Treatment of Uveitis
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Introduction
The goal of treatment in uveitis is to control inflammation in order to prevent vision loss while also limiting the side effects of therapy.[1][2] Treatments include medical management with ocular or systemic therapy, as well as surgical interventions for diagnostic or therapeutic purposes and for the treatment of complications of uveitis. Treatment strategies depend on the etiology of inflammation and the disease severity and course. If the underlying etiology is infectious, then this must first be treated with appropriate therapy. If the underlying etiology is idiopathic or associated with systemic autoimmune/inflammatory diseases, then a stepladder approach utilizing anti-inflammatory or immunomodulatory therapy may be necessary, often times in coordination with other specialists.
Mydriatic and Cycloplegic Agents
Mydriatic and cycloplegic agents are utilized in uveitis to relieve symptoms of pain and photophobia (by relieving spasm of the ciliary muscle and pupillary sphincter).[3] They are also used to prevent or break posterior synechiae. The choice of agent and frequency of use is tailored to the severity and course of inflammation. Preparations of short-acting and long-acting agents include:
| Agent | Duration |
|---|---|
| Tropicamide 0.5% and 1% | 6 hours |
| Cyclopentolate 0.5% and 1% | 24 hours |
| Phenylephrine 2.5% and 10% | 3 hours (but no cycloplegia) |
| Homatropine 2% | up to 2 days |
| Atropine 1% | up to 2 weeks |
Nonsteroidal Anti-inflammatory Drugs (NSAIDs)
As a primary treatment modality for ocular inflammatory diseases, NSAIDSs are generally ineffective in both local and systemic formulations; however, an exception might be some cases of non-necrotizing anterior scleritis.[1][4] NSAIDs might also provide some utility as an adjunct to other forms of therapy, such as the use of topical NSAIDs in the treatment of macular edema. The use of systemic NSAIDs with systemic corticosteroids increases the risk of gastric ulcers; therefore, histamine-H2 receptor antagonists or proton-pump inhibitors should be prescribed to reduce the risk.
Corticosteroids
Corticosteroids are the mainstay of treatment in uveitis and can be administered via multiple routes: topical, local injections (periocular or intraocular), or systemically via oral or intravenous routes.[1]
Topical steroids
Several steroids exist in topical ophthalmic preparations, and each has unique properties that may provide advantages and disadvantages in specific clinical scenarios.[2][3] Examples include difluprednate, dexamethasone, prednisolone acetate, fluorometholone, and loteprednol. Generally, topical steroid therapy should be started at high doses and then slowly tapered according to clinical evolution:
- Mild inflammation: administer q6h
- Moderate to severe inflammation: administer q1-2h
- A loading dose can be considered (eg, q1min for 5 minutes, then q30min-1h)
- A steroid ophthalmic ointment given at night can also be considered
- A commonly adopted regimen might consist of [3]:
- One drop q1h for 3 days, then
- One drop q2h for 3 days, then
- One drop q6h for 3 days, then
- One drop q8h for 7 days, then
- One drop q12h for 7 days, then
- One drop qday for 7 days, then stop.
Of note, difluprednate 0.05% 4 times daily has been found to be equivalent to prednisolone acetate 1% 8 times daily in anterior uveitis.[5]
Local steroid injections
Periocular or intraocular steroid injections through subconjunctival, transseptal, sub-Tenon, or intravitreal routes can be considered in the following clinical scenarios[3]:
- Severe unilateral uveitis
- Uveitis complicated by cystoid macular edema
- To supplement systemic therapy or when systemic therapy is contraindicated
- Poor patient compliance with topical or systemic therapy
Complications may include subconjunctival or retrobulbar hemorrhage, globe perforation, optic nerve injury, cutaneous changes, orbital fat atrophy, cataract, elevation of intraocular pressure, ptosis, and retinal vascular occlusion.
Inferior transseptal approach
- Administer topical anaesthesia (eg, tetracaine).
- Disinfect of the skin of the lower eyelid and maxillary area (eg, povidone-iodine 5%).
- Shake the vial containing the steroid.
- Draw 1 mL steroid (triamcinolone acetonide or methylprednisolone acetate 40 mg/mL) into a 2 mL syringe.
- Replace the drawing-up needle with a 25-gauge needle.
