Solcia E, Rindi G, Silini E, Villani L
Surgical and Anatomical Pathology Service, IRCCS Policlinico San Matteo, Pavia, Italy.
Baillieres Clin Gastroenterol. 1993 Mar;7(1):149-65. doi: 10.1016/0950-3528(93)90035-q.
ECL cells are argyrophilic endocrine cells of the stomach. Their distribution is species specific, however they are consistently located in the oxyntic mucosa and, in particular, in very close contact with the adenomeres of acidopeptic glands. ECL cells store histamine and are considered a key element in the mechanisms of gastric acid secretion as controlled by gastrin stimulus. Their peculiar anatomical disposition and secretory properties strongly suggest that ECL cells exert their function by a paracrine mechanism, i.e. by releasing histamine in the extracellular spaces surrounding acid-producing parietal cells. ECL cell activity is strongly stimulated by gastrin, which, once applied as a long-standing stimulus, also exerts a potent proliferating effect. Long-lasting hypergastrinaemia has been demonstrated to elicit ECL cell proliferation in laboratory animals, inducing ECL cell hyperplasia, dysplasia and ECL cell tumours, i.e. argyrophilic gastric carcinoids. However, in experimental rodents it is believed that hypergastrinaemia is not per se a stimulus capable of inducing ECL cell transformation, a predisposing genetic background being required for tumour development in endocrine organs. In man, long-standing hypergastrinaemia exerts the same proliferative pressure on ECL cells and is associated with hyperplasia with or without dysplastic changes and carcinoid development. Clinical evidence suggests that other factors, both genetic and environmental, are required to induce ECL cell transformation and carcinoid development. For this reason human gastric argyrophilic ECL carcinoids are subdivided into three main groups depending on their clinical background: (1) gastric carcinoids in patients with chronic atrophic gastritis; (2) gastric carcinoids in patients with Zollinger-Ellison and multiple endocrine neoplasia type 1 syndrome (MEN-ZES); and (3) solitary, sporadic gastric carcinoids. The clinical assessment of carcinoid-bearing patients is strongly recommended for better diagnosis and management of patients.
肠嗜铬样(ECL)细胞是胃的嗜银内分泌细胞。它们的分布具有物种特异性,但始终位于胃底黏膜,特别是与泌酸腺的腺泡紧密接触。ECL细胞储存组胺,被认为是胃泌素刺激控制胃酸分泌机制中的关键要素。它们独特的解剖位置和分泌特性强烈表明,ECL细胞通过旁分泌机制发挥功能,即通过在产酸壁细胞周围的细胞外空间释放组胺。胃泌素强烈刺激ECL细胞活性,长期应用胃泌素作为刺激物时,还会产生强大的增殖作用。在实验动物中已证明,长期高胃泌素血症可引发ECL细胞增殖,导致ECL细胞增生、发育异常和ECL细胞瘤,即嗜银性胃类癌。然而,在实验啮齿动物中,人们认为高胃泌素血症本身并非能够诱导ECL细胞转化的刺激因素,内分泌器官肿瘤的发生需要有易患的遗传背景。在人类中,长期高胃泌素血症对ECL细胞施加相同的增殖压力,并与伴有或不伴有发育异常改变的增生以及类癌的发生相关。临床证据表明,诱导ECL细胞转化和类癌发生还需要其他遗传和环境因素。因此,根据临床背景,人类胃嗜银性ECL类癌可分为三大类:(1)慢性萎缩性胃炎患者的胃类癌;(2)卓艾综合征和1型多发性内分泌肿瘤综合征(MEN-ZES)患者的胃类癌;(3)孤立性、散发性胃类癌。强烈建议对类癌患者进行临床评估,以更好地诊断和管理患者。