Hirschowitz B I, Haber M M
Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, 35294, USA.
Aliment Pharmacol Ther. 2001 Jan;15(1):87-103. doi: 10.1046/j.1365-2036.2001.00876.x.
Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor.
To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger-Ellison syndrome) or normal gastrin (non-Zollinger-Ellison syndrome) before and during long-term treatment with lansoprazole.
Lansoprazole was individually titrated to reduce basal acid output to < 5 mmol/h (< 1 mmol/h in post-surgical Zollinger-Ellison syndrome). Gastric corpus biopsies were obtained every 6 months before treatment and up to 8 years later.
H. pylori was present in corpus biopsies in approximately 50%, causing active gastritis which resolved rapidly in 15 subjects after elimination of H. pylori. Patchy mild/moderate corpus atrophy was present at entry in two and at the end in four out of 60 patients, one being H. pylori-positive. Intestinal metaplasia (< 10%) was seen in six isolated biopsies (1% of total). H. pylori did not affect serum gastrin, enterochromaffin-like cell density or hyperplasia. Enterochromaffin-like cell density was twice as high in Zollinger-Ellison syndrome as in non-Zollinger-Ellison syndrome patients (241 vs. 126 cells/mm2, P < 0.001). Enterochromaffin-like cells remained normal in the non-Zollinger-Ellison syndrome hypersecretors regardless of H. pylori status.
Corpus enterochromaffin-like cell increases were related to serum gastrin elevation, but neither H. pylori nor long-term treatment with lansoprazole alone or together had any effect on enterochromaffin-like cell density or hyperplasia. Corpus acute gastritis resulted from H. pylori infection, but did not result in mucosal atrophy despite long-term proton pump inhibitor treatment and promptly resolved with loss of H. pylori.
据说幽门螺杆菌会导致长期接受质子泵抑制剂治疗的胃食管反流病（GERD）患者胃体萎缩和肠嗜铬样细胞增殖。
确定幽门螺杆菌感染对胃酸分泌过多（基础酸排量>15 mmol/h）且伴有高胃泌素血症（佐林格-埃利森综合征）或胃泌素正常（非佐林格-埃利森综合征）的患者在使用兰索拉唑长期治疗之前和期间的胃炎、肠嗜铬样细胞密度和增生、黏膜萎缩及血清胃泌素的影响。
个体化滴定兰索拉唑剂量，以使基础酸排量降至<5 mmol/h（手术后的佐林格-埃利森综合征患者降至<1 mmol/h）。在治疗前每6个月获取胃体活检样本，直至8年后。
约50%的胃体活检样本中存在幽门螺杆菌，导致活动性胃炎，15名患者根除幽门螺杆菌后胃炎迅速消退。60名患者中，2名患者在入组时存在散在的轻度/中度胃体萎缩，4名患者在治疗结束时出现胃体萎缩，其中1名患者幽门螺杆菌呈阳性。6份单独的活检样本中可见肠化生（<10%）（占总数的1%）。幽门螺杆菌不影响血清胃泌素、肠嗜铬样细胞密度或增生。佐林格-埃利森综合征患者的肠嗜铬样细胞密度是非佐林格-埃利森综合征患者的两倍（241对126个细胞/mm²，P<0.001）。在非佐林格-埃利森综合征胃酸分泌过多患者中，无论幽门螺杆菌状态如何，肠嗜铬样细胞均保持正常。
胃体肠嗜铬样细胞增加与血清胃泌素升高有关，但幽门螺杆菌以及单独或联合使用兰索拉唑长期治疗均对肠嗜铬样细胞密度或增生无任何影响。胃体急性胃炎由幽门螺杆菌感染引起，但尽管长期使用质子泵抑制剂治疗，并未导致黏膜萎缩，且随着幽门螺杆菌的清除迅速消退。
