Osadchuk M A, Panfilov Iu A, Kvetnoĭ I M, Iakovleva N D, Pogudina N A
Sov Med. 1989(3):8-13.
A study has been carried out to substantiate the assumption that excessive proliferation of major gastroduodenal endocrine cells may be predetermined genetically. Hereditary predisposition to the hyperplasia of cells belonging to the APUD system may be inherited both through the male and female lines. Duodenal ulcers (DU) undoubtedly involves multifactorial inheritance. Acquired capacity for endocrine cell hyperplasia cannot be excluded in some of DU patients. The development of DU is, apparently, related to the formation of a pathological system, based on pathologic structure-linked neurohormonal relationships between the duodenum and peripheral and central nervous systems that enhance nerve impulses in the duodenal bulbar portion. A sudden "total" catecholamine release occurs at a certain stage and is followed by a change of production/utilization ratios of various hormones that weakens pathologic neurohormonal relationships, destroys the pathologic system and activates the healing process around the ulcer. The pathologic system, active in peptic ulcers, is doubtless counteracted by a system, whose activity must be determined by the number of endocrine cells with beta-endorphine-like and, perhaps, serotonin-like immunoreactivity. The antagonistic regulation principle is of great universal significance for general biology. It is essential for healing and chronization processes.
一项研究已经开展，以证实这样一种假设，即胃十二指肠主要内分泌细胞的过度增殖可能由基因预先决定。属于APUD系统的细胞增生的遗传易感性可能通过父系和母系遗传。十二指肠溃疡（DU）无疑涉及多因素遗传。在一些DU患者中，不能排除内分泌细胞增生的后天获得性能力。DU的发生显然与一个病理系统的形成有关，该病理系统基于十二指肠与外周和中枢神经系统之间与病理结构相关的神经激素关系，这种关系增强了十二指肠球部的神经冲动。在某个阶段会突然发生“全”儿茶酚胺释放，随后各种激素的产生/利用比率发生变化，这削弱了病理神经激素关系，破坏了病理系统并激活了溃疡周围的愈合过程。在消化性溃疡中活跃的病理系统无疑会受到另一个系统的对抗，其活性必须由具有β-内啡肽样以及可能具有5-羟色胺样免疫反应性的内分泌细胞数量来决定。拮抗调节原则对普通生物学具有重要的普遍意义。它对愈合和慢性病过程至关重要。
