Ono Shigeru, Fumino Shigehisa, Iwai Naomi
Department of Pediatric Surgery, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, Japan.
Pediatr Surg Int. 2011 Mar;27(3):237-40. doi: 10.1007/s00383-010-2782-3.
Pancreaticobiliary maljunction (PBM) is associated with an increased frequency of gallbladder malignancy. Intestinal metaplasia is often observed in gallbladder disease and is a risk factor for gallbladder carcinoma in adults. The hyperplasia-dysplasia-carcinoma progression is one of the possible mechanisms involved in biliary carcinogenesis. In this study, we evaluate the gallbladders of children with PBM for intestinal metaplasia and other histological changes.
From January 1997 to July 2010, 45 children with PBM were treated at our institution. A total of 42 children were included in our analysis which included histology and medical record review.
The median age was 2.9 years (range 1 month-16.5 years). The most common histological finding was villous-type mucosal hyperplasia, found in 24 patients (57.1%). Mucous gland metaplasia and goblet cell metaplasia were observed in 12 (28.6%) and 7 (16.7%) patients, respectively. There were no cases of malignancy. The intra-gallbladder amylase level in patients with mucosal hyperplasia was significantly elevated (81,373 ± 92,442 vs. 38,932 ± 61,466; p = 0.042). Patients with mucous gland metaplasia had significantly higher serum amylase levels (833 ± 1,214 vs. 343 ± 358; p = 0.024).
The incidence of intestinal metaplasia is relatively high even in children with PBM. Such mucosal changes are related to cholangitis resulting from the regurgitation of pancreatic juice into the bile duct, which also causes hyperamylasemia via cholangio-venous reflux.
胰胆管合流异常(PBM)与胆囊恶性肿瘤发生率增加相关。肠化生在胆囊疾病中常可见,且是成人胆囊癌的危险因素。增生 - 发育异常 - 癌进展是胆管癌发生的可能机制之一。在本研究中,我们评估了患有PBM的儿童胆囊的肠化生及其他组织学变化。
1997年1月至2010年7月,45例患有PBM的儿童在我们机构接受治疗。我们的分析共纳入42例儿童,包括组织学检查和病历回顾。
中位年龄为2.9岁(范围1个月至16.5岁)。最常见的组织学表现是绒毛型黏膜增生,见于24例患者(57.1%)。分别在12例(28.6%)和7例(16.7%)患者中观察到黏液腺化生和杯状细胞化生。无恶性肿瘤病例。黏膜增生患者的胆囊内淀粉酶水平显著升高(81,373 ± 92,442 vs. 38,932 ± 61,466;p = 0.042)。黏液腺化生患者的血清淀粉酶水平显著更高(833 ± 1,214 vs. 343 ± 358;p = 0.024)。
即使在患有PBM的儿童中,肠化生的发生率也相对较高。此类黏膜变化与胰液反流至胆管导致的胆管炎有关,胆管炎还通过胆管 - 静脉反流引起高淀粉酶血症。