Glaucoma Secondary to Intraocular Tumors

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Article initiated by:
Ahmad A. Aref, MD, MBA, Eric G. Feinstein MD
All contributors:
Brad H. Feldman, M.D., Ahmad A. Aref, MD, MBA, Daniel B. Moore, MD, Jill Wells, MD, Qi N. Cui, MD PhD
Assigned editor:
Caroline M Craven, MD, Mark Slabaugh, MD
Review:
Assigned status Update Pending
 by Qi N. Cui, MD PhD on November 17, 2022.


Ocular tumors or systemic malignancies that spread to the eye can lead to intraocular pressure elevation through many different mechanisms. If not diagnosed early, the tumor’s effect on eye pressure or spread of the tumor itself can be sight or life threatening. In patients with highly asymmetric glaucoma or eye pressure elevation that is resistant to standard medical therapy, a thorough history and ocular exam (including pertinent imaging) should be performed to rule out intraocular malignancies.


Disease

Tumors within the globe can lead to elevation in intraocular pressure (IOP) and permanent damage to the ocular structures. In patients who present with atypical, unilateral or highly asymmetric glaucoma, suspicion for intraocular malignancies must be high.[1] [2] The type of tumor, the location of the malignancy and the size of the mass affects the amount of pressure elevation within the globe. The pressure can be further increased depending on the amount of inflammation, necrosis, or hemorrhage present.[1][3] [4] [5] The prevalence of ocular metastasis from systemic tumors is estimated to be around 4%.[6]

Etiology

The majority of tumors that are found within ocular tissues are generally from distant sources that spread to the eye through the vascular/lymphatic system or rarely by direct invasion from surrounding tissues. Most systemic tumors affect the choroid with breast, lung and kidney being the most common primary sites.[7]

Overall, in eyes which have intraocular tumors the prevalence of elevation in IOP is around 5%.[8] The type as well as location of the intraocular malignancy affect the likelihood of causing elevations in IOP.[3][4] For patients with metastasis or uveal melanoma, an increase in IOP is much more common in tumors affecting the anterior uveal tract including the ciliary body and the iris.[8] [9] For iris metastasis or melanoma the rate of secondary glaucoma can be as high as one-third.[10] [11]

Pathophysiology

Open Angle Glaucoma

Direct Invasion of Anterior Chamber Angle

In tumors located in the anterior segment of the eye, the most common mechanism for secondary IOP elevation is direct invasion of the anterior chamber angle by tumor cells. This mechanically prevents aqueous humor from egressing the eye, which directly causes a rise in IOP. This can been seen clinically on gonioscopy as well as at the ultrastructural level using immunohistochemistry and electron microscopy of affected ocular tissues.[12]

For all anteriorly located metastatic tumors and iris melanomas, mechanical obstruction is the most common cause of secondary glaucoma.[2] Ring melanoma, which involves most of the ciliary body and iris, blocks aqueous outflow as it spreads circumferentially.[9][10][13] Not every patient with seeding of the angle will develop glaucoma. Tumors with the following characteristics are more likely to develop elevated IOP: larger tumor base, iris root location of tumor base, flat contour of tumors and tumors with a large number of clock hours of angle seeding.[8][11][14][15]

Secondary Pigmentary Glaucoma

Massive dispersion of pigment from pigmented tumor cells (i.e.- melanoma and melanocytoma) can lead to obstruction of the anterior chamber angle and iris heterochromia.[7][12][16][17] In ciliary body melanomas this is the most common cause of secondary glaucoma.[2]

Melanomalytic Glaucoma

Melanomalytic glaucoma is secondary to the release of pigment from tumor cells which are subsequently phagocytosed by macrophages.[18] [19] Based on studies using immunohistochemistry and electron microscopy, these pigment-laden macrophages cause blockage of the trabecular meshwork which leads to increased IOP.[7][18][19][12]

Anterior Chamber Angle Epithelialization

A sheet-like plaque of malignant tumor cells that spread over an open anterior chamber angle can cause mechanical obstruction of the trabecular meshwork. This causes IOP elevation and secondary open-angle glaucoma.[14]

