Subretinal Fibrosis and Uveitis Syndrome

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Article initiated by:
Hashem Abu Serhan
All contributors:
djihane machane, Osama Elaraby, Nagi Ahmed, Hashem Abu Serhan
Assigned editor:
Review:
Assigned status Update Pending
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Subretinal fibrosis and uveitis syndrome (SFUS) is a rare, progressive, bilateral inflammatory chorioretinal disorder characterized by intraocular inflammation and the development of extensive subretinal fibrosis. It typically affects young to middle-aged adults and may lead to severe, irreversible visual loss, particularly with macular involvement. The pathogenesis is thought to involve an immune-mediated inflammatory response causing fibroblast activation and subretinal scar formation. Management relies on early aggressive immunosuppression with corticosteroids and steroid-sparing agents to control inflammation and prevent progression.

Disease Entity

Disease

Diffuse subretinal fibrosis and uveitis syndrome (SFUS) is a rare inflammatory chorioretinal disorder characterized by multifocal inflammatory lesions that progressively evolve into subretinal fibrosis and permanent visual impairment. These lesions may enlarge and coalesce into extensive fibrotic plaques, progressively disrupting the retinal pigment epithelium (RPE), outer retina, and normal chorioretinal architecture.[1][2][3]

Recurrent inflammatory activity frequently accompanies disease progression and may promote ongoing fibrotic expansion. Vision loss is often severe when fibrosis involves the posterior pole and macula. Long-term series have attributed profound visual impairment principally to macular fibrosis, chorioretinal atrophy, and irreversible retinal damage.[2][4][5]

Etiology

The etiology of SFUS remains unknown. Despite extensive investigation in reported patients, no consistent infectious, environmental, or systemic cause has been identified.[1][2][4]

Clinicopathologic evidence supports an immune-mediated inflammatory process involving the choroid, RPE, and outer retina. Histopathologic studies have demonstrated chronic choroidal inflammation, lymphocytic and plasma-cell infiltration, immunoglobulin and complement deposition, and extensive subretinal fibrous proliferation.[3][6]

Reported systemic associations include ulcerative colitis, HLA-B27-associated spondyloarthropathy, pregnancy-associated disease activity, and Hodgkin lymphoma.

A secondary SFUS-like fibrosing phenotype has also been described in two patients with rheumatoid arthritis and concurrent renal dysfunction.[7][8][9][10][11]

Risk Factors

No established risk factors have been consistently identified. Most cases occur sporadically, and the rarity of the disease limits identification of reproducible demographic, environmental, infectious, or genetic predispositions.[1][2][4] Female predominance and young-adult onset were noted in early series, but later reports documented disease in males, children, and older adults.[1][2][4][5][12][13][14][15]

General Pathology

Histopathologic studies demonstrate chronic inflammation involving the choroid, RPE, and outer retina, accompanied by progressive subretinal fibrous proliferation. Choroidal infiltrates include lymphocytes and plasma cells, with immunoglobulin and complement deposition in affected tissue.[3][6]

Progressive RPE disruption appears central to plaque formation. Advanced cases show photoreceptor loss, retinal gliosis, interruption of Bruch membrane, and replacement of normal retinal architecture by fibrous tissue. Immunohistochemistry demonstrates both T- and B-cell participation and Müller-cell activation.[3][6][16]

Pathophysiology

The pathophysiology remains incompletely understood. Evidence suggests a dysregulated inflammatory response involving the choroid, RPE, and outer retina that culminates in progressive subretinal fibrosis. An autoimmune mechanism has been suspected because infectious causes have not been consistently identified and tissue studies demonstrate inflammatory infiltrates, immunoglobulin deposition, and complement activation.[3][6]

RPE injury may promote migration and proliferation of RPE-derived cells in the subretinal space. Cellular and humoral immunity both appear relevant, with T cells, B cells, plasma cells, and activated Müller cells identified in affected tissue.[3][6][16]

Reported responses to tumor necrosis factor-alpha inhibition and detection of elevated intraocular inflammatory mediators provide limited clinical support for cytokine involvement. These observations remain hypothesis-generating because they derive from individual cases.[8][14]

