Ocular Manifestations of Sarcoidosis

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Article initiated by:
Andrew Go Lee, MD, MacGregor Hall, Nita Bhat, MBBS, MS, Shruthi Harish Bindiganavile, MBBS, MS
All contributors:
Paul Phelps, MD, FACS, Ghazala A. D. O'Keefe, MD, Joobin Khadamy, MD, FEBO, FEBOS-CR, Edmund Tsui, MD, Nita Bhat, MBBS, MS, Michael T Yen, MD, Nahyoung Grace Lee, MD, Meghan Berkenstock M.D., William Kretzschmar M.D.
Assigned editor:
Meghan Berkenstock M.D., Hans Heymann, MD
Review:
Assigned status Update Pending
 by Meghan Berkenstock M.D. on June 16, 2025.


(A) Exterior photograph showing a Koeppe nodule with granulomatous changes on the pupil margin (yellow arrow).[1] (B) Fundus image revealing vitritis with snowball opacities (green arrows), characteristic of intermediate uveitis in sarcoidosis. (C) Fundus photograph demonstrating chorioretinitis, vascular sheathing, candle wax dripping phlebitis, granulomas as yellowish lesions, and diffuse vitreous haze in the posterior pole. (D) Wide-field fundus image illustrating peripheral multifocal chorioretinal scars, described as punch-out lesions, which are not pathognomonic of sarcoidosis and can also be seen in other conditions such as Histoplasmosis (Presumed Ocular Histoplasmosis Syndrome - POHS), Fuchs' Heterochromic Iridocyclitis (FHI), toxoplasmosis, syphilis, or tuberculosis (red arrows) in sarcoid-associated posterior uveitis. (Courtesy of J. Khadamy)
(A) Exterior photograph showing a Koeppe nodule with granulomatous changes on the pupil margin (yellow arrow). (B) Fundus image revealing vitritis with snowball opacities (green arrows), characteristic of intermediate uveitis in sarcoidosis. (C) Fundus photograph demonstrating chorioretinitis, vascular sheathing, candle wax dripping phlebitis, granulomas as yellowish lesions, and diffuse vitreous haze in the posterior pole. (D) Wide-field fundus image illustrating peripheral multifocal chorioretinal scars, described as punch-out lesions, which are not pathognomonic of sarcoidosis and can also be seen in other conditions such as Histoplasmosis (Presumed Ocular Histoplasmosis Syndrome - POHS), Fuchs' Heterochromic Iridocyclitis (FHI), toxoplasmosis, syphilis, or tuberculosis (red arrows) in sarcoid-associated posterior uveitis. (Courtesy of J. Khadamy)

Disease Entity

Sarcoidosis is a systemic inflammatory disease characterized by the formation of noncaseating granulomas. The pathophysiology of the disease has not been fully elucidated, but it is considered an immune mediated granulomatous disease with some autoimmune components and is the result of dysregulated antigenic response to unknown environmental exposures.[2] The disease most commonly affects the skin, lungs, lymph nodes, and eyes but can involve virtually any organ[3]. Within the eye, sarcoidosis can result in clinical manifestations from the posterior to anterior pole of the eye including retinitis to interstitial keratitis. The first patient with confirmed sarcoidosis was described by dermatologist Jonathan Hutchinson in early 1880, whose skin lesions Hutchinson named “Mortimer’s malady” after the patient[3]. Later, Caesar Boeck coined the term “sarcoid” because of the lesion’s resemblance to sarcoma on histology[4]. In 1909, Heerfordt described the first ocular manifestation of sarcoid in three men with uveitis, parotid enlargement, and fever[5].

