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Uveitis: Treatment

Author: James T Rosenbaum, MD

Section Editor: Jonathan Trobe, MD
Deputy Editor: Paul L Romain, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2017. | This topic last updated: Aug 14, 2017.

INTRODUCTION — Intraocular inflammation (ie, uveitis) results from many causes. The approach to therapy
depends upon the etiology, location, and severity of the inflammation [1]. The management of a patient with
uveitis will require consultation with an ophthalmologist or other specialist in uveal eye disease. Ideally, therapy
should be initiated within 24 hours of the onset of acute, anterior uveitis, and infectious causes of uveitis should
be treated promptly.

This topic will focus primarily on the treatment of uveitis that is not related to an active infection. A general
approach to evaluation and treatment of the patient presenting with a painful red eye is discussed separately.
Treatment of uveitis that is due to infection is discussed in more detail in topic reviews that address
management of the specific infection. The etiology, clinical manifestations, and diagnostic approach to a patient
with uveitis are presented separately. (See "Evaluation of the red eye" and "Uveitis: Etiology, clinical
manifestations, and diagnosis".)

DEFINITIONS — The uvea is the middle portion of the eye. The anterior portion of the uvea includes the iris and
ciliary body. The pars plana is the tissue just posterior to the ciliary body and just anterior to the retina. The
posterior portion of the uvea is known as the choroid (figure 1).

● Inflammation of the anterior uveal tract is called anterior uveitis and is synonymous with iritis. When the
adjacent ciliary body is also inflamed, the process is known as iridocyclitis.

● Terms used to describe uveitis posterior to the lens include vitritis, intermediate uveitis, pars planitis,
choroiditis, retinitis, chorioretinitis, or retinochoroiditis. Panuveitis refers to inflammation in the anterior
chamber, vitreous humor, and choroid or retina simultaneously. The presence of inflammatory cells in the
vitreous humor posterior to the lens is termed intermediate uveitis, even though the vitreous humor is not
technically part of the uveal tract.

UVEITIS DUE TO INFECTION — Infectious causes of uveitis are shown in the table (table 1).

● Viral infections may cause either anterior or posterior uveitis. The most common viruses causing uveitis are
cytomegalovirus (CMV), herpes zoster, and herpes simplex. These infections should be treated promptly
with appropriate antiviral agents. CMV is being increasingly recognized in Asian populations as a cause of a
chronic, unilateral anterior uveitis associated with elevated intraocular pressure [2]. Fuchs heterochromic
iridocyclitis, a form of chronic unilateral, primarily anterior uveitis, is now considered to be most often
secondary to a remote infection with rubella [3]. In herpetic infection of the retina, retinal destruction (acute
retinal necrosis) may otherwise progress rapidly. Although immunosuppressed patients are at greater risk
for acute retinal necrosis, it may also occur on occasion in patients with an intact immune system.
 CMV retinitis is seen only rarely in immunocompetent patients, while herpes simplex and herpes zoster may
affect both immunocompetent and immunocompromised patients.

● In addition to treating the underlying infection, patients with anterior uveitis due to an infection are often
treated with topical glucocorticoids after initiation of antiviral medication. Treatment of ocular involvement
due to these viral infections is discussed in the appropriate topic reviews. (See "Treatment of AIDS-related
cytomegalovirus retinitis" and "Treatment of herpes zoster in the immunocompetent host", section on
'Herpes zoster ophthalmicus' and "Herpes simplex keratitis".)

● Treatment of chorioretinitis due to Toxoplasmosis gondii in patients with HIV infection and in
immunocompetent adults is discussed separately. Higher doses and longer duration of treatment are
generally used in patients with HIV infection. (See "Toxoplasmosis in HIV-infected patients", section on
'Chorioretinitis' and "Toxoplasmosis in immunocompetent hosts".)

Other treatable infectious causes of uveitis in the immunocompetent host include syphilis, and, less commonly,
cat scratch fever, tuberculosis, leprosy, and Lyme disease. (See "Uveitis: Etiology, clinical manifestations, and
diagnosis".)

