Ординатура / Офтальмология / Английские материалы / Primary Intraocular Lymphoma_Chan, Gonzales_2007

74Primary Intraocular Lymphoma

33.Fine HA, Mayer RJ. (1993) Primary central nervous system lymphoma. Ann Intern Med 119(11): 1093–1104.

34.Akpek EK, Ahmed I, Hochberg FH, et al. (1999) Intraocular-central nervous system lymphoma: clinical features, diagnosis, and outcomes. Ophthalmology 106(9): 1805–1810.

35.Buggage RR, Chan CC, Nussenblatt RB. (2001) Ocular manifestations of central nervous system lymphoma. Curr Opin Oncol 13(3): 137–142.

36.Chan CC. (2003) Molecular pathology of primary intraocular lymphoma.

Trans Am Ophthalmol Soc 101: 275–292.

37.Char DH, Ljung BM, Miller T, Phillips T. (1988) Primary intraocular lymphoma (ocular reticulum cell sarcoma) diagnosis and management.

Ophthalmology 95: 625–630.

38.Char DH, Margolis L, Newman AB. (1981) Ocular reticulum cell sarcoma.

Am J Ophthalmol 91(4): 480–483.

39.Freeman LN, Schachat AP, Knox DL, Michels RG, Green WR. (1987) Clinical features, laboratory investigations, and survival in ocular reticulum cell sarcoma. Ophthalmology 94: 1631–1639.

40.Hormigo A, Abrey L, Heinemann MH, DeAngelis LM. (2004) Ocular presentation of primary central nervous system lymphoma: diagnosis and treatment. Br J Haematol 126(2): 202–208.

41.Jahnke K, Korfel A, Komm J, et al. (2005) Intraocular lymphoma 2000–2005: results of a retrospective multicentre trial. Graefes Arch Clin Exp Ophthalmol: 1–7.

42.Siegel MJ, Dalton J, Friedman AH, et al. (1989) Ten-year experience with primary ocular ‘reticulum cell sarcoma’ (large cell non-Hodgkin’s lymphoma). Br J Ophthalmol 73(5): 342–346.

43.Peterson K, Gordon KB, Heinemann MH, DeAngelis LM. (1993) The clinical spectrum of ocular lymphoma. Cancer 72(3): 843–849.

44.Matsuo T, Yamaoka A, Shiraga F, Matsuo N. (1998) Two types of initial ocular manifestations in intraocular-central nervous system lymphoma. Retina 18(4): 301–307.

45.Velez G, de Smet MD, Whitcup SM, et al. (2000) Iris involvement in primary intraocular lymphoma: report of two cases and review of the literature. Surv Ophthalmol 44(6): 518–526.

46.Wegelius C. (1964) Case findings and roentgen diagnostics of pulmonary sarcoidosis. Acta Med Scand Suppl 425: 92–95.

47.Szwarcberg JB, Glajchen N, Teirstein AS. (2005) Pleural involvement in chronic sarcoidosis detected by thoracic CT scanning. Sarcoidosis Vasc Diffuse Lung Dis 22(1): 58–62.

48.Ridley ME, McDonald HR, Sternberg P, Jr., et al. (1992) Retinal manifestations of ocular lymphoma (reticulum cell sarcoma). Ophthalmology 99(7): 1153–1160; discussion 1160–1151.

Clinical Manifestations of PIOL 75

49.Lang GK, Surer JL, Green WR, et al. (1985) Ocular reticulum cell sarcoma. Clinicopathologic correlation of a case with multifocal lesions. Retina 5(2): 79–86.

50.Buggage RR, Velez G, Myers-Powell B, et al. (1999) Primary intraocular lymphoma with a low interleukin 10 to interleukin 6 ratio and heterogeneous IgH gene rearrangement. Arch Ophthalmol 117(9): 1239–1242.

51.Cassoux N, Merle-Beral H, Leblond V, et al. (2000) Ocular and central nervous system lymphoma: clinical features and diagnosis. Ocul Immunol Inflamm 8(4): 243–250.

52.Tuaillon N, Chan CC. (2001) Molecular analysis of primary central nervous system and primary intraocular lymphoma. Curr Mol Med 1(2): 259–272.

53.Char DH, Ljung BM, Deschenes J, Miller TR. (1988) Intraocular lymphoma: immunological and cytological analysis. Br J Ophthalmol 72(12): 905–911.

54.Gass JD, Sever RJ, Grizzard WS, et al. (1984) Multifocal pigment epithelial detachments by reticulum cell sarcoma. A characteristic funduscopic picture. Retina 4(3): 135–143.

