Uveitis medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Faizan Sheraz, M.D. [2] Basir Gill, M.B.B.S, M.D.[3]

Overview

Treatment choice should be determined by anatomical subtype, severity, infectious risk, comorbidities, and sight-threatening features (e.g., macular edema, severe vitritis, retinochoroiditis, Behçet disease), with the primary goal of rapid inflammation control to prevent vision loss.[1] The mainstay of therapy for uveitis is steroids, either as topical eye drops or oral therapy with Prednisolone. Acyclovir is the drug of choice for empiric therapy in anterior uveitis. The treatment for intermediate and posterior uveitis generally depends on the underlying disease.[2]

Medical therapy

Uveitis is typically treated with glucocorticoids, either as topical eye drops (such as betamethasone, dexamethasone or prednisolone) or oral therapy with Prednisolone tablets. In addition, topical cycloplegics, such as atropine or homatropine, may be used. If the uveitis is caused by a body-wide infection, treatment may involve antibiotics and powerful anti-inflammatory medicines corticosteroids. In some cases, an injection of PSTTA can also be given to reduce the swelling of the eye.[3]

Antimetabolite medications, such as Methotrexate are often used for recalcitrant or more aggressive cases of uveitis. Experimental treatment with Infliximab infusions may prove helpful.

More specifically, the treatment regimen differs among the various forms of uveitis:

Noninfectious Anterior Uveitis

First-Line Therapy: Topical Corticosteroids

  • The mainstay of therapy for anterior uveitis is topical corticosteroid drops (Prednisolone acetate 1%). Rimexolone 1% can also achieve meaningful improvement.[4][5][6]
Typical regimen
  • One drop hourly while awake in the affected eye for 7 days.
  • Followed by a gradual taper, usually decreasing by one drop per day each week.
  • Tapering should be individualized based on clinical response.

Second-Line Therapy: Local Ocular Corticosteroids

Local corticosteroid therapy is used when topical drops are ineffective or cannot be used adequately.[7]

Available Options (in the order of preference):[8][9]
  • Periocular (sub-Tenon or orbital floor) injections e.g., triamcinolone acetonide for ~1-2 months
  • Intravitreal dexamethasone implant for ~3 - 6 months
  • Intravitreal fluocinolone acetonide implant for up to 36 months

Systemic Corticosteroids for Severe Anterior Uveitis[10][11]

Systemic corticosteroids are indicated when inflammation is severe, non-responsive to topical or regional therapy and/or threatens vision.

Typical regimen

Oral prednisone 1 mg/kg/day (maximum 60-80 mg/day) with gradual taper over 4-10 months.

Prolonged corticosteroid (topical, periocular, intravitreal, or systemic) use may cause Ocular hypertension, Glaucoma and Cataracts. Up to 18-24% of patients treated with corticosteroids require cataract or glaucoma surgery.[12][13][14] Trials have shown Suprachondrial triamcinolone to be safer than intravitreal dexamethasone implants and periocular triamcinolone. [8][9]

Noninfectious Intermediate, Posterior Uveitis, and Panuveitis

Patients with moderate to severe disease are at high risk of permanent vision loss and usually require systemic therapy.[1]

Systemic Corticosteroids[10][15]

Systemic corticosteroids are used to rapidly induce remission, especially in severe vision-threatening disease (e.g., Behçet disease, Vogt–Koyanagi–Harada disease):

  • Intravenous methylprednisolone 1 g daily for 3 days. Followed by oral prednisone taper over 4–10 months.

Disease-Modifying Antirheumatic Drugs (DMARDs)[16][17][18][19][20][21][22][23][24]

Guidelines recommend systemic corticosteroids combined with DMARDs as first-line therapy to maintain remission and reduce corticosteroid exposure.

  • Methotrexate

Weekly dosing of methotrexate, controlled inflammation at 12 months in

  • 52.1% of posterior/panuveitis
  • 74.9% of intermediate uveitis

40–50% maintained control with ≤10 mg prednisone daily with ~15% discontinued due to adverse effects.

  • Mycophenolate Mofetil

Achieved inflammation control at 12 months in:

  • 70.9% of posterior/panuveitis
  • 76.7% of intermediate uveitis

It also lowered relapse rate when combined with prednisone vs prednisone alone.