NONINFECTIOUS UVEITIS — The approach to treating noninfectious uveitis varies depending upon the location
of the inflammation. There are limited available data from controlled trials. The following strategies are generally
consistent with the approach advocated by a consensus panel of both ophthalmologists and rheumatologists
that convened in 2000, prior to any extensive testing of biologic therapies, such as tumor necrosis factor (TNF)
inhibitors, for uveitis [4]. An expert panel subsequently summarized the role of biologic therapies in the treatment
of uveitis [5]. These are potentially complex decisions that require consultation and ongoing care with an
ophthalmologist or other specialist in uveitis.

Initial treatment — Noninfectious causes of anterior uveitis are generally treated with topical glucocorticoids
such as prednisolone acetate (1 percent). The frequency for the drops depends upon the intensity of the
inflammation. A dilating drop such as scopolamine (0.25 percent) or cyclopentolate (1 percent) can relieve pain
due to spasm of the muscles controlling the pupil and will also help to prevent the formation of posterior
synechiae that may interfere with the function of the pupil.

Uveitis that is primarily posterior to the lens is generally not responsive to topical medication, although some
experts are increasingly using difluprednate (0.05 percent) [6]. Difluprednate has better vitreous humor
penetration for inflammation posterior to the lens compared with other topical corticosteroids, but it also has a
greater tendency to raise intraocular pressure or to cause a cataract. Additional options for initial treatment of
intermediate or posterior uveitis, or of panuveitis, include observation only or treatment with periocular injection
of a glucocorticoid such as triamcinolone (subconjunctival, subtenon, or peribulbar). Intraocular injection of
glucocorticoids entails more risk than a periocular injection, but this approach can also provide more potent and
more sustained benefit. Some patients, however, may decline a periocular or intraocular injection. The US Food
and Drug Administration (FDA) has approved two glucocorticoids for intraocular injection, a formulation of
triamcinolone and a polymer that slowly releases dexamethasone. Complications from glucocorticoid injections
in or around the eye include glaucoma and cataractogenesis.

Systemic treatment is generally reserved for resistant inflammation and may be indicated in patients with
glaucoma who cannot be treated with local injection. In addition, patients with bilateral disease are often treated
with systemic therapy. Some specific forms of inflammation such as Behçet's syndrome or serpiginous
choroiditis are more likely to require systemic therapy. The approach to therapy is generally not affected by the
etiology of the uveitis, but there are important exceptions. As examples, Behçet's syndrome is especially
responsive to infliximab [7-10]; Vogt-Koyanagi-Harada disease may benefit from intravenous methylprednisolone
when the illness first begins, and pars planitis is often managed just by observation or periocular glucocorticoid
injections to treat the complication of macular edema. One study found that interferon beta was more effective
than methotrexate in controlling macular edema associated with intermediate uveitis [11].

Disease resistant to initial treatment — Patients with ongoing inflammation may require systemic glucocorticoid
therapy or additional antiinflammatory or immunosuppressive agents, such as an antimetabolite and/or a
calcineurin antagonist (eg, cyclosporine). In patients with uveitis who are resistant to such therapy, subsequent
therapeutic options include a TNF inhibitor, such as adalimumab; a switch to a different antimetabolite; a
glucocorticoid, either regionally or orally, usually on a temporary basis; or the combination of an antimetabolite
with a calcineurin antagonist. The choice between these options depends on many variables such as patient and
provider preference, etiology of the uveitis, patient cost and regulatory or insurance restrictions, and the cause of
any visual loss. (See 'Oral glucocorticoids' below and 'Antimetabolites or cytotoxic agents' below and 'Anti-tumor
necrosis factor-alpha' below and 'Intraocular glucocorticoid releasing implant' below.)

In one study of patients with noninfectious uveitis, over half of the patients required a change in treatment after
their initial course of systemic therapy [12]. Disease in a large majority of these patients was effectively
controlled with a switch to a different immunosuppressive drug or the use of combinations of
immunosuppressive agents.

Oral glucocorticoids — Oral glucocorticoids are generally reserved for patients with bilateral disease that has
not responded to topical medications and that is interfering with the activities of daily living. A risk-benefit ratio
must be considered for any therapeutic decision. Some patients function well with a visual acuity of 20/70, while
others are functionally impaired with a visual acuity of 20/25.

Toxicity related to oral glucocorticoid use may limit acceptance by patients. Body weight, blood pressure, blood
glucose, bone mineral density, and lipids should be monitored if patients require chronic oral glucocorticoid
therapy. (See "Major side effects of systemic glucocorticoids".)