Increased Episcleral Venous Pressure

Aqueous humor outflow is dependent on the pressure gradient between IOP and episcleral venous pressure. Orbital tumors or extraocular extension of an intraocular tumor can cause an increase in episcleral venous pressure through direct compression. [20] Resulting elevation of episcleral venous pressure causes a pressure gradient reduction, contributing to secondary glaucoma.[21]

Closed Angle Glaucoma

Uveitic

Inflammation secondary to intraocular tumors can cause obstruction of the outflow pathway by inflammatory cells as well as peripheral anterior synechiae, which can lead to secondary angle closure. In patients with uveal melanoma and uveitis, secondary angle closure is common from peripheral anterior synechiae.[7] Metastatic tumors have also been shown to cause significant inflammation leading to outflow obstruction and synechial angle closure.[22]

Secondary Neovascularization

Patients with intraocular tumors can often develop neovascularization of the iris and angle, which can lead to chronic angle closure glaucoma. This is commonly true in tumors which cause a chronic retinal detachment (especially choroidal melanomas) leading to ischemia and resultant secondary neovascularization.[1][22] Metastatic cutaneous melanomas are also highly associated with neovascularization.[23] Neovascularization can also be present as a complication of tumor treatment (i.e., after radiation).[5][24][25][26][27]

Anterior Displacement of Lens-Iris Diaphragm

The most common mechanism of angle closure in patients with intraocular tumor is forward displacement of the lens-iris diaphragm. The displacement is usually from a large mass in the posterior segment of the eye causing forward pressure on iris and lens structures leading to pupillary block, iris bombé, and/or peripheral anterior synechiae closing the anterior chamber angle.[7][22][28]

Diagnosis

History

The workup begins with a thorough history, which should be performed in all patients with elevated IOP from atypical cases of glaucoma. A thorough history includes all of the following:

  • Complete history of present illness (including current and past symptoms)
  • Past medical and ocular history (focusing specifically on risk factors for cancer)
  • Past surgical history (including radiation treatments)
  • Medications (including eye drops)
  • Family history (especially cancer history)
  • Complete review of systems
  • Social history (including drugs, tobacco use, alcohol and occupation)

Symptoms

The symptoms that the patient experience depend greatly on the type and location of the malignancy as well as the amount of ocular involvement. The most frequently recorded symptoms are blurred vision, pain, redness and floaters. [8][11][14][29] Some patients, however, are asymptomatic.

Physical examination

Extraocular and slit lamp biomicroscopy exams of the anterior and posterior segments of each eye should be performed as well as a thorough gonioscopy of the angle. A complete dilated exam should be performed in all patients, as long as the anterior chamber angle is not occludable. The following findings are essential to note for any patient suspected of having tumor induced secondary glaucoma. [1][7][8][9][11][14][17][18][30]

Anterior Segment Exam Findings

  • Pigment dispersion (in anterior chamber or angle)
  • Dilated episcleral vessels
  • Intraocular inflammation (noting cell/flare, hypopyon, or keratic precipitates)
  • Hyphema
  • Heterochromia
  • Neovascularization of Iris or Angle
  • Mass lesions of the iris/ciliary body/angle
  • Abnormal transillumination of the globe (noting shadows suggestive of a masses)
  • Closed/narrow angle

Posterior segment Findings:

  • Retinal detachment
  • Posterior segment masses
  • Vitritis
  • Vitreous hemorrhage

Ophthalmic Imaging

B-Scan Ultrasonography (B-Scan)

In patients in whom dilation is not possible (patients at risk for angle closure) or if there is opacification of the media obstructing the view to the posterior pole, B-scan ultrasound can be used to examine the posterior segment. Specifically, it is helpful in taking measurements of the posterior segment tumors like uveal melanomas and looking for concurrent retinal detachments, vitreous hemorrhage or vitritis.