55.Michelson JB, Michelson PE, Bordin GM, Chisari FV. (1981) Ocular reticulum cell sarcoma. Presentation as retinal detachment with demonstration of monoclonal immunoglobulin light chains on the vitreous cells. Arch Ophthalmol 99(8): 1409–1411.

56.Gass JD, Trattler HL. (1991) Retinal artery obstruction and atheromas associated with non-Hodgkin’s large cell lymphoma (reticulum cell sarcoma).

Arch Ophthalmol 109(8): 1134–1139.

57.Madhavan HN, Priya K, Bagyalakshmi R. (2003) Phenotypic and genotypic methods for the detection of herpes simplex virus serotypes. J Virol Methods 108(1): 97–102.

58.Madhavan HN, Priya K, Anand AR, Therese KL. (1999) Detection of herpes simplex virus (HSV) genome using polymerase chain reaction (PCR) in clinical samples comparison of PCR with standard laboratory methods for the detection of HSV. J Clin Virol 14(2): 145–151.

59.Dean JM, Novak MA, Chan CC, Green WR. (1996) Tumor detachments of the retinal pigment epithelium in ocular/central nervous system lymphoma. Retina 16(1): 47–56.

60.Loh KY, Ogle J. (2004) Age related visual impairment in the elderly. Med J Malaysia 59(4): 562–568; quiz 569.

61.Coupland SE, Heimann H, Bechrakis NE. (2004) Primary intraocular lymphoma: a review of the clinical, histopathological and molecular biological features. Graefes Arch Clin Exp Ophthalmol 242(11): 901–913.

62.Chan CC, Buggage RR, Nussenblatt RB. (2002) Intraocular lymphoma. Curr Opin Ophthalmol 13(6): 411–418.

76Primary Intraocular Lymphoma

63.Raju VK, Green WR. (1982) Reticulum cell sarcoma of the uvea. Ann Ophthalmol 14(6): 555–560.

64.Henderly DE, Genstler AJ, Smith RE, Rao NA. (1987) Changing patterns of uveitis. Am J Ophthalmol 103(2): 131–136.

65.Rothova A, Buitenhuis HJ, Meenken C, et al. (1992) Uveitis and systemic disease. Br J Ophthalmol 76(3): 137–141.

66.Culbertson WW, Blumenkranz MS, Pepose JS, et al. (1986) Varicella zoster virus is a cause of the acute retinal necrosis syndrome. Ophthalmology 93(5): 559–569.

67.Garweg J, Bohnke M. (1997) Varicella-zoster virus is strongly associated with atypical necrotizing herpetic retinopathies. Clin Infect Dis 24(4): 603–608.

68.Hellinger WC, Bolling JP, Smith TF, Campbell RJ. (1993) Varicella-zoster virus retinitis in a patient with AIDS-related complex: case report and brief review of the acute retinal necrosis syndrome. Clin Infect Dis 16(2): 208–212.

69.Kaiser PK, Lee MS, Martin DA. (2003) Occlusive vasculitis in a patient with concomitant West Nile virus infection. Am J Ophthalmol 136(5): 928–930.

70.Garg S, Jampol LM. (2005) Systemic and intraocular manifestations of West Nile virus infection. Surv Ophthalmol 50(1): 3–13.

71.Anninger WV, Lomeo MD, Dingle J, et al. (2003) West Nile virus-associated optic neuritis and chorioretinitis. Am J Ophthalmol 136(6): 1183–1185.

72.de Smet MD, Nussenblatt RB, Davis JL, Palestine AG. (1990) Large cell lymphoma masquerading as a viral retinitis. Int Ophthalmol 14(5–6): 413–417.

73.Margo CE, Hamed LM. (1992) Ocular syphilis. Surv Ophthalmol 37(3): 203–220.

74.Poulsen A. (1950) Some clinical features of tuberculosis. 1. Incubation period. Acta Tuberc Scand 24(3–4): 311–346.

75.Poulsen A. (1957) Some clinical features of tuberculosis. Acta Tuberc Scand 33(1–2): 37–92; concl.

76.Arango L, Brewin AW, Murray JF. (1973) The spectrum of tuberculosis as currently seen in a metropolitan hospital. Am Rev Respir Dis 108(4): 805–812.

77.Ormerod LD, Dailey JP. (1999) Ocular manifestations of cat-scratch disease.

Curr Opin Ophthalmol 10(3): 209–216.