- Instruct the patient to look straight ahead.
- Insert the 25-gauge needle through the skin at the junction of the other third and the inner two-thirds of the lower orbital rim, entering close to the bony margin, while clearing the margin itself (note: some authors inject via the conjunctiva).
- Advance the needle slowly and tangentially to the globe.
- Slightly withdraw the plunger to ascertain that no blood enters the syringe and inject the full 1 mL of steroid slowly.
- Withdraw the needle carefully.
Posterior sub-Tenon approach
- Administer topical anaesthesia (eg, tetracaine).
- Place a small cotton pledget impregnated with an anaesthetic agent (eg, tetracaine, lidocaine 2% gel) in the superior fornix at the site of injection for 2 minutes.
- Shake the vial containing the steroid.
- Draw 1 mL steroid (triamcinolone acetonide or methylprednisolone acetate 40 mg/mL) into a 2 mL syringe.
- Replace the drawing-up needle with a 25-gauge needle.
- Instruct the patient to look in the nasal inferior direction (ie, the direction opposite to the superotemporal injection site).
- Penetrate the bulbar conjunctiva with the needle tip, bevel toward the eye globe.
- Slowly insert the needle posteriorly, following the contour of the globe, making side-to-side motions to prevent globe penetration.
- Slightly withdraw the plunger to ascertain that no blood enters the syringe and inject the full 1 mL of steroid slowly.
- Withdraw the needle carefully.
Intravitreal Steroid Injections
There are several options of intravitreal steroid delivery utilized in the treatment of uveitis[1]:
| Implant | Medication and Dosage | Duration |
|---|---|---|
| Triesence | triamcinolone acetonide intravitreal suspension, 40 mg/mL | 3 months |
| Ozurdex | dexamethasone intravitreal implant, 0.7mg | 6 months |
| Iluvien | fluocinolone acetonide intravitreal implant, 0.19mg | 36 months |
| Retisert | fluocinolone acetonide intravitreal implant, 0.59mg | 30 months |
The use of intravitreal steroids is effective in the treatment of uveitis and uveitic macular edema (see below).
Systemic Steroids
Systemic steroid therapy may be indicated in cases of vision-threatening uveitis, when there is poor response to topical or local steroid therapy, and in cases of bilateral or systemic involvement.[1][3][4] Treatment should consist of high dosage initially and then tapering according to clinical effect. In cases of severe uveitis, intravenous methylprednisolone may be considered (typically 1 g/day for 3 days). Initial dosing of oral prednisone is typically 1-1.5 mg/kg/day. Too rapid tapering or early discontinuation of systemic steroids may lead to disease recurrence. If steroid therapy is continued at a dose of more than 7.5 mg/day for a duration of more than 3 months, then steroid-sparing agents should be considered. A typically adopted steroid tapering schedule is as follows[6]:
| Prednisone dose (mg/day) | Decrement (mg/day) | Taper Interval | |
|---|---|---|---|
| RAPID | STANDARD | ||
| 60-30 | 10 | 2 days | weekly |
| 30-15 | 5 | 2 days | weekly |
| 15-7.5 | 2.5 | 2 days | weekly |
| < 7.5 | 2.5-1 | 2-7 days | weekly-monthly |
Side effects of corticosteroid therapy
Side effects of corticosteroid therapy are related to the route of administration and relative potency of the drugs.[1][3] Ocular side effects include cataract, elevation of intraocular pressure (IOP), and glaucoma. Systemic side effects of corticosteroid therapy include diabetes, hypertension, peptic ulcer, insomnia, osteoporosis, and others. Patients on long-term steroid treatment should receive calcium and vitamin D supplementation to prevent osteoporosis.
