Magrey Marina N, Khan Muhammad A
Case Western Reserve University School of Medicine, Cleveland, OH, 44109, USA.
MetroHealth Medical Center, Cleveland, OH, 44109, USA.
Curr Rheumatol Rep. 2017 Apr;19(4):17. doi: 10.1007/s11926-017-0644-x.
The purpose of the study is to briefly review the molecular mechanisms that leads to structural damage in ankylosing spondylitis (AS), defined as new bone formation resulting in complete or incomplete ankylosis of the spine, and the impact of treatment with biologics to retard this process.
The understanding of molecular mechanisms leading to new bone formation in AS has significantly improved but is still incomplete. Availability of biologics has greatly enhanced the treatment of patients with AS, but its impact on slowing the structural damage is still a matter of debate, although a few observational studies have shown that long term use of TNF-α blockers may slow radiographic progression. The availability of newer biologics targeting IL-17/1L23 has shown some promising results in slowing radiographic progression in AS. Although the availability of TNF-inhibitors has greatly enhanced the treatment options for patients with AS, their impact on slowing the structural damage is still not clearly established. However, preliminary results using newer biologics targeting IL-17/1L23 axis are more encouraging but longer follow-up is needed.
本研究旨在简要回顾导致强直性脊柱炎(AS)结构损伤的分子机制,AS的定义为新骨形成导致脊柱完全或不完全强直,以及生物制剂治疗对延缓这一过程的影响。
对导致AS中新骨形成的分子机制的理解有了显著改善,但仍不完整。生物制剂的可用性极大地改善了AS患者的治疗,但其对减缓结构损伤的影响仍存在争议,尽管一些观察性研究表明长期使用TNF-α阻滞剂可能减缓影像学进展。靶向IL-17/IL-23的新型生物制剂的出现,在减缓AS的影像学进展方面显示出一些有前景的结果。尽管TNF抑制剂的可用性极大地增加了AS患者的治疗选择,但其对减缓结构损伤的影响仍未明确确立。然而,使用靶向IL-17/IL-23轴的新型生物制剂的初步结果更令人鼓舞,但需要更长时间的随访。