Department of Pediatric Gastroenterology, Hepatology and Nutrition, Assistance Publique-Hôpitaux de Paris, Necker-Enfants Malades Hospital, Université Paris Descartes, Sorbonne Paris Cité, 149 rue de Sèvres, 75015, Paris, France,
Hum Genet. 2014 Mar;133(3):299-310. doi: 10.1007/s00439-013-1380-6. Epub 2013 Oct 19.
Congenital tufting enteropathy (CTE) is a rare and severe enteropathy recently ascribed to mutations in the epcam gene. Here we establish SPINT2, previously ascribed to congenital sodium diarrhea, as a second gene associated with CTE and report molecular and immunohistochemistry data in 57 CTE patients. Inclusion criteria were early onset diarrhea and intestinal insufficiency with the typical histological CTE abnormalities. The clinical phenotype was registered, the entire coding regions of epcam and SPINT2 sequenced, and immunostaining of EpCAM and SPINT2 performed on intestinal biopsies. An epcam mutation was involved in 41 patients (73 %) who mainly displayed isolated digestive symptoms. Mutations severely affected gene expression since the EpCAM signal on intestinal tissues was either undetectable or low and irregular. Twelve other patients (21 %) carried mutations in SPINT2, and were phenotypically characterized by systematic association with keratitis (p < 10(-4)) and, for half of them, with choanal atresia (p < 10(-4)). Dependency on parenteral nutrition (PN) was comparable in patients with epcam or SPINT2 mutations, but the frequent epcam mutation c.556-14A>G (abnormal splicing) was significantly associated with a better outcome (p = 0.032) with milder PN dependency to weaning in some cases. Finally, four patients (7 %) with isolated digestive symptoms had no detectable epcam or SPINT2 mutation. Two candidate genes, Elf3 and Claudin7, were excluded from this population. Our study allows us to separate CTE patients into at least three genetic classes, each with specific phenotypes. The genetics approach raises the question of the distinction between two congenital enteropathies. Our findings should help improve the diagnosis of CTE, guide toward strategies of long-term PN management, and limit indications for intestinal transplantation to life-threatening PN complications.
先天性簇状肠病(CTE)是一种罕见且严重的肠病,最近归因于 epcam 基因突变。在这里,我们将先前归因于先天性钠腹泻的 SPINT2 确立为与 CTE 相关的第二个基因,并在 57 例 CTE 患者中报告了分子和免疫组织化学数据。纳入标准为早发性腹泻和伴有典型组织学 CTE 异常的肠功能不全。登记了临床表型,对 epcam 和 SPINT2 的整个编码区进行了测序,并对肠活检进行了 EpCAM 和 SPINT2 的免疫染色。41 例患者(73%)存在 epcam 突变,主要表现为孤立性消化症状。突变严重影响基因表达,因为肠组织上的 EpCAM 信号要么无法检测到,要么低且不规则。其他 12 例患者(21%)携带 SPINT2 突变,其表型特征为与角膜炎(p < 10(-4))系统相关,其中一半患者与鼻后孔闭锁(p < 10(-4))相关。epcam 或 SPINT2 突变患者对肠外营养(PN)的依赖性相当,但频繁的 epcam 突变 c.556-14A>G(异常剪接)与更好的结局显著相关(p = 0.032),在某些情况下,PN 依赖性较弱,更容易断奶。最后,4 例(7%)有孤立性消化症状的患者未检测到 epcam 或 SPINT2 突变。这部分患者排除了两个候选基因 Elf3 和 Claudin7。我们的研究允许将 CTE 患者分为至少三种遗传类型,每种类型都有特定的表型。遗传学方法提出了区分两种先天性肠病的问题。我们的发现应有助于改善 CTE 的诊断,指导长期 PN 管理策略,并将肠移植的适应证限制为危及生命的 PN 并发症。