The goal of glucocorticoid therapy is not to cure but to limit the inflammation. Many forms of uveitis that are
severe enough to warrant oral glucocorticoid or other immunosuppressive drugs are chronic, such as
sarcoidosis. Thus, the clinician should strive to use the lowest dose of medication that provides acceptable
benefit. The dose of oral glucocorticoid varies based on the underlying disease, the disease severity, the patient
profile, and the clinician and patient preference. A common initial dose is the equivalent of 40 to 60 mg of
prednisone per day, with gradual tapering after response to the lowest dose that controls inflammation.

If remission has been achieved for 6 to 12 months, the maintenance dose of glucocorticoid may be gradually
discontinued. A shorter course of therapy is usually sufficient in patients with severe iritis associated with the
human leukocyte antigen (HLA)-B27 spectrum of spondyloarthritis. It is rarely necessary to treat such patients
with oral therapy for more than two weeks because the eye inflammation generally remits spontaneously.

Antimetabolites or cytotoxic agents — A small percentage of patients with uveitis may require
immunosuppressive medications. Indications for their use include bilateral disease, active inflammation, failure
to respond to oral glucocorticoid therapy, or severe disease that interferes with activities of daily living.
Additionally, patients who require a daily dose of 10 mg or more of prednisone to control their ocular
inflammation may benefit from a glucocorticoid-sparing agent, such as an antimetabolite, as a safer long-term
alternative. This recommendation is consistent with the consensus of a group of international experts on uveitis
management [13].

We prefer methotrexate, azathioprine, mycophenolate, or a calcineurin antagonist, such as cyclosporine or

tacrolimus, rather than a TNF inhibitor because of concerns regarding cost and toxicity of the biologic agent.

Immunosuppressive agents that may be employed include antimetabolites, such as azathioprine [14],
mycophenolate mofetil [15], or methotrexate [16]; calcineurin inhibitors, such as cyclosporine or tacrolimus; or
alkylating agents, such as cyclophosphamide. These medications should be used with appropriate caution and
careful monitoring. There should be no specific contraindication to the therapy, such as active liver disease when
using methotrexate, or hypertension or renal disease when using cyclosporine. (See "Chemotherapy
hepatotoxicity and dose modification in patients with liver disease" and "Pharmacology of cyclosporine and
tacrolimus" and "General principles of the use of cyclophosphamide in rheumatic diseases".)

Anti-tumor necrosis factor-alpha — In patients with uveitis who are resistant to therapy with antimetabolites
and/or a calcineurin antagonist such as cyclosporine, one major option is the use of a TNF inhibitor such as
adalimumab (an 80 mg subcutaneous initial injection followed one week later by 40 mg subcutaneously every
other week). In patients with intermediate uveitis/pars planitis, we obtain baseline brain magnetic resonance
imaging (MRI) before starting a TNF inhibitor because of the association of such findings with demyelinating
disease.

Two well-designed, randomized trials showed that adalimumab was effective in the treatment of noninfectious
intermediate, posterior, and pan-uveitis [17,18]. In these trials, adalimumab significantly improved the time-to-
treatment failure in patients with uveitis who followed a tapering schedule for oral glucocorticoids. In mid-2016,
both the European Medicines Agency (EMA) and the FDA recommended approval of adalimumab for adults with
these forms of uveitis [19,20].

Additional evidence supporting the use of TNF inhibitors for uveitis includes:

● In patients with juvenile idiopathic arthritis, the SYCAMORE trial demonstrated benefit from the addition of
adalimumab to ongoing therapy with methotrexate in children with active uveitis [21]. In this 18-month trial
involving 90 patients, therapy with methotrexate was continued, and patients were randomly assigned to
also receive adalimumab or placebo. The addition of adalimumab delayed the time to treatment failure
(hazard ratio [HR] 0.25, 95% CI 0.12-0.49), which was less frequent in the adalimumab-treated patients (27
versus 60 percent). The median time to failure was not reached in the adalimumab group during the trial
period but was 24.1 weeks with placebo. Enrollment in the trial was stopped early due to the degree of
benefit. Serious adverse events were more common in patients receiving adalimumab (0.29 versus 0.19
events per patient-year).

