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This review examines how the management of childhood uveitis has evolved over the past two decades, focusing on changes in treatment strategies, escalation pathways, safety, and the expanding role of biologic response modifiers
Over the past two decades, the management of paediatric non- infectious uveitis has undergone a fundamental transformation
Childhood uveitis is a rare, but potentially sight-threatening, condition, accounting for approximately 1–5 per cent of uveitis cases worldwide, while contributing disproportionately to visual morbidity. The disease is often chronic, asymptomatic, and associated with systemic conditions such as juvenile idiopathic arthritis (JIA), frequently presenting with complications including cataract, glaucoma, and cystoid macular oedema. Historically, management relied heavily on prolonged corticosteroid therapy and conventional immunosuppressive agents, which were associated with significant adverse effects and variable efficacy. Over the past two decades, the introduction of biologic response modifiers (BRMs) has transformed the therapeutic landscape of paediatric non-infectious uveitis. This review examines the evolution of treatment strategies, using early cohort evidence, including the fundamental work of Michael J Gallagher and colleagues, as a reference point, and tracing the shift towards evidence-based, stepwise management algorithms. The emergence of high-quality randomised controlled trials, notably SYCAMORE and ADJUVITE, has established anti-tumour necrosis factor (TNF-a) agents, particularly adalimumab in combination with methotrexate (MTX), as the cornerstone of therapy in refractory disease. In addition, this review explores the expanding role of newer biologic agents targeting alternative inflammatory pathways, including interleukin-6 (IL-6) inhibition with tocilizumab, as well as emerging therapies for treatment-resistant cases. Despite these advances, limitations remain, particularly the lack of large-scale paediatric trials and the need for long-term safety data. Overall, the management of childhood uveitis has evolved from empiric immunosuppression to a structured, targeted approach aimed at achieving sustained remission and preventing irreversible visual loss.
…the management of childhood uveitis has evolved from empiric immunosuppression to a structured, targeted approach aimed at achieving sustained remission and preventing irreversible visual loss
Introduction
While childhood uveitis is uncommon, it carries disproportionately high morbidity and poor visual outcomes.1 The disease is often asymptomatic and chronic, frequently presenting late with complications such as cataract, glaucoma, and cystoid macular oedema, which may result in permanent visual loss. This underlines the importance of early detection and regular screening, particularly in children with underlying systemic disease.1,2
The most common systemic association is JIA, an autoimmune condition conferring a high risk of chronic anterior uveitis and its complications.2-4 Non-infectious causes, although less common overall, tend to be more severe, often bilateral, recurrent, and resistant to conventional therapies requiring a more aggressive immunomodulatory approach.5
First-line treatment remains topical glucocorticoids, preferred over systemic corticosteroids such as prednisolone.5 However, their role is largely limited to short-term disease control due to significant adverse effects, including cataract formation, raised intraocular pressure, glaucoma, and, with systemic exposure, growth suppression and endocrine complications.6 Consequently, modern management has shifted towards early introduction of steroid-sparing therapies, particularly BRMs.5
One of the earliest structured reports on BRMs in paediatric uveitis was the study by Gallagher et al, which demonstrated benefit in refractory cases across a heterogeneous cohort, albeit with limitations of small sample size and retrospective design.7 Since then, treatment strategies have evolved substantially. BRMs, particularly anti-tumour necrosis factor (TNF)-a monoclonal antibodies, are now established as the key escalation step following failure of conventional immunosuppressive therapy such as MTX.5,8
This review examines how the management of childhood uveitis has evolved over the past two decades, focusing on changes in treatment strategies, escalation pathways, safety, and the expanding role of BRMs, using the Gallagher et al study as a reference point.
Early biologics: Where it all began
In the early 2000s, BRMs for childhood uveitis were largely limited to three key agents: Infliximab and adalimumab, both tumour necrosis factor (TNF)-a inhibitors, and daclizumab, an interleukin-2 (IL-2) receptor antagonist.7 These agents dominated early biologic therapy and were supported by the available evidence at the time. However, this evidence base was limited, consisting predominantly of small, retrospective studies with heterogeneous patient cohorts, which restricted the generalisability of findings.9-12
At a mechanistic level, it had already been established that the pathophysiology of uveitis, particularly in HLA-B27-associated and other systemic inflammatory uveitides, involves elevated levels of TNF-a in the aqueous humour.13 This provided a strong biological rationale for the early adoption of anti-TNF therapies. Among these, infliximab had the most robust paediatric evidence-base at the time. High-dose infliximab in refractory non-infectious uveitis demonstrated significant reductions in intraocular inflammation and was generally well tolerated in paediatric cohorts.9,10 These findings were reflected in early reports where infliximab produced some of the most favourable outcomes, including remission in three paediatric cases.7
In contrast, adalimumab appeared less effective in early cohort literature, although interpretation is limited by the small sample size.7 Nonetheless, contemporary studies reported up to an 80.8 per cent reduction in inflammatory activity with no significant adverse effects.11 Additionally, early evidence suggested potential advantages of adalimumab over infliximab, including subcutaneous administration, reduced dosing frequency, and improved cost-effectiveness.12 Despite these theoretical and practical benefits, the absence of robust randomised controlled trials (RCTs) at the time meant that paediatric clinical evidence remained stronger for infliximab.