Ultrasound Biomicroscopy (UBM)

To further characterize tumors in the anterior segment including the ciliary body, ultrasound biomicroscopy can be performed. UBM uses a high frequency wavelength which allows for accurate measurements of lesion size and is helpful for diagnosis (solid versus cystic masses) and follow up.[1][28][31]

Diagnostic procedures

If diagnostic uncertainty remains after a full history, physical exam, and imaging, a diagnostic biopsy can be performed for most tumors (it is contraindicated in retinoblastoma). The use of fine needle aspiration biopsy with either a 25-gauge needle or a vitrector can be performed, and the sample analyzed with or without immunohistochemistry to help with diagnosis. This method has proven to be especially helpful in leukemia/lymphoma.[32] [33][34] [35]

Differential diagnosis

Leukemia

Involvement of the eye can occur in just under one-third of cases of systemic leukemia.[6] Secondary glaucoma is generally caused by anterior chamber angle obstruction from leukemic cells.[30] Acute lymphoblastic (ALL) and acute myelogenous (AML) leukemias are the most common causes of secondary glaucoma in patients with leukemia.[1][6] On examination, due to layering of the leukemic cells, there may be a pseudohypopyon present in the anterior chamber.[20] Secondary angle closure glaucoma has also been reported.[8]

Lymphoma

Non-Hodgkin lymphoma of the central nervous system (NHL-CNS) tend to more commonly affect the eye compared to non-CNS involving lymphoma.[1][6][8][36] NHL-CNS classically affects the retina and vitreous with patients complaining of floaters.[36][37][38] On anterior segment examination, there can be signs of inflammation (cell/flare, keratic precipitates), hyphema, corneal edema and/or a pseudohypopyon (layered tumor cells). On posterior segment exam, vitritis and subretinal infiltrates may be present.[20] [38][37] Non-CNS intraocular lymphoma often metastasize through the choroidal circulation to the uveal tissue. Symptoms usually include pain, blurred vision and eye redness.[36][38][37]

Lymphoma with metastasis to the eye tends to occur at a lower rate compared to leukemia. Secondary elevation of IOP more commonly occurs from tumor seeding of the trabecular meshwork, but angle closure and iris neovascularization have also been reported. [8][20][31][34][37]

Metastatic Tumors

The most common type of intraocular tumor results from metastases. These tumors are most frequently located in the uveal tract, with the most common primary sites being breast and lung.[3][4][7][10][39] Besides leukemia and lymphoma, carcinomas are more common than sarcomas in terms of metastasis to the eye.[6][35] These patients have symptoms of decreased vision and pain and may have exophthalmos, retinal detachment, mass lesions, uveitis, and secondary glaucoma on exam.[3]

Secondary IOP elevations is much more common in anteriorly located metastatic tumors.[3][4] The mechanism of IOP elevation is generally from direct invasion of the anterior chamber angle but neovascularization has also been reported.[3][4][9] In one histopathological study of patients with metastatic carcinomas to the eye, high IOP was present in 7.5%.[3] Due to the general health and infrequent ophthalmic exams received by these patients, many metastatic tumors and secondary glaucomas may go undetected.

Uveal Melanoma

The most common primary intraocular malignancy in adults is uveal melanoma with the majority located within the choroid.[1][2][8][40][41] Elevation of IOP has been reported in up to one-fourth of patients with uveal melanoma through a variety of mechanisms causing both open and closed angle glaucomas.[2][8]

Open angle glaucoma in uveal melanoma patients can occur due to tumor seeding of the anterior chamber angle, direct invasion of the tumor into the angle and melanomalytic obstruction.[2][8][12][14][18][19][42] Ciliary body, iris, and ring melanomas tend to cause IOP elevation by direct invasion of the anterior chamber angle or pigment dispersion.[8][12]

Angle closure glaucoma is also common and can occur from a variety of mechanisms. It can be from neovascularization (usually with chronic retinal detachment), anterior displacement of the lens-iris diaphragm from large posterior segment tumors, and/or synechial angle closure.[1][2][8]

Retinoblastoma

Retinoblastoma is the most common primary intraocular tumor in children and most commonly presents with strabismus and leukocoria. Patients also rarely can have a red, painful eye either from inflammation or elevated IOP.[43]

In a large retrospective study it was shown that 17% of retinoblastoma patients had elevation of IOP.[8] The majority of pressure elevation is secondary to neovascularization followed by displacement of the iris-lens diaphragm.[8][43] Other less common causes of secondary glaucoma include tumor seeding of the anterior chamber angle, uveitis, and vitreous hemorrhage.