78.Cunningham ET, Koehler JE. (2000) Ocular bartonellosis. Am J Ophthalmol 130(3): 340–349.

79.Bar S, Segal M, Shapira R, Savir H. (1990) Neuroretinitis associated with cat scratch disease. Am J Ophthalmol 110(6): 703–705.

80.Davis JL, Solomon D, Nussenblatt RB, et al. (1992) Immunocytochemical staining of vitreous cells. Indications, techniques, and results. Ophthalmology 99(2): 250–256.

Clinical Manifestations of PIOL 77

81.Priem HA, Oosterhuis JA. (1988) Birdshot chorioretinopathy: clinical characteristics and evolution. Br J Ophthalmol 72(9): 646–659.

82.LeHoang P, Ozdemir N, Benhamou A, et al. (1992) HLA-A29.2 subtype associated with birdshot retinochoroidopathy. Am J Ophthalmol 113(1): 33–35.

83.Rizzato G, Angi M, Fraioli P, et al. (1996) Uveitis as a presenting feature of chronic sarcoidosis. Eur Respir J 9(6): 1201–1205.

84.Obenauf CD, Shaw HE, Sydnor CF, Klintworth GK. (1978) Sarcoidosis and its ophthalmic manifestations. Am J Ophthalmol 86(5): 648–655.

85.James DG. (1986) Ocular sarcoidosis. Ann N Y Acad Sci 465: 551–563.

86.Behçet H. (1940) Some observations on clinical picture of the so-called triple symptom complex. Dermatologica 81: 73–83.

87.Tugal-Tutkun I, Onal S, Altan-Yaycioglu R, et al. (2004) Uveitis in Behcet disease: an analysis of 880 patients. Am J Ophthalmol 138(3): 373–380.

88.Haim S. (1968) Contribution of ocular symptoms in the diagnosis of Behcet’s disease. Study of 23 cases. Arch Dermatol 98(5): 478–480.

89.Harada H. (1926) Beitrag zur klinischen kenntis von nichteitriger Choroiditis (Choroidtis diffusa acuta). Acta Soc Ophthalmol Jpn 30: 356–378.

90.Koyanagi Y. (1906) Dysakusis, alopecia und poliosis bei schwerer uveitis nicht traumatischen Ursprungs. Klin Monatsbl Augenheilkd 44: 228–242.

91.Vogt A. (1906) Fruhzeitiges Ergrauen der Zilien und Bemerkungen uber den sogenannten plotzlichen Eintritt diser Veranderung. Klin Monatsbl Augenheilkd 44: 228–242.

92.Rubsamen PE, Gass JD. (1991) Vogt-Koyanagi-Harada syndrome. Clinical course, therapy, and long-term visual outcome. Arch Ophthalmol 109(5): 682–687.

93.Coupland SE, Joussen A, Anastassiou G, Stein H. (2005) Diagnosis of a primary uveal extranodal marginal zone B-cell lymphoma by chorioretinal biopsy: case report. Graefes Arch Clin Exp Ophthalmol 243(5): 482–486.

94.Crookes GP, Mullaney J. (1967) Lymphoid hyperplasia of the uveal tract simulating malignant lymphoma. Am J Ophthalmol 63(5): 962–967.

95.Cheung MK, Martin DF, Chan CC, et al. (1994) Diagnosis of reactive lymphoid hyperplasia by choroidal biopsy. Am J Ophthalmol 118(4): 457–462.

96.Ryan SJ, Jr., Frank RN, Green WR. (1971) Bilateral inflammatory pseudotumors of the ciliary body. Am J Ophthalmol 72(3): 586–591.

97.Jakobiec FA, Sacks E, Kronish JW, et al. (1987) Multifocal static creamy choroidal infiltrates. An early sign of lymphoid neoplasia. Ophthalmology 94(4): 397–406.

98.Coupland SE, Anastassiou G, Bornfeld N, et al. (2005) Primary intraocular lymphoma of T-cell type: report of a case and review of the literature.

Graefes Arch Clin Exp Ophthalmol 243(3): 189–197.

78Primary Intraocular Lymphoma

99.Wiznia RA, Freedman JK, Mancini AD, Shields JA. (1978) Malignant melanoma of the choroid in neurofibromatosis. Am J Ophthalmol 86(5): 684–687.

100.Reeser FH, Aaberg TM, Van Horn DL. (1978) Astrocytic hamartoma of the retina not associated with tuberous sclerosis. Am J Ophthalmol 86(5): 688–698.