Another TNF inhibitor, etanercept, was also explored for use in childhood uveitis. However, even early studies suggested inferior efficacy compared to monoclonal antibody TNF inhibitors such as infliximab.14 This has since been reinforced by more recent guidelines, which recommend monoclonal anti-TNF agents (infliximab, adalimumab) over etanercept for uveitis management.5
Finally, daclizumab emerged in initial early studies as a promising therapeutic option. As an IL-2 receptor antagonist, it demonstrated efficacy across a heterogeneous cohort of paediatric patients.7 Notably, at the time, this study represented the only available clinical evidence evaluating daclizumab in paediatric uveitis. While initial results were encouraging, the limited evidence-base and lack of subsequent large-scale studies restricted its early clinical adoption.
The evidence shift
The key shift in the evidence-base supporting biologic therapies in childhood uveitis came with the emergence of large RCTs that were double-blind and placebo-controlled, particularly in paediatric populations. This represented a significant advancement from earlier observational and retrospective studies, providing more robust and less biased data on efficacy and safety.
The most influential of these trials include SYCAMORE (2017) and ADJUVITE (2018), both evaluating the role of adalimumab, particularly in combination with MTX, in JIA-associated uveitis.15,16
In contrast to the Gallagher et al paper,7 which was exploratory and aimed to establish whether biologics had a safe and effective role in refractory childhood uveitis, these later RCTs were designed to directly assess clinical efficacy using stricter inclusion criteria and significantly larger cohorts. Although the early cohort data reported adalimumab as the least effective biologic in its cohort,7 this finding must be interpreted in the context of small sample size and limited early evidence, as prior supporting studies were not sufficiently powered or comparable.11,12 Subsequent large-scale RCTs have since redefined treatment guidelines.5
The SYCAMORE trial was a multicentre, double-blind, randomised placebo-controlled trial involving children over the age of two years with active uveitis despite MTX therapy.15 It compared adalimumab plus MTX versus MTX plus placebo. The trial was terminated early due to clear evidence of efficacy: Treatment failure occurred in 27 per cent of patients receiving adalimumab compared to 60 per cent in the placebo group, demonstrating a significant reduction in disease progression. While adverse events were more frequent in the adalimumab group, they were consistent with the known safety profile. This trial was pivotal in establishing the combination of MTX and adalimumab as a standard of care, subsequently reflected in international guidelines.5,16
Similarly, the ADJUVITE trial,17 another double-blind RCT, reinforced the findings of SYCAMORE. It evaluated children aged ≥four years with chronic JIA-associated uveitis refractory to MTX. A key methodological strength was the use of laser flare photometry (≥30 photons/ms) as a sensitive and objective measure of intraocular inflammation. This highlighted the importance of detecting subclinical (‘silent’) inflammation, supporting the need for early and regular screening in paediatric uveitis.
Results demonstrated a 56 per cent response rate with adalimumab versus 20 per cent with placebo, with rapid improvement observed within two months. The subsequent open-label phase, in which all patients received adalimumab, showed improvement in the initial placebo group, further reinforcing its efficacy. Importantly, no new safety concerns were identified, strengthening its favourable safety profile in paediatric populations.17
The VISUAL I and VISUAL II trials,18,19 although conducted in adult populations, were high-quality phase 3 RCTs that further supported the role of adalimumab in non-infectious uveitis. These studies demonstrated that adalimumab significantly reduced the risk of treatment failure and uveitic flare following glucocorticoid withdrawal, as well as reducing the risk of visual impairment. While not paediatric-specific, their comprehensive framework and large sample sizes provide strong supportive evidence for the broader efficacy of anti-TNF therapies in uveitis.
In the early 2000s, infliximab had a stronger evidence base in paediatric uveitis, a finding also reflected in the Gallagher et al paper.7 Early studies demonstrated sustained control of inflammation, although relapses were common upon discontinuation.10 Long-term safety data did not reveal major new toxicities, but these studies highlighted an important limitation being maintenance dependence.
Subsequent evidence refined the use of infliximab, particularly regarding dosing strategies. Studies demonstrated that dose escalation (up to four-fold increases) was often required to achieve adequate disease control and was not associated with increased adverse events, with doses <10mg/kg every four weeks often proving insufficient.20 Although later follow-up studies suggested that early high-dose therapy may be beneficial, optimal dosing regimens remained unclear.20 These findings illustrate a progression from initial efficacy signals to a more nuanced understanding of dosing requirements.
