Efficacy of adalimumab in chronic non-infectious anterior uveitis: a retrospective study

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Methods This was a retrospective, single-center observational study. A total of 114 patients with chronic NIAU who were treated at Baoji People’s Hospital between May 2022 and May 2025 and had complete electronic medical records were included. The cohort comprised 45 males and 69 females, with a mean age of 42.15 ± 14.28 years (range, 7–86 years). Patients were divided into two groups according to whether ADA was administered. The control group (n = 56) received conventional therapy with topical corticosteroids and mydriatic/cycloplegic agents, while the study group (n = 58) received additional subcutaneous ADA on the basis of conventional treatment. Demographic characteristics, disease duration, Anterior chamber cell count(AC cell count), and best-corrected visual acuity (BCVA) were collected. AC cell count, BCVA, treatment efficacy, and recurrence rates were compared at baseline and at 1, 2, and 3 weeks, as well as 3 and 6 months after treatment. Statistical analyses were performed using independent-sample t-tests, Mann–Whitney U tests, and χ² tests, with P 0.05), while disease duration was longer in the study group (P = 0.017). Idiopathic NIAU was the most common etiology (58.62% in the study group and 69.64% in the control group), followed by ankylosing spondylitis, rheumatoid arthritis, juvenile idiopathic arthritis, and psoriatic arthritis. During the first 2 weeks of treatment, AC cell count decreased markedly in both groups, with no significant intergroup differences (all P > 0.05). From week 3 onward, AC cell count improvement was significantly greater in the study group than in the control group (all P < 0.05). BCVA improved in both groups during the first 3 weeks without significant differences; however, at 3 and 6 months, BCVA was significantly better in the study group (both P < 0.05). At 6 months, the study group demonstrated a higher complete remission rate (84.48% vs. 64.29%), a lower recurrence rate (13.79% vs. 28.57%), and a higher overall treatment efficacy (96.55% vs. 87.50%) compared with the control group (all P < 0.05). Conclusions Adalimumab appears to be an effective therapeutic option for recurrent chronic non-infectious anterior uveitis, particularly in patients with underlying autoimmune diseases. ADA can achieve better inflammation control, improve treatment efficacy, reduce recurrence, and decrease the need for corticosteroids and immunosuppressive therapy. chronic non-infectious anterior uveitis adalimumab treatment efficacy recurrence Figures Figure 1 Background Non-infectious anterior uveitis (NIAU) is an immune-mediated form of uveitis that primarily involves the iris and anterior segment of the ciliary body. Unlike infectious uveitis, its onset is not directly related to bacterial, viral, fungal, or parasitic pathogens, but is mainly associated with autoimmune responses, dysregulated immune regulation, or systemic immune-related diseases. NIAU represents the most common subtype of uveitis, accounting for approximately 50% of all uveitis cases [ 1 ]. Clinically, patients typically present with ocular pain, redness, photophobia, blurred vision, keratic precipitates, and inflammatory cells or fibrinous exudates in the anterior chamber. According to the Standardization of Uveitis Nomenclature, anterior uveitis is defined as chronic when the natural disease course exceeds 3 months [ 1 ]. Without timely and adequate treatment, chronic NIAU may lead to posterior synechiae, cataract formation, and secondary glaucoma, resulting in irreversible visual impairment. Conventional management of NIAU relies primarily on topical corticosteroids combined with mydriatic or cycloplegic agents, with systemic therapy reserved for selected patients. However, in cases characterized by recurrent episodes, association with systemic autoimmune diseases, or refractory idiopathic NIAU, disease control is often suboptimal. Adalimumab (ADA) is a fully human monoclonal antibody targeting tumor necrosis factor-α (TNF-α), which specifically binds both soluble and transmembrane TNF-α, thereby preventing its interaction with TNF receptors and suppressing inflammatory signaling pathways. Previous studies have demonstrated that ADA can effectively reduce disease activity, lower relapse rates, and decrease the requirement for corticosteroids and immunosuppressive agents in non-infectious uveitis [ 2 – 7 ]. Nevertheless, most existing evidence has focused on non-infectious intermediate uveitis, posterior uveitis, or panuveitis, whereas data specifically addressing chronic non-infectious anterior uveitis remain limited. Therefore, the present study retrospectively summarizes clinical outcomes in patients with chronic NIAU treated with ADA over a recent 3-year period, aiming to provide practical evidence for clinical management. Methods This retrospective case-series study included patients with chronic non-infectious anterior uveitis (NIAU) who were treated at Baoji People’s Hospital between May 2022 and May 2025 and had complete electronic medical records. A total of 114 patients were enrolled, including 45 males and 69 females, with a mean age of 42.15 ± 14.28 years (range, 7–86 years). Patients were divided into two groups according to whether a tumor necrosis factor-α (TNF-α) antagonist was administered. The control group (n = 56) received conventional local therapy with topical corticosteroids and mydriatic/cycloplegic agents, whereas the study group (n = 58) received additional subcutaneous adalimumab (ADA) on the basis of conventional treatment. In patients with bilateral involvement, only the eye with more severe disease was included for analysis (eyes with irreversible blindness were excluded).Follow-up was conducted through regular outpatient visits and routine examinations, including visits scheduled for ADA administration. The follow-up period was calculated from the initial clinical evaluation, with a minimum duration of 6 months and a maximum duration of 42 months. The median follow-up time was 21 (interquartile range, 16–26) months, and the follow-up endpoint was November 2025. Inclusion criteria Patients were eligible for inclusion if they met all of the following criteria: (1) A diagnosis of active non-infectious anterior uveitis according to the Standardization of Uveitis Nomenclature (SUN) criteria; (2) At least two episodes of disease relapse with a natural disease course longer than 3 months; (3) A treatment duration of at least 3 months and a follow-up period of not less than 6 months, with complete clinical records available. Exclusion criteria Patients were excluded if one or more of the following conditions were present: (1) A disease duration of less than 3 months, or a disease duration greater than 3 months with only a first episode; (2) Infectious uveitis or other conditions that may cause anterior segment inflammatory reactions, including posterior corneal dystrophy, corneal endothelial pigment deposition or pseudoexfoliative material, pseudoexfoliation syndrome, anterior segment ischemia, or primary or secondary intraocular tumors; (3) Active systemic infection (e.g., tuberculosis or active hepatitis B), malignancy, congestive heart failure (New York Heart Association class III–IV), uncontrolled hyperglycemia, gastric ulcer, or psychiatric disorders that precluded or resulted in refusal of systemic corticosteroids, immunosuppressive agents, or biological therapy; (4) A follow-up duration of less than 6 months, loss to follow-up, or incomplete medical records. Treatment regimens Patients in the control group were primarily treated with topical corticosteroids (tobramycin–dexamethasone ophthalmic suspension or fluorometholone eye drops) combined with mydriatic/cycloplegic agents (compound tropicamide eye drops). When necessary, topical non-steroidal anti-inflammatory drugs (bromfenac sodium eye drops) were added. Periocular corticosteroid injections (triamcinolone acetonide or dexamethasone, administered via subconjunctival or posterior sub-Tenon routes) were used in selected cases. Systemic therapy included oral corticosteroids (prednisone) or non-steroidal anti-inflammatory drugs (ibuprofen, diclofenac, celecoxib, or etoricoxib). For patients with severe systemic manifestations of rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), or psoriatic arthritis (PsA), immunosuppressive therapy with methotrexate was administered as appropriate. In the study group, adalimumab was added to conventional therapy and administered via subcutaneous abdominal injection following a standardized dosing regimen. An initial dose of 80 mg was given, followed by 40 mg one week later, and then 40 mg every two weeks. In some patients who achieved complete remission of anterior segment inflammation after 2–3 months and were not receiving oral corticosteroids, the dosing interval was extended to 40 mg every 4 weeks, followed by gradual tapering and discontinuation. Clinical assessments Demographic data, including age, sex, and disease duration, were collected for all patients. Anterior chamber cell count(AC cell count), best-corrected visual acuity (BCVA), treatment response, and recurrence were evaluated at baseline and at 1, 2, and 3 weeks, as well as at 3 and 6 months after treatment initiation. Assessment of AC cell count AC cell count was evaluated in a dark room using a slit-lamp biomicroscope with high magnification (16×) and a narrow slit beam (1 mm width × 2 mm height) positioned at a 45° angle. Inflammatory cells floating in the anterior chamber were counted within a 1 mm × 1 mm field. Mild to severe inflammation was defined as 6–50 cells per field, and very severe inflammation as more than 50 cells per field. AC cell count was graded from 0 to 4 + according to the SUN criteria. Evaluation of treatment response Treatment response was assessed according to previously published