● The response of uveitis associated with Behçet's syndrome to infliximab has been encouraging in
observational studies [7-10,22-24]. For example, in an open-label observational study of 43 patients, 33
patients responded to conventional therapy (oral glucocorticoids, cyclosporine, azathioprine, or
methotrexate) [10]. Ten patients who failed to respond were subsequently treated with infliximab (5 mg/kg)
every two weeks for a total of six doses. Patients treated with infliximab had fewer relapses and longer
remissions than patients who were treated conventionally. Infliximab has been approved in Japan to treat
Behçet's syndrome, which is a relatively common cause of uveitis in that country.

● Several reports suggest that infliximab may be more effective than etanercept for the treatment of uveitis
[25,26]. An unusual increase in adverse effects, including drug-induced lupus, was reported in one
prospective study using infliximab to treat uveitis [27].

● Etanercept, adalimumab, certolizumab, or infliximab appear to reduce the risk of developing eye
inflammation in patients with ankylosing spondylitis, a disease frequently associated with acute anterior
uveitis [28,29].

Intraocular glucocorticoid releasing implant — In 2005, the FDA approved an intraocular fluocinolone implant
for patients with refractory posterior uveitis. The surgically implanted device delivers a glucocorticoid into the
vitreous humor continuously for about 2.5 years [30].
We reserve use of the fluocinolone implant for patients whose noninfectious posterior or intermediate uveitis
requires frequent local glucocorticoid injection and in whom systemic use of glucocorticoids or other immune
modulators may be particularly problematic. An ideal candidate is an individual with unilateral disease, no
systemic illness requiring immunosuppression, and disease that would otherwise require frequent local
glucocorticoid injections.

Cataract and glaucoma are common complications, but the implant does not cause systemic toxicity and can be
effective in selected patients. In a randomized trial involving 255 patients with severe noninfectious intermediate,
posterior, or panuveitis, improvement in visual acuity over 24 months was comparable in patients receiving the
implants to those treated with systemic glucocorticoids and glucocorticoid-sparing immunosuppressive agents
[31], with visual outcomes remaining similar in a follow-up study at 54 months [32,33]. However, after seven
years of extended follow-up, visual acuity was better in patients initially allocated to receive systemic therapy,
although the study was limited by 30 percent loss to follow-up in both groups [34].

The implant carries a slight risk of surgical complications, including endophthalmitis. Almost all patients who
have not had prior cataract surgery will develop a cataract, and about 30 percent of patients will require
additional surgery for glaucoma. The safety of multiple implantations and continuous steroid exposure beyond
2.5 years requires additional study.

Investigational approaches — Ongoing clinical trials include the evaluation of an antibody to interleukin (IL)-1
beta (gevokizumab). An antibody to IL-17 was tested in several randomized trials with disappointing results [35].
An intravitreal injection of sirolimus showed benefit at the lower of two dosages tested in one randomized trial
[36].

Alpha interferon is used, primarily in Europe, for refractory posterior uveitis or Behçet's syndrome, if the response
to other agents is inadequate. It has also been used to treat persistent cystoid macular edema, a common
complication of uveitis that can limit visual acuity. Cystoid macular edema usually responds to control of the
underlying inflammation or to the local injection of glucocorticoids [37]. Alpha interferon requires frequent
injections and its use is associated with flu-like symptoms and depression. (See "Treatment of Behçet's
syndrome", section on 'Posterior uveitis'.)

Prevention of recurrent episodes — Several small studies have found that sulfasalazine can help prevent attacks
of HLA-B27-associated iritis [38,39]. This prophylactic approach is appropriate for patients whose attacks are
especially frequent or severe. TNF inhibitors are highly effective in reducing the frequency of HLA-B27-
associated iritis, but the risk and cost usually do not justify their use if the purpose is solely to prevent iritis.
Some evidence also indicates that methotrexate or oral nonsteroidal antiinflammatory drugs (NSAIDs) could
reduce the frequency of iritis attacks.

PROGNOSIS — Prognosis varies depending upon the etiology and severity of the uveitis. In patients with new-
onset anterior uveitis, factors associated with a lower rate of medication-free remission and persistent
inflammation include diagnosis with juvenile idiopathic arthritis, Behçet's syndrome, bilateral uveitis, history of
cataract surgery, and findings at presentation of either 1+ or greater vitreous cells or visual acuity of 20/200 or
worse [40].

