Dear Editor, We read with great interest the article by Rocha et al. entitled “Tumor necrosis factor inhibitors prevent structural damage in hips in ankylosing spondylitis—time to reconsider treatment guidelines?… Click to show full abstract
Dear Editor, We read with great interest the article by Rocha et al. entitled “Tumor necrosis factor inhibitors prevent structural damage in hips in ankylosing spondylitis—time to reconsider treatment guidelines? A case series and review of literature.” The authors sought to assess the potential structural effect of TNF inhibitors on hip joint damage in patients with spondyloarthritis (SpA). Three out of the four reported patients had no worsening in hip damage under TNF inhibitors. In this context, we would like to emphasize a few points that can make these conclusions more generalizable. Hip involvement is the most frequent extraspinal arthritic complication of SpA, affecting approximately 24 to 36% of patients [1]. Despite the postoperative improvements in pain, functioning, and hip range of motion, total hip replacement (THR) should no longer be considered the optimal therapeutic option, especially in young patients. Given the potential need for revision surgery and the limited life span of the hip prosthesis [2], conservative treatment should be the preferred option. In fact, anti-TNF agents have revolutionized the management and radically changed the prognosis of SpA. While their ability to decelerate the spinal progression is well-established, their positive impact on the hip involvement is a matter of great debate. The first point we would like to draw attention to is the decline in the incidence of hip replacement surgery over the last few decades, suggesting a possible structural effect of the novel treatments, mainly TNF-alpha blockers. Furthermore, previous studies have shown that the synovial hip joint membrane in SpA shares comparable histological features to those seen in rheumatoid arthritis (RA) [3]. Given the welldocumented ability of TNF inhibitors to reduce destructive processes in RA, we hypothesize they can decelerate hip joint damage in SpA patients. Besides, the structural TNF inhibitor effect has been demonstrated not only by the case reports and series reported by this paper [4–6] but also by several retrospective or prospective studies, including up to 136 patients [7–9]. According to Rocha and colleagues, it would be difficult to conduct long-term placebo-controlled trials specifically for the treatment of hip involvement, and the radiographic progression at hips can only be a secondary outcome even in future clinical trials. This is generally the case, but not always. Indeed, we have recently published a retrospective cohort study of 94 patients comparing hip joint damage in patients under TNF inhibitors and anti-TNF-naïve patients [10]. Our results are consistent with those of Rocha et al. and show the absence of structural damage under long-term anti-TNF alpha therapy. We assessed hip joint progression by the Bath Ankylosing Spondylitis Radiology Index (BASRI)-hip, an accurate assessment tool of hip joint damage used by several studies. However, we have to admit that MRI remains the preferred imaging tool to detect the initial and subtle hip lesions such as synovial enhancement, joint effusion, and subchondral bone marrow edema. Therefore, further welldesigned prospective studies with MRI hip joint assessment are required to confirm these findings. Given the significant functional impotence and impaired quality of life of SpA patients with hip involvement, current data encourage the wider use of TNF inhibitors. We believe that adopting this new perspective as a strong recommendation can be immensely helpful in significantly decreasing the incidence of hip replacement surgery in this young population. * Dorra Ben Nessib [email protected]
               
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