Other Tumors

  • Medulloepithelioma. A congenital embryonal tumor of the ciliary body, these tumors cause IOP elevation in just under half of patients usually through direct tumor invasion of the angle or neovascularization.[8][44]
  • Iris melanocytoma. These tumors cause elevated IOP through pigmentary or melanomalytic glaucoma.[8][16][45]
  • Multiple Myeloma are a malignant proliferation of plasma cells, and have been reported to cause secondary glaucoma by anterior chamber angle invasion or secondary angle-closure.[39]
  • Juvenile Xanthogranuloma is a benign skin disorder that presents with cutaneous lesions, can have iris lesions, spontaneous hyphema, uveitis and secondary glaucoma.[25] Cellular infiltration of the angle, hyphema, or peripheral anterior synechiae and angle closure lead to secondary glaucoma.[46]

Management

For intraocular tumors with secondary glaucoma, elimination of the viable tumor cells is of primary importance. Control of IOP can be done either medically or surgically.

Medical therapy

Treatment of the secondary glaucoma should begin with topical eye drops (alpha-agonists, beta-blockers and carbonic anhydrase inhibitors) which decrease aqueous humor production. If the pressure remains uncontrolled on topical medication then oral hypotensive agents like acetazolamide or methazolamide should be tried. Prostaglandin analogues are not strictly contradicted, however, there is controversy over whether this class of medication should be given in ocular tumor patients, as a theoretical concern for metastasis due to the increased uveoscleral outflow is present.[43]

For metastases with multiple lesions in the eye, systemically chemotherapy can play a large role. In eyes that have poor visual potential and elevated pressure, treatment for secondary glaucoma should only be given if pain is present.

Surgery

Surgical intervention should only be considered if the patient failed more conservative treatment options. Successful en-bloc resections of the iris and ciliary body tumors have been reported with large tectonic corneoscleral grafts. These surgeries do carry a risk of hypotony if more than 5 clock hours are removed.[47] Transscleral cyclophotocoagulation or cryotherapy to the ciliary body offer less invasive ways to control IOP.[1][42][43]

Incisional glaucoma surgery, including filtration procedures and aqueous tube shunts, are generally contraindicated, except in cases of metastases, due to the potential risk of facilitating tumor spread outside of the globe.[1][35][43][44][48] Minimally invasive glaucoma procedures may play a role, however the risk for tumor spread remains.[45]

Sometimes treatment of the underlying tumors with plaque brachytherapy, external beam radiation, chemotherapy, or radiation can improve the IOP. For certain tumors like large uveal melanomas, retinoblastoma, or a blind painful eye primary enucleation may be the appropriate option.

Complications

A significant number of patients will develop neovascular glaucoma (NVG) following treatment of the original tumor with brachytherapy and proton beam radiation.[5][24][25][26][27][49] Heightened vigilance and appropriate follow-up in these patients is key. Other systemic medications including docetaxel, paclitaxel and imatinib as well as intravitreal rituximab/methotrexate have been reported to elevate IOP.[17][31][50]

Prognosis

Prognosis is highly variable and depends upon the type of tumor, the degree of ocular involvement, and the treatment received. The primary goal for any treatment is to control the tumor first and then control the IOP. Management of any intraocular tumor must be done concurrently with an oncologist to treat systemic diseases as well.