criteria [ 2 , 8 ] and classified as complete remission, partial remission, non-response, recurrence, or overall treatment efficacy. Complete remission was defined as complete resolution of anterior segment inflammatory symptoms, an AC cell count grade of 0, complete resolution of inflammatory macular edema, and no requirement for systemic therapy at 6 months. Partial remission was defined as marked improvement of anterior segment inflammation, resolution or marked improvement of inflammatory macular edema, and a daily oral corticosteroid dose of ≤ 10 mg at 6 months. Non-response was defined as no improvement or progression of disease despite treatment. Recurrence was defined as the reappearance of an AC cell count grade ≥ 1 + or recurrent symptoms such as photophobia, ocular pain, or decreased vision after complete remission, confirmed by slit-lamp examination and requiring treatment escalation. Overall treatment efficacy was defined as the proportion of patients who achieved complete or partial remission. Statistical analysis Continuous variables are presented as mean ± standard deviation. BCVA values were converted to logarithm of the minimum angle of resolution (LogMAR) units for statistical analysis. Statistical analyses were performed using SPSS version 20.0 (IBM Corp., Armonk, NY, USA). Normality was assessed using the Shapiro–Wilk test. As AC cell count and BCVA at post-treatment time points showed non-normal distributions, intergroup comparisons were performed using the Mann–Whitney U test. Independent-sample t-tests were used for other normally distributed continuous variables. Categorical variables were compared using the χ² test, and Fisher’s exact test was applied when expected cell counts were less than five. A P value < 0.05 was considered statistically significant. Results Table 1 A total of 114 patients with chronic NIAU were included in the study. females outnumbered males in both groups. Disease duration was significantly longer in the study group than in the control group (t = 2.44, P = 0.017). No significant differences were observed between the two groups in terms of age, baseline anterior chamber cell count(AC cell count), or LogMAR best-corrected visual acuity (BCVA) (all P > 0.05). Table 1 Baseline characteristics of patients with chronic NIAU in the two groups Variable Study group ( N = 58) Control group ( N = 56) t value P value Sex(male),n 21 24 — — Disease duration(years) 2.02 ± 2.57 1.08 ± 1.34 2.44 0.017 Age(years) 42.56 ± 16.73 43.17 ± 15.37 0.20 0.840 AC cell count(cells/field) 32.56 ± 14.64 31.74 ± 13.52 0.31 0.757 LogMAR BCVA 0.39 ± 0.18 0.38 ± 0.22 0.36 0.718 Table 2 Idiopathic NIAU was the most common subtype in both groups, accounting for 58.62% (34/58) in the study group and 69.64% (39/56) in the control group. The second most common subtype was ankylosing spondylitis–associated uveitis, comprising 22.41% (13/58) and 17.86% (10/56) in the two groups, respectively. Rheumatoid arthritis–associated uveitis ranked third (8.6% vs. 5.4%). Juvenile idiopathic arthritis and psoriatic arthritis were also represented among both groups. Overall, the proportion of NIAU cases associated with systemic autoimmune diseases was higher in the study group than in the control group. Table 2 Distribution of uveitis subtypes in patients with chronic NIAU according to SUN classification (n) Uveitis subtype Study group ( N = 58) Control group ( N = 56) Total ( N = 114) Idiopathic 34 39 73 Ankylosing spondylitis 13 10 23 Rheumatoid arthritis 5 3 8 Juvenile idiopathic arthritis 2 1 3 Psoriatic arthritis 2 1 3 Autoimmune thyroiditis 1 0 1 Other* 1 2 2 * In the study group, one case was Behçet’s disease–associated anterior uveitis. In the control group, one case was chronic recurrent anterior uveitis triggered by postoperative inflammation, and another case was recurrent chronic Fuchs’ uveitis syndrome. Figure 1 AC cell count decreased markedly in both groups during the first two weeks of treatment, with no significant between-group differences at any early time point (all P > 0.05). From week 3 onward, AC cell count improvement was significantly greater in the Study group than in the control group (week 3: U = 1889.0, P = 0.039; month 3: U = 1909.5, P = 0.017; month 6: U = 1926.5, P = 0.010). Regarding LogMAR BCVA, both groups demonstrated notable improvement during the first three weeks, and no significant difference was observed between the groups during this period (all P > 0.05). However, at 3 months and 6 months, BCVA in the study group was significantly better than that in the control group (month 3: U = 1394.0, P = 0.046; month 6: U = 1326.5, P = 0.019). Table 3 At the 6-month follow-up, 49 patients in the study group achieved complete remission, yielding a complete remission rate of 84.48% (49/58). The recurrence rate was 13.79% (8/58), and the overall treatment efficacy was 96.55% (56/58). In the control group, the complete remission rate was 64.29% (36/56), the recurrence rate was 28.57% (16/56), and the overall efficacy was 87.50% (49/56). The differences between the two groups were statistically significant for complete remission rate (P = 0.024), recurrence rate (P = 0.029), and overall treatment efficacy (P = 0.045). No significant between-group differences were observed in the proportions of patients with partial remission or no response (both P > 0.05). A total of seven patients (2 in the study group and 5 in the control group) showed no response to treatment and required adjustment of corticosteroid or immunosuppressive regimens. Table 3 Comparison of treatment response between the study and control groups Treatment response Study group(%) ( N = 58) Control group(%) ( N = 56) χ² P value No response 2 (3.45%) 7 (12.50%) 0.165* Partial remission 7 (12.07%) 13 (23.21%) 2.09 0.148 Complete remission 49 (84.48%) 36 (64.29%) 5.06 0.024 Recurrence 8 (13.79%) 16 (28.57%) 4.76 0.029 Overall efficacy 56 (96.55%) 49 (87.50%) 4.03 0.045 *Fisher’s exact test Discussion Adalimumab (ADA) is a tumor necrosis factor-alpha (TNF-α) inhibitor [ 3 – 4 , 9 – 10 ]. TNF-α is a potent, multifunctional cytokine that plays a pivotal role in maintaining immune homeostasis. Under physiological conditions, TNF-α is produced by almost all immune cells and various non-immune cells, but it is rapidly consumed, and its serum level is usually undetectable in healthy individuals. When inflammatory stimuli occur, activated monocyte–macrophages, T cells, NK cells, mast cells, and endothelial cells secrete large amounts of TNF-α. Anti–TNF-α research began in the late 1980s and early 1990s, when Keffer, Beutler, and others elucidated the role of TNF-α in inflammation and demonstrated the efficacy of anti–TNF-α therapy in immune-mediated arthritis [ 11 – 12 ]. These findings directly led to the clinical application of TNF-α inhibitors in immune-inflammatory diseases. Currently available TNF-α inhibitors can be broadly divided into soluble TNF receptor fusion proteins (sTNFR-Fc) and monoclonal antibodies (mAbs). The former is represented by etanercept, whereas mAbs include ADA, infliximab, golimumab, and certolizumab pegol. ADA is a full-length, bivalent, fully human IgG1 monoclonal antibody and remains the only biologic agent approved specifically for the treatment of non-infectious uveitis (NIU). Non-infectious anterior uveitis (NIAU) results from the combined effects of genetic susceptibility, dysregulated immune regulation, and environmental triggers. In genetically predisposed individuals, ocular infection, trauma, or stress can activate innate immunity and excessively stimulate Th1/Th17 pathways, leading to sustained elevation of TNF-α, interleukin (IL)-1β, IL-6, IL-17, and other inflammatory cytokines. These mediators disrupt the blood–aqueous barrier and induce iris and ciliary body inflammation, ultimately resulting in NIAU. Topical corticosteroids and mydriatic/cycloplegic agents remain the basic treatment for NIAU; however, some patients are intolerant or poorly responsive to steroids, leading to recurrent or chronic inflammation, cataract formation, and secondary refractory glaucoma, with consequent visual impairment. In our clinical practice, ADA is generally considered for patients who have experienced at least two relapses, have a disease duration > 3 months, and remain in an active inflammatory phase despite treatment with corticosteroids and/or immunosuppressants. Many of these patients have concomitant systemic autoimmune diseases. In addition, ADA provides an important alternative for chronic NIAU patients who cannot receive systemic corticosteroids because of comorbid hyperglycemia, peptic ulcer disease, or psychiatric disorders, as well as for some young women who decline systemic corticosteroids or immunosuppressants due to concerns about appearance or weight gain and opt for ADA as an adjunct to local therapy. In this study, idiopathic NIAU was the most frequent subtype, in line with previous reports [ 13 ]. Idiopathic disease likely reflects undetected immune abnormalities rather than the absence of immune involvement. Ankylosing spondylitis (AS) was the second most common association; approximately 20–25% of patients with AS develop anterior uveitis, more often in males, typically unilateral with alternating laterality, and the severity of ocular inflammation often does not parallel joint disease activity [ 14 ]. More than 90% of affected patients carry the HLA-B27 allele [ 15 ]. HLA-B27 can cause abnormal antigen presentation and protein misfolding [ 16 ], activating cytotoxic T lymphocytes and inducing immune misrecognition of self-antigens [ 17 – 18 ]. In addition, HLA-B27 can form cell-surface homodimers that activate NK cells and Th cells, resulting in excessive TNF-α production. TNF-α is one of the key pro-inflammatory cytokines in the pathogenesis of uveitis; it promotes inflammatory cell recruitment, triggers inflammatory cascades (including induction of IL-1 and IL-6), upregulates adhesion molecules, and leads