Epidemiology

Sarcoidosis is a global disease but is more common in Nordic and African American populations[6]. The incidence and prevalence are heavily influenced by sex, race, and geography. In the U.S. incident rates range from 7.6 to 11 per 100,000[7] One U.S. study demonstrated the increased risk in African American patients with incidence ranging from 8.1 per 100,000 in Caucasians to 17.8 in African Americans[8]. Women are also at a higher risk particularly those of African American descent. White individuals have a prevalence of 59 women per 100 000 and 40 men per 100 000 while Black individuals were found to have a prevalence of 179 women per 100 000 and 93 men per 100 000.[9] Sarcoidosis can affect individuals of any age, but has long been reported to primarily affect adults under the age of 40.[7] The prevalence of ocular involvement in systemic sarcoidosis ranges from 12%-76% with ocular involvement being the presenting symptom in 30-40%[10][11][12]. The most common types of ocular involvement are lacrimal gland involvement, uveitis, and conjunctival nodules[12].

Pathophysiology

The pathophysiology of sarcoidosis involves a dysregulated immune response to unknown environmental antigens in genetically susceptible individuals, culminating in the formation of noncaseating granulomas. The process begins when antigen-presenting cells (APCs), particularly macrophages and dendritic cells, ingest putative sarcoid antigens and present them as peptide fragments in the context of HLA class II molecules to CD4+ T cells. This results in the activation of the granulomatous inflammatory response triggered by the release of cytokines and chemokines including interferon-γ, tumor necrosis factor (TNF)-α, transforming growth factor-β, etc.[2] The proposed environmental triggers have not yet been elucidated, however, the ACCESS study found higher rates of sarcoid in agricultural workers, healthcare workers, bird breeder, automotive industry, and middle/high school teachers, as well as with exposures to insecticides, mildew, mold, musty odors, and home central air conditioning. There are also proposed infectious triggers such as Mycobacterium tuberculosis and Cutibacterium acnes [13] Tattoos have also been proposed as a possible trigger.[14]

Ocular manifestations

The granulomatous inflammation of sarcoidosis can affect any part of the eye and its adnexa and can progress to severe visual impairment and blindness. It is important for ophthalmologists and non-ophthalmologists to recognize the manifestations of ocular sarcoidosis, as well as consider sarcoidosis in any patient presenting with uveitis. A study from a uveitis clinic at Casey Eye Institute analyzed 249 patients and found that 72% of patients referred to their clinic came with a diagnosis of idiopathic uveitis. After further examination and CT imaging on 53 of these patients, 19 of the 53 patients (36.2%) had imaging findings consistent with a diagnosis of sarcoidosis. The study went on to demonstrate that these patients were then referred for EKG despite a presenting complaint of uveitis and 4 of the 19 went on to develop Ventricular Tachycardia requiring an ICD. [15] This study demonstrates It is common for the ocular manifestations of sarcoidosis to be the presenting complaint despite the patient having prominent systemic disease. This can be vision threatening even with asymptomatic pulmonary involvement. Patient's with ocular sarcoidosis can often be asymptomatic in other organ systems despite multiorgan involvement that can be life threatening.[11]

Intraocular manifestations

The most common ocular manifestation overall is uveitis, reported in 30-70% of cases. [16] Sarcoidosis can present with anterior, intermediate, posterior or panuveitis, however, the most common type is bilateral anterior uveitis without posterior segment involvement. [16] Anterior uveitis typically presents with pain, redness and photophobia, but these signs may be absent and thus delay diagnosis. Slit-lamp exam may show cell and flare, hypopyon, granulomatous keratic precipitates, iris nodules, and anterior or posterior synechiae. [17] Intermediate uveitis presents with floaters and blurry vision. Characteristic fundoscopic findings in intermediate uveitis include vitreous opacities, snow balls (aggregates of inflammatory cells in the vitreous humor posterior to the lens), and snow banks (accumulation of white exudates over the pars plana and ora serrata).[17] Posterior Uveitis involves the retina and choroid and can present with blurred vision, visual distortion, eye pain, photophobia, but can often be asymptomatic. Characteristic fundoscopic findings in posterior uveitis include, chorioretinitis, retinal exudates or hemorrhages, disc edema, periphlebitis and “candle wax drippings” (scattered whitish-yellow perivascular retinal exudates along the retinal veins).[11][12] Posterior involvement in sarcoid uveitis is usually bilateral but can be asymmetric. Choroidal granulomas vary widely in size and can lead to visual impairment if they are centrally located and possibly retinal detachment if the granulomas are large. [11]