Primary Prevention

No established method of primary prevention exists because the cause is unknown and no modifiable causal factor has been confirmed. Early recognition and treatment target active inflammation and disease progression rather than true primary prevention.[1][2][4]

Diagnosis

History

Patients most commonly report blurred or reduced vision of gradual or acute onset. Scotomas, metamorphopsia, photopsias, and floaters may occur according to lesion location and inflammatory activity.[1][2][4][17][8][14]

Disease may begin unilaterally and involve the fellow eye months or years later. Recurrent episodes may follow periods of apparent stability, with renewed visual deterioration accompanying inflammatory reactivation or fibrotic progression.[1][2][4][14]

A systemic history should assess autoimmune or inflammatory disease, including rheumatoid arthritis and inflammatory bowel disease; pregnancy or postpartum timing; malignancy; infection risk; renal disease; and previous ocular trauma or surgery.[18][19][7][8][9][10][11]

Physical Examination

Visual acuity ranges from mild impairment to profound loss when fibrosis involves the macula. The anterior segment may be normal or show mild anterior uveitis or posterior synechiae. Vitreous inflammation ranges from minimal cells to clinically significant vitritis.[1][2][4][5][20][12][14]

Fundus examination typically shows multiple yellow-white lesions that enlarge and coalesce into broad subretinal fibrotic plaques. Additional findings include punched-out scars, pigmentary changes, retinal folds, subretinal fluid, and hemorrhage.[1][2][10][11]

Choroidal neovascularization, retinal neovascularization, and vitreoretinal traction have also been reported.[12][13][14][15]

Signs

Hallmark signs are multifocal yellow-white inflammatory chorioretinal lesions and their evolution into broad areas of subretinal fibrosis. Advanced disease may show RPE alterations, chorioretinal atrophy, macular fibrosis, optic disc hyperemia or edema, cystoid macular edema, subretinal fluid, serous retinal detachment, retinal folds, and hemorrhage.[1][2][4][5][20][12][14] Secondary choroidal or retinal neovascularization may occur in selected cases.[12][13][14][15]

Symptoms

Blurred vision is the most frequently reported symptom. Central or paracentral scotomas, metamorphopsia, photopsias, and floaters may accompany macular involvement, retinal distortion, subretinal fluid, or vitreous inflammation. Symptoms may initially be unilateral, with later fellow-eye involvement.[1][2][4][17][8][12][14][10]

Clinical Diagnosis

SFUS is a clinical diagnosis based on the characteristic evolution of multifocal inflammatory chorioretinal lesions into progressive subretinal fibrosis. No universally accepted diagnostic criteria or confirmatory laboratory test exists. Diagnosis integrates history, ophthalmic examination, serial multimodal imaging, and exclusion of alternative causes.[1][2][21]

Diagnostic Procedures

A .Fundus Photography

Serial fundus photography documents lesion morphology, enlargement, coalescence, scar formation, and expansion of fibrotic plaques.[1][2][4]

b. Fluorescein Angiography

Fluorescein angiography may demonstrate hyperfluorescence or leakage from active inflammatory lesions, staining or blockage associated with fibrosis, optic disc or retinal vascular leakage, and cystoid macular edema.[1][2][4][7][14][11] Angiography may also identify secondary choroidal or retinal neovascularization in selected cases.[12][13][14]

c. Indocyanine Green Angiography

Indocyanine green angiography can reveal hypofluorescent choroidal lesions, including abnormalities not apparent clinically or on fluorescein angiography.[22]

d. Optical Coherence Tomography

OCT may demonstrate subretinal or sub-RPE fibrotic material, RPE and outer-retinal disruption, photoreceptor loss, intraretinal cysts, macular edema, subretinal fluid, atrophy, and associated neovascular or tractional changes.[20][23][12][13][14][15]

e. Optical Coherence Tomography Angiography

OCTA may characterize vascular or neocapillary networks associated with chronic lesions and assist in evaluating suspected secondary choroidal neovascularization. Evidence remains limited.[24]

f. Fundus Autofluorescence

Fundus and near-infrared autofluorescence may demonstrate hypoautofluorescence over fibrotic or atrophic tissue and hyperautofluorescence associated with active or evolving lesions.[23][24][15]