  • Azathioprine

Reduced development and recurrence of uveitis in Behçet disease with:

  • 69% control in intermediate uveitis
  • 44% in posterior/panuveitis
  • Cyclosporine
  • Controlled inflammation in ~52% of intermediate and posterior/panuveitis cases
  • Noninferior to IV steroid pulse therapy in Vogt–Koyanagi–Harada disease

Biologic Therapy

Biologic agents are second-line therapy for patients who do not respond adequately to DMARDs.

  • Adalimumab

FDA-approved for noninfectious uveitis

  • VISUAL I trial:
    • Time to treatment failure: 24 weeks vs 13 weeks with placebo
  • VISUAL II trial:
    • Longer remission duration in inactive disease
  • Increased risk of serious infections and demyelinating disease

Other TNF inhibitors (golimumab, certolizumab) reduced uveitis flares in patients with axial spondyloarthritis.

DMARDS and Biologics for Uveitis[1]
Category/Drug Adult dose and administration Adverse effects Monitoring Contraindications/Cautions Special Considerations
Disease-Modifying Antirheumatic drugs
Antimetabolites
Methotrexate 7.5-25 mg/wk Embryofetal toxicity, gastrointestinal reaction (10%), bone marrow suppression (2%), hepatotoxicity (15%), interstitial pneumonitis, opportunistic infections Complete blood cell count, kidney panel, liver panel Pregnancy, breastfeeding, alcoholism or liver disease, immunodeficiencies, blood dyscrasias, Caution in active infection Considered first-line alongside mycophenolate mofetil. Subcutaneous administration more effective than oral administration
Mycophenolate Mofetil 1-1.5 g Twice daily Embryofetal toxicity, gastrointestinal reaction (20%), bone marrow suppression (2%), hepatotoxicity (20%), Malignancies (lymphoma and skin), opportunistic infections Complete blood cell count.

Mycophenolate levels can be measured for patients not responding to therapy

Pregnancy, breastfeeding, blood dyscrasias, active infection Considered first-line alongside methotrexate
Azathioprine 150-200 mg once daily Embryofetal toxicity, gastrointestinal reaction (10%), bone marrow suppression (5%), hepatotoxicity (4%), Complete blood cell count Pregnancy, previous alkylating agents (cyclophosphamide, chlorambucil) Consider thiopurine methyltransferase (TPMT) testing before starting azathioprine, as reduced TPMT activity can lead to severe bone marrow toxicity
Calcineurin Inhibitors
Cyclosporine 1.5 mg/kg Twice daily Nephrotoxicity (4%), hypertension (3%), hepatotoxicity (1.5%), gum hyperplasia (1%), skin cancer Complete blood cell count, kidney panel, blood pressure.

Cyclosporine trough levels can be measured for patients not responding to therapy

Uncontrolled hypertension, kidney disease, malignancy
Biologics
TNF blockers
Adalimumab 40 mg Subcutaneously every 2 wk Infusion reactions (20%), gastrointestinal reaction (15%), hepatotoxicity (10%), demyelination, increased risk of malignancy and infection (including tuberculosis, hepatitis B) Complete blood cell count, kidney panel, liver panel, Ongoing vigilance for serious or opportunistic infections. Repeat tuberculosis serology and chest radiography if pulmonary symptoms occur. Consider brain MRI in cases of neurologic symptoms compatible with demyelinating disorders. Anti-adalimumab antibodies can be measured for patients not responding to therapy Initiation contraindicated during an active infection Caution during infection (stop if serious), caution for hepatitis B carriers (reactivation may occur), caution for demyelinating disease and heart failure (may worsen) First-line biologic with the strongest evidence in both adults and children
Golimumab 50 mg Subcutaneously monthly Hepatotoxicity, bone marrow suppression, infusion reactions (2%), hypertension (2%), demyelination, increased risk of malignancy and infection (including tuberculosis, hepatitis B) Complete blood cell count, kidney panel, liver panel. Ongoing vigilance for serious or opportunistic infections. Repeat tuberculosis serology and chest radiography if pulmonary symptoms occur. Consider brain MRI in cases of neurologic symptoms compatible with demyelinating disorders. Initiation contraindicated during an active infection. Caution during infection (stop if serious), caution for hepatitis B carriers (reactivation may occur), caution for demyelinating disease and heart failure (may worsen)
Certolizumab 200 mg Subcutaneously every 2 wk