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and
"Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond
the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written
at the 10th to 12th grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Uveitis (The Basics)" and "Patient education: Chorioretinitis (The
Basics)")

SUMMARY AND RECOMMENDATIONS

● The optimal management of a patient with uveitis will require consultation with an ophthalmologist or other
specialist in eye disease. Ideally, therapy should be initiated within 24 hours of the onset of acute, anterior
uveitis, and most infectious causes of uveitis should be treated promptly. (See 'Introduction' above.)

● Treatment of uveitis due to an infectious agent is directed toward the responsible organism. Infection with
herpes simplex or herpes zoster may cause retinal destruction (acute retinal necrosis). Antiviral therapy is
especially important in the setting of retinitis in order to limit retinal damage. (See 'Uveitis due to infection'
above.)

● Uveitis is generally classified as anterior, intermediate, or posterior or as panuveitis (involving all anatomic
segments of the uveal tract). Anterior uveitis not due to infection is treated with topical glucocorticoids.
Dilating ophthalmic drops are indicated if ciliary spasm is causing pain or if there is risk for posterior
synechiae. Posterior or intermediate uveitis and panuveitis are generally not responsive to topical treatment.
Initial management of uveitis posterior to the lens usually includes observation, as well as periocular and,
occasionally, intraocular glucocorticoid injections. (See 'Initial treatment' above.)

● Oral glucocorticoids are frequently recommended for patients with uveitis that is resistant to topical therapy.
Other immunomodulatory agents are suggested in patients who have active inflammation that interferes
with activities of daily living and who have one of the following indications (see 'Disease resistant to initial
treatment' above):

• Refractory uveitis

• Drug-related adverse effects from systemic glucocorticoids or persistent requirement for a dose of
prednisone greater than 10 mg/day or equivalent

● An intraocular fluocinolone-releasing implant offers an alternative to systemic therapy, but it may

necessitate multiple surgeries for its complications (cataract and glaucoma) and its long-term safety has
not been fully studied. (See 'Intraocular glucocorticoid releasing implant' above.)