Laboratory Test

No laboratory test confirms SFUS. Testing is directed by the differential diagnosis and is used to exclude infectious, autoimmune, inflammatory, and neoplastic mimics. Reported evaluations include blood counts, inflammatory markers, ACE and lysozyme, syphilis and tuberculosis testing, toxoplasmosis and other infection testing, autoimmune antibody panels, HLA-B27, chest imaging, and selected neurologic or oncologic investigations.[1][2][7][8][14][9][10][11]

Differential Diagnosis

The differential diagnosis includes multifocal choroiditis, punctate inner choroidopathy, serpiginous or serpiginous-like choroiditis, presumed ocular histoplasmosis syndrome, sympathetic ophthalmia, Vogt-Koyanagi-Harada disease, sarcoidosis, tuberculosis-associated choroiditis, and primary vitreoretinal lymphoma. Distinction depends on lesion pattern, degree of inflammation, systemic features, exposure or surgical history, imaging, and targeted testing.[2][21][18][19][9]

Multifocal choroiditis is closely related clinically, and some authors regard SFUS as an aggressive fibrosing phenotype within that spectrum.[2][4][21] A history of trauma or surgery with bilateral granulomatous inflammation favors sympathetic ophthalmia.[18][19] Other mimics require correlation with their characteristic lesion distributions, systemic manifestations, and laboratory findings.[21]

Management

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General Treatment

Treatment aims to suppress active intraocular inflammation, limit fibrotic progression, preserve retinal structure, and manage complications. Because controlled trials are unavailable, treatment is individualized according to activity, structural damage, vision, previous response, and associated systemic disease.[1][2][4][7][8][25]

Medical Therapy

a.    Corticosteroids

Acute inflammatory or exudative findings may improve with corticosteroid treatment, but established fibrosis may persist or continue to progress, and the response varies among reported patients.[1][2][4][5][22][12][13][10][11]

b.   Conventional Immunosuppressive Therapy

Methotrexate, azathioprine, cyclosporine, cyclophosphamide, and other steroid-sparing regimens have been used in recurrent or severe disease. Evidence derives from uncontrolled reports, and treatment effects cannot be separated reliably from concomitant therapy or natural history.[3][4][5][19][26][8][12][14][9]

c.    Biologic Therapy

Infliximab was associated with reduced inflammation and improved visual acuity in one refractory HLA-B27-positive case. Rituximab was reported as successful in two bilateral cases, although patient-level details were unavailable in the abstract. Adalimumab was used in the Hodgkin lymphoma-associated case, but multiple treatment changes and systemic disease preclude efficacy conclusions.[8][25][9]

d.   Anti-VEGF Therapy

Anti-VEGF agents have been used for secondary choroidal neovascularization or exudative complications. Ranibizumab showed minimal benefit in one case, whereas bevacizumab and newer agents were associated with control of selected neovascular or edema findings in other reports. Anti-VEGF therapy does not treat the underlying inflammatory process and has not been shown to reverse established fibrosis.[20][12][14]

Medical Follow-up

Long-term surveillance is warranted because inflammatory reactivation, fibrotic progression, and fellow-eye involvement may occur after apparent stability. Follow-up should document visual acuity, anterior and vitreous inflammation, fundus findings, and serial imaging. OCT is particularly useful for monitoring fibrosis, edema, subretinal fluid, outer-retinal integrity, and neovascular or tractional complications..[1][2][4][20][23][12][24][14][15]

Surgery

Surgery is not a primary therapy. Procedures may be required for cataract, retinal detachment, vitreoretinal traction, neovascular complications, or diagnostic tissue sampling. In a recent case, pars plana vitrectomy resolved traction and retinal neovascularization, although fibrosis initially progressed.[6][3][16][7][14]

Prior ocular surgery must be interpreted carefully because postoperative inflammatory fibrosing phenotypes may represent sympathetic ophthalmia.[18][19]

Surgical Follow-up

Postoperative monitoring should assess visual acuity, inflammation, retinal attachment, edema, neovascularization, traction, and progression of fibrosis. OCT and fundus imaging are appropriate when structural complications are present. Evidence specific to postoperative management is limited.[7][20][14]