to endothelial activation, tissue injury, and fibrosis [ 19 ]. Rheumatoid arthritis (RA)–associated NIAU is not uncommon [ 20 ]. Approximately 90% of RA patients carry HLA-DR4/DR1 alleles with the “shared epitope,” which is believed to compromise immune tolerance and drive chronic inflammation. Autoantibodies such as rheumatoid factor further amplify immune activation, and 10–20% of patients develop extra-articular involvement, including ocular disease [ 21 ]. RA-associated NIAU is typically chronic or recurrent and may be accompanied by peripheral keratitis or scleritis. In our clinical experience, careful history taking and examination of hand and foot joints in patients with refractory, chronic anterior uveitis—particularly those with peripheral corneal involvement—often reveal long-standing, previously under-recognized RA. In this study, all three RA patients had severe corneal lesions. One 74-year-old man was initially diagnosed elsewhere with keratitis, corneal ulcer, and hypopyon; based on typical RA deformities and positive anti-cyclic citrullinated peptide and RF tests, we initiated combined local therapy and ADA, which led to rapid resolution of ciliary injection and healing of the corneal ulcer with visual improvement. The other two elderly patients (86-year-old woman and 82-year-old man) presented with dense fibrin in the pupillary area, and the latter had secondary refractory glaucoma; both responded well to ADA plus local therapy. In juvenile idiopathic arthritis (JIA), TNF-α, Th17/IL-17, and IL-6 pathways are central to disease persistence and progression, and associated uveitis is a prototypical form of chronic, insidious anterior uveitis. Children are often asymptomatic in the early stage, and delayed diagnosis can quickly lead to fibrinous exudation in the anterior chamber, posterior synechiae, cataract, band keratopathy, hypotony, or glaucoma. Therefore, when local therapy is insufficient, systemic treatment (oral corticosteroids, methotrexate, or ADA) should be initiated promptly [ 22 – 23 ]. All three psoriatic arthritis (PsA) patients in our study were HLA-B27 positive; two had recurrent uveitis and one presented with peripheral corneal ulceration. One patient with autoimmune thyroiditis had Hashimoto thyroiditis (HT). Uveitis associated with HT is currently thought to reflect shared systemic autoimmune susceptibility and network imbalance rather than a confirmed organ-specific antigen cross-reaction, and its pathogenesis requires further basic and clinical investigation [ 24 ]. One patient with Fuchs’ uveitis syndrome required topical steroid therapy due to recurrent fibrin in the pupillary area with visual impairment. Most Fuchs’ cases, however, have a long disease course but preserved vision, and although topical steroids can partially reduce keratic precipitates, they often recur after discontinuation and long-term treatment is usually unnecessary. In the present study, AC cell count improved substantially in both groups during the first 2 weeks, with no significant between-group differences. This likely reflects the rapid onset and high bioavailability of frequently administered topical corticosteroids during the early phase, while ADA had not yet reached full efficacy. From week 3 onward, AC cell count was consistently lower in the study group than in the control group, indicating that ADA exerted an additional anti-inflammatory effect and helped prevent anti-drug antibody formation, thereby reducing inflammation and recurrence [ 3 – 7 ]. At 3 and 6 months, BCVA was significantly better in the study group. By weeks 3–4, nearly half of the patients in the study group could discontinue topical steroids or maintain inflammation control with only 1–2 drops per day. In contrast, patients in the control group—particularly those with systemic autoimmune diseases—often required prolonged topical and systemic corticosteroids or immunosuppressants. Long-term or high-dose corticosteroid therapy may lead to elevated intraocular pressure, cataract formation, weight gain, metabolic disturbances, hypertension, osteoporosis, gastrointestinal discomfort, and psychiatric symptoms. These adverse effects can reduce adherence, prompting patients to self-reduce or discontinue medication. Furthermore, some patients exhibit primary poor responsiveness to steroids or develop secondary tachyphylaxis and steroid resistance, resulting in suboptimal inflammation control, recurrent disease, posterior synechiae, cataract, and glaucoma, ultimately impairing vision. Corticosteroids remain the mainstay of NIAU treatment. By binding to glucocorticoid receptors and regulating gene transcription, they inhibit pro-inflammatory signaling pathways such as NF-κB and activator protein-1 (AP-1), reduce the production of multiple cytokines and inflammatory mediators, and upregulate anti-inflammatory proteins including I-κB, IL-10, and annexin A1 (ANXA1). They also suppress T-cell, B-cell, and phagocyte activation and infiltration, decrease inflammatory cell migration, and stabilize vascular permeability, thereby alleviating tissue edema and damage. These properties make corticosteroids particularly effective for rapidly controlling acute inflammation. However, their efficacy depends on sustained drug exposure; rapid tapering or discontinuation often leads to reactivation of suppressed inflammatory pathways and disease relapse. This pattern is especially evident in AS-, JIA-, and RA-associated anterior uveitis, which are typically steroid-dependent and prone to chronic recurrence [ 25 ]. TNF-α acts as a common inflammatory amplifier across multiple etiologies, representing a shared pathological pathway regardless of whether the initial trigger is autoimmune or unknown. By specifically blocking TNF-α–mediated cascades, ADA disrupts the central inflammatory axis that drives persistent uveitis, controls intraocular inflammation, and helps restore immune homeostasis, producing consistent therapeutic effects across different forms of NIU [ 2 ]. Accordingly, in our study the study group showed significantly higher overall efficacy and lower recurrence rates than the control group. Throughout ADA treatment and up to 6 months after the last injection, the most frequently reported adverse event was mild injection-site pain. No patients experienced metabolic disorders, osteoporosis, marked immunosuppression, or other systemic adverse events commonly associated with long-term corticosteroids or traditional immunosuppressants [ 2 ], consistent with previous findings [ 3 – 7 , 26 – 29 ]. A major unresolved issue is how best to taper or discontinue ADA once disease remission is achieved, and the optimal strategy remains under investigation worldwide [ 25 ]. As a biologic agent, ADA is costly. Our hospital is located in Northwest China, and most patients come from less-developed regions of western Shaanxi and eastern Gansu, where economic status and educational level are relatively low and disease awareness is limited. Clinical observation suggests that patients who discontinue therapy prematurely for financial reasons have a markedly higher recurrence rate than those who maintain continuous treatment. In our cohort, patients who were able to adhere to long-term ADA were mostly employed or retired workers, whereas many rural patients frequently asked when they could stop treatment once their disease stabilized. At treatment initiation, we inform patients that ADA may be required for a prolonged period; if disease remains stable for a substantial time, we gradually extend the dosing interval before discontinuation. In chronic NIAU patients without systemic autoimmune disease who refuse systemic steroids due to intolerance or cosmetic concerns, we generally administer continuous ADA for 2–3 months; if complete remission is achieved, ADA is discontinued, and disease control can often be maintained with 1–2 daily instillations of topical corticosteroids. For recurrent chronic idiopathic NIAU or NIAU with definite systemic autoimmune disease, once corticosteroids are discontinued or reduced to ≤ 10 mg/day and complete remission has been maintained for more than 3 months, we extend the ADA dosing interval to once monthly for an additional 2–3 months. If the disease remains stable, ADA is then withdrawn, and most patients maintain long-term remission. In the few patients who experience relapse after dose reduction or discontinuation, temporary dose escalation or shortening of the dosing interval has been effective [ 10 ]. This study has several limitations inherent to its retrospective design. First, treatment histories were mainly derived from records at our institution and may not fully capture therapies received elsewhere. Second, some patients were concurrently taking medications for other systemic conditions, which could have influenced ocular outcomes. Despite these limitations, our findings suggest that although most NIAU cases can be effectively managed with local corticosteroids and mydriatic agents alone, ADA is a valuable option for recurrent chronic idiopathic NIAU. In particular, for chronic NIAU associated with systemic autoimmune diseases, proactive use of ADA can effectively control ocular inflammation, reduce systemic disease activity, improve vision and ocular structural outcomes, and reduce the need for corticosteroids and immunosuppressants, with a favorable safety profile. However, strategies to further reduce recurrence, optimize tapering and discontinuation protocols, and achieve more precise individualized treatment require further prospective and mechanistic studies. Declarations Conflict of interest The authors declare no competing interests. Ethics approval and Consent to participate This study was conducted in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of Baoji People’s Hospital. Owing to the retrospective nature of the study, the requirement for written informed consent was waived. Author Contribution DGP and DGL contributed to the conception and design of the study and manuscript writing. XGJ and LS contributed to data collection, interpretation of the results, and statistical analysis. Data Availability The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request. 