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REFERENCES

1. Smith JR, Rosenbaum JT. Management of uveitis: a rheumatologic perspective. Arthritis Rheum 2002;
46:309.
2. Chee SP, Jap A. Cytomegalovirus anterior uveitis: outcome of treatment. Br J Ophthalmol 2010; 94:1648.
3. Quentin CD, Reiber H. Fuchs heterochromic cyclitis: rubella virus antibodies and genome in aqueous humor.
Am J Ophthalmol 2004; 138:46.
4. Jabs DA, Rosenbaum JT, Foster CS, et al. Guidelines for the use of immunosuppressive drugs in patients
with ocular inflammatory disorders: recommendations of an expert panel. Am J Ophthalmol 2000; 130:492.
 5. Levy-Clarke G, Jabs DA, Read RW, et al. Expert panel recommendations for the use of anti-tumor necrosis
factor biologic agents in patients with ocular inflammatory disorders. Ophthalmology 2014; 121:785.
6. Sheppard JD, Toyos MM, Kempen JH, et al. Difluprednate 0.05% versus prednisolone acetate 1% for
endogenous anterior uveitis: a phase III, multicenter, randomized study. Invest Ophthalmol Vis Sci 2014;
55:2993.
7. Sfikakis PP, Theodossiadis PG, Katsiari CG, et al. Effect of infliximab on sight-threatening panuveitis in
Behçet's disease. Lancet 2001; 358:295.
8. Ohno S, Nakamura S, Hori S, et al. Efficacy, safety, and pharmacokinetics of multiple administration of
infliximab in Behçet's disease with refractory uveoretinitis. J Rheumatol 2004; 31:1362.
9. Tugal-Tutkun I, Mudun A, Urgancioglu M, et al. Efficacy of infliximab in the treatment of uveitis that is
resistant to treatment with the combination of azathioprine, cyclosporine, and corticosteroids in Behçet's
disease: an open-label trial. Arthritis Rheum 2005; 52:2478.
10. Tabbara KF, Al-Hemidan AI. Infliximab effects compared to conventional therapy in the management of
retinal vasculitis in Behçet disease. Am J Ophthalmol 2008; 146:845.
11. Mackensen F, Jakob E, Springer C, et al. Interferon versus methotrexate in intermediate uveitis with macular
edema: results of a randomized controlled clinical trial. Am J Ophthalmol 2013; 156:478.
12. Joshi L, Talat L, Yaganti S, et al. Outcomes of changing immunosuppressive therapy after treatment failure
in patients with noninfectious uveitis. Ophthalmology 2014; 121:1119.
13. Jabs DA, Nussenblatt RB, Rosenbaum JT, Standardization of Uveitis Nomenclature (SUN) Working Group.
Standardization of uveitis nomenclature for reporting clinical data. Results of the First International
Workshop. Am J Ophthalmol 2005; 140:509.
14. Pasadhika S, Kempen JH, Newcomb CW, et al. Azathioprine for ocular inflammatory diseases. Am J
Ophthalmol 2009; 148:500.
15. Daniel E, Thorne JE, Newcomb CW, et al. Mycophenolate mofetil for ocular inflammation. Am J Ophthalmol
2010; 149:423.
16. Ali A, Rosenbaum JT. Use of methotrexate in patients with uveitis. Clin Exp Rheumatol 2010; 28:S145.
17. Jaffe GJ, Dick AD, Brézin AP, et al. Adalimumab in Patients with Active Noninfectious Uveitis. N Engl J Med
2016; 375:932.
18. Nguyen QD, Merrill PT, Jaffe GJ, et al. Adalimumab for prevention of uveitic flare in patients with inactive
non-infectious uveitis controlled by corticosteroids (VISUAL II): a multicentre, double-masked, randomised,
placebo-controlled phase 3 trial. Lancet 2016; 388:1183.
19. HIGHLIGHTS OF PRESCRIBING INFORMATION. HUMIRA (adalimumab) injection, for subcutaneous use. htt
p://www.accessdata.fda.gov/drugsatfda_docs/label/2016/125057s397lbl.pdf (Accessed on July 25, 2016).
20. European Medicines Agency. Humira. http://www.ema.europa.eu/ema/index.jsp?curl=pages/medicines/hu
man/medicines/000481/smops/Positive/human_smop_000983.jsp&mid=WC0b01ac058001d127 (Access
ed on July 25, 2016).
21. Ramanan AV, Dick AD, Jones AP, et al. Adalimumab plus Methotrexate for Uveitis in Juvenile Idiopathic
Arthritis. N Engl J Med 2017; 376:1637.
22. Joseph A, Raj D, Dua HS, et al. Infliximab in the treatment of refractory posterior uveitis. Ophthalmology
2003; 110:1449.
23. Lindstedt EW, Baarsma GS, Kuijpers RW, van Hagen PM. Anti-TNF-alpha therapy for sight threatening
uveitis. Br J Ophthalmol 2005; 89:533.
24. Bodaghi B, Bui Quoc E, Wechsler B, et al. Therapeutic use of infliximab in sight threatening uveitis:
retrospective analysis of efficacy, safety, and limiting factors. Ann Rheum Dis 2005; 64:962.
25. Foeldvari I, Nielsen S, Kümmerle-Deschner J, et al. Tumor necrosis factor-alpha blocker in treatment of
juvenile idiopathic arthritis-associated uveitis refractory to second-line agents: results of a multinational
survey. J Rheumatol 2007; 34:1146.
26. Galor A, Perez VL, Hammel JP, Lowder CY. Differential effectiveness of etanercept and infliximab in the
treatment of ocular inflammation. Ophthalmology 2006; 113:2317.
27. Suhler EB, Smith JR, Wertheim MS, et al. A prospective trial of infliximab therapy for refractory uveitis:
preliminary safety and efficacy outcomes. Arch Ophthalmol 2005; 123:903.
28. Braun J, Baraliakos X, Listing J, Sieper J. Decreased incidence of anterior uveitis in patients with ankylosing
spondylitis treated with the anti-tumor necrosis factor agents infliximab and etanercept. Arthritis Rheum
2005; 52:2447.
29. van Denderen JC, Visman IM, Nurmohamed MT, et al. Adalimumab significantly reduces the recurrence rate
of anterior uveitis in patients with ankylosing spondylitis. J Rheumatol 2014; 41:1843.
30. Fluocinolone acetonide ophthalmic--Bausch & Lomb: fluocinolone acetonide Envision TD implant. Drugs R
D 2005; 6:116.
31. Multicenter Uveitis Steroid Treatment (MUST) Trial Research Group, Kempen JH, Altaweel MM, et al.
Randomized comparison of systemic anti-inflammatory therapy versus fluocinolone acetonide implant for
intermediate, posterior, and panuveitis: the multicenter uveitis steroid treatment trial. Ophthalmology 2011;
118:1916.
32. Multicenter Uveitis Steroid Treatment (MUST) Trial Research Group, Kempen JH, Altaweel MM, et al.
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; 122:1967.
33. Multicenter Uveitis Steroid Treatment (MUST) Trial Follow-up Study Research Group. Quality of Life and
Risks Associated with Systemic Anti-inflammatory Therapy versus Fluocinolone Acetonide Intraocular
Implant for Intermediate Uveitis, Posterior Uveitis, or Panuveitis: Fifty-four-Month Results of the Multicenter
Uveitis Steroid Treatment Trial and Follow-up Study. Ophthalmology 2015; 122:1976.
34. Writing Committee for the Multicenter Uveitis Steroid Treatment (MUST) Trial and Follow-up Study
Research Group, Kempen JH, Altaweel MM, et al. 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; 317:1993.
35. Dick AD, Tugal-Tutkun I, Foster S, et al. Secukinumab in the treatment of noninfectious uveitis: results of
three randomized, controlled clinical trials. Ophthalmology 2013; 120:777.
36. Bodaghi B, Ali Y, Yang Y, et al. Changes in vitreous haze over time with intravitreal sirolimus in non-
infectious posterior uveitis: results of SAKURA Study I. Acta Ophthalmol 2014; 92:s253.
37. Deuter CM, Kötter I, Günaydin I, et al. Efficacy and tolerability of interferon alpha treatment in patients with
chronic cystoid macular oedema due to non-infectious uveitis. Br J Ophthalmol 2009; 93:906.
38. Muñoz-Fernández S, Hidalgo V, Fernández-Melón J, et al. Sulfasalazine reduces the number of flares of
acute anterior uveitis over a one-year period. J Rheumatol 2003; 30:1277.
39. Benitez-Del-Castillo JM, Garcia-Sanchez J, Iradier T, Bañares A. Sulfasalazine in the prevention of anterior
uveitis associated with ankylosing spondylitis. Eye (Lond) 2000; 14 ( Pt 3A):340.
40. Artornsombudh P, Pistilli M, Foster CS, et al. Factors predictive of remission of new-onset anterior uveitis.
Ophthalmology 2014; 121:778.
Topic 5592 Version 27.0
GRAPHICS

