H.pylori阳性组的糖尿病性脂肪肝发生率71.0%(44/62),H.pylori阴性组糖尿病性脂肪肝发生率50.7%(35/69),差异有统计学意义(P<0.05);H.pylori阳性组甘油三酯、HOMR-IR均明显高于H.pylori阴性组,血清C肽低于H.pylori阴性组,差异均有统计学意义(P<0.05),而胆固醇及低密度脂蛋白(lowdensity lipoprotein,LDL)、高密度脂蛋白(high-density lipoprotein,HDL)、BMI在两组间均无统计学差异(P>0.05).结论:糖尿病性脂肪肝患者中H.pylori感染率高,高H.pylori感染加重糖尿病性糖脂代谢紊乱及胰岛素抵抗,加重脂肪肝进展,或许积极抗H.pylori治疗,有利于缓解或减少糖尿病性脂肪肝的发生、发展.
文摘Giant duodenal ulcers （GDUs） are a subset of duodenal ulcers that have historically resulted in greater morbidity than usual duodenal ulcers. Until recently, few cases had been successfully treated with medical therapy. However, the widespread use of endoscopy, the introduction of H-2 receptor blockers and proton p^Jmp inhibitors, and the improvement in surgical techniques all have revolutionized the diagnosis, treatment and outcome of this condition. Nevertheless, GDUs are still associated with high rates of morbidity, mortality and complications. Thus, surgical evaluation of a patient with a GDU should remain an integral part of patient care. These giant variants, while usually benign, can frequently harbor malignancy. A careful review of the literature highlights the important differences when comparing GDUs to classical peptic ulcers and why they must be thought of differently than their more common counterpart.
