Section of Pediatric Gastroenterology, Hepatology, and Nutrition, Digestive Health Institute, Children's Hospital Colorado, Aurora, CO 80045, USA.
J Pediatr Gastroenterol Nutr. 2013 Feb;56(2):166-72. doi: 10.1097/MPG.0b013e3182716b7a.
Differentiation between the common etiologies of dense esophageal eosinophilia such as gastroesophageal reflux disease (GERD) and eosinophilic esophagitis can be difficult. We hypothesized that histologic features may provide diagnostic clues concerning the etiology of esophageal eosinophilia.
: We performed a retrospective chart review of 204 children with the diagnosis of esophagitis characterized by ≥ 15 eosinophils (eos) per high-power field (HPF) in at least 1 biopsy. We then restricted our analysis to subjects who had received at least 8 weeks of only proton pump inhibitors (PPIs) followed by endoscopy and who had a clinicopathologic response to this treatment. Symptoms, endoscopic findings, and pathologic descriptions were reviewed and an eosinophil peroxidase (EPX) index was determined to assess for degranulation/eosinophil activation.
Of the 204 identified charts, 7 subjects identified met the inclusion criteria. Five of these 7 patients showed a clinicopathologic response to PPIs after their follow-up endoscopy, (mean peak eosinophil count: 92 vs 5 eos/HPF, and EPX index: 39.2 vs 14.6, pre- and posttreatment, respectively). Two patients experienced initial resolution of symptoms and esophageal eosinophilia with PPI therapy; however, within 17-23 months they redeveloped symptoms and esophageal eosinophilia while receiving PPI therapy at the time of a third endoscopy (mean peak eosinophil count: 40 vs 11 vs 36 eos/HPF, and EPX index: 44 vs 21 vs 36.5, pre-, post- and posttreatment, respectively). No clinicopathologic features or degranulation patterns differentiated subjects with GERD/PPI responsive esophageal eosinophilia from those who had transient response to PPI treatment.
No clinicopathologic features differentiated subjects who responded to PPI treatment. PPI treatment can be helpful to exclude GERD and PPI responsive esophageal eosinophilia but long-term follow-up is critical in the management of esophagitis.
胃食管反流病（GERD）和嗜酸性食管炎等食管嗜酸性粒细胞增多的常见病因之间的鉴别可能很困难。我们假设组织学特征可能为食管嗜酸性粒细胞增多的病因提供诊断线索。
我们对 204 例诊断为食管炎的患儿进行了回顾性图表审查，这些患儿的食管炎特征为至少 1 次活检中每高倍视野（HPF）≥ 15 个嗜酸性粒细胞（EOS）。然后，我们将分析仅限于至少接受 8 周质子泵抑制剂（PPI）治疗后进行内镜检查且对这种治疗有临床病理反应的患者。回顾了症状、内镜检查结果和病理描述，并确定了嗜酸性粒细胞过氧化物酶（EPX）指数以评估脱颗粒/嗜酸性粒细胞活化。
在确定的 204 份图表中，有 7 份符合纳入标准。这 7 例患者中有 5 例在随访内镜检查后对 PPI 有临床病理反应（平均峰值嗜酸性粒细胞计数：92 与 5 eos/HPF，和 EPX 指数：39.2 与 14.6，分别为治疗前和治疗后）。2 例患者在接受 PPI 治疗后最初缓解了症状和食管嗜酸性粒细胞增多症；然而，在 17-23 个月内，他们在第三次内镜检查时再次出现症状和食管嗜酸性粒细胞增多症，同时正在接受 PPI 治疗（平均峰值嗜酸性粒细胞计数：40 与 11 与 36 eos/HPF，和 EPX 指数：44 与 21 与 36.5，分别为治疗前、治疗后和治疗后）。没有临床病理特征或脱颗粒模式可以区分对 PPI 治疗有反应的 GERD/PPI 相关食管嗜酸性粒细胞增多症与对 PPI 治疗有短暂反应的患者。
没有临床病理特征可以区分对 PPI 治疗有反应的患者。PPI 治疗有助于排除 GERD 和 PPI 反应性食管嗜酸性粒细胞增多症，但长期随访对食管炎的治疗至关重要。