Hepatotoxicity, bone marrow suppression, gastrointestinal reaction, infusion reactions, demyelination, increased risk of malignancy and infection (including tuberculosis) Complete blood cell count, kidney panel, liver panel. Ongoing vigilance for serious or opportunistic infections. Repeat tuberculosis serology and chest radiography if pulmonary symptoms occur. Consider brain MRI in cases of neurologic symptoms compatible with demyelinating disorders. Initiation contraindicated during an active infection. Caution during infection (stop if serious), caution for hepatitis B carriers (reactivation may occur), caution for demyelinating disease, blood dyscrasias, and heart failure (may worsen)
JAK Inhibitor
Filgotinib 200 mg by mouth Major cardiovascular events, malignancy, venous thromboembolism, serious infections (adverse effects currently considered as class-effect from tofacitinib) Embryofetal toxicity, gastrointestinal reaction (4%), bone marrow suppression (1%), nephrotoxicity, hepatotoxicity, hyperlipidemia Complete blood cell count, kidney panel, liver panel, glucose, blood pressure. High suspicion index to investigate venous thromboembolism, cardiac events, or new skin lesion. Repeat tuberculosis serology and chest radiography if pulmonary symptoms occur Avoid use in patients 65 y or older, in patients who are current or past long-time smokers, and in patients with other cardiovascular disease or malignancy risk factors, unless there are no suitable alternatives. Use with caution in patients with risk factors for venous thromboembolism

Infectious Uveitis

General Principles[25]

  • Treat the infection first with appropriate antimicrobials
  • Corticosteroids may be added only when indicated
  • Corticosteroids must never be used alone in viral retinitis or toxoplasmosis
  • In the case of infectious anterior uveitis, antimicrobial therapy is recommended.[2]

Infectious Panuveitis (Endophthalmitis)[26]

  • Exogenous cases: intravitreal antimicrobials
  • Endogenous cases: systemic antimicrobials + source control
  • Empiric broad-spectrum therapy should be started promptly

In a study of 278 cases:

  • 78.5% were gram-positive (100% sensitive to vancomycin)
  • 11.8% were gram-negative
  • Remaining cases were fungal Uveitis

Tuberculosis-Associated Uveitis[27][28][29]

Uveitis may result from direct ocular infection or Immune-mediated reaction to systemic tuberculosis. Decisions regarding antitubercular therapy should be individualized based on clinical, microbiological, and epidemiologic findings. The WHO recommends a 6-month regimen: isoniazid/rifampicin/pyrazinamide/ethambutol for 2 months, followed by isoniazid/rifampicin for 4 months, achieving 85% success for drug susceptible tuberculosis.

Antimicrobial regimens

  • Infectious uveitis
  • 1. Empiric antimicrobial therapy
  • Preferred regimen: Acyclovir 800 mg PO q5h for 7-10 days
  • Note: Long-term prophylactic acyclovir 400 mg PO bid may be beneficial in preventing recurrences of herpetic uveitis and development of complications.
  • 2. Pathogen-directed antimicrobial therapy
  • 2.1 Lyme uveitis

Intermediate and Posterior Uveitis

Treatment often depends on the underlying cause of the inflammation. If the cause is infectious, treatment must involve an anti-infective agent.

