Bufka J, Sýkora J, Vaňková L, Gutová V, Kačerová Š, Daum O, Schwarz J
Department of Pediatrics, Faculty of Medicine in Pilsen, Faculty Hospital, Charles University in Prague, Alej Svobody 80, Pilsen, 323 00, Czech Republic.
Department of Histology and Embryology, Faculty of Medicine in Pilsen, Charles University, Pilsen, Czech Republic.
Eur J Pediatr. 2024 Feb;183(2):515-522. doi: 10.1007/s00431-023-05324-2. Epub 2023 Nov 10.
We would like to provide an updated comprehensive perspective and identify the components linked to chronic spontaneous urticaria (CSU) without specific triggers in autoimmune atrophic gastritis (AAG). AAG is an organ-specific autoimmune disease that affects the corpus-fundus gastric mucosa. Although we lack a unified explanation of the underlying pathways, when considering all paediatric patients reported in the literature, alterations result in gastric neuroendocrine enterochromaffin-like (ECL) cell proliferation and paracrine release of histamine. Several mechanisms have been proposed for the pathogenesis of CSU, with much evidence pointing towards AAG and ECL cell responses, which may be implicated as potential factors contributing to CSU. The excessive production/release of histamine into the bloodstream could cause or trigger exacerbations of CSU in AAG, independent of Helicobacter pylori; thus, the release of histamine from ECL cells may be the primary modulator.
Considering the understanding of these interactions, recognising the respective roles of AAG in the pathogenesis of CSU may strongly impact the diagnostic workup and management of unexplained/refractory CSU and may inform future research and interventions in the paediatric population.
• Autoimmune atrophic gastritis is a chronic immune-mediated inflammatory disease characterised by the destruction of the oxyntic mucosa in the gastric body and fundus, mucosal atrophy, and metaplastic changes. • Autoimmune atrophic gastritis in paediatric patients is important because of the poor outcome and risk of malignancy and possibly underestimated entities primarily reported in single-case reports.
• Upper gastrointestinal inflammatory disorders, independent of H. pylori, have been implicated as potential inducing factors in the development of chronic spontaneous urticaria. • If a paediatric patient presents with symptoms such as anaemia, reduced vitamin B12 levels, recurrent urticaria with no other detectable aetiology, positive anti-parietal cell antibodies, and elevated gastrin levels, autoimmune atrophic gastritis should be considered a possible cause of chronic urticaria.
我们希望提供一个更新的全面观点，并确定自身免疫性萎缩性胃炎（AAG）中与无特定触发因素的慢性自发性荨麻疹（CSU）相关的组成部分。AAG是一种器官特异性自身免疫性疾病，会影响胃体-胃底黏膜。尽管我们对潜在途径缺乏统一的解释，但考虑文献中报道的所有儿科患者时，病变会导致胃神经内分泌肠嗜铬样（ECL）细胞增殖和组胺的旁分泌释放。已经提出了几种CSU发病机制，许多证据指向AAG和ECL细胞反应，这可能是导致CSU的潜在因素。组胺过度产生/释放到血液中可能会导致或引发AAG中CSU的加重，与幽门螺杆菌无关；因此，ECL细胞释放组胺可能是主要调节因素。
考虑到对这些相互作用的理解，认识到AAG在CSU发病机制中的各自作用可能会对不明原因/难治性CSU的诊断检查和管理产生重大影响，并可能为儿科人群的未来研究和干预提供信息。
• 自身免疫性萎缩性胃炎是一种慢性免疫介导的炎症性疾病，其特征是胃体和胃底的泌酸黏膜破坏、黏膜萎缩和化生改变。
• 儿科患者的自身免疫性萎缩性胃炎很重要，因为其预后不良和恶性肿瘤风险，且可能主要在单病例报告中报道的实体被低估。
• 独立于幽门螺杆菌的上消化道炎症性疾病被认为是慢性自发性荨麻疹发展的潜在诱发因素。
• 如果儿科患者出现贫血、维生素B12水平降低、无其他可检测病因的复发性荨麻疹、抗壁细胞抗体阳性和胃泌素水平升高等症状，应考虑自身免疫性萎缩性胃炎是慢性荨麻疹的可能原因。
