Ординатура / Офтальмология / Английские материалы / Shields Textbook of Glaucoma, 6th edition_Allingham, Damji, Freedman_2010

P.323

case of a 16-year-old girl has been reported in which an aggressive iris nevus caused glaucoma by invading the trabecular meshwork (85).

A specific form of iris nevus with associated glaucoma is the iris nevus syndrome. In these cases, diffuse nevi of the iris are associated with progressive synechial closure of the angle and subsequent IOP elevation (86). A subset of the iridocorneal endothelial syndrome, the Cogan-Reese syndrome, has a similar clinical appearance, but the pedunculated nodules on the surface of the iris are composed of tissue resembling iris stroma (87). The benign lesions of the iris in both of these conditions have been mistaken for malignant melanomas, which has led to enucleation in some patients. (These conditions are discussed further in Chapter 16.)

Cysts

Cysts of the iris are classified as primary and secondary, with the former arising from the epithelial layers of the iris and ciliary body or, less often, from the iris stroma (88). Most primary cysts are stationary lesions, rarely progressing or causing visual complications. However, families have been described in which multiple cysts of the iris and ciliary body, presumably of autosomal dominant inheritance, caused angle-closure glaucoma (89). Other reported mechanisms of IOP elevation associated with iris cysts include pigment dispersion (90) and a mucusproducing epithelial cyst of the iris stroma of unknown origin (91). Iris cysts have been successfully treated by laser cystotomy, although others may require surgical excision if uncontrolled IOP or other symptoms persist. Secondary cysts of the iris may result from surgery, trauma, or neoplasia and are more likely than primary cysts to lead to inflammation and glaucoma (88, 92). Ultrasonography has been a useful diagnostic adjunct for primary and secondary iris cysts.

Melanocytomas

These tumors are classified as benign nevi and are seen clinically as darkly pigmented lesions, usually on the optic nerve head and, less often, in the choroid, ciliary body, or iris. Tumors in the latter location can cause glaucoma by direct spread into the anterior chamber angle or by dispersion of pigment into the angle from a necrotic melanocytoma (93, 94).

Melanoses

Melanosis iridis is characterized by verrucous-like elevations on the surface of a darkly pigmented, velvety iris. It is usually unilateral and sometimes sectorial, although bilateral involvement has been reported (95). Melanosis oculi has additional hyperpigmentation of the episclera, choroid, or both and has been reported in association with open-angle glaucoma in which the mechanism appears to be heavy pigmentation of the trabecular meshwork (96). A similar condition has been observed in oculodermal melanocytosis (nevus of Ota, which is considered later in this chapter).

Adenomas

Benign adenomas may arise from the epithelium of the anterior uvea, especially the ciliary body (Fuchs adenoma) (97). They occur predominantly in adults, although they have been observed in a child with associated hyperplastic primary vitreous (98). Although common among the elderly, adenomas are rarely observed clinically (99). Some can involve the iris primarily or secondarily and have caused glaucoma from pigment dispersion (100, 101). Adenomas must be distinguished from anterior uveal cysts and melanomas (100). Adenocarcinomas may also arise from the ciliary body epithelium and may cause glaucoma (102).

Leiomyomas

These rare tumors may appear as a slow-growing grayish-white, vascularized nodule on the surface of the iris. Glaucoma is not a typical complication.

PHAKOMATOSES

In 1932, Van der Hoeve (103) coined the term phakomatosis, meaning “mother spot” or “birthmark,” to denote a group of disorders that are characterized by hamartomas, which are congenital tumors arising from tissue that is normally found in the involved area. The hamartomas primarily involve the eye, skin, and nervous system, although other systems may be involved to a lesser degree, including pulmonary,

cardiovascular, gastrointestinal, renal, and skeletal. In some cases, the anomalies are present at birth, whereas others become manifest later in life. The four conditions that traditionally comprise the phakomatoses are the von Hippel-Lindau syndrome, von Recklinghausen neurofibromatosis, tuberous sclerosis or Bourneville disease, and the Sturge-Weber syndrome. Several other disorders subsequently have been included by various investigators. The following discussion is limited to phakomatoses that frequently or occasionally are associated with glaucoma.