Despite early data suggesting superior efficacy of infliximab compared to adalimumab,7 more recent comparative studies and long-term follow-up data have demonstrated that adalimumab has a more favourable efficacy and safety profile, particularly for long-term management of JIA-associated uveitis.21 While infliximab remains effective in reducing inflammation, adalimumab is now generally preferred due to lower adverse event rates and more consistent long-term outcomes.
Finally, the potential of daclizumab, highlighted in early observational studies,7 has not translated into long-term clinical use. Post-marketing surveillance identified rare but severe immune-mediated adverse events, including inflammatory encephalitis and meningoencephalitis, some of which were fatal. As a result, daclizumab (Zinbryta) was withdrawn from the European market in 2018 following a review by the European Medicines Agency.22
This highlights an important limitation of early biologic trials: Rare but serious adverse effects may only become apparent through long-term pharmacovigilance, emphasising the need for continued safety monitoring even after initial trial approval.
Beyond anti-TNF: Emerging biologics
As discussed previously, adalimumab has become the primary first-line BRM in refractory paediatric uveitis. Despite its central role, a number of newer biologic agents have been investigated for cases refractory to anti-TNF-a therapy, several of which are now incorporated into more recent treatment guidelines.16,23 However, the evidence base for these agents remains limited, and they are generally reserved for failure of first-line anti-TNF therapy, most commonly adalimumab.16,23
One of the most extensively studied second-line agents is tocilizumab, an (IL-6) receptor inhibitor that blocks IL-6-mediated inflammatory signalling.24 Tocilizumab initially demonstrated efficacy in rheumatological conditions, particularly systemic JIA, which led to its investigation in uveitis.25 The APTITUDE trial (2020), a phase 2 study in paediatric patients with JIA-associated uveitis refractory to both MTX and adalimumab, evaluated its efficacy in this setting.25 Although the trial did not meet its primary endpoint, only 33 per cent of patients achieved a predefined reduction in intraocular inflammation, clinically meaningful responses were observed in approximately one-third of participants. Notably, among the 19 per cent of patients with cystoid macular oedema, 75 per cent experienced resolution; highlighting a potential role for tocilizumab in macular oedema control.25 In terms of safety, adverse events were reported in 95 per cent of patients; however, none were classified as serious.25 These findings suggest that while tocilizumab may not be broadly effective for all refractory cases, it has a valuable role in selected patients, particularly those with macular oedema, and is therefore best positioned as a second- or third-line agent.25,26 This has been reflected in updated guidelines, where tocilizumab is now recommended following anti-TNF failure, alongside infliximab.23,26
Another biologic explored in this context is abatacept, which inhibits T-cell activation by binding to CD80/CD86 on antigen-presenting cells, thereby blocking co-stimulatory signalling.24 Evidence for abatacept in refractory uveitis is limited to small case series and cohort studies, but these suggest a favourable safety profile and potential efficacy.27 In one small cohort, the majority of patients tolerated treatment well, with only one out of seven patients discontinuing due to intolerance.27 While promising, the paucity of data and absence of controlled trials limit its current role, and abatacept remains an emerging option in highly refractory disease.
Golimumab, another anti-TNF-a agent, has also been investigated as an alternative following adalimumab failure.16 As a fully human monoclonal antibody, it offers a theoretical advantage in reduced immunogenicity. Evidence from small cohort studies suggests efficacy in refractory uveitis, with intravenous golimumab demonstrating high response rates in JIA, achieving remission in up to 84.6 per cent of patients.28 However, data specific to uveitis remain limited, and its use is currently restricted to selected non-responders.16
Finally, rituximab, which targets CD20-positive B-cells, has shown benefit in non-infectious uveitis, particularly in refractory posterior uveitis, Behçet’s disease, and JIA-associated cases unresponsive to TNF-a inhibitors.24 Retrospective studies suggest that rituximab may be particularly beneficial in oligoarticular and polyarticular JIA-associated uveitis.29 However, its use is tempered by safety concerns, including infusion reactions and immunosuppression-related risks, and some studies suggest that multiple treatment cycles (up to four) may be required to optimise efficacy while mitigating adverse effects.29
Current management: A stepwise approach
The contemporary management of refractory childhood uveitis follows a structured, stepwise escalation approach, significantly shaped by the introduction of BRMs. Current international guidelines emphasise early control of inflammation while minimising corticosteroid-related toxicity.5,16,30
Topical glucocorticoids, most commonly prednisolone acetate 1 per cent, remain first-line for rapid suppression of intraocular inflammation. However, early tapering and transition to steroid-sparing therapy are strongly recommended to reduce complications such as glaucoma and cataract formation.5,6,16