  • Acute retinal necrosis (ARN) due to Herpes simplex or Varicella zoster virus: intravenous acyclovir 10 mg/kg every 8 hours with normal renal function for 1 to 2 weeks followed by Valacyclovir or Famciclovir for 6 weeks to several months. In case of ARN due to CMV, IV Ganciclovir should replace Acyclovir.
  • Progressive outer retinal necrosis: prolonged intravenous antiviral agents, in addition to intravitreal injections with Foscarnet and Ganciclovir, and the initiation of HAART in HIV-positive patients.
  • Ocular syphilis: intravenous penicillin 4 million U every 4 hours for 10 to 14 days. Corticosteroids are given to decrease intraocular inflammation as a result of Jarisch-Herxheimer reaction
  • Ocular TB: treated with the same medications and duration of therapy as TB meningitis
  • Lyme uveitis:Preferred regimen: Ceftriaxone 2 g IV q24h for 14 days

If the cause is non-infectious, treatment is administered to reduce inflammation, often through the use of corticosteroids. Intermediate uveitis is often treated with steroid eye drops, whereas posterior uveitis would have to be treated with steroid pills, as eye drops and ointments cannot reach the back of the eye.

References

  1. ↑ 1.0 1.1 1.2 Maghsoudlou, P., Epps, S. J., Guly, C. M., & Dick, A. D. (2025). Uveitis in adults: A review: A review. The Journal of the American Medical Association, 334(5), 419–434. https://doi.org/10.1001/jama.2025.4358
  2. ↑ 2.0 2.1 Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 978-0-443-06839-3.
  3. ↑ BNF 45 March 2003
  4. ↑ Gutteridge, I. F., & Hall, A. J. (2007). Acute anterior uveitis in primary care. Clinical & Experimental Optometry: Journal of the Australian Optometrical Association, 90(2), 70–82. https://doi.org/10.1111/j.1444-0938.2006.00128.x
  5. ↑ Maghsoudlou, P., Epps, S. J., Guly, C. M., & Dick, A. D. (2025). Uveitis in adults: A review: A review. The Journal of the American Medical Association, 334(5), 419–434. https://doi.org/10.1001/jama.2025.4358
  6. ↑ Biswas, J., Ganeshbabu, T. M., Raghavendran, S. R., Raizada, S., Mondkar, S. V., & Madhavan, H. N. (2004). Efficacy and safety of 1% rimexolone versus 1% prednisolone acetate in the treatment of anterior uveitis--a randomized triple masked study. International Ophthalmology, 25(3), 147–153. https://doi.org/10.1007/s10792-004-5195-2
  7. ↑ Takase, H., Acharya, N. R., Babu, K., Bodaghi, B., Khairallah, M., McCluskey, P. J., Tesavibul, N., Thorne, J. E., Tugal-Tutkun, I., Yamamoto, J. H., Rao, N. A., Smith, J. R., & Mochizuki, M. (2021). Recommendations for the management of ocular sarcoidosis from the International Workshop on Ocular Sarcoidosis. The British Journal of Ophthalmology, 105(11), 1515–1519. https://doi.org/10.1136/bjophthalmol-2020-317354
  8. ↑ 8.0 8.1 Thorne, J. E., Sugar, E. A., Holbrook, J. T., Burke, A. E., Altaweel, M. M., Vitale, A. T., Acharya, N. R., Kempen, J. H., Jabs, D. A., & Multicenter Uveitis Steroid Treatment Trial Research Group. (2019). 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, 126(2), 283–295. https://doi.org/10.1016/j.ophtha.2018.08.021
  9. ↑ 9.0 9.1 Yeh, S., Khurana, R. N., Shah, M., Henry, C. R., Wang, R. C., Kissner, J. M., Ciulla, T. A., Noronha, G., & PEACHTREE Study Investigators. (2020). Efficacy and safety of suprachoroidal CLS-TA for macular edema secondary to noninfectious uveitis: Phase 3 randomized trial. Ophthalmology, 127(7), 948–955. https://doi.org/10.1016/j.ophtha.2020.01.006