Sturge-Weber Syndrome General Features

The hamartoma occurring in the Sturge-Weber syndrome (i.e., encephalotrigeminal angiomatosis) arises from vascular tissue and produces a characteristic port-wine hemangioma of the skin along the trigeminal distribution (Fig. 21.7) and an ipsilateral leptomeningeal angioma. The angiomata are present at birth and are usually unilateral, although bilateral cases also occur. In one review of 51 patients, the condition was recognized before 24 months of age in more than half the cases (104). The nervous system involvement frequently causes seizure disorders, hemispheric motor or sensory defects, and intellectual deficiency. A characteristic radiographic finding is cortical calcifications that develop after several years and appear as double densities or “ra ilroad tracks.” There is no race or sex predilectio n, and no hereditary pattern has been established.

P.324

Figure 21.7 Child with the Sturge-Weber syndrome and unilateral glaucoma. Notice the typical portwine hemangioma of the skin along the distribution of the left trigeminal nerve.

Ocular Features

Glaucoma occurs in approximately one half of the cases in which the port-wine stain involves the ophthalmic and maxillary divisions of the trigeminal nerve. Slitlamp examination typically reveals a dense episcleral vascular plexus and occasional ampulliform dilatations of conjunctival vessels. These findings are on the side of the cutaneous lesion. Some patients also have a choroidal hemangioma. In the study of 51 patients previously mentioned, 69% had conjunctival or episcleral hemangiomas, 55% had choroidal hemangiomas, and 71% had glaucoma (104).

Theories of Glaucoma Mechanism

The cause of glaucoma in the Sturge-Weber syndrome has been a controversial issue. Weiss (105) described two mechanisms, the more common of which occurs in infants, with a developmental anomaly of the anterior chamber angle similar to that of congenital glaucoma. One histopathologic report described a partial developmental anomaly of the anterior chamber angle (106), and another study revealed neovascularization in the trabecular meshwork (107). Cibis and associates (108) found aging changes, similar to those seen in chronic openangle glaucoma in the trabecular meshwork of three eyes with the Sturge-Weber syndrome.

The other mechanism of glaucoma appears later in life and is associated with an open anterior chamber angle and small arteriovenous fistulas in the episcleral vessels. Phelps (109) observed episcleral hemangiomas in all cases and elevated episcleral venous pressure whenever this parameter could be studied but saw no abnormalities of the anterior chamber angle. He thought that elevated episcleral venous pressure was the most common glaucoma mechanism in all ages of patients with the SturgeWeber syndrome.

Management

Medical therapy may suffice to control glaucoma that occurs in later life, whereas the infantile form usually requires surgical intervention (105). In most cases of glaucoma associated with elevated episcleral venous pressure, medical therapy has limited efficacy, and this appears to be true for prostaglandins (110). In one report, use of latanoprost was associated with development of an anterior uveal effusion (111). Success has been reported with a trabeculectomy in children and adults (112, 113). However, filtering surgery in these patients is associated with intraoperative choroidal effusion and occasionally with expulsive hemorrhage. In one study of 30 patients, goniotomy was not associated with these complications and was the investigator's first choice in most cases (113). Because whether the glaucoma is caused by an anterior chamber angle anomaly or elevated episcleral venous pressure is not certain, a combined trabeculotomy-trabeculectomy may improve the chances of success by treating both possible sources of elevated IOP (114, 115), although it does not reduce the potential for serious complications.

Some surgeons prefer to perform one or more prophylactic posterior sclerotomies just before filtration surgery or any other intraocular procedure to reduce the risk for choroidal or retinal effusion and expulsive hemorrhage. Another surgical approach to reduce pressure in these patients, while minimizing intraocular complications, is implantation of a valved or nonvalved glaucoma drainage device. One case series reported good outcomes after two-staged implantation of Baerveldt glaucoma drainage devices (116). In this situation, the Baerveldt implant is placed in the appropriate location; the tube is reflected to an adjacent subconjunctival location and anchored to sclera. Six weeks later, the tube is dissected free and inserted into the anterior chamber. A final technique that may be considered is a cyclodestructive procedure that avoids incisional surgery.