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 Radcliffe NM, Finger PT. Eye cancer related glaucoma: current concepts. Surv Ophthalmol. 2009;54(1):47-73.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Shields CL, Materin MA, Shields JA et al. Factors associated with elevated intraocular pressure in eyes with iris melanoma. Br. J Ophthalmol. 2001;85(6):666-9.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Ferry AP, Font RL. Carcinoma metastatic to the eye and orbit II. A clinicopathological study of 26 patients with carcinoma metastatic to the anterior segment of the eye. Arch Ophthalmol. 1975;93(7):472-82.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 Ferry AP, Font RL. Carcinoma metastatic to the eye and orbit II. A clinicopathological study of 26 patients with carcinoma metastatic to the anterior segment of the eye. Arch Ophthalmol. 1975;93(7):472-82.
  5. ↑ 5.0 5.1 5.2 Bollinger, Kathryn, Annapurna Singh, and Arun D. Singh. "Glaucoma and Intraocular Tumors." Ed. Tarek M. Shaarawy, Mark B. Sherwood, Roger A. Hitchings, and Jonathan G. Crowston. Glaucoma: Medical Diagnosis and Therapy. Philadelphia: Saunders/Elsevier, 2009. 441-47. Print.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 Nelson CC, Hertzberg BS, Klintworth GK. A histopathologic study of 716 unselected eyes in patients with cancer at the time of death. Am J Ophthalmol. 1983;95:788-793.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 Shields CL, Shields JA, Gross NE, Schwartz GP, Lally SE. Survey of 520 eyes with uveal metastases. Ophthalmology. 1996 Aug; 104(8):1265-76.
  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 8.12 8.13 8.14 8.15 8.16 Shields CL, Shields JA, Shields MB, Augsburger JJ. Prevalence and mechanisms of secondary intraocular pressure elevation in eyes with intraocular tumors. Ophthalmology. 1987;94(7):839-846.
  9. ↑ 9.0 9.1 9.2 9.3 Shields CL, Materin MA, Shields JA et al. Factors associated with elevated intraocular pressure in eyes with iris melanoma. Br. J Ophthalmol. 2001;85(6):666-9.
  10. ↑ 10.0 10.1 10.2 Shields CL et al. Iris Metastasis From Systemic Cancer in 104 Patients: The 2014 Jerry A. Shields Lecture. Cornea. 2015 Jan;34 (1).
  11. ↑ 11.0 11.1 11.2 11.3 Shields CL, Kaliki S, Furuta M, et al. Iris melanoma features and prognosis in children and adults in 317 patients. J Am Assoc Pediatr Ophthalmol Strabismus 2012;16:10-6.
  12. ↑ 12.0 12.1 12.2 12.3 12.4 Krohn J, Mørk SJ. Acute glaucoma caused by massive pigment dispersion from necrotic choroidal melanoma. Can J Ophthalmol. 2010 Aug;45(4):417-8.
  13. ↑ Demirci H, Shields CL, Shields JA, Honavar SG, Eagle RC. Ring Melanoma of the Ciliary Body. Report of Twenty-Three Patients. Retina 22:689-706, 2002.
  14. ↑ 14.0 14.1 14.2 14.3 14.4 McMenamin PG, Lee WR. Ultrastructural pathology of melanomalytic glaucoma. Br J Ophthalmol. 1986 Dec;70(12):895-906.
  15. ↑ Lee V, Cree IA, Hungerford JL. Ring Melanoma- A Rare Cause of Refractory Glaucoma. Br J Ophthalmol. 1999;84:194-198.
  16. ↑ 16.0 16.1 de A Alves LF, Fernandes BF, Menezes MS, Ribeiro AS, Leal MM, Burnier JV, Burnier MN Jr. Management of glaucoma in an eye with diffuse iris melanocytoma. Br J Ophthalmol. 2011 Oct;95(10):1471, 1479.
  17. ↑ 17.0 17.1 17.2 Fabre-Guillevin E, Tchen N, Anibali-Charpiat MF, Calluaud L, Ravaud A. Taxane-induced glaucoma. Lancet. 1999 Oct 2;354(9185):1181-2.