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Chinese expert consensus on the diagnosis and treatment of juvenile idiopathic arthritis–associated uveitis (2023). Medical Journal of Peking Union Medical College Hospital[J].2023,14(2):247256.DOI: 10.12290/xhyxzz.2023-0090 . Durga S Borkar,Gelareh Homayounfar,Vivien M Tham,et al.Association between thyroid disease and uveitis: results from the pacific ocular inflammation study[J].JAMA Ophthalmol.2017,135(6):594–599.Doi: 10.1001/jamaophthalmol.2017.1009 . Wang XZ,Zheng WJ,Zhang XM.Interpretation of the Chinese expert consensus on treatment of non-infectious uveitis with anti-tumor necrosis factor-alpha monoclonal antibody.Chin J Ocular Fundus Dis[J]. 2024,40(1):20–26.Doi: 10.3760/cma.j.cn511434-20240104-00005 . Renton WD,Jung J,Palestine AG.Tumor necrosis factor (TNF) inhibitors for juvenile idiopathic arthritis-associated uveitis[J].Cochrane Database Syst Rev,2022,10(10): CD013818.DOI:10.1002/14651858.CD013818.pub2 . Suhler EB,Adán A,Brézin AP,et al.Safety and efficacy of Adalimumab in patients with noninfectious uveitis in an ongoing open-label study:VISUAL III[J].Ophthalmology,2018,125(7):1075–1087.DOI: 10.1016/j.ophtha.2017.12.039 . Suhler EB,Jaffe GJ,Fortin E,et al.Long-term safety and efficacy of Adalimumab in patients with noninfectious intermediate uveitis, posterior uveitis, or panuveitis[J].Ophthalmology,2021,128(6):899–909.DOI: 10.1016/j.ophtha.2020.10.036 . Burmester GR,Panaccione R,Gordon KB,et al.Adalimumab:long-term safety in 23458 patients from global clinical trials in rheumatoid arthritis,juvenile idiopathic arthritis,ankylosing spondylitis,psoriatic arthritis,psoriasis and Crohn’s disease[J].Ann Rheum Dis,2013,72(4):517–524.DOI: 10.1136/annrheumdis-2011-201244 . Additional Declarations No competing interests reported. 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Hospital","correspondingAuthor":false,"prefix":"","firstName":"Xie","middleName":"","lastName":"Guijun","suffix":""},{"id":565248047,"identity":"373f9438-0008-4282-b1b3-bf44dfff36b8","order_by":2,"name":"Ding Guolong","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA5ElEQVRIiWNgGAWjYBACewYGxgcfDGzs2NgbgNwCBgYJQloMGxiYDWdUpCXz8xxgYDhgQIQWgwMMbNI8Zw4xzpyRQKyWG+nPJGe2HWA2uPn4mDTQhXKSDcwPH93Ap+XMGWOLj213+Axup6VJHDBIM5ZmYDM2zsGn5XgP482Zbc+YDW7nmAG1HE6cx8DDJo1Xy2H2B9K8bYcZN9w8Q6yW4w1GQO8fBnqfB6JlNiEthj1njKGBnJZscQboF8lmAn6xl0h/CI3KwwdvVFTYyEkcb374GJ8WLICZNOWjYBSMglEwCrAAAOsnULH1eS8AAAAAAElFTkSuQmCC","orcid":"","institution":"The First Hospital of Xi’an","correspondingAuthor":true,"prefix":"","firstName":"Ding","middleName":"","lastName":"Guolong","suffix":""},{"id":565248048,"identity":"77b86b31-4061-4132-868f-c962ebdfa942","order_by":3,"name":"Lei Shu","email":"","orcid":"","institution":"Baoji Maternal and 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09:10:38","extension":"xml","order_by":5,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":87400,"visible":true,"origin":"","legend":"","description":"","filename":"6a698483e0c44554897b09d4adbe04621structuring.xml","url":"https://assets-eu.researchsquare.com/files/rs-8297406/v1/c36b06274cb2fdd15a896336.xml"},{"id":99217465,"identity":"c5f20045-7c48-4ea8-8da1-dddb68bff660","added_by":"auto","created_at":"2025-12-30 09:10:38","extension":"html","order_by":6,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":100595,"visible":true,"origin":"","legend":"","description":"","filename":"earlyproof.html","url":"https://assets-eu.researchsquare.com/files/rs-8297406/v1/22ef577d2c598c75e7d87c24.html"},{"id":99318165,"identity":"fc4c2525-7cf2-4031-b1dc-7df430969cd5","added_by":"auto","created_at":"2025-12-31 16:31:42","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":206843,"visible":true,"origin":"","legend":"\u003cp\u003eComparison of AC cell count and LogMAR BCVA between the two groups over time\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e*\u003c/strong\u003e \u003cem\u003eP \u003c/em\u003evalue \u0026lt; 0.05\u003c/p\u003e","description":"","filename":"floatimage1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8297406/v1/c58e44d628a9adbe4c2ff148.jpeg"},{"id":104740322,"identity":"14800adc-7cf1-4a46-9910-e44f67d65c80","added_by":"auto","created_at":"2026-03-16 16:16:35","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":750155,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8297406/v1/93e9346e-5664-43eb-9da6-90d47cca15d9.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Efficacy of adalimumab in chronic non-infectious anterior uveitis: a retrospective study","fulltext":[{"header":"Background","content":"\u003cp\u003eNon-infectious anterior uveitis (NIAU) is an immune-mediated form of uveitis that primarily involves the iris and anterior segment of the ciliary body. Unlike infectious uveitis, its onset is not directly related to bacterial, viral, fungal, or parasitic pathogens, but is mainly associated with autoimmune responses, dysregulated immune regulation, or systemic immune-related diseases. NIAU represents the most common subtype of uveitis, accounting for approximately 50% of all uveitis cases [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Clinically, patients typically present with ocular pain, redness, photophobia, blurred vision, keratic precipitates, and inflammatory cells or fibrinous exudates in the anterior chamber. According to the Standardization of Uveitis Nomenclature, anterior uveitis is defined as chronic when the natural disease course exceeds 3 months [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Without timely and adequate treatment, chronic NIAU may lead to posterior synechiae, cataract formation, and secondary glaucoma, resulting in irreversible visual impairment.\u003c/p\u003e \u003cp\u003eConventional management of NIAU relies primarily on topical corticosteroids combined with mydriatic or cycloplegic agents, with systemic therapy reserved for selected patients. However, in cases characterized by recurrent episodes, association with systemic autoimmune diseases, or refractory idiopathic NIAU, disease control is often suboptimal. Adalimumab (ADA) is a fully human monoclonal antibody targeting tumor necrosis factor-α (TNF-α), which specifically binds both soluble and transmembrane TNF-α, thereby preventing its interaction with TNF receptors and suppressing inflammatory signaling pathways. Previous studies have demonstrated that ADA can effectively reduce disease activity, lower relapse rates, and decrease the requirement for corticosteroids and immunosuppressive agents in non-infectious uveitis [\u003cspan additionalcitationids=\"CR3 CR4 CR5 CR6\" citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Nevertheless, most existing evidence has focused on non-infectious intermediate uveitis, posterior uveitis, or panuveitis, whereas data specifically addressing chronic non-infectious anterior uveitis remain limited. Therefore, the present study retrospectively summarizes clinical outcomes in patients with chronic NIAU treated with ADA over a recent 3-year period, aiming to provide practical evidence for clinical management.\u003c/p\u003e"},{"header":"Methods","content":"\u003cp\u003eThis retrospective case-series study included patients with chronic non-infectious anterior uveitis (NIAU) who were treated at Baoji People\u0026rsquo;s Hospital between May 2022 and May 2025 and had complete electronic medical records. A total of 114 patients were enrolled, including 45 males and 69 females, with a mean age of 42.15\u0026thinsp;\u0026plusmn;\u0026thinsp;14.28 years (range, 7\u0026ndash;86 years). Patients were divided into two groups according to whether a tumor necrosis factor-α (TNF-α) antagonist was administered. The control group (n\u0026thinsp;=\u0026thinsp;56) received conventional local therapy with topical corticosteroids and mydriatic/cycloplegic agents, whereas the study group (n\u0026thinsp;=\u0026thinsp;58) received additional subcutaneous adalimumab (ADA) on the basis of conventional treatment. In patients with bilateral involvement, only the eye with more severe disease was included for analysis (eyes with irreversible blindness were excluded).Follow-up was conducted through regular outpatient visits and routine examinations, including visits scheduled for ADA administration. The follow-up period was calculated from the initial clinical evaluation, with a minimum duration of 6 months and a maximum duration of 42 months. The median follow-up time was 21 (interquartile range, 16\u0026ndash;26) months, and the follow-up endpoint was November 2025.\u003c/p\u003e \u003cp\u003eInclusion criteria\u003c/p\u003e \u003cp\u003ePatients were eligible for inclusion if they met all of the following criteria: (1) A diagnosis of active non-infectious anterior uveitis according to the Standardization of Uveitis Nomenclature (SUN) criteria; (2) At least two episodes of disease relapse with a natural disease course longer than 3 months; (3) A treatment duration of at least 3 months and a follow-up period of not less than 6 months, with complete clinical records available.\u003c/p\u003e \u003cp\u003eExclusion criteria\u003c/p\u003e \u003cp\u003ePatients were excluded if one or more of the following conditions were present: (1) A disease duration of less than 3 months, or a disease duration greater than 3 months with only a first episode; (2) Infectious uveitis or other conditions that may cause anterior segment inflammatory reactions, including posterior corneal dystrophy, corneal endothelial pigment deposition or pseudoexfoliative material, pseudoexfoliation syndrome, anterior segment ischemia, or primary or secondary intraocular tumors; (3) Active systemic infection (e.g., tuberculosis or active hepatitis B), malignancy, congestive heart failure (New York Heart Association class III\u0026ndash;IV), uncontrolled hyperglycemia, gastric ulcer, or psychiatric disorders that precluded or resulted in refusal of systemic corticosteroids, immunosuppressive agents, or biological therapy; (4) A follow-up duration of less than 6 months, loss to follow-up, or incomplete medical records.