The anatomical pattern of sarcoid uveitis shows striking racial differences. In Black patients, anterior uveitis accounts for 70-75% of cases, while in White patients, posterior uveitis predominates, accounting for 65-83% of cases. [18]

Complications of chronic uveitis include cataract formation, glaucoma and cystoid macular edema (CME), related to the chronic intraocular inflammation. Sarcoid uveitis can lead to increased intraocular pressure and glaucoma related to edema or inflammatory cells that cause trabecular meshwork obstruction, or peripheral anterior synechiae. Out of 159 patients in one Japanese study, 61% of patients had trabecular meshwork nodules and 55% had tent-shaped peripheral anterior synechiae leading to abnormal gonioscopic findings. [11]

Ocular surface manifestations

Conjunctival manifestations can include conjunctival nodules, acute follicular conjunctivitis, symblepharon, and chronic cicatricial conjunctivitis. Nodules are another common ocular manifestations of sarcoidosis and are typically asymptomatic.[16] Scleritis can occur with ocular sarcoidosis but is rare and has mostly been associated with older female patients aged 53 to 64 years old. [11] Sarcoidosis-related scleritis can present as anterior diffuse, anterior nodular, or posterior scleritis and is usually non-necrotizing. [11]

Corneal manifestations include superficial punctate keratitis secondary to keratoconjunctivitis sicca, interstitial keratitis, exposure keratopathy (related to granuloma formation or facial nerve involvement), band keratopathy, and peripheral ulcerative keratitis. [11] Chronic inflammation and hypercalcemia in sarcoidosis can also result in subepithelial deposition of calcium, leading to calcific band keratopathy. [16][19]

Adnexal and orbital manifestations

Eyelid manifestations of sarcoidosis include: granulomas, madarosis (loss of eyelashes), poliosis (whitening of lashes), entropion, trichiasis, and lagophthalmos (if associated with facial palsy). [11] Lacrimal gland/nasolacrimal drainage system involvement is the most common ocular manifestation of ocular sarcoidosis. The inflammation and/or granuloma formation and can lead to Keratoconjunctivitis sicca, epiphora, dacryoadenitis, Nasolacrimal duct obstruction.[11][12][20]. Patients may be asymptomatic or may present with symptoms due to mass effect or inflammation.[11] Keratoconjunctivitis sicca (KCS) is commonly associated with sarcoidosis and is a result of decreased aqueous tear production secondary to lacrimal gland inflammation. Epiphora due to granulomatous inflammation of the lacrimal drainage system has also been reported. [11]

Extraocular muscle and orbital tissue involvement (orbital fat, optic nerve sheath) can lead to ptosis, proptosis, strabismus, optic nerve compression, pain, and limited eye movements once again related to granuloma formation.[11] These manifestations can mimic other orbital inflammatory conditions like thyroid ophthalmopathy, which can occur simultaneously with ocular sarcoidosis.[12] Complications of orbital masses caused by ocular sarcoid include central retinal artery occlusion and permanent blindness[11].

Neuro-ophthalmic manifestations

Neurosarcoidosis causes a wide range of signs and symptoms depending on the areas of the nervous system affected and can mimic many other conditions. The most common manifestation, however, is cranial neuropathy most commonly of the facial and optic nerves[21]. However, any of the cranial nerves can be affected and will present with their corresponding deficits. Cranial nerve involvement can occur due to direct infiltration by sarcoid tissue or compression from space-occupying lesions. Neurosarcoidosis can also manifest as papilledema, nystagmus, RAPD, and visual field defects[16].

