Digestive Diseases and Nutrition Center, Women and Children's Hospital of Buffalo, University at Buffalo, NY 14222, USA.
J Pediatr Gastroenterol Nutr. 2009 Oct;49(4):393-9. doi: 10.1097/MPG.0b013e31819c4b3e.
Eosinophilic esophagitis (EE) is a clinical entity that is recognized increasingly in children. The treatment of EE has been debated since its identification as a clinical entity separate from reflux esophagitis. We hypothesize that the treatment with a high-dose proton pump inhibitor (HDPPI) helps differentiate EE from noneosinophilic esophagitis (NEE).
Retrospective review of 2221 patients who underwent esophagogastroduodenoscopy (EGD) with biopsies was undertaken. Sixty-nine patients had more than or equal to 15 eosinophils/high-power field (eos/HPF) in 1 or more esophageal levels. Of those, 36 were initially treated with HDPPI for 3 months followed by repeat EGD. Patients who demonstrated histologic response were classified as NEE. Patients with no histologic response were diagnosed as having EE and treated with HDPPI+swallowed fluticasone for 3 months followed by repeat EGD.
Of the 36 patients, histologic response was seen in 14 (39%) after treatment with HDPPI; 95% confidence interval (0.23-0.54). Swallowed fluticasone was added to the treatment of the 22 patients who did not show histologic response to HDPPI alone. Of those, 15 patients underwent repeat endoscopies. Seven patients were lost to follow-up or did not have repeated EGDs. Histologic response was observed in 9 of 15 (60%) patients. Of the nonresponders (6 of 15), 5 of 6 (83%) self-reported noncompliance with the swallowed fluticasone. Patients with more than or equal to 15 eos/HPF at all 3 levels (25 of 36) were less likely to respond to HDPPI alone and more likely to be categorized as EE (18 of 25), P=or<0.043. Symptomatically, 28 of 36 patients reported resolution of symptoms after HDPPI therapy alone, P=or<0.0001, regardless of histology. Visual endoscopic findings during the first and second EGDs did not show any significance in differentiating EE from NEE, P=0.625 and P=0.2405, respectively.
The study demonstrates that HDPPI can be used to help differentiate EE from NEE histologically. Moreover, patients with more than or equal to 15 eos/HPF at all 3 levels are less likely to respond to HDPPI than patients with more than or equal to 15 eos/HPF at fewer than 3 levels. Therefore, having more than or equal to 15 eos/HPF at 1 or 2 biopsy levels does not necessarily establish the diagnosis of EE. Symptomatic response to HDPPI does not correlate with histologic findings. Clinical management guided by EGD with biopsy helps distinguish patients with EE from those with NEE.
嗜酸性食管炎（EE）是一种在儿童中越来越被认识到的临床实体。自被确定为一种与反流性食管炎不同的临床实体以来，EE 的治疗一直存在争议。我们假设高剂量质子泵抑制剂（HDPPI）的治疗有助于将 EE 与非嗜酸性食管炎（NEE）区分开来。
对 2221 例接受食管胃十二指肠镜检查（EGD）并进行活检的患者进行了回顾性分析。69 例患者在 1 个或多个食管水平的 1 个或多个高倍视野（HPF）中嗜酸性粒细胞大于或等于 15 个/HPF。其中，36 例最初接受 HDPPI 治疗 3 个月，然后重复 EGD。表现出组织学反应的患者被归类为 NEE。没有组织学反应的患者被诊断为 EE，并接受 HDPPI+吞咽氟替卡松治疗 3 个月，然后重复 EGD。
在接受 HDPPI 治疗的 36 例患者中，有 14 例（39%）出现组织学反应；95%置信区间（0.23-0.54）。对单独使用 HDPPI 治疗无组织学反应的 22 例患者加用吞咽氟替卡松治疗。其中，15 例患者接受了重复内镜检查。7 例患者失访或未行重复 EGD。9 例（60%）患者观察到组织学反应。在未反应者（15 例中的 6 例）中，5 例（83%）自述不遵守吞咽氟替卡松的规定。所有 3 个水平嗜酸性粒细胞大于或等于 15 个/HPF 的患者（36 例中的 25 例）更不可能单独对 HDPPI 有反应，更有可能被归类为 EE（25 例中的 18 例），P=或<0.043。症状上，28 例患者在单独接受 HDPPI 治疗后报告症状缓解，P=或<0.0001，无论组织学如何。第一次和第二次 EGD 期间的可视内镜检查结果在区分 EE 与 NEE 方面均无显著意义，P=0.625 和 P=0.2405。
本研究表明，HDPPI 可用于帮助组织学上区分 EE 和 NEE。此外，与在少于 3 个水平有大于或等于 15 个/HPF 的患者相比，在所有 3 个水平有大于或等于 15 个/HPF 的患者对 HDPPI 的反应性较低。因此，在 1 或 2 个活检水平有大于或等于 15 个/HPF 的嗜酸性粒细胞并不一定能确立 EE 的诊断。对 HDPPI 的症状反应与组织学发现不相关。以 EGD 结合活检为指导的临床管理有助于区分 EE 患者与 NEE 患者。