101.Ferreri AJ, Campo E, Seymour JF, et al. (2004) Intravascular lymphoma: clinical presentation, natural history, management and prognostic factors in a series of 38 cases, with special emphasis on the ‘cutaneous variant’. Br J Haematol 127(2): 173–183.

102.Al-Hazzaa SAF, Green WR, Wann RB. (1993) Uveal involvement in systemic angiotropic large cell lymphoma. Ophthalmology 100(6): 961–965.

103.Domizio P, Hall PA, Cotter F, et al. (1989) Angiotropic large cell lymphoma (ALCL): morphological, immunohistochemical and genotypic studies with analysis of previous reports. Hematol Oncol 7(3): 195–206.

104.Ko YH, Han JH, Go JH, et al. (1997) Intravascular lymphomatosis: a clinicopathological study of two cases presenting as an interstitial lung disease.

Histopathology 31(6): 555–562.

105.Sepp N, Schuler G, Romani N, et al. (1990) “Intravascular lymphomatosis” (angioendotheliomatosis): evidence for a T-cell origin in two cases. Hum Pathol 21(10): 1051–1058.

106.O’Grady JT, Shahidullah H, Doherty VR, al-Nafussi A. (1994) Intravascular histiocytosis. Histopathology 24(3): 265–268.

107.Snowden JA, Angel CA, Winfield DA, et al. (1997) Angiotropic lymphoma: report of a case with histiocytic features. J Clin Pathol 50(1): 67–70.

108.Wu H, Said JW, Ames ED, et al. (2005) First reported cases of intravascular large cell lymphoma of the NK cell type: clinical, histologic, immunophenotypic, and molecular features. Am J Clin Pathol 123(4): 603–611.

109.Chapin JE, Davis LE, Kornfeld M, Mandler RN. (1995) Neurologic manifestations of intravascular lymphomatosis. Acta Neurol Scand 91(6): 494–499.

110.Elner VM, Hidayat AA, Charles NC, et al. (1986) Neoplastic angioendotheliomatosis. A variant of malignant lymphoma immunohistochemical and ultrastructural observations of three cases. Ophthalmology 93(9): 1237–1245.

111.Gass JD, Weleber RG, Johnson DR. (1987) Non-Hodgkin’s lymphoma causing fundus picture simulating fundus flavimaculatus. Retina 7(4): 209–214.

Imaging 81

Ophthalmoscopic imaging is both necessary and important for evaluating PIOL.

Ultrasound

In cases where vitritis is severe (as when vitreous cells form clumps or sheets that obscure a view of the fundus) or a dense cataract precludes view of the fundus, one simple technique to begin with is B-scan ultrasonography. Ultrasound can help determine whether there are any masses or lesions intraocularly or extraocularly (e.g., associated with ocular adnexa as in extranodal marginal zone lymphoma). Intraocular masses visualized with ultrasonography may represent PIOL or may signal a systemic metastasis, such as a systemic NHL that has affected the eye, usually the choroid.3,4 In addition, choroidal or subretinal masses may be visualized upon ophthalmoscopic examination and fundus photography, but details of the lesions may be unattainable due to overlying retinal changes, e.g. retinal detachments. Ultrasound can help further characterize these lesions. However, ultrasonography is nonspecific and while it may help in determining whether a process is occurring intraor extraocularly, other modalities are more often employed to document PIOL. Nevertheless, there are some ultrasonographic features associated with PIOL. Vitreous cells, the most common feature of PIOL, may appear as vitreous debris upon ultrasound. Thickening of the choroid and sclera as well as chorioretinal lesions secondary to reactive inflammatory reaction may rarely be revealed. When significant infiltration by lymphoma cells occurs, exudative, serous, or bullous retinal detachments can occur. The retinal detachment may be partial or may be significant enough to be noted as a funnel retinal detachment on ultrasound. Of course, funnel and serous retinal detachments can occur in other secondary lymphomatous processes as well, such as those that can occur with extranodal marginal zone lymphoma (EMZL) of mucosa-associated lymphoid tissue (MALT) with intraocular involvement.5,6 Primary uveal EMZL MALT can impart a low to medium reflectivity to a thickened choroid on ultrasound.7 Ultrasound can help demonstrate how extensive the tumor is. Typically, a lymphomatous lesion will be low-reflective.8 As the lesion of PIOL is not vascularized, color Doppler imaging would not be expected to show vascularity in this case as compared with cases of systemic metastases.3 In primary uveal lymphoma, ultrasonographic features may be different than those in