Diagnosis

Diagnosis of sarcoidosis is usually based on history and physical exam findings along with histological confirmation in affected tissue along with exclusion of other granulomatous diseases such as tuberculosis or syphilis. Since most patients with sarcoidosis have pulmonary involvement, chest X-rays are frequently used as a screening tool. Computerized tomography (CT) is more sensitive but is typically not recommended unless clinical suspicion is high and chest X-ray is negative.[22] Serum ACE, calcium, and ESR may also be used and tissue biopsy is considered the gold standard. In 2017, the International Workshop on Ocular Sarcoidosis (IWOS) published criteria for diagnosing ocular sarcoidosis based on seven clinic signs, eight systemic investigation results, and three diagnostic criteria listed below. These criteria were revised from those previously suggested in 2009 due to limitations suggested by two validation studies.[23]

Revised International Workshop on Ocular Sarcoidosis (IWOS) criteria for the diagnosis of ocular sarcoidosis (OS):

I. Other causes of granulomatous uveitis must be ruled out.

II. Intraocular clinical signs suggestive of OS:

  1. Mutton-fat keratic precipitates (large and small) and/or iris nodules at pupillary margin (Koeppe) or in stroma (Busacca).
  2. Trabecular mesh work nodules and/or tent-shaped peripheral anterior synechia.
  3. Snowballs/string of pearls vitreous opacities.
  4. Multiple chorioretinal peripheral lesions (active and atrophic).
  5. Nodular and/or segmental periphlebitis (candle wax drippings) and/or macroaneurysm in an inflamed eye.
  6. Optic disc nodule(s)/granuloma(s) and/or solitary choroidal nodule.
  7. Bilaterality (assessed by ophthalmological examination including ocular imaging showing subclinical inflammation).

III. Systemic investigation results in suspected OS:

  1. Bilateral hilar lymphadenopathy (BHL) by chest X-ray and/or chest computed CT scan.
  2. Negative tuberculin test or interferon-gamma releasing assays.
  3. Elevated serum angiotensin-converting enzyme (ACE).
  4. Elevated serum lysozyme.
  5. Elevated CD4/CD8 ratio (>3.5) in bronchoalveolar lavage fluid.
  6. Abnormal accumulation of gallium-67 scintigraphy or 18F-fluorodeoxyglucose positron emission tomography imaging.
  7. Lymphopenia.
  8. Parenchymal lung changes consistent with sarcoidosis, as determined by pulmonologists or radiologists.

IV. Diagnostic criteria:

Definite OS: diagnosis supported by biopsy with compatible uveitis.

Presumed OS: diagnosis not supported by biopsy, but BHL present with two intraocular signs.

Probable OS: diagnosis not supported by biopsy and BHL absent, but three intraocular signs and two systemic investigations selected from two to eight are present.

At this time there is no indication for characterization of gene expression or the measurement of proteins such as cytokines in the intraocular fluid due to uncertain sensitivity and specificity when compared to control. [11]

Screening EKG is also recommended at the time of diagnosis. [11]

Management

Treatment of ocular sarcoidosis aims to restore vision and prevent complications from inflammation, particularly uveitis because it is the most common vision threatening presentation.

Treatment of intraocular manifestations

Corticosteroids

Corticosteroids are the firstline treatment for sarcoid uveitis and can be administered topically in the form of eye drops, regionally in the form of periocular and intraocular injections or implants, or systemically in the form of oral corticosteroids. Topical corticosteroids are the first line treatment for anterior uveitis but can be ineffective in treating posterior segment inflammation[11]. Dose and frequency may vary based on the severity of the disease. Adverse effects include elevated IOP, early-onset cataract and delayed wound healing. Prednisolone acetate is the preferred topical steroid due to cost and low risk profile, while difluprednate is an alternative with great vitreous humor penetration, but greater risk of cataract and glaucoma.[11]

Corticosteroid injections and implants may be considered in posterior segment involvement or in those who respond poorly to topical solutions. Periocular injections are most commonly administered into the sub-Tenon’s capsule or the orbital floor[16]. The most common preparation is triamcinolone acetonide (TA) 20-40mg which typically lasts 2-4 months. TA can also be administered via 1-4mg intravitreal injections, which can last 3-6 months. Adverse effects include elevated IOP, cataract progression, and injection-related side effects. Dexamethasone can also be administered in the form of a biodegradable implant through the pars plana, which has been shown to improve vision and macular edema in patients with non-infectious uveitis. The main disadvantage appears to be recurrence of macular edema, which occurred in 65% of patients within 6 months in one study[17].