Von Recklinghausen Neurofibromatosis General Features

The principal systemic lesions in this condition involve the skin and include café-au-lait spots, which are flat, hyperpigmented lesions with well-circumscribed borders, and neurofibromas, which appear as soft, flesh-colored, pedunculated masses. The latter lesions arise from Schwann cells. Central nervous system involvement is uncommon, although neurofibromas may develop from cranial nerves, especially the acoustic nerve. Two subsets of neurofibromatosis have been distinguished: peripheral (von Recklinghausen neurofibromatosis), characterized by the skin lesions, and central, characterized by bilateral acoustic schwannomas (117). Both are inherited by an autosomal dominant mode with variable expressivity. Genetic analysis of a kindred with von Recklinghausen neurofibromatosis indicated that the responsible gene is located near the centromere on chromosome 17 (118).

Ocular Features

In the peripheral form, the eyelids, conjunctiva, iris, ciliary body, and choroid may be involved with the neurofibromas. The hamartomatous lesions of the iris are called Lisch nodules (119). They are usually bilateral and characterized by welldefined, clear to yellow or brown, dome-shaped, gelatinous elevations

on the iris stroma (Fig 21.8). An ultrastructural study indicates that they are of melanocytic origin (120). Lisch nodules are a nearly constant feature of von Recklinghausen neurofibromatosis, occurring in 92% of one series of 77 patients (121). In another study of 64 patients, the nodules were seen

P.325

in 95% and in all patients aged 16 years or older (122). Chorioretinal hamartomas and gliomas of the optic nerve are occasionally present. A fluorescein angiographic study of the choroidal lesions revealed avascular patches of hypofluorescence similar to multiple, small choroidal nevi (122). The central form of neurofibromatosis does not typically have ocular findings other than presenile posterior subcapsular or nuclear cataracts (117).

Figure 21.8 Slitlamp view of Lisch nodules on the iris of a patient with von Recklinghausen neurofibromatosis. (Courtesy of George Rosenwasser, MD.)

IOP elevation is more likely to occur in neurofibromatosis when the lids are involved with neurofibromas. Possible mechanisms of glaucoma include infiltration of the angle with neurofibromatous tissue, closure of the anterior chamber angle caused by nodular thickening of the ciliary body and choroid, fibrovascular membrane resembling neovascular glaucoma, and failure of normal anterior chamber angle development (123, 124).

Management

In treating the glaucoma, medical measures should be attempted first, because surgical approaches are often not satisfactory. An infant with unilateral glaucoma underwent five unsuccessful operations before ocular neurofibromatosis was discovered 2 years later (125).

Von Hippel-Lindau Disease

This phakomatosis is characterized by angiomatosis of the retina and, in a small percentage of cases, the cerebellum. Most cases are not familial. Glaucoma may occur as a late sequela of rubeosis iridis or iridocyclitis.

Nevus of Ota

The nevus of Ota (i.e., oculodermal melanocytosis) is not included in all reported classifications of the phakomatoses, but it does fit the broader definition of the disease group.

General Features

The hamartoma in this condition represents an abnormally large accumulation of melanocytes in ocular tissues, especially the episclera (Fig. 21.9), the skin in the distribution of the trigeminal nerve, and occasionally the nasal or buccal mucosa. In a study of 194 patients, 67 had only dermal involvement, 12 had only ocular involvement, and 115 had both (126). The condition is nearly always unilateral with a preponderance of females and a tendency toward races with darker pigmentation (127). Degeneration to malignant melanomas may occur in white patients but are rare in nonwhite patients (128).

Figure 21.9 Abnormal pigmentation of the episclera in a patient with oculodermal melanocytosis (nevus of Ota).

Glaucoma

Evidence of chronic glaucoma has been observed in patients with the nevus of Ota (129). Elevated IOP, with or without glaucomatous damage, was seen in 10% of cases in one series (124). The involved eye typically has unusually heavy pigmentation of the trabecular meshwork, and histopathologic studies have revealed melanocytes in the meshwork (130, 131).