  18. ↑ 18.0 18.1 18.2 18.3 Yanoff M, Scheie HG. Melanomalytic glaucoma. Report of a case. Arch Ophthalmol. 1970 Oct;84(4):471-3.
  19. ↑ 19.0 19.1 19.2 Fineman MS, Eagle RC Jr, Shields JA, Shields CL, De Potter P. Melanocytomalytic glaucoma in eyes with necrotic iris melanocytoma. Ophthalmology. 1998 Mar;105(3):492-6.
  20. ↑ 20.0 20.1 20.2 20.3 Matano S, Ohta T, Nakamura S, et al. Leukemic hypopyon in acute myelogenous leukemia. Ann Hematol. 2000;79(8): 455--8
  21. ↑ Jørgensen JS, Guthoff R. [The role of episcleral venous pressure in the development of secondary glaucomas]. Klin Monbl Augenheilkd. 1988 Nov;193(5):471-5.
  22. ↑ 22.0 22.1 22.2 Girkin CA, Goldberg I, Mansberger SL, Shields JA, Shields CL. Management of iris melanoma with secondary glaucoma. J Glaucoma. 2002 Feb;11(1):71-4.
  23. ↑ Garrison LM, Christensen RE, Allen RA. Angle-closure glaucoma from metastatic carcinoma. Am J Ophthalmol. 1967 Mar;63(3):503-7.
  24. ↑ 24.0 24.1 Bergmann U, Guthoff R. [Ultrasound biomicroscopy for evaluation of space-occupying lesions of the anterior eye segment. Initial results]. Ophthalmologe. 1995 Dec;92(6):844-8.
  25. ↑ 25.0 25.1 25.2 Chang MW, Frieden IJ, Good W. The risk intraocular juvenile xanthogranuloma: survey of current practices and assessment of risk. J Am Acad Dermatol. 1996 Mar;34(3):445-9.
  26. ↑ 26.0 26.1 Albert DM, Gangnon RE, Zimbric ML, Damico CM, Fisher MR, Gleiser J, Grossniklaus HE, Green WR. A study of iridectomy histopathologic features of latanoprost- and non-latanoprost-treated patients. Arch Ophthalmol. 2004 Nov;122(11):1680-5.
  27. ↑ 27.0 27.1 Naumann GO, Rummelt V. Block excision of tumors of the anterior uvea. Report on 68 consecutive patients. Ophthalmology. 1996 Dec;103(12):2017-27.
  28. ↑ 28.0 28.1 Gündüz K, Shields JA, Shields CL, Eagle RC Jr. Cutaneous melanoma metastatic to the vitreous cavity. Ophthalmology. 1998 Apr;105(4):600-5.
  29. ↑ Puusaari I, Heikkonen J, Kivelä T. Ocular complications after iodine brachytherapy for large uveal melanomas. Ophthalmology. 2004 Sep;111(9):1768-77.
  30. ↑ 30.0 30.1 Schuman JS, Wang N, Eisenberg DL. Leukemic glaucoma: the effects on outflow facility of chronic lymphocytic leukemia lymphocytes. Exp Eye Res. 1995;61(5):609-17.
  31. ↑ 31.0 31.1 31.2 van Oterendorp C, Ness T, Illerhaus G, Neuburger M, Jordan JF. The trabectome as treatment option in secondary glaucoma due to intraocular lymphoma. J Glaucoma. 2014 Sep;23(7):482-4
  32. ↑ Ellsworth RM. The practical management of retinoblastoma. Trans Am Ophthalmol Soc. 1969;67:462-534.
  33. ↑ Conway RM, Poothullil AM, Daftari IK, Weinberg V, Chung JE, O'Brien JM. Estimates of ocular and visual retention following treatment of extra-large uveal melanomas by proton beam radiotherapy. Arch Ophthalmol. 2006 Jun;124(6):838-43.
  34. ↑ 34.0 34.1 Sullivan SF, Dallow RI. Intraocular reticulum cell sarcoma: its dramatic response to systemic chemotherapy and its angiogenic potential. Ann Ophthalmol. 1977 Apr;9(4):401-6.
  35. ↑ 35.0 35.1 35.2 Feinstein E, Kaliki S, Shields CL, Ehya H, Shields JA. Choroidal metastasis from leiomyosarcoma in two cases. Oman J Ophthalmol. 2014 Jan;7(1):19-21.