\u003c/p\u003e \u003cp\u003eTreatment regimens\u003c/p\u003e \u003cp\u003ePatients in the control group were primarily treated with topical corticosteroids (tobramycin\u0026ndash;dexamethasone ophthalmic suspension or fluorometholone eye drops) combined with mydriatic/cycloplegic agents (compound tropicamide eye drops). When necessary, topical non-steroidal anti-inflammatory drugs (bromfenac sodium eye drops) were added. Periocular corticosteroid injections (triamcinolone acetonide or dexamethasone, administered via subconjunctival or posterior sub-Tenon routes) were used in selected cases. Systemic therapy included oral corticosteroids (prednisone) or non-steroidal anti-inflammatory drugs (ibuprofen, diclofenac, celecoxib, or etoricoxib). For patients with severe systemic manifestations of rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), or psoriatic arthritis (PsA), immunosuppressive therapy with methotrexate was administered as appropriate.\u003c/p\u003e \u003cp\u003eIn the study group, adalimumab was added to conventional therapy and administered via subcutaneous abdominal injection following a standardized dosing regimen. An initial dose of 80 mg was given, followed by 40 mg one week later, and then 40 mg every two weeks. In some patients who achieved complete remission of anterior segment inflammation after 2\u0026ndash;3 months and were not receiving oral corticosteroids, the dosing interval was extended to 40 mg every 4 weeks, followed by gradual tapering and discontinuation.\u003c/p\u003e \u003cp\u003eClinical assessments\u003c/p\u003e \u003cp\u003eDemographic data, including age, sex, and disease duration, were collected for all patients. Anterior chamber cell count(AC cell count), best-corrected visual acuity (BCVA), treatment response, and recurrence were evaluated at baseline and at 1, 2, and 3 weeks, as well as at 3 and 6 months after treatment initiation.\u003c/p\u003e \u003cp\u003eAssessment of AC cell count\u003c/p\u003e \u003cp\u003eAC cell count was evaluated in a dark room using a slit-lamp biomicroscope with high magnification (16\u0026times;) and a narrow slit beam (1 mm width \u0026times; 2 mm height) positioned at a 45\u0026deg; angle. Inflammatory cells floating in the anterior chamber were counted within a 1 mm \u0026times; 1 mm field. Mild to severe inflammation was defined as 6\u0026ndash;50 cells per field, and very severe inflammation as more than 50 cells per field. AC cell count was graded from 0 to 4\u0026thinsp;+\u0026thinsp;according to the SUN criteria.\u003c/p\u003e \u003cp\u003eEvaluation of treatment response\u003c/p\u003e \u003cp\u003eTreatment response was assessed according to previously published criteria [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e] and classified as complete remission, partial remission, non-response, recurrence, or overall treatment efficacy. Complete remission was defined as complete resolution of anterior segment inflammatory symptoms, an AC cell count grade of 0, complete resolution of inflammatory macular edema, and no requirement for systemic therapy at 6 months. Partial remission was defined as marked improvement of anterior segment inflammation, resolution or marked improvement of inflammatory macular edema, and a daily oral corticosteroid dose of \u0026le;\u0026thinsp;10 mg at 6 months. Non-response was defined as no improvement or progression of disease despite treatment. Recurrence was defined as the reappearance of an AC cell count grade\u0026thinsp;\u0026ge;\u0026thinsp;1\u0026thinsp;+\u0026thinsp;or recurrent symptoms such as photophobia, ocular pain, or decreased vision after complete remission, confirmed by slit-lamp examination and requiring treatment escalation. Overall treatment efficacy was defined as the proportion of patients who achieved complete or partial remission.\u003c/p\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStatistical analysis\u003c/h2\u003e \u003cp\u003eContinuous variables are presented as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation. BCVA values were converted to logarithm of the minimum angle of resolution (LogMAR) units for statistical analysis. Statistical analyses were performed using SPSS version 20.0 (IBM Corp., Armonk, NY, USA). Normality was assessed using the Shapiro\u0026ndash;Wilk test. As AC cell count and BCVA at post-treatment time points showed non-normal distributions, intergroup comparisons were performed using the Mann\u0026ndash;Whitney U test. Independent-sample t-tests were used for other normally distributed continuous variables. Categorical variables were compared using the χ\u0026sup2; test, and Fisher\u0026rsquo;s exact test was applied when expected cell counts were less than five. A P value\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was considered statistically significant.\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cp\u003eTable\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003eA total of 114 patients with chronic NIAU were included in the study. females outnumbered males in both groups. Disease duration was significantly longer in the study group than in the control group (t\u0026thinsp;=\u0026thinsp;2.44, P\u0026thinsp;=\u0026thinsp;0.017). No significant differences were observed between the two groups in terms of age, baseline anterior chamber cell count(AC cell count), or LogMAR best-corrected visual acuity (BCVA) (all P\u0026thinsp;\u0026gt;\u0026thinsp;0.05).\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eBaseline characteristics of patients with chronic NIAU in the two groups\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVariable\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eStudy group (\u003cem\u003eN\u003c/em\u003e\u0026thinsp;=\u0026thinsp;58)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eControl group (\u003cem\u003eN\u003c/em\u003e\u0026thinsp;=\u0026thinsp;56)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cem\u003et\u003c/em\u003e value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cem\u003eP\u003c/em\u003e value\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSex(male),n\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e21\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e24\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026mdash;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u0026mdash;\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDisease duration(years)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2.02\u0026thinsp;\u0026plusmn;\u0026thinsp;2.57\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1.08\u0026thinsp;\u0026plusmn;\u0026thinsp;1.34\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e2.44\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.017\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAge(years)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e42.56\u0026thinsp;\u0026plusmn;\u0026thinsp;16.73\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e43.17\u0026thinsp;\u0026plusmn;\u0026thinsp;15.37\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.20\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.840\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAC cell count(cells/field)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e32.56\u0026thinsp;\u0026plusmn;\u0026thinsp;14.64\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e31.74\u0026thinsp;\u0026plusmn;\u0026thinsp;13.52\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.31\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.757\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLogMAR BCVA\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.39\u0026thinsp;\u0026plusmn;\u0026thinsp;0.18\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.38\u0026thinsp;\u0026plusmn;\u0026thinsp;0.22\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.36\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.718\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eTable\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e Idiopathic NIAU was the most common subtype in both groups, accounting for 58.62% (34/58) in the study group and 69.64% (39/56) in the control group. The second most common subtype was ankylosing spondylitis\u0026ndash;associated uveitis, comprising 22.41% (13/58) and 17.86% (10/56) in the two groups, respectively. Rheumatoid arthritis\u0026ndash;associated uveitis ranked third (8.6% vs. 5.4%). Juvenile idiopathic arthritis and psoriatic arthritis were also represented among both groups. Overall, the proportion of NIAU cases associated with systemic autoimmune diseases was higher in the study group than in the control group.