Eye anatomy in cross section

Graphic 57690 Version 5.0

Representative infectious causes of uveitis

Bacterial/spirochetal Viral Fungal Parasitic

Atypical mycobacteria Anellovirus Aspergillosis (protozoan/helminthic)

Brucellosis Chikungunya Blastomycosis Acanthamoeba

Cat scratch disease Cytomegalovirus Candidiasis Cystercercosis

Leprosy Ebola Coccidioidomycosis Onchocerciasis

Leptospirosis Epstein-Barr Cryptococcosis Toxocariasis

Lyme disease Herpes simplex Histoplasmosis Toxoplasmosis

Cutibacterium (formerly Herpes zoster Pneumocystis jirovecii (PCP)

Propionibacterium)
HIV-1 Sporotrichosis
Rocky Mountain spotted
Human T cell leukemia virus
fever
Mumps
Syphilis
Parechovirus
Tuberculosis
Rubella
Whipple's disease
Rubeola

Vaccinia

West Nile virus

Zika virus

HIV: human immunodeficiency virus.

Graphic 61247 Version 11.0

Contributor Disclosures
James T Rosenbaum, MD Grant/Research/Clinical Trial Support: Alcon Research Institute [Uveitis]. Speaker's
Bureau: Abbvie [Uveitis (Adalimumab)]; Mallinckrodt [Uveitis (Acthar)]. Consultant/Advisory Boards: UCB [Uveitis
(Certolizumab)]; Abbvie [Uveitis (Adalimumab)]; Regeneron [Uveitis (Dupilumab)]; Santen [Uveitis (Intravitreal
rapamycin)]; Gilead [Uveitis (Filgotinib)]. Jonathan Trobe, MD Nothing to disclose Paul L Romain, MD Nothing to
disclose

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