Management

Medical management, as with other forms of open-angle glaucoma, should be tried first. If this fails, laser trabeculoplasty may be effective (96), although filtering surgery will most likely be required. Phakomatosis Pigmentovascularis

Phakomatosis pigmentovascularis represents an overlap syndrome with combined oculodermal vascular malformation (nevus flammeus, similar to Klippel-Trenaunay-Weber syndrome and Sturge-Weber syndrome) and oculodermal melanocytosis (132). It has only been described in Asian patients. Congenital glaucoma developed in all eyes that had 360-degree involvement of the episclera by the vascular malformation and melanocytosis. When one or both are present with only partial involvement, elevated IOP may develop later in life. Vascular malformation plays a more important role in the predisposition to glaucoma in these patients than does oculodermal melanocytosis.

KEY POINTS

Glaucoma secondary to intraocular tumor should be considered in all cases of unilateral or heavily

asymmetric glaucoma, particularly in the context of certain features: lack P.326

of response to IOP-lowering treatment, chronic pseudouveitis that is unresponsive to steroid treatment, iris heterochromia, unilateral pigment dispersion, serous retinal detachment with elevated IOP, dilated episcleral sentinel vessels, or media opacity precluding a good view of posterior segment.

In general, management of glaucoma related to intraocular malignant tumors involves treatment of the underlying tumor and managing IOP with medical therapy, cyclophotocoagulation, or both. Incisional glaucoma procedures, such as trabeculectomy and glaucoma drainage-device surgery, are contraindicated in most cases of intraocular malignant tumors. In refractory cases, enucleation may be the preferred option.

Primary malignant melanomas of the uvea may cause openangle forms of glaucoma by direct extension or seeding of tumor cells, pigment granules, or macrophages into the anterior chamber angle. Less often, these tumors may cause angle-closure glaucoma by a mass effect behind the iris or lens or via iris neovascularization.

Ultrasonography and cytology of aqueous aspirates are useful diagnostic adjuncts, and most confirmed cases are managed by enucleation. B-scan ultrasonography and UBM should be considered in all blind or painful eyes, particularly when a cloudy media prevents a clear view of the fundus and ciliary body region.

Systemic malignancies, including metastatic carcinomas and melanomas, leukemias, and lymphomas, may occasionally cause glaucoma, usually by invasion of the anterior chamber angle.

Ocular tumors of childhood that may cause glaucoma include retinoblastoma and medulloepithelioma.

Some of the phakomatoses—most notably Sturge-Weber syndrome, von Recklinghausen neurofibromatosis, and nevus of Ota—may also have a ssociated glaucoma.

REFERENCES

1.Radcliffe NM, Finger PT. Eye cancer related glaucoma: current concepts [review]. Surv Ophthalmol. 2009;54(1):47-73.

2.Shields CL, Shields JA, Shields MB, et al. Prevalence and mechanisms of secondary intraocular pressure elevation in eyes with intraocular tumors. Ophthalmology. 1987;94(7):839-846.

3.Yanoff M. Glaucoma mechanisms in ocular malignant melanomas. Am J Ophthalmol. 1970;70 (6):898-904.

4.Shields MB, Klintworth GK. Anterior uveal melanomas and intraocular pressure. Ophthalmology. 1980;87(6):503-517.

5.Demirci H, Shields CL, Shields JA, et al. Ring melanoma of the anterior chamber angle: a report of fourteen cases. Am J Ophthalmol. 2001;132(3):336-342.

6.Chaudhry IM, Moster MR, Augsburger JJ. Iris ring melanoma masquerading as pigmentary glaucoma. Arch Ophthalmol. 1997;115(11): 1480-1481.

7.Omulecki W, Pruszczynski M, Borowski J. Ring melanoma of the iris and ciliary body. Br J Ophthalmol. 1985;69(7):514-518.

8.Nguyen QD, Foster CS. Ciliary body melanoma masquerading as chronic uveitis. Ocul Immunol Inflamm. 1998;6(4):253-256.

9.Yanoff M, Scheie HG. Melanomalytic glaucoma. Report of a case. Arch Ophthalmol. 1970;84 (4):471-473.