Given the safety profile of this class of drugs and the risks of ocular and systemic complications, relative potencies (as established compared to the reference of hydrocortisone) must also be taken into account.[7] Corticosteroids are presented in decreasing order of relative potency in the table below:
| Relative potencies of corticosteroids | ||
|---|---|---|
| Corticosteroid | Systemic Equivalent (mg) | Relative Potency |
|
Bethamethasone |
0.6 |
33.0 |
|
Dexamethasone |
0.75 |
26.0 |
|
Methylprednisolone |
4 |
5.0 |
|
Triamcinolone |
4 |
5.0 |
|
Prednisolone |
4 |
5.0 |
|
Prednisone |
5 |
4.0 |
|
Hydrocortisone |
20 |
1.0 |
|
Cortisone |
25 |
0.8 |
Immunomodulatory Therapy (IMT)
An important goal in the treatment of uveitis is to minimize the use of corticosteroids and its myriad ocular and systemic adverse effects.[2][7] The use of immunomodulatory therapy is an essential treatment strategy in the management of noninfectious uveitis (NIU). The Fundamentals of Care for Uveitis (FOCUS) International Consensus Group of uveitis specialists (both ophthalmologists and rheumatologists) outlined the following indications for noncorticosteroid systemic immunomodulatory therapy (NCSIT)[8]:
- Ocular factors such as acute sight-threatening disease, chronic persistent inflammation, exudative retinal detachment, posterior and macular involvement, and binocular sight-threatening disease
- Therapeutic needs such as failure of regional or systemic steroid therapy, high dosage of systemic steroid therapy, relapse after reduction of systemic steroid therapy, and steroid intolerance or need for steroid-sparing effect
Immunomodulatory therapies for the treatment on NIU include the following[6]:
| Class | Name |
|---|---|
| Antimetabolites | Azathioprine |
| Methotrexate | |
| Mycophenolate Mofetil | |
| Calcineurin Inhibitors | Cyclosporine |
| Tacrolimus | |
| Alkylating Agents | Chlorambucil |
| Cyclophosphamide |
Additionally, biologic therapies for the treatment of NIU include the following[9]:
| Class | Name |
|---|---|
| Anti-TNFα | Infliximab |
| Adalimumab | |
| Golimumab | |
| Certolizumab | |
| Anti-IL-1β | Anakinra |
| Canakinumab | |
| Anti-IL-2 | Daclizumab |
| Anti-IL-6 | Tocilizumab |
| Sarilumab | |
| Anti-IL-17A | Secukinumab |
| Anti-IL-12/ IL-23 | Ustekinumab |
| Anti-CD20 | Rituximab |
| Selective co-stimulator modulator | Abatacept |
| Interferons | IFN α-2a |
| IFN α-2b | |
| IFN β | |
| Janus kinase inhibitors | Tofacitinib |
| Baricitinib | |
| Other | Intravenous immunoglobulin |
The FOCUS Initiative Group has provided information on the level of evidence for each NCSIT available for the treatment of intermediate and posterior NIU, excluding biologics. [8] An adapted version is showed below:
| Evidence levels of NCSITs in the treatment of noninfectious uveitis | |||
|---|---|---|---|
|
SYSTEMIC NCSITs |
LEVEL OF EVIDENCE FOR NIU |
RECOMMENDATION LEVEL |
CLINICAL EFFECTS |
|
2B |
B |
Control of inflammation, steroid-sparing, improved VA | |
|
AZATHIOPRINE |
2B |
C |
Control of inflammation, steroid-sparing |
|
2B |
B |
Control of inflammation, steroid-sparing, improved VA | |
|
2B |
B |
Control of inflammation, steroid-sparing, improved VA | |
|
TACROLIMUS |
2B |
B |
Control of inflammation, steroid-sparing, improved VA |
|
CYCLOPHOSPHAMIDE |
4 |
C |
Control of inflammation, steroid-sparing |
|
CHLORAMBUCIL |
4 (for panuveitis in sympathetic ophthalmia) |
C |
Control of inflammation, steroid-sparing, improved VA |
In addition, the FOCUS Initiative group has provided information regarding the level of evidence supporting the use of biologics in uveitis.[8] A simplified version is presented below:
| Evidence Levels of biologic agents in the treatment of noninfectious uveitis | |||
|---|---|---|---|
|
BIOLOGIC AGENTS |
LEVEL OF EVIDENCE FOR NIU |
RECOMMENDATION LEVEL |
CLINICAL EFFECTS |
|
1B |
A |
Control of inflammation, steroid-sparing, improved VA | |
|
2B |
B-C |
Control of inflammation, steroid-sparing, improved VA | |
|
ETANERCEPT |
4 |
C |
Not recommended (EL2B) |
| ANAKINRA |
4 (for Behçet disease) |
C |
Control of inflammation |
| GEVOKIZUMAB |
2B (for Behçet disease) |
C |
Control of inflammation |
| DACLIZUMAB |
2B |
B |
Control of inflammation, steroid-sparing, improved VA |
| TOCILIZUMAB |
4 |
C |
Control of inflammation, improved VA |
| RITUXIMAB |
2B (for Behçet disease) |
C |
Control of inflammation |
| ALEMTUZUMAB |
2B (for Behçet disease) |
C |
Control of inflammation, steroid-sparing |
| INTERFERON-ALFA |
2B |
B |
Control of inflammation, steroid-sparing, improved VA |
| INTERFERON-BETA |
2B (IU or MS-related uveitis) |
C |
Control of inflammation, improved VA |
The choice of IMT must be individualized, taking into account the patient’s history, cause of uveitis, and comorbidities.