  10. ↑ 10.0 10.1 Jabs, D. A., Rosenbaum, J. T., Foster, C. S., Holland, G. N., Jaffe, G. J., Louie, J. S., Nussenblatt, R. B., Stiehm, E. R., Tessler, H., Van Gelder, R. N., Whitcup, S. M., & Yocum, D. (2000). Guidelines for the use of immunosuppressive drugs in patients with ocular inflammatory disorders: recommendations of an expert panel. American Journal of Ophthalmology, 130(4), 492–513. https://doi.org/10.1016/s0002-9394(00)00659-0
  11. ↑ Zhang, H., Nicholson, C. M., Kempen, J. H., Ying, G.-S., & Gangaputra, S. S. (2025). Management of acute non-infectious anterior uveitis in adults - practice patterns among uveitis specialists in North America. Ocular Immunology and Inflammation, 33(7), 1153–1158. https://doi.org/10.1080/09273948.2024.2346819
  12. ↑ Gutteridge, I. F., & Hall, A. J. (2007). Acute anterior uveitis in primary care. Clinical & Experimental Optometry: Journal of the Australian Optometrical Association, 90(2), 70–82. https://doi.org/10.1111/j.1444-0938.2006.00128.x
  13. ↑ Urban, R. C., Jr, & Cotlier, E. (1986). Corticosteroid-induced cataracts. Survey of Ophthalmology, 31(2), 102–110. https://doi.org/10.1016/0039-6257(86)90077-9
  14. ↑ Prieto-Del-Cura, M., & González-Guijarro, J. J. (2020). Risk factors for ocular complications in adult patients with uveitis. European Journal of Ophthalmology, 30(6), 1381–1389. https://doi.org/10.1177/1120672119899379
  15. ↑ Charkoudian, L. D., Ying, G.-S., Pujari, S. S., Gangaputra, S., Thorne, J. E., Foster, C. S., Jabs, D. A., Levy-Clarke, G. A., Nussenblatt, R. B., Rosenbaum, J. T., Suhler, E. B., & Kempen, J. H. (2012). High-dose intravenous corticosteroids for ocular inflammatory diseases. Ocular Immunology and Inflammation, 20(2), 91–99. https://doi.org/10.3109/09273948.2011.646382
  16. ↑ 1 Recommendations | Adalimumab and dexamethasone for treating non-infectious uveitis | Guidance | NICE. (n.d.). Retrieved January 27, 2026, from https://www.nice.org.uk/guidance/ta460/chapter/1-Recommendations
  17. ↑ Dick, A. D., Rosenbaum, J. T., Al-Dhibi, H. A., Belfort, R., Jr, Brézin, A. P., Chee, S. P., Davis, J. L., Ramanan, A. V., Sonoda, K.-H., Carreño, E., Nascimento, H., Salah, S., Salek, S., Siak, J., Steeples, L., & Fundamentals of Care for Uveitis International Consensus Group. (2018). Guidance on noncorticosteroid systemic immunomodulatory therapy in noninfectious uveitis: Fundamentals of care for UveitiS (FOCUS) initiative. Ophthalmology, 125(5), 757–773. https://doi.org/10.1016/j.ophtha.2017.11.017
  18. ↑ Gangaputra, S., Newcomb, C. W., Liesegang, T. L., Kaçmaz, R. O., Jabs, D. A., Levy-Clarke, G. A., Nussenblatt, R. B., Rosenbaum, J. T., Suhler, E. B., Thorne, J. E., Foster, C. S., Kempen, J. H., & Systemic Immunosuppressive Therapy for Eye Diseases Cohort Study. (2009). Methotrexate for ocular inflammatory diseases. Ophthalmology, 116(11), 2188-98.e1. https://doi.org/10.1016/j.ophtha.2009.04.020
  19. ↑ Daniel, E., Thorne, J. E., Newcomb, C. W., Pujari, S. S., Kaçmaz, R. O., Levy-Clarke, G. A., Nussenblatt, R. B., Rosenbaum, J. T., Suhler, E. B., Foster, C. S., Jabs, D. A., & Kempen, J. H. (2010). Mycophenolate mofetil for ocular inflammation. American Journal of Ophthalmology, 149(3), 423-32.e1-2. https://doi.org/10.1016/j.ajo.2009.09.026
