Authors’ Response

We appreciate the insightful letter-to-editor¹ on our study of the efficacy and safety of an adalimumab biosimilar in axial spondyloarthritis (axSpA).²

We acknowledge the concern regarding the duration of latent tuberculosis infection (LTBI) prophylaxis. The three-month daily isoniazid plus rifampicin (3HR) regimen used in our cohort is a WHO-recommended LTBI treatment and is endorsed by the Indian National TB Elimination Programme, particularly in high TB-burden settings.^3,4 Short-course rifamycin-based regimens are prioritized globally to maximize treatment completion and safety, factors that are paramount in managing chronic inflammatory diseases. While international guidelines often cite rifapentine-based regimens (such as 3HP) as a standard, these are currently not widely available in the Indian market, making the 3HR regimen the most evidence-based and pragmatic short-course option in our setting.

The occurrence of multidrug-resistant tuberculosis in one patient likely reflects reinfection or primary infection with a resistant strain rather than failure of latent tuberculosis infection prophylaxis, as preventive therapy does not protect against new exposure. Furthermore, as noted in our original report, one patient had a history of chronic steroid abuse, which is an additional well-recognised risk factor for tuberculosis. From a clinical perspective, the urgency of initiating tumour necrosis factor inhibitors to prevent irreversible structural damage necessitates timely intervention; delaying therapy for a traditional nine-month course would significantly compromise the ‘window of opportunity’ for these patients. Nonetheless, we agree that vigilant post-biologic surveillance remains essential in endemic regions.

Regarding neurological screening, axSpA primarily causes inflammation of axial structures, such as the sacroiliac and facet joints, vertebral bodies, and entheses; it does not directly affect neural structures. While complications such as cauda equina syndrome are documented, they are rare in clinical practice. Consistent with our safety protocols, patients with a history of demyelinating disease were excluded, and no neurological adverse events were identified. Current guidelines do not mandate routine baseline neuroimaging in asymptomatic patients; we maintain that clinical pharmacovigilance is the most sustainable model for high-volume settings.

We proactively identified attrition and selection bias as primary limitations in our manuscript. In real-world settings, loss to follow up is frequently driven by financial and geographic barriers. As stated, financial constraints likely skewed our 24-wk results toward patients who responded favourably and could afford long-term treatment. This is compounded by the ‘burst’ nature of state-funded relief (CMRF), which can lead to abrupt discontinuation when funds are exhausted. Regarding immunogenicity, while anti-drug antibodies contribute to secondary non-response, therapeutic drug monitoring was not routinely available during the study period; thus, decisions were guided by clinical response. In contemporary practice, treatment decisions are often guided by clinical response because of the high cost and limited accessibility of these assays.

We respectfully disagree with this interpretation. Juvenile spondyloarthritis (JSpA) is a biologically distinct phenotype characterized by higher rates of peripheral arthritis and radiographic hip involvement, a feature we specifically noted as being significantly prevalent in our cohort. Both manifestations are associated with poorer Bath Ankylosing Spondylitis Disease Activity Index (BASDAI)-based responses despite effective control of inflammation. BASDAI is known to underperform in patients with predominant peripheral or hip disease, potentially underestimating the true clinical benefit in JSpA.^5,6 Existing evidence does not demonstrate superior efficacy of alternative biologics over TNF inhibitors in juvenile-onset axial disease, and tumour necrosis factor inhibitors remain the recommended first-line biologic therapy. Therefore, the lower BASDAI50 response observed likely reflects limitations in disease phenotype and outcome measures rather than suboptimal therapeutic choice or delayed intervention.