Major Studies in the Treatment of Uveitis
The long-term safety of immunosuppression was addressed by the Systemic Immunosuppressive Therapy for Eye Disease (SITE) Cohort Study, which evaluated 9250 patients with ocular inflammation with up to 30 years of follow-up.[10] Alkylating agents did not have a significantly increased risk of overall mortality but had a borderline significant increased risk of cancer-related mortality. The study found no increased malignancy risk with antimetabolites or calcineurin inhibitors in patients without an inherent increased risk, nor increased risk of mortality or cancer mortality.
The Multicenter Uveitis Steroid Treatment (MUST) Trial demonstrated that systemic therapy (including corticosteroid-supplemented immunomodulatory therapy and biologic agents) improved visual outcomes, controlled inflammation, and reduced macular edema similarly to local treatment using sustained-release intravitreal fluocinolone acetonide implant in patients with noninfectious intermediate uveitis, posterior uveitis, or panuveitis.[11][12] The implant was slightly better for the first 5 years, after which they were similar with uveitis control in 87% of patients at 7 years. Data from the MUST studies suggest that oral corticosteroids and immunosuppression can be administered relatively safely for at least 7 years. Interestingly, a Cochrane systematic review was unable to conclude that the implants are superior to traditional systemic therapy for the treatment of noninfectious uveitis, and findings regarding safety outcomes suggest increased risks of post-implant surgery for cataract and elevated intraocular pressure, compared with standard-of-care systemic therapy including corticosteroids.
The FAST trial demonstrated that mycophenolate and methotrexate are equally effective for the treatment of noninfectious intermediate, posterior, or panuveitis. The study compared oral methotrexate 25 mg weekly vs mycophenolate mofetil 3 g daily for corticosteroid-sparing control at 6 months. Treatment success occurred in 66.7% with methotrexate vs 57.1% with mycophenolate, a nonsignificant difference, supporting methotrexate noninferiority. At 12 months, most initial responders in both groups maintained success, and among early failures who switched therapy, success was higher when switching from mycophenolate to methotrexate than the reverse (69% vs 35%, P=.02). Elevated liver enzymes were the most frequent lab adverse event occurring in 13.0% of the patients in the methotrexate group and in 7.4% of the patients in the mycophenolate group.[13]
The VISUAL I, II, and III Trials demonstrated the efficacy of adalimumab in the control of inflammation in patients with noninfectious intermediate uveitis, posterior uveitis, or panuveitis.[14] The percentage of patients showing quiescence increased from 34% at week 0 to 85% at week 150, and the average daily dose of systemic steroids decreased from 9.4 ± 17.1 mg/day at week 0 to 1.5 ± 3.9 mg/day at week 150. Infections were the most commonly reported adverse event. The SYCAMORE Trial demonstrated that combined use of adalimumab with methotrexate in children with juvenile idiopathic arthritis associated uveitis decreased the likelihood of treatment failure over the use of methotrexate alone.[15] Patients on adalimumab were more likely to report adverse events than those on placebo.