Complications

The principal complication is progressive subretinal fibrosis, especially when plaques involve the posterior pole and macula. Other Reported inflammatory and structural complications include cystoid macular edema, subretinal fluid, serous or bullous retinal detachment, retinal folds, chorioretinal atrophy, pigmentary abnormalities, cataract, and profound visual loss.[1][2][3][4][27][28][10][29] Secondary choroidal neovascularization, retinal neovascularization, and vitreoretinal traction have been described in selected cases.[12][13][14][15]

Prognosis

Visual prognosis is generally poor when fibrosis reaches the fovea or central macula. Longitudinal series attributed severe impairment mainly to dense macular fibrosis and chorioretinal atrophy.[2][4][5]

Disease course is variable. Some eyes show recurrent inflammation and progressive lesion enlargement, whereas others develop extensive fibrosis with minimal clinically apparent inflammation. Established photoreceptor loss, RPE destruction, atrophy, and dense fibrosis are generally irreversible.[1][2][3][4]

Individual reports describe stabilization or visual improvement after corticosteroids, infliximab, or rituximab, but these uncontrolled observations do not establish comparative efficacy. No treatment has been proven to reverse established subretinal fibrosis.[8][25][13]

Global Variants

SFUS has been reported in North America, Europe, Asia, and South America, but evidence is insufficient to establish geographic or ethnic differences in incidence, phenotype, or treatment response. Ethnicity and refractive status were inconsistently reported.[1][2][27][26][10][11][30]

Pediatric cases demonstrate that SFUS can occur in very young children and may be complicated by rapid fibrosis and secondary choroidal neovascularization. Adult and older-patient reports broaden the age range, although some older cases have atypical or systemic disease-associated phenotypes.[26][12][13][14][15][11]

Reported systemic or host associations include ulcerative colitis, HLA-B27-positive spondyloarthropathy, pregnancy or postpartum disease activity, and Hodgkin lymphoma.[7][8][9][10] In addition, a secondary SFUS-like fibrosing phenotype has been reported in two patients with rheumatoid arthritis and concurrent renal dysfunction.[11] These isolated observations expand the clinical spectrum but do not establish causality.

Additional Resources

Because SFUS is rare and no consensus treatment guideline exists, evaluation by an ophthalmologist experienced in uveitis and inflammatory chorioretinal disease is appropriate. Multidisciplinary consultation may be needed when systemic inflammatory, infectious, autoimmune, or neoplastic disease is suspected.

PubMed: search “subretinal fibrosis and uveitis syndrome,” “diffuse subretinal fibrosis syndrome,” and “multifocal choroiditis with progressive subretinal fibrosis.”

American Academy of Ophthalmology: educational resources concerning posterior uveitis, multifocal choroiditis, and inflammatory choroidal neovascularization.

National Eye Institute: patient-oriented information about uveitis and related inflammatory eye disease.

ClinicalTrials.gov: information about studies of noninfectious uveitis; disease-specific SFUS trials may be unavailable because of its rarity.

Treatment decisions must be individualized. Favorable outcomes reported with corticosteroids, conventional immunosuppression, infliximab, or rituximab should not be interpreted as established treatment guidelines.[8][25][13]