Systemic corticosteroids may be considered in chronic, bilateral uveitis, in those who respond poorly to topical or regional therapy, or in systemic disease that also requires therapy. Systemic therapy usually entails short term courses of prednisone dosed at 1-1.5mg/kg/day that is then tapered down to the lowest effective dose. Systemic steroid therapy requiring prolonged courses or higher doses may be associated with many systemic adverse effects[16].

Immunosuppressive agents

Systemic immunosuppressive agents may be considered in patients requiring long term courses of corticosteroids or when corticosteroids fail to treat patients with ocular sarcoidosis. The most common agents include methotrexate, mycophenolate mofetil, azathioprine and cyclosporine. Rosenbaum and Pasadhika prefer to start with methotrexate by subQ injection at 20 to 25 mg/wk as tolerated with the addition of calcineurin antagonists like cyclosporine or tacrolimus.[11]

Biologic agents

Biologic agents may be considered when corticosteroids or immunosuppressive agents fail to induce or sustain remission in patients with ocular sarcoidosis. Rosenbaum and Pasadhika mention that in the case that the ocular manifestations remain vision threatening they will often skip the addition of calcineurin antagonists and move straight to monoclonal antibiodies.[11] Most of the agents studied to treat uveitis are Tumor Necrosis Factor (TNF)-α inhibitors, including adalimumab, infliximab, etanercept, and golimumab. These agents bind TNFα or block its receptor which may prevent granulomatous inflammation in sarcoidosis. Adalimumab is the only agent of these that is FDA approved for the treatment of non-infectious uveitis. Two Phase III trials reported that adalimumab lowered the risk of uveitic flare or loss of visual acuity in patients with active (VISUAL I) or inactive (VISUAL II) non-infectious intermediate uveitis, posterior uveitis, or pan-uveitis[16][17]. However, these agents still remain second-line due to limited long-term safety and efficacy data[11]. Interestingly, anti-TNFα agents have been associated with causing uveitis[24].

Treatment of ocular surface manifestations

Conjunctival lesions may respond to topical cyclosporine eye drops[25]. Scleritis is usually treated with systemic corticosteroids or systemic immunomodulators. One case report suggested thalidomide as a possible therapy for scleritis after a woman in her early 50’s showed complete remission of bilateral nodular scleritis after treatment with thalidomide[26]. Treatment of Keratoconjunctivitis sicca involves typical dry eye treatments.

Treatment of adnexal and orbital manifestations

Cutaneous lesions on the eyelids may be treated with systemic corticosteroids, intralesional triamcinolone injections, or oral chloroquine[11]. KCS may respond to topical cyclosporine eye drops. Orbital lesions may be treated with systemic corticosteroids and biopsy or removal if suspicious for malignancy. These choices are often empiric as there are no comparative studies. [11]

Treatment of complications

Chronic ocular inflammation secondary to sarcoidosis and treatment thereof can lead to a number of vision-threatening complications such as cataract, glaucoma, and CME which must also be considered. Steroid-sparing agents may be considered in patients with elevated IOP. Cataract surgery in patients with ocular sarcoidosis may be considered after ocular inflammation is quiescent for at least 3 months, similar to other causes of uveitis[27]. CME, the major cause of vision loss in ocular sarcoidosis patients, can be monitored with Optical coherence tomography (OCT)[12][17]. Treatment options for uveitic macular edema include dexamethasone implants, immunomodulatory drugs, anti-vascular endothelial growth-factor agents, and pars plana vitrectomy in refractory cases[28].