The Adalimumab vs. Conventional Immunosuppression for Uveitis (ADVISE) Trial was a comparative effectiveness trial that compared adalimumab to conventional immunosuppressive drugs (antimetabolites and/or calcineurin inhibitors) for non-infectious intermediate, posterior, or panuveitides. The primary outcome was successful corticosteroid sparing at 6 months, which occurred in 69% of participants assigned to adalimumab versus 54% in the conventional immunosuppression group. By 12 months, successful corticosteroid discontinuation occurred in 55% of the adalimumab group versus 40% of the conventional therapy group. The trial concluded that for patients requiring immunosuppression, adalimumab treatment resulted in a greater proportion of participants achieving successful corticosteroid sparing at 6 months and discontinuation at 12 months, compared to conventional agents.[16]
Surgical Interventions in the Treatment of Uveitis
Surgical interventions may also be necessary in the treatment of complications of uveitis. [1] This can include the treatment of calcific band keratopathy with chelation therapy with disodium ethylene diamine tetraacetic acid (EDTA), cataract surgery, glaucoma surgery, surgical interventions for hypotony, pars plana vitrectomy and membrane peel for epiretinal membrane, retinal detachment repair, and others.
Selected Uveitis-Related Complications
Uveitic Cataract
Uveitic Glaucoma
Uveitic Macular Edema
Macular edema is a frequent complication and a major cause of vision loss in patients with uveitis, and treatment includes both control of intraocular inflammation and treatments directed toward macular edema. The Periocular Versus Intravitreal Corticosteroids for Uveitic Macular Edema (POINT) Trial demonstrated that periocular triamcinolone acetonide, intravitreal triamcinolone acetonide, and the intravitreal dexamethasone implant reduced central subfield thickness by 23%, 39%, and 46% (respectively) at 8 weeks, compared to baseline in patients with uveitic macular edema.[17] Although the MUST trial suggested that 0.59 mg implants provided no significantly increased efficacy compared to systemic treatment, a few studies have shown implanted eyes have improved uveitic macular edema. [18][19]
Some studies examined the impact of intravitreal anti-VEGF injections in the treatment of uveitic macular edema. They suggested that repeat bevacizumab injections improved visual acuity and reduced macular thickness in refractory uveitic macular edema.[20][21] Ranibizumab injections were studied in the PROMETHEUS trial to evaluate its efficacy in patients with macular edema from causes other than diabetic retinopathy, retinal vein occlusion, or neovascular age-related macular degeneration.[22] At 12 months, ranibizumab showed superiority in visual acuity gain over sham, reaching +5.45 letters of visual acuity treatment effect in the inflammatory or post-uveitis macular edema subgroup. However, more recently, the MERIT trial directly compared intravitreal ranibizumab 0.5 mg, methotrexate 400 μg, and dexamethasone implant in inactive or minimally active noninfectious uveitis with persistent or recurrent macular edema. At 12 weeks, dexamethasone achieved greater anatomic improvement, reducing central subfield thickness to 0.65 of baseline versus 0.78 with ranibizumab and 0.89 with methotrexate, and it was the only treatment to produce a significant visual gain (+4.9 letters). Dexamethasone was superior to methotrexate (P < 0.001) and ranibizumab (P ≈ 0.01–0.02), though it carried a higher incidence of intraocular pressure elevation.[23]
The PEACHTREE phase 3 randomized trial evaluated suprachoroidal triamcinolone acetonide (CLS-TA) versus sham for macular edema secondary to noninfectious uveitis. At 24 weeks, 47% of CLS-TA–treated eyes gained ≥15 ETDRS letters, compared with 16% of controls, with mean CST reduction of 153 μm versus 18 μm. Rescue therapy was needed in 14% versus 72%, and no treatment-related serious adverse events occurred. Cataract and IOP events were similar between groups.[24]
Uveitic Choroidal and Retinal Neovascularization
Intravitreal anti-VEGF injections have also been utilized in the treatment of uveitic choroidal and retinal neovascularization[25] Most studies involve bevacizumab, and a few involve ranibizumab, while the use of aflibercept is scarce, with only 1 small case series suggesting clinical benefit from a switch strategy from ranibizumab to aflibercept in refractory uveitic CNV.[26] The MINERVA study was designed to evaluate the efficacy of ranibizumab in patients with CNV from uncommon causes, including inflammatory disease.[27] In the postinflammatory CNV subgroup, a treatment effect of +6.5 letters at month 2 was noted in the ranibizumab treatment group.