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eDistribution of uveitis subtypes in patients with chronic NIAU according to SUN classification (n)\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eUveitis subtype\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eStudy group (\u003cem\u003eN\u003c/em\u003e\u0026thinsp;=\u0026thinsp;58)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eControl group (\u003cem\u003eN\u003c/em\u003e\u0026thinsp;=\u0026thinsp;56)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eTotal (\u003cem\u003eN\u003c/em\u003e\u0026thinsp;=\u0026thinsp;114)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colspan=\"1\" nameend=\"c5\" namest=\"c5\"\u003e\u0026nbsp;\u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIdiopathic\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e34\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e39\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e73\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c5\" namest=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAnkylosing spondylitis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e13\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e23\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c5\" namest=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRheumatoid arthritis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c5\" namest=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eJuvenile idiopathic arthritis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c5\" namest=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePsoriatic arthritis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c5\" namest=\"c4\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAutoimmune thyroiditis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c5\" namest=\"c4\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eOther*\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c5\" namest=\"c4\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e* In the study group, one case was Beh\u0026ccedil;et\u0026rsquo;s disease\u0026ndash;associated anterior uveitis. In the control group, one case was chronic recurrent anterior uveitis triggered by postoperative inflammation, and another case was recurrent chronic Fuchs\u0026rsquo; uveitis syndrome.\u003c/p\u003e \u003cp\u003eFigure \u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e AC cell count decreased markedly in both groups during the first two weeks of treatment, with no significant between-group differences at any early time point (all P\u0026thinsp;\u0026gt;\u0026thinsp;0.05). From week 3 onward, AC cell count improvement was significantly greater in the Study group than in the control group (week 3: U\u0026thinsp;=\u0026thinsp;1889.0, P\u0026thinsp;=\u0026thinsp;0.039; month 3: U\u0026thinsp;=\u0026thinsp;1909.5, P\u0026thinsp;=\u0026thinsp;0.017; month 6: U\u0026thinsp;=\u0026thinsp;1926.5, P\u0026thinsp;=\u0026thinsp;0.010). Regarding LogMAR BCVA, both groups demonstrated notable improvement during the first three weeks, and no significant difference was observed between the groups during this period (all P\u0026thinsp;\u0026gt;\u0026thinsp;0.05). However, at 3 months and 6 months, BCVA in the study group was significantly better than that in the control group (month 3: U\u0026thinsp;=\u0026thinsp;1394.0, P\u0026thinsp;=\u0026thinsp;0.046; month 6: U\u0026thinsp;=\u0026thinsp;1326.5, P\u0026thinsp;=\u0026thinsp;0.019).\u003c/p\u003e \u003cp\u003eTable\u0026nbsp;\u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e At the 6-month follow-up, 49 patients in the study group achieved complete remission, yielding a complete remission rate of 84.48% (49/58). The recurrence rate was 13.79% (8/58), and the overall treatment efficacy was 96.55% (56/58). In the control group, the complete remission rate was 64.29% (36/56), the recurrence rate was 28.57% (16/56), and the overall efficacy was 87.50% (49/56).\u003c/p\u003e \u003cp\u003eThe differences between the two groups were statistically significant for complete remission rate (P\u0026thinsp;=\u0026thinsp;0.024), recurrence rate (P\u0026thinsp;=\u0026thinsp;0.029), and overall treatment efficacy (P\u0026thinsp;=\u0026thinsp;0.045). No significant between-group differences were observed in the proportions of patients with partial remission or no response (both P\u0026thinsp;\u0026gt;\u0026thinsp;0.05).\u003c/p\u003e \u003cp\u003eA total of seven patients (2 in the study group and 5 in the control group) showed no response to treatment and required adjustment of corticosteroid or immunosuppressive regimens.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab3\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eComparison of treatment response between the study and control groups\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTreatment response\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eStudy group(%) (\u003cem\u003eN\u003c/em\u003e\u0026thinsp;=\u0026thinsp;58)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eControl group(%) (\u003cem\u003eN\u003c/em\u003e\u0026thinsp;=\u0026thinsp;56)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eχ\u0026sup2;\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cem\u003eP\u003c/em\u003e value\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNo response\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2 (3.45%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e7 (12.50%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.165*\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePartial remission\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e7 (12.07%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e13 (23.21%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e2.09\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.148\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eComplete remission\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e49 (84.48%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e36 (64.29%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e5.06\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.024\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRecurrence\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e8 (13.79%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e16 (28.57%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.76\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.029\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eOverall efficacy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e56 (96.55%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e49 (87.50%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.03\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.045\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003ctfoot\u003e \u003ctr\u003e\u003ctd colspan=\"5\"\u003e*Fisher\u0026rsquo;s exact test\u003c/td\u003e\u003c/tr\u003e \u003c/tfoot\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eAdalimumab (ADA) is a tumor necrosis factor-alpha (TNF-α) inhibitor [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. TNF-α is a potent, multifunctional cytokine that plays a pivotal role in maintaining immune homeostasis. Under physiological conditions, TNF-α is produced by almost all immune cells and various non-immune cells, but it is rapidly consumed, and its serum level is usually undetectable in healthy individuals. When inflammatory stimuli occur, activated monocyte\u0026ndash;macrophages, T cells, NK cells, mast cells, and endothelial cells secrete large amounts of TNF-α. Anti\u0026ndash;TNF-α research began in the late 1980s and early 1990s, when Keffer, Beutler, and others elucidated the role of TNF-α in inflammation and demonstrated the efficacy of anti\u0026ndash;TNF-α therapy in immune-mediated arthritis [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. These findings directly led to the clinical application of TNF-α inhibitors in immune-inflammatory diseases. Currently available TNF-α inhibitors can be broadly divided into soluble TNF receptor fusion proteins (sTNFR-Fc) and monoclonal antibodies (mAbs). The former is represented by etanercept, whereas mAbs include ADA, infliximab, golimumab, and certolizumab pegol. ADA is a full-length, bivalent, fully human IgG1 monoclonal antibody and remains the only biologic agent approved specifically for the treatment of non-infectious uveitis (NIU).\u003c/p\u003e \u003cp\u003eNon-infectious anterior uveitis (NIAU) results from the combined effects of genetic susceptibility, dysregulated immune regulation, and environmental triggers. In genetically predisposed individuals, ocular infection, trauma, or stress can activate innate immunity and excessively stimulate Th1/Th17 pathways, leading to sustained elevation of TNF-α, interleukin (IL)-1β, IL-6, IL-17, and other inflammatory cytokines. These mediators disrupt the blood\u0026ndash;aqueous barrier and induce iris and ciliary body inflammation, ultimately resulting in NIAU. Topical corticosteroids and mydriatic/cycloplegic agents remain the basic treatment for NIAU; however, some patients are intolerant or poorly responsive to steroids, leading to recurrent or chronic inflammation, cataract formation, and secondary refractory glaucoma, with consequent visual impairment.\u003c/p\u003e \u003cp\u003eIn our clinical practice, ADA is generally considered for patients who have experienced at least two relapses, have a disease duration\u0026thinsp;\u0026gt;\u0026thinsp;3 months, and remain in an active inflammatory phase despite treatment with corticosteroids and/or immunosuppressants. Many of these patients have concomitant systemic autoimmune diseases. In addition, ADA provides an important alternative for chronic NIAU patients who cannot receive systemic corticosteroids because of comorbid hyperglycemia, peptic ulcer disease, or psychiatric disorders, as well as for some young women who decline systemic corticosteroids or immunosuppressants due to concerns about appearance or weight gain and opt for ADA as an adjunct to local therapy.