References

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  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 Palestine AG, Nussenblatt RB, Parver LM, Knox DL. Progressive subretinal fibrosis and uveitis. Br J Ophthalmol. 1984;68(9):667-673. doi:10.1136/bjo.68.9.667.
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 Cantrill HL, Folk JC. Multifocal choroiditis associated with progressive subretinal fibrosis. Am J Ophthalmol. 1986;101(2):170-180. doi:10.1016/0002-9394(86)90590-8.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 Kim MK, Chan CC, Belfort R Jr, et al. Histopathologic and immunohistopathologic features of subretinal fibrosis and uveitis syndrome. Am J Ophthalmol. 1987;104(1):15-23. doi:10.1016/0002-9394(87)90287-X.
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 4.17 4.18 4.19 Reddy CV, Brown J Jr, Folk JC, et al. Enlarged blind spots in chorioretinal inflammatory disorders. Ophthalmology. 1996;103(4):606-617. doi:10.1016/S0161-6420(96)30645-3.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 Brown J Jr, Folk JC, Reddy CV, Kimura AE. Visual prognosis of multifocal choroiditis, punctate inner choroidopathy, and diffuse subretinal fibrosis syndrome. Ophthalmology. 1996;103(7):1100-1105. doi:10.1016/S0161-6420(96)30561-7.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 Palestine AG, Nussenblatt RB, Chan CC, Hooks JJ, Friedman L, Kuwabara T. Histopathology of the subretinal fibrosis and uveitis syndrome. Ophthalmology. 1985;92(6):838-844. doi:10.1016/S0161-6420(85)33969-6.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Fuentes-Páez G, Martínez-Osorio H, Herreras JM, Calonge M. Subretinal fibrosis and uveitis syndrome associated with ulcerative colitis. Int J Colorectal Dis. 2007;22(3):333-334. doi:10.1007/s00384-006-0137-2.
  8. ↑ 8.00 8.01 8.02 8.03 8.04 8.05 8.06 8.07 8.08 8.09 8.10 8.11 Adán A, Sanmartí R, Burés A, Casaroli-Marano RP. Successful treatment with infliximab in a patient with diffuse subretinal fibrosis syndrome. Am J Ophthalmol. 2007;143(3):533-534. doi:10.1016/j.ajo.2006.10.047.
  9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 Socci da Costa D, Turchetti Moraes R, Zajdenweber ME, Land Curi AL, Menezes de Souza J, Rosa Gameiro Filho A. Progressive subretinal fibrosis and uveitis associated with Hodgkin lymphoma. Case Rep Ophthalmol. 2025;16(1):728-738. doi:10.1159/000548315.
  10. ↑ 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 Ono K, Kunimatsu S, Numaga J, Kaburaki T, Fujino Y, Kawashima H. Multifocal choroiditis with subretinal fibrosis before, during and after pregnancy. Clin Exp Ophthalmol. 2003;31(4):365-366. doi:10.1046/j.1442-9071.2003.00674.x.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 Matsuo T, Matsuo N. Progressive subretinal fibrosis in patients with rheumatoid arthritis and renal dysfunction. Ophthalmologica. 1998;212(4):289-294. doi:10.1159/000027310.
  12. ↑ 12.00 12.01 12.02 12.03 12.04 12.05 12.06 12.07 12.08 12.09 12.10 12.11 12.12 12.13 Steeples LR, Ashworth J, Jones N. Multifocal chorioretinitis with progressive subretinal fibrosis in a young child. BMJ Case Rep. 2015;2015:bcr2015212526. doi:10.1136/bcr-2015-212526.
  13. ↑ 13.0 13.1 13.2 13.3 13.4 13.5 13.6 13.7 13.8 13.9 Stolowy ND, Donnadieu BP, Comet AC, et al. Diffuse subretinal fibrosis syndrome: a rare entity. Eur J Ophthalmol. 2018;28(6):NP1-NP6. doi:10.1177/1120672118777418.
  14. ↑ 14.00 14.01 14.02 14.03 14.04 14.05 14.06 14.07 14.08 14.09 14.10 14.11 14.12 14.13 14.14 14.15 14.16 14.17 14.18 14.19 Zhang X, Hu Y, Li J. Case Report: A case of diffuse subretinal fibrosis and uveitis syndrome with vitreoretinal traction syndrome. Front Med. 2026;13:1671793. doi:10.3389/fmed.2026.1671793.