Conclusions
Uncontrolled uveitis is a leading cause of vision loss in the United States and worldwide.[1] These data reinforce the importance of prompt and aggressive treatment of uveitis. The management of the uveitis patient represents a challenge for both the patient and the clinician; therefore, referral to a uveitis specialist should be considered early in the course of the disease. The ultimate goals of treatment of uveitis are to preserve vision, prevent significant vision-related morbidity, and prevent the iatrogenic effects of local and systemic therapies. Finally, treatment of the uveitis patient must always consider the underlying systemic disease. Thus, close collaboration with infectious disease specialists, autoimmune disease specialists, and other medical specialties dedicated to these diseases is of the utmost importance.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 American Academy of Ophthalmology. Basic and Clinical Science Course. Uveitis and Ocular Inflammation. American Academy of Ophthalmology; 2026-2027.
- ↑ 2.0 2.1 2.2 Foster CS, Vitale AT. Diagnosis & Treatment of Uveitis. 2nd Edition. JP Medical Ltd. 2013.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Salmon JF. Kanski's Clinical Ophthalmology: A Systematic Approach, 10th ed. Elsevier; 2025. ISBN: 978-0-443-11,099-3.
- ↑ 4.0 4.1 Yanoff M, Duker JS. Ophthalmology. 6th Edition. Elsevier; 2022.
- ↑ Sheppard JD, Toyos MM, Kempen JH, Kaur P, Foster CS. Difluprednate 0.05% versus prednisolone acetate 1% for endogenous anterior uveitis: a phase III, multicenter, randomized study. Invest Ophthalmol Vis Sci. 2014 May 6;55(5):2993-3002. doi: 10.1167/iovs.13-12660. PMID: 24677110; PMCID: PMC4581692.
- ↑ 6.0 6.1 Jabs DA. Immunosuppression for the Uveitides. Ophthalmology. 2018 Feb;125(2):193-202. doi: 10.1016/j.ophtha.2017.08.007. Epub 2017 Sep 20. PMID: 28942074; PMCID: PMC5794515.
- ↑ 7.0 7.1 Lee FF, Foster CS. Pharmacotherapy of uveitis. Expert Opin Pharmacother. 2010 May;11(7):1135-46. doi: 10.1517/14656561003713534. PMID: 20367272.
- ↑ 8.0 8.1 8.2 Dick AD, Rosenbaum JT, Al-Dhibi HA, Belfort R Jr, Brézin AP, Chee SP, Davis JL, Ramanan AV, Sonoda KH, Carreño E, Nascimento H, Salah S, Salek S, Siak J, Steeples L; Fundamentals of Care for Uveitis International Consensus Group. Guidance on Noncorticosteroid Systemic Immunomodulatory Therapy in Noninfectious Uveitis: Fundamentals Of Care for UveitiS (FOCUS) Initiative. Ophthalmology. 2018 May;125(5):757-773. doi: 10.1016/j.ophtha.2017.11.017. Epub 2018 Jan 6. PMID: 29310963.
- ↑ Ferreira LB, Smith AJ, Smith JR. Biologic Drugs for the Treatment of Noninfectious Uveitis. Asia Pac J Ophthalmol (Phila). 2021 Jan 19;10(1):63-73. doi: 10.1097/APO.0000000000000371. PMID: 33481396.
- ↑ Kempen JH, Daniel E, Gangaputra S, Dreger K, Jabs DA, Kaçmaz RO, Pujari SS, Anzaar F, Foster CS, Helzlsouer KJ, Levy-Clarke GA, Nussenblatt RB, Liesegang T, Rosenbaum JT, Suhler EB. Methods for identifying long-term adverse effects of treatment in patients with eye diseases: the Systemic Immunosuppressive Therapy for Eye Diseases (SITE) Cohort Study. Ophthalmic Epidemiol. 2008 Jan-Feb;15(1):47-55. doi: 10.1080/09286580701585892. PMID: 18300089.
- ↑ Multicenter Uveitis Steroid Treatment (MUST) Trial Research Group; Kempen JH, Altaweel MM, Drye LT, Holbrook JT, Jabs DA, Sugar EA, Thorne JE. Benefits of Systemic Anti-inflammatory Therapy versus Fluocinolone Acetonide Intraocular Implant for Intermediate Uveitis, Posterior Uveitis, and Panuveitis: Fifty-four-Month Results of the Multicenter Uveitis Steroid Treatment (MUST) Trial and Follow-up Study. Ophthalmology. 2015 Oct;122(10):1967-75. doi: 10.1016/j.ophtha.2015.06.042. Epub 2015 Aug 20. PMID: 26298715; PMCID: PMC4581989.