82 Primary Intraocular Lymphoma

PIOL and can include choroidal changes, such as diffuse thickening of the choroid and serous detachment.9 However, even in PIOL there can be choroidal or scleral thickening.1

A few case series exist on the ultrasonographic features of PIOL. Ursea and colleagues performed both A- and B-scan ultrasonography on 16 eyes in 13 patients with PIOL.10 Vitreous debris was the most common ultrasonographic finding, with 87.5% of the eyes exhibiting this feature. Vitreous debris was evidenced by low reflective scattered echoes within the vitreous. Half of the eyes studied showed choroidal and scleral thickening and a quarter of the eyes showed a widened optic nerve shadow on ultrasound. Irregular retrobulbar fat, an elevated lesion, retinal detachment, and Tenon capsule accentuation were each found in 18.7% of the eyes. Posterior vitreous detachment was found in 12.5% of the eyes, and a vitreous membrane was found in one eye (6.2%).

While ultrasound is a useful tool that can help the ophthalmologist view the extent of lesions or disease not viewed during slit lamp or ophthalmoscopic examination, many of its findings, such as, vitreous debris and choroidal thickening are non-specific. For example, vitreous debris can certainly be due to uveitis of myriad etiologies and choroidal thickening can be due to other tumors. Therefore, other imaging techniques are more commonly employed, including fluorescein angiography and magnetic resonance imaging (MRI). Nevertheless, ultrasound can help an ophthalmologist consider whether a lymphomatous process is likely affecting the eye and, importantly, it can be used to document response to treatment.

While definitely useful in some instances, ultrasound is an optional imaging test in PIOL and is not routinely obtained when this diagnosis is pursued.

Fluorescein Angiography

Often when no retinal lesions are identified during direct or indirect ophthalmoscopic exam, fluorescein angiography may provide useful clues. Fluorescein angiography (FA) is widely used in retinal vascular diseases, such as diabetic retinopathy, choroidal neovascularization, and retinal vasculitis. Even when obvious retinal lesions are present, such as the characteristic creamy yellow-whitish sub-RPE infiltrates, FA is an important tool in confirming an ophthalmologist’s suspicion of a malignant

Imaging 83

lymphoid process. FA in PIOL seems to have a characteristic appearance. Commonly, RPE disturbances are noted and include granularity, mottling, and late staining patterns.11,12 “Leopard spot” patterns have also been described,13 although this term has been used to describe the hyperfluorescent spots in ocular syphilis.14,15 Blockage of fluorescence at the level of the RPE, termed mottling, due to tumor infiltration can correspond to the deep retinal or subretinal creamy colored lesions noted on fundus photography. Early staining of the subretinal infiltrates may show nonfluorescence1 as viable tumor cells are not easily penetrated by fluorescein dye because their cell membranes remain intact.16 Late staining may show some weak staining of the borders of the lesions or incomplete staining of the lesions, imparting a hypofluorescent appearance. Late staining may also occur near the macula or outside the macula.1,2,17,18 FA is also used to confirm the location of the lesions as being at the level of the RPE.2 In areas where tumor infiltration has caused detachment of the overlying RPE and retina, blocked fluorescence will be noted and there may be staining at the detachment’s borders.19 There may also be small hyperfluorescent lesions representing window defects from RPE atrophy.2 The combination of blocked fluorescence and hyperfluorescence produces a pattern of granularity.2,12 Small branch artery occlusions, which have been noted to occasionally occur in PIOL,20 can be documented with FA.2 In a study of five patients with PIOL, Ridley et al. found FA to be important in documenting retinal changes over time.2 For example, in some patients there was vascular sheathing with little perivascular exudate and leakage on initial FA. When FA was performed at a later stage, vascular leakage had increased. However, others have reported that vascular leakage is less common in PIOL compared with inflammatory conditions.12 Velez et al. analyzed the angiographic findings of 31 eyes in 17 patients at the National Eye Institute (NEI).12 The most common angiographic finding was disturbance of the RPE in 65% of the eyes. RPE disturbances included granularity, late staining at the level of the RPE, and blockage of fluorescence. Unlike viable tumor, nonviable tumor cells will take up fluorescein dye and can appear hyperfluorescent. FA has been shown to reveal RPE changes when none were noted upon ophthalmoscopic examination in patients with vitritis.12 Importantly, although FA is a valuable tool in the diagnosis of PIOL, occasionally no abnormalities are noted in patients with PIOL. For example, in the study by Velez et al. 14% of the eyes with