10.Zakka KA, Foos RY, Sulit H. Metastatic tapioca iris melanoma. Br J Ophthalmol. 1979;63(11):744-

11.Reese AB, Mund ML, Iwamoto T. Tapioca melanoma of the iris. 1. Clinical and light microscopy studies. Am J Ophthalmol. 1972;74(5):840-850.

12.Shields MB, Proia AD. Neovascular glaucoma associated with an iris melanoma. A

clinicopathologic report. Arch Ophthalmol. 1987;105(5): 672-674.

13.Hopkins RE, Carriker FR. Malignant melanoma of the ciliary body. Am J Ophthalmol. 1958;45 (6):835-843.

14.Foos RY, Hull SN, Straatsma BR. Early diagnosis of ciliary body melanomas. Arch Ophthalmol. 1969;81(3):336-344.

15.Gupta K, Hoepner JA, Streeten BW. Pseudomelanoma of the iris in herpes simplex keratoiritis. Ophthalmology. 1986;93(12):1524-1527.

16.Shields JA, Sanborn GE, Augsburger JJ. The differential diagnosis of maignant melanoma of the iris. A clinical study of 200 patients. Ophthalmology. 1983;90(6):716-720.

17.el Baba F, Hagler WS, De la Cruz A, et al. Choroidal melanoma with pigment dispersion in vitreous and melanomalytic glaucoma. Ophthalmology. 1988;95(3):370-377.

18.Fraser DJ Jr, Font RL. Ocular inflammation and hemorrhage as initial manifestations of uveal malignant melanoma. Incidence and prognosis. Arch Ophthalmol. 1979;97(7):1311-1314.

19.Alward WL, Byrne SF, Hughes JR, et al. Dislocated lens nuclei simulating choroidal melanomas. Arch Ophthalmol. 1989;107(10):1463-1464.

20.Pavlin CJ, McWhae JA, McGowan HD, et al. Ultrasound biomicroscopy of anterior segment tumors. Ophthalmology. 1992;99(8):1220-1228.

21.Maberly DA, Pavlin CJ, McGowan HD, et al. Ultrasound biomicroscopic imaging of the anterior aspect of peripheral choroidal melanomas. Am J Ophthalmol. 1997;123(4):506-514.

22.Marigo FA, Finger PT, McCormick SA, et al. Iris and ciliary body melanomas: ultrasound biomicroscopy with histopathologic correlation. Arch Ophthalmol. 2000;118(11):1515-1521.

23.Marigo FA, Esaki K, Finger PT, et al. Differential diagnosis of anterior segment cysts by ultrasound biomicroscopy. Ophthalmology. 1999; 106(11):2131-2135.

24.Gitter KA, Meyer D, Sarin LK. Ultrasound to evaluate eyes with opaque media. Am J Ophthalmol. 1967;64(1):100-113.

25.Christiansen JM, Wetzig PC, Thatcher DB, et al. Diagnosis and management of anterior uveal tumors. Ophthalmic Surg. 1979;10(1):81-88.

26.Brovkina AF, Chichua AG. Value of fluorescein iridography in diagnosis of tumours of the iridociliary zone. Br J Ophthalmol. 1979;63(3):157-160.

27.Jakobiec FA, Depot MJ, Henkind P, et al. Fluorescein angiographic patterns of iris melanocytic tumors. Arch Ophthalmol. 1982;100(8): 1288-1299.

28.Char DH, Schwartz A, Miller TR, et al. Ocular metastases from systemic melanoma. Am J Ophthalmol. 1980;90(5):702-707.

29.Green WR. Diagnostic cytopathology of ocular fluid specimens. Ophthalmology. 1984;91(6):726-

30.Midena E, Segato T, Piermarocchi S, et al. Fine needle aspiration biopsy in ophthalmology. Surv Ophthalmol. 1985;29(6):410-422.

31.Karcioglu ZA, Caldwell DR. Frozen section diagnosis in ophthalmic surgery. Surv Ophthalmol. 1984;28(4):323-332.

32.Barr CC, McLean IW, Zimmerman LE. Uveal melanoma in children and adolescents. Arch Ophthalmol. 1981;99(12):2133-2136.