- ↑ Writing Committee for the Multicenter Uveitis Steroid Treatment (MUST) Trial and Follow-up Study Research Group; Kempen JH, Altaweel MM, Holbrook JT, Sugar EA, Thorne JE, Jabs DA. Association Between Long-Lasting Intravitreous Fluocinolone Acetonide Implant vs Systemic Anti-inflammatory Therapy and Visual Acuity at 7 Years Among Patients With Intermediate, Posterior, or Panuveitis. JAMA. 2017 May 16;317(19):1993-2005. doi: 10.1001/jama.2017.5103. PMID: 28477440; PMCID: PMC5540027.
- ↑ Rathinam SR, Gonzales JA, Thundikandy R, Kanakath A, Murugan SB, Vedhanayaki R, Lim LL, Suhler EB, Al-Dhibi HA, Doan T, Keenan JD, Rao MM, Ebert CD, Nguyen HH, Kim E, Porco TC, Acharya NR; FAST Research Group. Effect of Corticosteroid-Sparing Treatment With Mycophenolate Mofetil vs Methotrexate on Inflammation in Patients With Uveitis: A Randomized Clinical Trial. JAMA. 2019 Sep 10;322(10):936-945. doi: 10.1001/jama.2019.12618. PMID: 31503307; PMCID: PMC6737523.
- ↑ Suhler EB, Jaffe GJ, Fortin E, Lim LL, Merrill PT, Dick AD, Brezin AP, Nguyen QD, Thorne JE, Van Calster J, Cimino L, Adan A, Goto H, Kaburaki T, Kramer M, Vitale AT, Kron M, Song AP, Liu J, Pathai S, Douglas KM, Schlaen A, Muccioli C, Van Velthoven MEJ, Zierhut M, Rosenbaum JT. Long-Term Safety and Efficacy of Adalimumab in Patients with Noninfectious Intermediate Uveitis, Posterior Uveitis, or Panuveitis. Ophthalmology. 2021 Jun;128(6):899-909. doi: 10.1016/j.ophtha.2020.10.036. Epub 2020 Nov 3. PMID: 33157077.
- ↑ Ramanan AV, Dick AD, Jones AP, McKay A, Williamson PR, Compeyrot-Lacassagne S, Hardwick B, Hickey H, Hughes D, Woo P, Benton D, Edelsten C, Beresford MW; SYCAMORE Study Group. Adalimumab plus Methotrexate for Uveitis in Juvenile Idiopathic Arthritis. N Engl J Med. 2017 Apr 27;376(17):1637-1646. doi: 10.1056/NEJMoa1614160. PMID: 28445659.
- ↑ Adalimumab versus Conventional Immunosuppression for Uveitis Trial Research Group; Jabs DA, Sugar EA, Burke AE, Altaweel M, Thorne JE, Baksh S, Lim L, Thomas A, Yeh S, Holbrook JT. Adalimumab versus Conventional Immunosuppression for Uveitis (ADVISE) Trial. Ophthalmology. 2026 Mar;133(3):310-325. doi: 10.1016/j.ophtha.2025.10.004. Epub 2025 Oct 11. PMID: 41077357; PMCID: PMC13001625. Available from: https://www.aaojournal.org/article/S0161-6420(25)00639-6/fulltext
- ↑ Thorne JE, Sugar EA, Holbrook JT, Burke AE, Altaweel MM, Vitale AT, Acharya NR, Kempen JH, Jabs DA; Multicenter Uveitis Steroid Treatment Trial Research Group. Periocular Triamcinolone vs. Intravitreal Triamcinolone vs. Intravitreal Dexamethasone Implant for the Treatment of Uveitic Macular Edema: The PeriOcular vs. INTravitreal corticosteroids for uveitic macular edema (POINT) Trial. Ophthalmology. 2019 Feb;126(2):283-295. doi: 10.1016/j.ophtha.2018.08.021. Epub 2018 Sep 27. PMID: 30269924; PMCID: PMC6348060.