Systemic conventional immunomodulatory therapy (DMARDs) is the next step, with MTX as the cornerstone first-line agent. This is supported by the FAST trial, a randomised controlled study demonstrating superior efficacy of MTX over mycophenolate mofetil, albeit in a predominantly adult cohort.31 Other agents, including tacrolimus, cyclosporine, and azathioprine, show comparatively reduced efficacy, with cyclosporine having limited value and tacrolimus retaining a potential role only in refractory cases.32,33
In cases of inadequate response to MTX, escalation to biologic therapy is recommended. Anti-TNF agents are the preferred first-line biologics, with adalimumab as the agent of choice, supported by trials such as SYCAMORE and ADJUVITE.15,17 Infliximab is typically reserved for patients refractory to adalimumab.5,16,30 Some guidelines include golimumab as an alternative, while etanercept is consistently not recommended due to inferior efficacy in uveitis.5,16,30
For persistent disease despite MTX and anti-TNF therapy, a stepwise intensification strategy is advised. Initial measures include dose escalation or increased dosing frequency, followed by within-class switching. If unsuccessful, transition to alternative biologic classes is recommended, most notably IL-6 inhibition with tocilizumab.23,25 Additional options include switching to or combining with other DMARDs such as mycophenolate mofetil, cyclosporine, or leflunomide.5,16,30
Escalation is guided by persistent inflammation, inability to taper corticosteroids, or lack of improvement in visual acuity. Long-term disease control is essential, with guidelines recommending at least two years of remission before tapering systemic therapy.5,18,30 Given the often asymptomatic nature of paediatric uveitis, regular monitoring is crucial to detect subclinical progression.
A key evolution from early 2000s practice is the emphasis on dose optimisation. In the early cohort literature infliximab dosing ranged from 100-700mg every two weeks initially, then every four to eight weeks.7 Subsequent evidence, including Sukumaran et al,20 demonstrated that dose escalation up to four-fold may be required for adequate control, a principle now embedded in modern algorithms. Similarly, adalimumab dosing (40mg/m² every other week) has remained consistent from early studies through to trials such as SYCAMORE.7,15 The major advancement lies not in initial dosing, but in recognising dose escalation as the most effective step following treatment failure, now explicitly incorporated into guideline recommendations.
Looking ahead
Over the past two decades, the management of paediatric non-infectious uveitis has undergone a fundamental transformation. What was once a condition managed primarily with prolonged corticosteroid therapy and limited immunosuppressive options has evolved into a structured, evidence-based, stepwise approach centred on early introduction of steroid-sparing therapies and targeted biologic agents.5,16,30
The transition from small retrospective cohorts, such as the original study by Gallagher et al,7 to high-quality RCTs including SYCAMORE and ADJUVITE has been pivotal in redefining clinical practice.15,17 These trials, supported by adult data from VISUAL I and II,18,19 have established anti-TNF-a therapy, particularly adalimumab in combination with MTX, as the standard of care in refractory disease, significantly improving disease control and long-term visual outcomes.5,16
Despite these advances, important limitations remain. Paediatric evidence is still relatively limited, with small sample sizes and a lack of direct comparative trials between BRMs, particularly in patients who fail first-line anti-TNF therapy.5,23 This represents a key gap in the current treatment framework and highlights the need for larger, well-designed paediatric studies to better guide escalation strategies.
Emerging therapeutic targets offer promising avenues for future management. IL-6 inhibition with tocilizumab has demonstrated potential in refractory disease, particularly in cases complicated by cystoid macular oedema, although its efficacy appears variable and requires further validation.23,25,26 Other cytokine pathways, including IL-1 and IL-27, as well as novel approaches such as exosome-based therapies and nanobodies, may allow for more targeted immunomodulation in the future.24 In addition, translating robust adult trial data into paediatric populations may help accelerate therapeutic development.18,19
Importantly, the evolution of biologics has not only expanded treatment options, but has reshaped therapeutic goals, shifting focus toward early intervention, sustained remission, and prevention of irreversible visual damage.5,16 However, long-term safety remains a critical consideration. The withdrawal of daclizumab following rare, but severe, immune-mediated adverse events highlights the importance of continued pharmacovigilance and long-term follow-up in paediatric populations.22
In conclusion, biologic therapies have transitioned from experimental interventions to a cornerstone of modern management in refractory childhood uveitis. Future progress will depend on strengthening the paediatric evidence base, refining treatment algorithms beyond anti-TNF therapy, and ensuring long-term safety while continuing to improve visual outcomes in this high-risk population.
Acknowledgments
The author would like to thank Michael J Gallagher for his guidance and supervision during the development of this manuscript.
Conflict of interest
The authors declare no conflicts of interest.
Corresponding author
Anna Macháček
Email: machacea@tcd.ie
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