Summary

It is important for the ophthalmologist to be aware of the ocular manifestations of sarcoidosis as they may be the first sign of systemic disease and can lead to severe complications. Early diagnosis using the IWOS criteria and intervention can be crucial in preventing severe vision loss. Appropriate management also requires long-term follow up to monitor for disease progression and drug-related adverse effects.

References

  1. ↑ Khadamy J (January 08, 2024) Anterior-Segment Optical Coherence Tomography Unlocks Novel Perspectives: Lacking Iris Anterior Limiting Layer Signal in Uveitis. Cureus 16(1): e51872. doi:10.7759/cureus.51872
  2. ↑ 2.0 2.1 Llanos O, Hamzeh N. Sarcoidosis. Med Clin North Am. 2019;103(3):527-534. doi:10.1016/j.mcna.2018.12.011
  3. ↑ 3.0 3.1 Zissel G, Müller-Quernheim J. Sarcoidosis: historical perspective and immunopathogenesis (part I). Respiratory Medicine. 1998;92(2):126-139. doi:10.1016/s0954-6111(98)90085-3. Accessed April 21, 2020.
  4. ↑ Llanos O, Hamzeh N. Sarcoidosis. Medical Clinics of North America.2019;103(3):527-534. doi:10.1016/j.mcna.2018.12.011. Accessed April 21, 2020.
  5. ↑ Ibitoye RT, Wilkins A, Scolding NJ. Neurosarcoidosis: a clinical approach to diagnosis and management. Journal of Neurology. 2016;264(5):1023-1028. doi:10.1007/s00415-016-8336-4. Accessed April 21, 2020.
  6. ↑ Arkema EV, Cozier YC. Epidemiology of sarcoidosis: current findings and future directions.Therapeutic Advances in Chronic Disease. 2018;9(11):227-240. doi:10.1177/2040622318790197. Accessed April 21, 2020.
  7. ↑ 7.0 7.1 Cozier YC, Arkema EV. Epidemiology of Sarcoidosis. Clin Chest Med. 2024;45(1):1-13. doi:10.1016/j.ccm.2023.06.004
  8. ↑ Baughman RP, Field S, Costabel U, et al. Sarcoidosis in America. Analysis Based on Health Care Use. Annals of the American Thoracic Society. 2016;13(8):1244-1252. doi:10.1513/annalsats.201511-760oc. Accessed April 21, 2020.
  9. ↑ Cozier  YC, Berman  JS, Palmer  JR, Boggs  DA, Serlin  DM, Rosenberg  L.  Sarcoidosis in black women in the United States: data from the Black Women's Health Study.   Chest. 2011;139(1):144-150. doi:10.1378/chest.10-0413
  10. ↑ Ungprasert P, Tooley AA, Crowson CS, Matteson EL, Smith WM. Clinical Characteristics of Ocular Sarcoidosis: A Population-Based Study 1976–2013. Ocular Immunology and Inflammation. 2017;27(3):389-395. Accessed April 21, 2020.
  11. ↑ 11.00 11.01 11.02 11.03 11.04 11.05 11.06 11.07 11.08 11.09 11.10 11.11 11.12 11.13 11.14 11.15 11.16 11.17 11.18 11.19 11.20 11.21 11.22 Pasadhika S, Rosenbaum JT. Ocular Sarcoidosis. Clinics in Chest Medicine. 2015;36(4):669-683. doi:10.1016/j.ccm.2015.08.009. Accessed April 21, 2020.
  12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 Rothova A. Ocular involvement in sarcoidosis. British Journal of Ophthalmology. 2000;84(1):110-116. doi:10.1136/bjo.84.1.110. Accessed April 21, 2020.
  13. ↑ Newman, Lee S., et al. "A case control etiologic study of sarcoidosis: environmental and occupational risk factors." American journal of respiratory and critical care medicine 170.12 (2004): 1324-1330.