33.Rones B, Zimmerman LE. The prognosis of primary tumors of the iris treated by iridectomy. Arch Ophthalmol. 1958;60(2):193-205.

34.Dunphy EB, Dryja TP, Albert DM, et al. Melanocytic tumor of the anterior uvea. Am J Ophthalmol. 1978;86(5):680-683.

35.Geisse LJ, Robertson DM. Iris melanomas. Am J Ophthalmol. 1985; 99(6):638-648.

36.Shields CL, Shields JA, Materin M, et al. Iris melanoma: risk factors for metastasis in 169 consecutive patients. Ophthalmology. 2001; 108(1):172-178.

37.Territo C, Shields CL, Shields JA, et al. Natural course of melanocytic tumors of the iris. Ophthalmology. 1988;95(9):1251-1255.

38.Charteris DG. Progression of an iris melanoma over 41 years. Br J Ophthalmol. 1990;74(9):566-567.

39.Memmen JE, McLean IW. The long-term outcome of patients undergoing iridocyclectomy. Ophthalmology. 1990;97(4):429-432.

40.Finger PT. Plaque radiation therapy for malignant melanoma of the iris and ciliary body. Am J Ophthalmol. 2001;132(3):328-335.

41.Zimmerman LE, McLean IW, Foster WD. Statistical analysis of follow-up data concerning uveal melanomas, and the influence of enucleation. Ophthalmology. 1980;87(6):557-564.

42.Kramer KK, La Piana FG, Whitmore PV. Enucleation with stabilization of intraocular pressure in the treatment of uveal melanomas. Ophthalmic Surg. 1980;11(1):39-43.

P.327

43.Blair CJ, Guerry RK, Stratford TP. Normal intraocular pressure during enucleation for choroidal melanoma. Arch Ophthalmol. 1983;101(12): 1900-1902.

44.Migdal C. Effect of the method of enucleation on the prognosis of choroidal melanoma. Br J Ophthalmol. 1983;67(6):385-388.

45.McGalliard JN, Johnston PB. A study of iris melanoma in Northern Ireland. Br J Ophthalmol. 1989;73(8):591-595.

46.Cleasby GW, Van Westenbrugge JA. Treatment of iris melanoma by photocoagulation: a case report. Ophthalmic Surg. 1987;18(1):42-44.

47.Grossniklaus HE, Brown RH, Stulting RD, et al. Iris melanoma seeding through a trabeculectomy site. Arch Ophthalmol. 1990;108(9):1287-1290.

48.Bloch RS, Gartner S. The incidence of ocular metastatic carcinoma. Arch Ophthalmol. 1971;85 (6):673-675.

49.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(6):788-793.

50.Foulds WS, Lee WR. The significance of glaucoma in the management of melanomas of the anterior segment. Trans Ophthalmol Soc UK. 1983;103(pt 1):59-63.

51.Scholz R, Green WR, Baranano EC, et al. Metastatic carcinoma to the iris. Diagnosis by aqueous paracentesis and response to irradiation and chemotherapy. Ophthalmology. 1983;90(12):1524-1527.

52.Ferry AP, Font RL. Carcinoma metastatic to the eye and orbit. I. A clinicopathologic study of 227 cases. Arch Ophthalmol. 1974;92(4):276-286.

53.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):472-482.

54.Johnson BL. Bilateral glaucoma caused by nasal carcinoma obstructing schlemm's canal. Am J Ophthalmol. 1983;96(4):550-552.

55.Wormald RP, Harper JI. Bilateral black hypopyon in a patient with self-healing cutaneous malignant melanoma. Br J Ophthalmol. 1983; 67(4):231-235.

56.Abramson A. Anterior chamber activity in children with acute leukemia. Ann Ophthalmol. 1980;12:553-556.

57.Ohkoshi K, Tsiaras WG. Prognostic importance of ophthalmic manifestations in childhood leukaemia. Br J Ophthalmol. 1992;76(11):651-655.

58.Rennie I. Ophthalmic manifestations of childhood leukaemia. Br J Ophthalmol. 1992;76(11):641.

59.Novakovic P, Kellie SJ, Taylor D. Childhood leukaemia: relapse in the anterior segment of the eye. Br J Ophthalmol. 1989;73(5):354-359.