\u003c/p\u003e \u003cp\u003eIn this study, idiopathic NIAU was the most frequent subtype, in line with previous reports [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. Idiopathic disease likely reflects undetected immune abnormalities rather than the absence of immune involvement. Ankylosing spondylitis (AS) was the second most common association; approximately 20\u0026ndash;25% of patients with AS develop anterior uveitis, more often in males, typically unilateral with alternating laterality, and the severity of ocular inflammation often does not parallel joint disease activity [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. More than 90% of affected patients carry the HLA-B27 allele [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]. HLA-B27 can cause abnormal antigen presentation and protein misfolding [\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e], activating cytotoxic T lymphocytes and inducing immune misrecognition of self-antigens [\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e]. In addition, HLA-B27 can form cell-surface homodimers that activate NK cells and Th cells, resulting in excessive TNF-α production. TNF-α is one of the key pro-inflammatory cytokines in the pathogenesis of uveitis; it promotes inflammatory cell recruitment, triggers inflammatory cascades (including induction of IL-1 and IL-6), upregulates adhesion molecules, and leads to endothelial activation, tissue injury, and fibrosis [\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eRheumatoid arthritis (RA)\u0026ndash;associated NIAU is not uncommon [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. Approximately 90% of RA patients carry HLA-DR4/DR1 alleles with the \u0026ldquo;shared epitope,\u0026rdquo; which is believed to compromise immune tolerance and drive chronic inflammation. Autoantibodies such as rheumatoid factor further amplify immune activation, and 10\u0026ndash;20% of patients develop extra-articular involvement, including ocular disease [\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]. RA-associated NIAU is typically chronic or recurrent and may be accompanied by peripheral keratitis or scleritis. In our clinical experience, careful history taking and examination of hand and foot joints in patients with refractory, chronic anterior uveitis\u0026mdash;particularly those with peripheral corneal involvement\u0026mdash;often reveal long-standing, previously under-recognized RA. In this study, all three RA patients had severe corneal lesions. One 74-year-old man was initially diagnosed elsewhere with keratitis, corneal ulcer, and hypopyon; based on typical RA deformities and positive anti-cyclic citrullinated peptide and RF tests, we initiated combined local therapy and ADA, which led to rapid resolution of ciliary injection and healing of the corneal ulcer with visual improvement. The other two elderly patients (86-year-old woman and 82-year-old man) presented with dense fibrin in the pupillary area, and the latter had secondary refractory glaucoma; both responded well to ADA plus local therapy.\u003c/p\u003e \u003cp\u003eIn juvenile idiopathic arthritis (JIA), TNF-α, Th17/IL-17, and IL-6 pathways are central to disease persistence and progression, and associated uveitis is a prototypical form of chronic, insidious anterior uveitis. Children are often asymptomatic in the early stage, and delayed diagnosis can quickly lead to fibrinous exudation in the anterior chamber, posterior synechiae, cataract, band keratopathy, hypotony, or glaucoma. Therefore, when local therapy is insufficient, systemic treatment (oral corticosteroids, methotrexate, or ADA) should be initiated promptly [\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e]. All three psoriatic arthritis (PsA) patients in our study were HLA-B27 positive; two had recurrent uveitis and one presented with peripheral corneal ulceration. One patient with autoimmune thyroiditis had Hashimoto thyroiditis (HT). Uveitis associated with HT is currently thought to reflect shared systemic autoimmune susceptibility and network imbalance rather than a confirmed organ-specific antigen cross-reaction, and its pathogenesis requires further basic and clinical investigation [\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e]. One patient with Fuchs\u0026rsquo; uveitis syndrome required topical steroid therapy due to recurrent fibrin in the pupillary area with visual impairment. Most Fuchs\u0026rsquo; cases, however, have a long disease course but preserved vision, and although topical steroids can partially reduce keratic precipitates, they often recur after discontinuation and long-term treatment is usually unnecessary.\u003c/p\u003e \u003cp\u003eIn the present study, AC cell count improved substantially in both groups during the first 2 weeks, with no significant between-group differences. This likely reflects the rapid onset and high bioavailability of frequently administered topical corticosteroids during the early phase, while ADA had not yet reached full efficacy. From week 3 onward, AC cell count was consistently lower in the study group than in the control group, indicating that ADA exerted an additional anti-inflammatory effect and helped prevent anti-drug antibody formation, thereby reducing inflammation and recurrence [\u003cspan additionalcitationids=\"CR4 CR5 CR6\" citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. At 3 and 6 months, BCVA was significantly better in the study group. By weeks 3\u0026ndash;4, nearly half of the patients in the study group could discontinue topical steroids or maintain inflammation control with only 1\u0026ndash;2 drops per day. In contrast, patients in the control group\u0026mdash;particularly those with systemic autoimmune diseases\u0026mdash;often required prolonged topical and systemic corticosteroids or immunosuppressants. Long-term or high-dose corticosteroid therapy may lead to elevated intraocular pressure, cataract formation, weight gain, metabolic disturbances, hypertension, osteoporosis, gastrointestinal discomfort, and psychiatric symptoms. These adverse effects can reduce adherence, prompting patients to self-reduce or discontinue medication. Furthermore, some patients exhibit primary poor responsiveness to steroids or develop secondary tachyphylaxis and steroid resistance, resulting in suboptimal inflammation control, recurrent disease, posterior synechiae, cataract, and glaucoma, ultimately impairing vision.\u003c/p\u003e \u003cp\u003eCorticosteroids remain the mainstay of NIAU treatment. By binding to glucocorticoid receptors and regulating gene transcription, they inhibit pro-inflammatory signaling pathways such as NF-κB and activator protein-1 (AP-1), reduce the production of multiple cytokines and inflammatory mediators, and upregulate anti-inflammatory proteins including I-κB, IL-10, and annexin A1 (ANXA1). They also suppress T-cell, B-cell, and phagocyte activation and infiltration, decrease inflammatory cell migration, and stabilize vascular permeability, thereby alleviating tissue edema and damage. These properties make corticosteroids particularly effective for rapidly controlling acute inflammation. However, their efficacy depends on sustained drug exposure; rapid tapering or discontinuation often leads to reactivation of suppressed inflammatory pathways and disease relapse. This pattern is especially evident in AS-, JIA-, and RA-associated anterior uveitis, which are typically steroid-dependent and prone to chronic recurrence [\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eTNF-α acts as a common inflammatory amplifier across multiple etiologies, representing a shared pathological pathway regardless of whether the initial trigger is autoimmune or unknown. By specifically blocking TNF-α\u0026ndash;mediated cascades, ADA disrupts the central inflammatory axis that drives persistent uveitis, controls intraocular inflammation, and helps restore immune homeostasis, producing consistent therapeutic effects across different forms of NIU [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Accordingly, in our study the study group showed significantly higher overall efficacy and lower recurrence rates than the control group.\u003c/p\u003e \u003cp\u003eThroughout ADA treatment and up to 6 months after the last injection, the most frequently reported adverse event was mild injection-site pain. No patients experienced metabolic disorders, osteoporosis, marked immunosuppression, or other systemic adverse events commonly associated with long-term corticosteroids or traditional immunosuppressants [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e], consistent with previous findings [\u003cspan additionalcitationids=\"CR4 CR5 CR6\" citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan additionalcitationids=\"CR27 CR28\" citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e]. A major unresolved issue is how best to taper or discontinue ADA once disease remission is achieved, and the optimal strategy remains under investigation worldwide [\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e]. As a biologic agent, ADA is costly. Our hospital is located in Northwest China, and most patients come from less-developed regions of western Shaanxi and eastern Gansu, where economic status and educational level are relatively low and disease awareness is limited. Clinical observation suggests that patients who discontinue therapy prematurely for financial reasons have a markedly higher recurrence rate than those who maintain continuous treatment. In our cohort, patients who were able to adhere to long-term ADA were mostly employed or retired workers, whereas many rural patients frequently asked when they could stop treatment once their disease stabilized. At treatment initiation, we inform patients that ADA may be required for a prolonged period; if disease remains stable for a substantial time, we gradually extend the dosing interval before discontinuation.