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Chuyển hóa xương trong bệnh lý histiocytosis tế bào Langerhans

Endocrine Connections - Tập 7 Số 7 - Trang R246-R253 - 2018

Athanasios D. Anastasilakis¹, Marina Tsoli², Gregory Kaltsas², Polyzois Makras³

¹1Department of Endocrinology, 424 General Military Hospital, Thessaloniki, Greece

²21st Propaedeutic Department of Internal Medicine, National and Kapodistrian University of Athens, Athens, Greece

³3Department of Endocrinology and Diabetes, 251 Hellenic Air Force & VA General Hospital, Athens, Greece

Tóm tắt

Bệnh histiocytosis tế bào Langerhans (LCH) là một bệnh hiếm với nguyên nhân chưa được xác định rõ ràng, liên quan đến sự kích hoạt tế bào miễn dịch và thường ảnh hưởng đến hệ xương. Sự tham gia của xương trong LCH thường xuất hiện dưới dạng tổn thương tiêu xương cùng với mật độ khoáng xương thấp. Nhiều phân tử liên quan đến chuyển hóa xương được cho là có vai trò trong cơ chế bệnh sinh của LCH hoặc có thể bị ảnh hưởng trong quá trình phát triển của bệnh, bao gồm các interleukin (IL), yếu tố hoại tử khối u α, kích hoạt thụ thể NF-κB (RANK) và ligand hòa tan RANKL của nó, osteoprotegerin (OPG), periostin và sclerostin. Trong số đó, IL-17A, periostin và RANKL đã được đề xuất như là các dấu ấn sinh học tiềm năng trong huyết thanh cho LCH, đặc biệt là vì sự tương tác giữa RANK, RANKL và OPG không chỉ điều chỉnh sự cân bằng xương thông qua tác động lên các tế bào tiêu xương mà còn ảnh hưởng đến sự kích hoạt và tồn tại của các tế bào miễn dịch. Sự thay đổi đáng kể về mức độ RANKL trong tuần hoàn và tổn thương đã được quan sát thấy ở bệnh nhân LCH bất kể có tổn thương xương hay không. Quản lý LCH tiêu chuẩn bao gồm việc sử dụng corticosteroid tại chỗ hoặc toàn thân và hóa trị liệu. Với sự liên quan của RANK, RANKL và OPG trong cơ chế bệnh và tính chất tiêu xương của các tổn thương xương, các tác nhân nhằm ức chế con đường RANKL và/hoặc kích hoạt tế bào tiêu xương, như bisphosphonates và denosumab, có thể có vai trò trong cách tiếp cận điều trị LCH mặc dù cần có điều tra lâm sàng thêm.

Từ khóa

#Langerhans cell histiocytosis; bone metabolism; osteolytic lesions; RANK; RANKL; OPG; biomarkers

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