循证医学文献评价作业胃溃疡

IntroductionBackgroundGastritis includes a myriad of disorders that involve inflammatory changes in the gastric mucosa, including erosive gastritis caused by Helicobacter pylori bacterial infections, other infectious gastritises, nonsteroidal anti-inflammatory drugs (NSAIDs), noxious irritants, reflux gastritis from exposure to bile and pancreatic fluids, infectious gastritis, and gastric mucosal Peptic ulcer disease (PUD) refers to a discrete mucosal defect in the portions of the gastrointestinal tract (gastric or duodenal) exposed to acid and pepsin Presentations of gastritis and PUD usually are indistinguishable in the ED, and thus the ED management is generally the Emergent complications include hemorrhagic shock and peritonitis secondary to a perforated The clinician should be concerned about other life-threatening conditions (eg, acute coronary syndromes and aortic aneurysms), which can mimic the presentation of For more information, see Medscape's Peptic Ulcer Disease Resource CPathophysiologyThe mechanisms of mucosal injury in gastritis and PUD are thought to be mainly caused by H pylori infections, coupled an imbalance of aggressive factors, such as acid production or pepsin, and defensive factors, such as mucus production, bicarbonate, and blood Erosive gastritis usually is associated with serious illness or with various Stress, ethanol, bile, and nonsteroidal anti-inflammatory drugs (NSAIDs) disrupt the gastric mucosal barrier, making it vulnerable to normal gastric Infection with H pylori, a short, spiral-shaped, microaerophilic gram-negative bacillus, is the leading cause of PUD and is associated with virtually all ulcers not induced by NSAID H pylori colonize the deep layers of the mucosal gel that coats the gastric mucosa and presumably disrupts its protective H pylori is thought to infect virtually all patients with chronic active Eradication of H pylori was thought to be the pathway to curing ulcer disease, but that has proven increasingly NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal Many people with known H pylori colonization or who are taking NSAIDs do not suffer from gastritis or PUD, which indicates other important causative factors must be FrequencyUnited StatesApproximately 10% of Americans eventually develop PUD, and about 10% of patients presenting to the ED with abdominal pain are diagnosed with PUD Prevalence has decreased in the United States over the last 30 InternationalFrequency of PUD is decreasing in the developed world but increasing in developing Mortality/MorbidityComplications of gastritis include PUD and, rarely, extensive PUD accounts for more than 50% of all causes of upper gastrointestinal bleeds in the United SComplications of peptic ulcer disease include bleeding, occasionally massive, and perforation leading to peritonitis and sepsis (rare)The mortality rate is SexMale-to-female ratio of gastritis is approximately 1:1Male-to-female ratio of PUD is approximately 2:1AgeAn estimated 60% of Americans older than 60 years harbor H Duodenal ulcers usually occur in those aged 25-75 Gastric ulcer prevalence peaks in those aged 55-65 ClinicalHistoryPatients typically present with abdominal pain that has the following characteristics:Epigastric to left upper quadrantFrequently described as burningMay radiate to the backUsually occurs 1-5 hours after mealsMay be relieved by food, antacids (duodenal), or vomiting (gastric)Typically follows a daily pattern specific to patientNSAID-induced gastritis or ulcers are usually Sudden onset of symptoms may indicate Gastritis may present as bleeding, which is more likely in elderly Symptoms consistent with anemia (eg, fatigue, dyspnea) may PhysicalEpigastric tenderness is present and usually Bowel sounds are Signs of peritonitis or GI bleeding may be Perform a rectal examination and Hemoccult CausesH pylori (most common cause of ulceration)NSAIDs, aspirinGastrinoma (Zollinger-Ellison syndrome)Severe stress (eg, trauma, burns), Curling ulcersAlcoholBile refluxPancreatic enzyme refluxRadiationStaphylococcus aureus exotoxinBacterial or viral infection

1979年，病理学医生Warren在慢性胃炎患者的胃窦黏膜组织切片上观察到一种弯曲状细菌，并且发现这种细菌邻近的胃黏膜总是有炎症存在，因而意识到这种细菌和慢性胃炎可能有密切关系。 1981年，消化科临床医生Marshall与Warren合作，他们以100例接受胃镜检查及活检的胃病患者为对象进行研究，证明这种细菌的存在确实与胃炎相关。此外他们还发现,这种细菌还存在于所有十二指肠溃疡患者、大多数胃溃疡患者和约一半胃癌患者的胃黏膜中。 经过多次失败之后，1982年4月，Marshall终于从胃黏膜活检样本中成功培养和分离出了这种细菌。为了进一步证实这种细菌就是导致胃炎的罪魁祸首，Marshall和另一位医生Morris不惜喝下含有这种细菌的培养液，结果大病一场。 基于这些结果，Marshall和Warren提出幽门螺杆菌涉及胃炎和消化性溃疡的病因学。1984年4月5号，他们的成果发表于在世界权威医学期刊《柳叶刀》（lancet）上。成果一经发表，立刻在国际消化病学界引起了轰动，掀起了全世界的研究热潮。世界各大药厂陆续投巨资开发相关药物，专业刊物《螺杆菌》杂志应运而生，世界螺杆菌大会定期召开，有关螺杆菌的研究论文不计其数。通过人体试验、抗生素治疗和流行病学等研究，幽门螺杆菌在胃炎和胃溃疡等疾病中所起的作用逐渐清晰，科学家对该病菌致病机理的认识也不断深入。 2005年10月3日，瑞典卡罗林斯卡研究院宣布，2005年度诺贝尔生理学或医学奖授予这两位科学家以表彰他们发现了幽门螺杆菌以及这种细菌在胃炎和胃溃疡等疾病中的作用。 所以应该是1979年发现的。

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