  14. ↑ Kluger N.: Tattoo-associated uveitis with or without systemic sarcoidosis: a comparative review of the literature . J Eur Acad Dermatol Venereol 2018; 32 (11): pp. 1852-1861.
  15. ↑ Han YS, Rivera-Grana E, Salek S, Rosenbaum JT. Distinguishing Uveitis Secondary to Sarcoidosis From Idiopathic Disease: Cardiac Implications. JAMA Ophthalmol. 2018;136(2):109-115. doi:10.1001/jamaophthalmol.2017.5466
  16. ↑ 16.0 16.1 16.2 16.3 16.4 16.5 16.6 16.7 Matsou A, Tsaousis KT. Management of chronic ocular sarcoidosis: challenges and solutions. Clinical Ophthalmology. 2018;Volume 12:519-532. doi:10.2147/opth.s128949. Accessed April 21, 2020.
  17. ↑ 17.0 17.1 17.2 17.3 17.4 Yang SJ, Salek S, Rosenbaum JT. Ocular sarcoidosis. Current Opinion in Pulmonary Medicine. 2017;23(5):458-467. doi:10.1097/mcp.0000000000000409. Accessed April 21, 2020.
  18. ↑ Belperio JA, Shaikh F, Abtin F, et al. Extrapulmonary sarcoidosis with a focus on cardiac, nervous system, and ocular involvement. EClinicalMedicine. 2021;37:100966. Published 2021 Jun 27. doi:10.1016/j.eclinm.2021.100966
  19. ↑ Anbar F, Dryden S. Calcific Band Keratopathy. EyeWiki. https://eyewiki.aao.org/Calcific_Band_Keratopathy. Accessed April 21, 2020.
  20. ↑ Mavrikakis I, Rootman J. Diverse Clinical Presentations of Orbital Sarcoid. American Journal of Ophthalmology. 2007;144(5). doi:10.1016/j.ajo.2007.07.019. Accessed April 21, 2020.
  21. ↑ Ferriby, D., et al. "Long-term follow-up of neurosarcoidosis." Neurology 57.5 (2001): 927-929.
  22. ↑ Patel S. Ocular Sarcoidosis. International Ophthalmology Clinics. 2015;55(3):15-24. doi:10.1097/iio.0000000000000069. Accessed April 21, 2020.
  23. ↑ Mochizuki M, Smith JR, Takase H, Kaburaki T, Acharya NR, Rao NA. Revised criteria of International Workshop on Ocular Sarcoidosis (IWOS) for the diagnosis of ocular sarcoidosis. British Journal of Ophthalmology. Accessed April 21, 2020.
  24. ↑ Lim LL, Fraunfelder FW, Rosenbaum JT. Do tumor necrosis factor inhibitors cause uveitis? A registry-based study. Arthritis & Rheumatism. 2007;56(10):3248-3252. doi:10.1002/art.22918. Accessed April 21, 2020.
  25. ↑ Oh JY, Wee WR. Cyclosporine for Conjunctival Sarcoidosis. Ophthalmology. 2008;115(1). doi:10.1016/j.ophtha.2007.08.024. Accessed April 21, 2020.
  26. ↑ Huddleston SM, Houser KH, Walton RC. Thalidomide for Recalcitrant Nodular Scleritis in Sarcoidosis. JAMA Ophthalmology. 2014;132(11):1377. doi:10.1001/jamaophthalmol.2014.2420. Accessed April 21, 2020.
  27. ↑ Chee S-P, Chan N-W, Ti S-E. Decision-making and management of uveitic cataract. Indian Journal of Ophthalmology. 2017;65(12):1329. doi:10.4103/ijo.ijo_740_17. Accessed April 21, 2020.
  28. ↑ Karim R, Sykakis, Lightman S, Fraserbell. Interventions for the treatment of uveitic macular edema: a systematic review and meta-analysis. Clinical Ophthalmology. 2013:1109. doi:10.2147/opth.s40268. Accessed April 21, 2020.
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