\u003c/p\u003e \u003cp\u003eIn chronic NIAU patients without systemic autoimmune disease who refuse systemic steroids due to intolerance or cosmetic concerns, we generally administer continuous ADA for 2\u0026ndash;3 months; if complete remission is achieved, ADA is discontinued, and disease control can often be maintained with 1\u0026ndash;2 daily instillations of topical corticosteroids. For recurrent chronic idiopathic NIAU or NIAU with definite systemic autoimmune disease, once corticosteroids are discontinued or reduced to \u0026le;\u0026thinsp;10 mg/day and complete remission has been maintained for more than 3 months, we extend the ADA dosing interval to once monthly for an additional 2\u0026ndash;3 months. If the disease remains stable, ADA is then withdrawn, and most patients maintain long-term remission. In the few patients who experience relapse after dose reduction or discontinuation, temporary dose escalation or shortening of the dosing interval has been effective [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThis study has several limitations inherent to its retrospective design. First, treatment histories were mainly derived from records at our institution and may not fully capture therapies received elsewhere. Second, some patients were concurrently taking medications for other systemic conditions, which could have influenced ocular outcomes. Despite these limitations, our findings suggest that although most NIAU cases can be effectively managed with local corticosteroids and mydriatic agents alone, ADA is a valuable option for recurrent chronic idiopathic NIAU. In particular, for chronic NIAU associated with systemic autoimmune diseases, proactive use of ADA can effectively control ocular inflammation, reduce systemic disease activity, improve vision and ocular structural outcomes, and reduce the need for corticosteroids and immunosuppressants, with a favorable safety profile. However, strategies to further reduce recurrence, optimize tapering and discontinuation protocols, and achieve more precise individualized treatment require further prospective and mechanistic studies.\u003c/p\u003e "},{"header":"Declarations","content":"\u003cp\u003e \u003cstrong\u003eConflict of interest\u003c/strong\u003e \u003cp\u003eThe authors declare no competing interests.\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eEthics approval and Consent to participate\u003c/strong\u003e \u003cp\u003e This study was conducted in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of Baoji People\u0026rsquo;s Hospital. Owing to the retrospective nature of the study, the requirement for written informed consent was waived.\u003c/p\u003e \u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eDGP and DGL contributed to the conception and design of the study and manuscript writing. XGJ and LS contributed to data collection, interpretation of the results, and statistical analysis.\u003c/p\u003e\u003ch2\u003eData Availability\u003c/h2\u003e\u003cp\u003eThe datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eEye Immunology Group, Ophthalmology Branch of the Chinese Medical Association. \u003cem\u003eExpert consensus on the clinical diagnosis and treatment of acute anterior uveitis in China (2016)\u003c/em\u003e.Chin J Ophthalmol[J].2016;52(3):164\u0026ndash;166.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDing GP, Xie GJ, Ju X, et al. Clinical observation on the efficacy of adalimumab in the treatment of non-infectious uveiti\u003cem\u003es\u003c/em\u003e. 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class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBurmester GR,Panaccione R,Gordon KB,et al.Adalimumab:long-term safety in 23458 patients from global clinical trials in rheumatoid arthritis,juvenile idiopathic arthritis,ankylosing spondylitis,psoriatic arthritis,psoriasis and Crohn\u0026rsquo;s disease[J].Ann Rheum Dis,2013,72(4):517\u0026ndash;524.DOI:\u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1136/annrheumdis-2011-201244\u003c/span\u003e\u003cspan address=\"10.1136/annrheumdis-2011-201244\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"international-ophthalmology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"inte","sideBox":"Learn more about [International Ophthalmology](https://www.springer.com/journal/10792)","snPcode":"10792","submissionUrl":"https://submission.nature.com/new-submission/10792/3","title":"International Ophthalmology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false},"keywords":"chronic non-infectious anterior uveitis, adalimumab, treatment efficacy, recurrence","lastPublishedDoi":"10.21203/rs.3.rs-8297406/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8297406/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eTo evaluate the clinical efficacy of adalimumab (ADA) in the treatment of chronic non-infectious anterior uveitis (NIAU).\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eThis was a retrospective, single-center observational study. A total of 114 patients with chronic NIAU who were treated at Baoji People\u0026rsquo;s Hospital between May 2022 and May 2025 and had complete electronic medical records were included. The cohort comprised 45 males and 69 females, with a mean age of 42.15\u0026thinsp;\u0026plusmn;\u0026thinsp;14.28 years (range, 7\u0026ndash;86 years). Patients were divided into two groups according to whether ADA was administered. The control group (n\u0026thinsp;=\u0026thinsp;56) received conventional therapy with topical corticosteroids and mydriatic/cycloplegic agents, while the study group (n\u0026thinsp;=\u0026thinsp;58) received additional subcutaneous ADA on the basis of conventional treatment. Demographic characteristics, disease duration, Anterior chamber cell count(AC cell count), and best-corrected visual acuity (BCVA) were collected. AC cell count, BCVA, treatment efficacy, and recurrence rates were compared at baseline and at 1, 2, and 3 weeks, as well as 3 and 6 months after treatment. Statistical analyses were performed using independent-sample t-tests, Mann\u0026ndash;Whitney U tests, and χ\u0026sup2; tests, with P\u0026thinsp;\u0026lt;\u0026thinsp;0.05 considered statistically significant.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eThere were no significant differences between the two groups in age, baseline AC cell count, or baseline BCVA (all P\u0026thinsp;\u0026gt;\u0026thinsp;0.05), while disease duration was longer in the study group (P\u0026thinsp;=\u0026thinsp;0.017). Idiopathic NIAU was the most common etiology (58.62% in the study group and 69.64% in the control group), followed by ankylosing spondylitis, rheumatoid arthritis, juvenile idiopathic arthritis, and psoriatic arthritis. During the first 2 weeks of treatment, AC cell count decreased markedly in both groups, with no significant intergroup differences (all P\u0026thinsp;\u0026gt;\u0026thinsp;0.05). From week 3 onward, AC cell count improvement was significantly greater in the study group than in the control group (all P\u0026thinsp;\u0026lt;\u0026thinsp;0.05). BCVA improved in both groups during the first 3 weeks without significant differences; however, at 3 and 6 months, BCVA was significantly better in the study group (both P\u0026thinsp;\u0026lt;\u0026thinsp;0.05). At 6 months, the study group demonstrated a higher complete remission rate (84.48% vs. 64.29%), a lower recurrence rate (13.79% vs. 28.57%), and a higher overall treatment efficacy (96.55% vs. 87.50%) compared with the control group (all P\u0026thinsp;\u0026lt;\u0026thinsp;0.05).\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e \u003cp\u003eAdalimumab appears to be an effective therapeutic option for recurrent chronic non-infectious anterior uveitis, particularly in patients with underlying autoimmune diseases. ADA can achieve better inflammation control, improve treatment efficacy, reduce recurrence, and decrease the need for corticosteroids and immunosuppressive therapy.\u003c/p\u003e","manuscriptTitle":"Efficacy of adalimumab in chronic non-infectious anterior uveitis: a retrospective study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-12-30 09:10:31","doi":"10.21203/rs.3.rs-8297406/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-01-12T10:02:38+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-01-10T20:56:07+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-01-09T10:05:43+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-01-01T10:41:28+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-12-29T06:46:24+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"193507089659694809576183844169128931846","date":"2025-12-26T06:27:06+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"176093680609943451650497538520881361271","date":"2025-12-24T13:06:39+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"273753059113622323978363511963513052631","date":"2025-12-24T08:03:42+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"261176062631947405560115795957142196155","date":"2025-12-24T02:22:48+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"178909077191189780583335546956996907708","date":"2025-12-23T17:00:24+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"79492849356948501186076958247529368499","date":"2025-12-23T13:01:39+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-12-23T11:26:54+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-12-08T10:36:52+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-12-08T10:34:14+00:00","index":"","fulltext":""},{"type":"submitted","content":"International Ophthalmology","date":"2025-12-07T02:39:57+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"international-ophthalmology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"inte","sideBox":"Learn more about [International Ophthalmology](https://www.springer.com/journal/10792)","snPcode":"10792","submissionUrl":"https://submission.nature.com/new-submission/10792/3","title":"International Ophthalmology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false}}],"origin":"","ownerIdentity":"b31e5044-51ba-401c-8e1f-c9eae2db6a0d","owner":[],"postedDate":"December 30th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2026-03-16T16:12:09+00:00","versionOfRecord":{"articleIdentity":"rs-8297406","link":"https://doi.org/10.1007/s10792-026-04013-x","journal":{"identity":"international-ophthalmology","isVorOnly":false,"title":"International Ophthalmology"},"publishedOn":"2026-03-12 15:59:44","publishedOnDateReadable":"March 12th, 2026"},"versionCreatedAt":"2025-12-30 09:10:31","video":"","vorDoi":"10.1007/s10792-026-04013-x","vorDoiUrl":"https://doi.org/10.1007/s10792-026-04013-x","workflowStages":[]},"version":"v1","identity":"rs-8297406","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8297406","identity":"rs-8297406","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}