  20. ↑ Deuter, C. M. E., Engelmann, K., Heiligenhaus, A., Lanzl, I., Mackensen, F., Ness, T., Pleyer, U., Stuebiger, N., Wilhelm, B., Luedtke, H., Zierhut, M., Doycheva, D., & MYCUV-IIT02 Study Group. (2018). Enteric-coated mycophenolate sodium in the treatment of non-infectious intermediate uveitis: results of a prospective, controlled, randomised, open-label, early terminated multicentre trial. The British Journal of Ophthalmology, 102(5), 647–653. https://doi.org/10.1136/bjophthalmol-2017-310156
  21. ↑ Yazici, H., Pazarli, H., Barnes, C. G., Tüzün, Y., Ozyazgan, Y., Silman, A., Serdaroğlu, S., Oğuz, V., Yurdakul, S., & Lovatt, G. E. (1990). A controlled trial of azathioprine in Behçet’s syndrome. The New England Journal of Medicine, 322(5), 281–285. https://doi.org/10.1056/NEJM199002013220501
  22. ↑ Pasadhika, S., Kempen, J. H., Newcomb, C. W., Liesegang, T. L., Pujari, S. S., Rosenbaum, J. T., Thorne, J. E., Foster, C. S., Jabs, D. A., Levy-Clarke, G. A., Nussenblatt, R. B., & Suhler, E. B. (2009). Azathioprine for ocular inflammatory diseases. American Journal of Ophthalmology, 148(4), 500-509.e2. https://doi.org/10.1016/j.ajo.2009.05.008
  23. ↑ Kaçmaz, R. O., Kempen, J. H., Newcomb, C., Daniel, E., Gangaputra, S., Nussenblatt, R. B., Rosenbaum, J. T., Suhler, E. B., Thorne, J. E., Jabs, D. A., Levy-Clarke, G. A., & Foster, C. S. (2010). Cyclosporine for ocular inflammatory diseases. Ophthalmology, 117(3), 576–584. https://doi.org/10.1016/j.ophtha.2009.08.010
  24. ↑ Ono, T., Goto, H., Sakai, T., Nitta, F., Mizuki, N., Takase, H., Kaneko, Y., Hori, J., Nakano, S., Nao-I, N., Ohguro, N., Miyata, K., Tomita, M., Mochizuki, M., & Japan VKH Disease Treatment Study Group. (2022). Comparison of combination therapy of prednisolone and cyclosporine with corticosteroid pulse therapy in Vogt-Koyanagi-Harada disease. Japanese Journal of Ophthalmology, 66(2), 119–129. https://doi.org/10.1007/s10384-021-00878-w
  25. ↑ Takakura, A., Tessler, H. H., Goldstein, D. A., Guex-Crosier, Y., Chan, C.-C., Brown, D. M., Thorne, J. E., Wang, R., & Cunningham, E. T., Jr. (2014). Viral retinitis following intraocular or periocular corticosteroid administration: a case series and comprehensive review of the literature. Ocular Immunology and Inflammation, 22(3), 175–182. https://doi.org/10.3109/09273948.2013.866256
  26. ↑ Benz, M. S., Scott, I. U., Flynn, H. W., Jr, Unonius, N., & Miller, D. (2004). Endophthalmitis isolates and antibiotic sensitivities: a 6-year review of culture-proven cases. American Journal of Ophthalmology, 137(1), 38–42. https://doi.org/10.1016/s0002-9394(03)00896-1
  27. ↑ Agrawal, R., Testi, I., Mahajan, S., Yuen, Y. S., Agarwal, A., Kon, O. M., Barisani-Asenbauer, T., Kempen, J. H., Gupta, A., Jabs, D. A., Smith, J. R., Nguyen, Q. D., Pavesio, C., Gupta, V., & Collaborative Ocular Tuberculosis Study Consensus Group. (2021). Collaborative Ocular Tuberculosis Study consensus guidelines on the management of tubercular uveitis-report 1: Guidelines for initiating antitubercular therapy in tubercular choroiditis. Ophthalmology, 128(2), 266–276. https://doi.org/10.1016/j.ophtha.2020.01.008
  28. ↑ Betzler, B. K., Putera, I., Testi, I., La Distia Nora, R., Kempen, J., Kon, O. M., Pavesio, C., Gupta, V., & Agrawal, R. (2023). Anti-tubercular therapy in the treatment of tubercular uveitis: A systematic review and meta-analysis. Survey of Ophthalmology, 68(2), 241–256. https://doi.org/10.1016/j.survophthal.2022.10.001
  29. ↑ World Health Organization. Guidelines for treatment of drug-susceptible tuberculosis. Published 2017. Accessed April 3, 2025. https:// www.who.int

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