- ↑ Callanan DG, Jaffe GJ, Martin DF, Pearson PA, Comstock TL. Treatment of posterior uveitis with a fluocinolone acetonide implant: three-year clinical trial results. Arch Ophthalmol. 2008 Sep;126(9):1191-201. doi: 10.1001/archopht.126.9.1191. PMID: 18779477.
- ↑ Pavesio C, Zierhut M, Bairi K, Comstock TL, Usner DW; Fluocinolone Acetonide Study Group. Evaluation of an intravitreal fluocinolone acetonide implant versus standard systemic therapy in noninfectious posterior uveitis. Ophthalmology. 2010 Mar;117(3):567-75, 575.e1. doi: 10.1016/j.ophtha.2009.11.027. Epub 2010 Jan 15. PMID: 20079922.
- ↑ Bae JH, Lee CS, Lee SC. Efficacy and safety of intravitreal bevacizumab compared with intravitreal and posterior sub-tenon triamcinolone acetonide for treatment of uveitic cystoid macular edema. Retina. 2011 Jan;31(1):111-8. doi: 10.1097/IAE.0b013e3181e378af. PMID: 20856170.
- ↑ Soheilian M, Rabbanikhah Z, Ramezani A, Kiavash V, Yaseri M, Peyman GA. Intravitreal bevacizumab versus triamcinolone acetonide for refractory uveitic cystoid macular edema: a randomized pilot study. J Ocul Pharmacol Ther. 2010 Apr;26(2):199-206. doi: 10.1089/jop.2009.0093. PMID: 20307215.
- ↑ Staurenghi G, Lai TYY, Mitchell P, Wolf S, Wenzel A, Li J, Bhaumik A, Hykin PG; PROMETHEUS Study Group. Efficacy and Safety of Ranibizumab 0.5 mg for the Treatment of Macular Edema Resulting from Uncommon Causes: Twelve-Month Findings from PROMETHEUS. Ophthalmology. 2018 Jun;125(6):850-862. doi: 10.1016/j.ophtha.2017.12.002. Epub 2018 Jan 20. PMID: 29371007.
- ↑ Multicenter Uveitis Steroid Treatment Trial (MUST) Research Group, Writing Committee:; Acharya NR, Vitale AT, Sugar EA, Holbrook JT, Burke AE, Thorne JE, Altaweel MM, Kempen JH, Jabs DA. Intravitreal Therapy for Uveitic Macular Edema-Ranibizumab versus Methotrexate versus the Dexamethasone Implant: The MERIT Trial Results. Ophthalmology. 2023 Sep;130(9):914-923. doi: 10.1016/j.ophtha.2023.04.011. Epub 2023 Jun 13. PMID: 37318415; PMCID: PMC10524707.
- ↑ Yeh S, Khurana RN, Shah M, Henry CR, Wang RC, Kissner JM, Ciulla TA, Noronha G; PEACHTREE Study Investigators. Efficacy and Safety of Suprachoroidal CLS-TA for Macular Edema Secondary to Noninfectious Uveitis: Phase 3 Randomized Trial. Ophthalmology. 2020 Jul;127(7):948-955. doi: 10.1016/j.ophtha.2020.01.006. Epub 2020 Jan 10. PMID: 32173113.
- ↑ Gulati N, Forooghian F, Lieberman R, Jabs DA. Vascular endothelial growth factor inhibition in uveitis: a systematic review. Br J Ophthalmol. 2011 Feb;95(2):162-5. doi: 10.1136/bjo.2009.177279. Epub 2010 May 21. PMID: 20494915.
- ↑ Hernández-Martínez P, Dolz-Marco R, Alonso-Plasencia M, Abreu-Gonzalez R. Aflibercept for inflammatory choroidal neovascularization with persistent fluid on intravitreal ranibizumab therapy. Graefes Arch Clin Exp Ophthalmol. 2014 Aug;252(8):1337-9. doi: 10.1007/s00417-014-2634-2. Epub 2014 May 1. PMID: 24789465.
- ↑ Lai TYY, Staurenghi G, Lanzetta P, Holz FG, Melissa Liew SH, Desset-Brethes S, Staines H, Hykin PG; MINERVA Study Group. Efficacy And Safety Of Ranibizumab For The Treatment Of Choroidal Neovascularization Due To Uncommon Cause: Twelve-Month Results Of The Minerva Study. Retina. 2017 Jul 12.