  36. ↑ 36.0 36.1 36.2 Velez G, de Smet MD, Whitcup SM, Robinson M, Nussenblatt RB, Chan CC. Iris involvement in primary intraocular lymphoma: report of two cases and review of the literature. Surv Ophthalmol. 2000 May-Jun;44(6):518-26.
  37. ↑ 37.0 37.1 37.2 37.3 Mashayekhi A, Shields CL, Shields JA. Iris involvement by lymphoma: a review of 13 cases. Clin Experiment Ophthalmol. 2013 Jan-Feb;41(1):19-26.
  38. ↑ 38.0 38.1 38.2 Cooper EL, Riker JL. Malignant Lymphoma of the Uveal Tract. Am J Ophthalmol. 1951 Aug;34(8):1153-8.
  39. ↑ 39.0 39.1 Chin KJ, Kempin S, Milman T, Finger PT. Ocular manifestations of multiple myeloma: three cases and a review of the literature. Optometry. 2011 Apr;82(4):224-30.
  40. ↑ Wanner JB, Pasquale LR. Glaucomas secondary to intraocular melanomas. Semin Ophthalmol. 2006 Jul-Sep;21(3):181-9.
  41. ↑ Faulkner-Jones BE, Foster WJ, Harbour JW, Smith ME, Dávila RM. Fine needle aspiration biopsy with adjunct immunohistochemistry in intraocular tumor management. Acta Cytol. 2005 May-Jun;49(3):297-308.
  42. ↑ 42.0 42.1 Lumbroso-Le Rouic L, Charif Chefchaouni M, Levy C, Plancher C, Dendale R, Asselain B, Solignac S, Mazal A, Desjardins L. 125I plaque brachytherapy for anterior uveal melanomas. Eye (Lond). 2004 Sep;18(9):911-6.
  43. ↑ 43.0 43.1 43.2 43.3 43.4 de Leon JM, Walton DS, Latina MA, Mercado GV. Glaucoma in retinoblastoma. Semin Ophthalmol. 2005 Oct-Dec;20(4):217-22.
  44. ↑ 44.0 44.1 Kaliki S, Shields CL, Eagle RC Jr, Vemuganti GK, Almeida A, Manjandavida FP, Mulay K, Honavar SG, Shields JA. Ciliary body medulloepithelioma: analysis of 41 cases. Ophthalmology. 2013 Dec;120(12):2552-9.
  45. ↑ 45.0 45.1 Demirci H, Mashayekhi A, Shields CL, Eagle RC Jr, Shields JA. Iris melanocytoma: clinical features and natural course in 47 cases. Am J Ophthalmol. 2005 Mar;139(3):468-75.
  46. ↑ Vendal Z, Walton D, Chen T. Glaucoma in juvenile xanthogranuloma. Semin Ophthalmol. 2006 Jul-Sep;21(3):191-4.
  47. ↑ Rennie IG. Clinically important ocular reactions to systemic drug therapy. Drug Saf. 1993 Sep;9(3):196-211.
  48. ↑ Grossniklaus HE, Brown RH, Stulting RD, Blasberg RD. Iris melanoma seeding through a trabeculectomy site. Arch Ophthalmol. 1990 Sep;108(9):1287-90.
  49. ↑ Gragoudas ES, Seddon JM, Egan K, Glynn R, Munzenrider J, Austin-Seymour M, Goitein M, Verhey L, Urie M, Koehler A. Long-term results of proton beam irradiated uveal melanomas. Ophthalmology. 1987 Apr;94(4):349-53."
  50. ↑ Fraunfelder FW, Solomon J, Druker BJ, Esmaeli B, Kuyl J. Ocular side-effects associated with imatinib mesylate (Gleevec). J Ocul Pharmacol Ther. 2003 Aug;19(4):371-5.
  1. Pasternak S, Erwenne CM, Nicolela MT. Subconjunctival spread of ciliary body melanoma after glaucoma filtering surgery: a clinicopathological case report. Can J Ophthalmol. 2005 Feb;40(1):69-71.
  2. Boonyaleephan S. Drug-induced secondary glaucoma. J Med Assoc Thai. 2010 Feb;93 Suppl 2:S118-22.
  3. Sharkawi E, Oleszczuk JD, Bergin C, Zografos L. Baerveldt shunts in the treatment of glaucoma secondary to anterior uveal melanoma and proton beam radiotherapy. Br J Ophthalmol. 2012 Aug;96(8):1104-7.
  4. Mantel I, Schalenbourg A, Bergin C, Petrovic A, Weber DC, Zografos L. Prophylactic use of bevacizumab to avoid anterior segment neovascularization following proton therapy for uveal melanoma. Am J Ophthalmol. 2014 Oct;158(4):693-701.
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