Ohsie Steven, Gerney Garrett, Gui Dorina, Kahana Doron, Martín Martín G, Cortina Galen
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at the University of California at Los Angeles, Los Angeles, CA 90095, USA.
Hum Pathol. 2009 Jul;40(7):1006-14. doi: 10.1016/j.humpath.2008.12.016. Epub 2009 Mar 17.
A generalized absence of enteroendocrine cells characterizes 2 diarrheal/malabsorptive diseases, namely, enteroendocrine cell dysgenesis and autoimmune polyglandular syndrome 1. However, it is not routine for pathologists to examine mucosal biopsies for enteroendocrine cells in cases of chronic diarrheal illness. Our primary aim was to prospectively examine colonic mucosa for loss of enteroendocrine cells using chromogranin A immunohistochemistry for diagnostic purposes. Our secondary aim was to investigate enterochromaffin cells as a subset of enteroendocrine cells, using serotonin (5HT) immunohistochemistry; we hypothesized that other causes of diarrhea due to loss of enteroendocrine cell subsets are missed by evaluating enteroendocrine cells alone. Our approach was limited to patients with chronic unexplained diarrhea partly selected by referring physicians who considered the patients problematic. Seven problematic patients with reduced enteroendocrine or enterochromaffin cells were collected over a 9-month period and placed in group A. Three group A patients demonstrated reduced enteroendocrine cells relative to controls, and they were later diagnosed as having enteroendocrine cell dysgenesis (n = 1) and autoimmune polyglandular syndrome 1 (n = 2). Four group A patients had reduced enterochromaffin cells but normal enteroendocrine cells. These 4 patients had conditions such as congenital diarrhea, mild graft-versus-host disease, acquired childhood chronic diarrhea, and diarrhea post lung transplant. The reduced enterochromaffin cells in the graft-versus-host disease patient inspired a third aim, that is, to investigate whether a loss of enterochromaffin cells would be a generalized defect seen in patients with mild colonic graft-versus-host disease (group B). However, no loss of enterochromaffin cells was detected in group B. Two methods of enumerating endocrine cells were used and demonstrated 67% agreement.
两种腹泻/吸收不良疾病的特征是肠内分泌细胞普遍缺失,即肠内分泌细胞发育不全和自身免疫性多腺体综合征1型。然而,对于慢性腹泻疾病患者,病理学家常规不会检查黏膜活检组织中的肠内分泌细胞。我们的主要目的是前瞻性地使用嗜铬粒蛋白A免疫组织化学检查结肠黏膜中肠内分泌细胞的缺失情况,以用于诊断。我们的次要目的是使用血清素(5HT)免疫组织化学研究作为肠内分泌细胞亚群的肠嗜铬细胞;我们假设仅评估肠内分泌细胞会遗漏因肠内分泌细胞亚群缺失导致腹泻的其他原因。我们的研究方法仅限于患有慢性不明原因腹泻的患者,部分患者由认为其病情棘手的转诊医生挑选。在9个月的时间里收集了7例肠内分泌或肠嗜铬细胞减少的棘手患者,并将其归入A组。A组中有3例患者相对于对照组肠内分泌细胞减少,后来被诊断为患有肠内分泌细胞发育不全(n = 1)和自身免疫性多腺体综合征1型(n = 2)。A组中有4例患者肠嗜铬细胞减少但肠内分泌细胞正常。这4例患者患有先天性腹泻、轻度移植物抗宿主病、儿童获得性慢性腹泻和肺移植后腹泻等疾病。移植物抗宿主病患者肠嗜铬细胞减少促使我们提出第三个目的,即研究肠嗜铬细胞缺失是否是轻度结肠移植物抗宿主病患者(B组)中普遍存在的缺陷。然而,在B组中未检测到肠嗜铬细胞缺失。我们使用了两种内分泌细胞计数方法,结果显示一致性为67%。