Division of Allergy and Clinical Immunology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Domino's Farms, 24 Frank Lloyd Wright Drive, PO Box 442, Suite H-2100, Ann Arbor, MI, 48106-0442, USA.
Clin Rev Allergy Immunol. 2019 Oct;57(2):194-212. doi: 10.1007/s12016-018-8695-y.
Hypereosinophilic syndrome and mastocytosis are relatively rare proliferative diseases encountered in the general population. However, allergists frequently consider these disorders in the differential of patients presenting with gastrointestinal, pulmonary, cutaneous, and allergic symptoms. Gastrointestinal symptoms are some of the most frequent and/or debilitating aspects of both disease states and in many cases lead to poor quality of life and functional limitation for the patient. They are the third most common clinical manifestation in hypereosinophilic syndrome and have been found to be the most distressful aspect of the disorder in those with systemic mastocytosis. Both eosinophils and mast cells play integral parts in normal gut physiology, but when and how exactly their effector functionality translates into clinically significant disease remains unclear, and the available literature regarding their pathophysiology remains sparse. Eosinophils and mast cells even, in fact, may not necessarily function in isolation from each other but can participate in bidirectional crosstalk. Both are affected by similar mediators and can also influence one another in a paracrine fashion. Their interactions include both production of soluble mediators for specific eosinophil and mast cell receptors (for example, eosinophil recruitment and activation by mast cells releasing histamine and eotaxin) as well as direct physical contact. The mechanistic relationship between clonal forms of hypereosinophilia and systemic mastocytosis has also been explored. The nature of gastrointestinal symptomatology in the setting of both hypereosinophilic syndrome and mast cell disease is frequently manifold, heterogeneous, and the lack of better targeted therapy makes diagnosis and management challenging, especially when faced with a substantial differential. Currently, the management of these gastrointestinal symptoms relies on the treatment of the overall disease process. In hypereosinophilia patients, systemic corticosteroids are mainstay, although steroid-sparing agents such as hydroxyurea, IFN-α, methotrexate, cyclosporine, imatinib, and mepolizumab have been utilized with varying success. In mastocytosis patients, anti-mediator therapy with antihistamines and mast cell stabilization with cromolyn sodium can be considered treatments of choice, followed by other therapies yet to be thoroughly studied, including the role of the low-histamine diet, corticosteroids, and treatment of associated IBS symptoms. Given that both eosinophils and mast cells may have joint pathophysiologic roles, they have the potential to be a combined target for therapeutic intervention in disease states exhibiting eosinophil or mast cell involvement.
高嗜酸性粒细胞综合征和肥大细胞增多症是在普通人群中相对罕见的增殖性疾病。然而,过敏症专家经常在鉴别出现胃肠道、肺部、皮肤和过敏症状的患者时考虑这些疾病。胃肠道症状是这两种疾病状态中最常见和/或使人虚弱的方面之一,在许多情况下会导致患者生活质量下降和功能受限。它们是高嗜酸性粒细胞综合征的第三大常见临床表现,并且在系统性肥大细胞增多症患者中被发现是该疾病最痛苦的方面。嗜酸性粒细胞和肥大细胞在正常肠道生理学中都发挥着不可或缺的作用,但它们的效应功能何时以及如何转化为临床上有意义的疾病尚不清楚,并且关于它们的病理生理学的可用文献仍然很少。事实上,嗜酸性粒细胞和肥大细胞甚至不一定彼此孤立地发挥作用,而是可以相互参与双向串扰。它们都受到相似介质的影响,并且可以以旁分泌方式相互影响。它们的相互作用包括为特定的嗜酸性粒细胞和肥大细胞受体产生可溶性介质(例如,肥大细胞释放组胺和嗜酸性粒细胞趋化因子使嗜酸性粒细胞募集和激活)以及直接的物理接触。克隆形式的高嗜酸性粒细胞增多症和系统性肥大细胞增多症之间的机制关系也得到了探讨。在高嗜酸性粒细胞综合征和肥大细胞疾病中,胃肠道症状的性质常常是多方面的、异质的,并且缺乏更好的靶向治疗使得诊断和管理具有挑战性,尤其是在面对大量差异时。目前,这些胃肠道症状的管理依赖于整体疾病过程的治疗。在高嗜酸性粒细胞增多症患者中,全身性皮质类固醇是主要治疗方法,尽管羟基脲、IFN-α、甲氨蝶呤、环孢素、伊马替尼和美泊利珠单抗等类固醇保留剂已被不同程度地成功应用。在肥大细胞增多症患者中,抗介质治疗可使用抗组胺药和肥大细胞稳定剂(如色甘酸钠),然后是其他尚未经过充分研究的治疗方法,包括低组胺饮食、皮质类固醇的作用以及相关 IBS 症状的治疗。鉴于嗜酸性粒细胞和肥大细胞都可能具有共同的病理生理作用,因此它们有可能成为表现出嗜酸性粒细胞或肥大细胞参与的疾病状态的联合治疗靶点。