  15. ↑ 15.0 15.1 15.2 15.3 15.4 15.5 15.6 15.7 Patel A, Kelgaonkar A, Pathengay A. Unilateral idiopathic progressive subretinal fibrosis: imaging characteristics. Retina. 2025;45(4):e23-e24. doi:10.1097/IAE.0000000000004277.
  16. ↑ 16.0 16.1 16.2 Chan CC, Matteson DM, Li Q, Whitcup SM, Nussenblatt RB. Apoptosis in patients with posterior uveitis. Arch Ophthalmol. 1997;115(12):1559-1567. doi:10.1001/archopht.1997.01100160729010.
  17. ↑ 17.0 17.1 Gandorfer A, Ulbig MW, Kampik A. Diffuse subretinal fibrosis syndrome. Retina. 2000;20(5):561-563. doi:10.1097/00006982-200005000-00028.
  18. ↑ 18.0 18.1 18.2 18.3 Wang RC, Zamir E, Dugel PU, et al. Progressive subretinal fibrosis and blindness associated with multifocal granulomatous chorioretinitis: a variant of sympathetic ophthalmia. Ophthalmology. 2002;109(8):1527-1531. doi:10.1016/S0161-6420(02)01108-9.
  19. ↑ 19.0 19.1 19.2 19.3 19.4 Lim WK, Chee SP, Sng I, Nussenblatt RB, Chan CC. Immunopathology of progressive subretinal fibrosis: a variant of sympathetic ophthalmia. Am J Ophthalmol. 2004;138(3):475-477. doi:10.1016/j.ajo.2004.04.013.
  20. ↑ 20.0 20.1 20.2 20.3 20.4 20.5 Symeonidis C, Dastiridou A, Konidaris V, et al. Subretinal fibrosis and uveitis: a spectral domain OCT study of its evolution and minimal therapeutic effect of ranibizumab. Ocul Immunol Inflamm. 2014;22(6):497-500. doi:10.3109/09273948.2013.841959.
  21. ↑ 21.0 21.1 21.2 21.3 Kaiser PK, Gragoudas ES. The subretinal fibrosis and uveitis syndrome. Int Ophthalmol Clin. 1996;36(1):145-152. doi:10.1097/00004397-199603610-00015
  22. ↑ 22.0 22.1 Amaro MH, Muccioli C, Motta MMS. Progressive subretinal fibrosis and multifocal granulomatous chorioretinitis. Arq Bras Oftalmol. 2006;69(3):413-415. doi:10.1590/S0004-27492006000300024.
  23. ↑ 23.0 23.1 23.2 Hua R, Yao K, Liu L, Li J. Near infrared autofluorescence findings in diffuse subretinal fibrosis syndrome. Lasers Med Sci. 2015;30(9):2395-2397. doi:10.1007/s10103-015-1718-5.
  24. ↑ 24.0 24.1 24.2 Moll-Udina A, Alba-Linero C, Llorenç V, Adán A. Multimodal imaging in diffuse subretinal fibrosis with uveitis syndrome. Retin Cases Brief Rep. 2023;17(1):13-17. doi:10.1097/ICB.0000000000001111
  25. ↑ 25.0 25.1 25.2 25.3 Cornish KS, Kuffova L, Forrester JV. Treatment of diffuse subretinal fibrosis uveitis with rituximab. Br J Ophthalmol. 2015;99(2):153-154. doi:10.1136/bjophthalmol-2013-304686.
  26. ↑ 26.0 26.1 26.2 Velillas S, Rodriguez de la Rua E, Carrasco B, et al. Progressive diffuse subretinal fibrosis syndrome: a case report. Arch Soc Esp Oftalmol. 2001;76(4):259-262.
  27. ↑ 27.0 27.1 Yamane I, Ishibashi T, Honda T, et al. A case of multifocal choroiditis associated with progressive subretinal fibrosis. Nippon Ganka Gakkai Zasshi. 1995;99(5):618-623.
  28. ↑ Gass JDM, Margo CE, Levy MH. Progressive subretinal fibrosis and blindness in patients with multifocal granulomatous chorioretinitis. Am J Ophthalmol. 1996;122(1):76-85. doi:10.1016/S0002-9394(14)71966-X.
  29. ↑ Salvador F, Garcia-Arumi J, Mateo C, et al. Multifocal choroiditis with progressive subretinal fibrosis: report of two cases. Ophthalmologica. 1994;208(3):163-167. doi:10.1159/000310476.
  30. ↑ Serracarbassa PD, Lagos C, Abujamra S. Síndrome da fibrose sub-retiniana difusa: relato de três casos. Arq Bras Oftalmol. 2002;65(4):475-478. doi:10.1590/S0004-27492002000400016.
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