60.Leonardy NJ, Rupani M, Dent G, et al. Analysis of 135 autopsy eyes for ocular involvement in leukemia. Am J Ophthalmol. 1990;109(4):436^44.

61.Kozlowski IM, Hirose T, Jalkh AE. Massive subretinal hemorrhage with acute angle-closure glaucoma in chronic myelocytic leukemia. Am J Ophthalmol. 1987;103(6):837-838.

62.Saga T, Ohno S, Matsuda H, et al. Ocular involvement by a peripheral T-cell lymphoma. Arch Ophthalmol. 1984;102(3):399-402.

63.Epstein DL, Grant WM. Secondary open-angle glaucoma in histiocytosis X. Am J Ophthalmol.

1977;84(3):332-336.

64.Moore AT, Pritchard J, Taylor DS. Histiocytosis X: an ophthalmological review. Br J Ophthalmol. 1985;69(1):7-14.

65.Shakin EP, Augsburger JJ, Eagle RC Jr, et al. Multiple myeloma involving the iris. Arch Ophthalmol. 1988;106(4):524-526.

66.Smith DL, Skuta GL, Trobe JD, et al. Angle-closure glaucoma as initial presentation of myelodysplastic syndrome. Can J Ophthalmol. 1990; 25(6):306-308.

67.Wohlrab TM, Pleyer U, Rohrbach JM, et al. Sudden increase in intraocular pressure as an initial manifestation of myelodysplastic syndrome. Am J Ophthalmol. 1995;119(3):370-372.

68.Yoshizumi MO, Thomas JV, Smith TR. Glaucoma-inducing mechanisms in eyes with retinoblastoma. Arch Ophthalmol. 1978;96(1):105-110.

69.Ellsworth RM. The practical management of retinoblastoma. Trans Am Ophthalmol Soc. 1969;67:462-534.

70.Pe'er J, Neufeld M, Baras M, et al. Rubeosis iridis in retinoblastoma. Histologic findings and the possible role of vascular endothelial growth factor in its induction. Ophthalmology. 1997;104(8):12511258.

71.Haik BG, Dunleavy SA, Cooke C, et al. Retinoblastoma with anterior chamber extension. Ophthalmology. 1987;94(4):367-370.

72.Roberts CW, Iwamoto M, Haik BC. Ultrastructural correlation of specular microscopy in retinoblastoma. Am J Ophthalmol. 1986; 102(2):182-187.

73.Moazed K, Albert D, Smith TR. Rubeosis iridis in “pseudogliomas”. Surv Ophthalmol. 1980;25 (2):85-90.

74.Shields JA. Ocular toxocariasis. A review. Surv Ophthalmol. 1984;28(5): 361-381.

75.Spaulding G. Rubeosis iridis in retinoblastoma and pseudoglioma. Trans Am Ophthalmol Soc. 1978;76:584-609.

76.Shields CL, Shields JA, Cater J, et al. Plaque radiotherapy for retinoblastoma: long-term tumor control and treatment complications in 208 tumors. Ophthalmology. 2001;108(11):2116-2121.

77.Broughton WL, Zimmerman LE. A clinicopathologic study of 56 cases of intraocular medulloepitheliomas. Am J Ophthalmol. 1978;85(3):407-418.

78.Jakobiec FA, Howard GM, Ellsworth RM, et al. Electron microscopic diagnosis of medulloepithelioma. Am J Ophthalmol. 1975;79(2):321-329.

79.Wilson ME, McClatchey SK, Zimmerman LE. Rhabdomyosarcoma of the ciliary body. Ophthalmology. 1990;97(11):1484-1488.

80.Bruner WE, Stark WJ, Green WR. Presumed juvenile xanthogranuloma of the iris and ciliary body in an adult. Arch Ophthalmol. 1982; 100(3):457-459.

81.Casteels I, Olver J, Malone M, et al. Early treatment of juvenile xanthogranuloma of the iris with subconjunctival steroids. Br J Ophthalmol. 1993;77(1):57-60.

82.Jakobiec FA, Silbert G. Are most iris “melanoma s” really nevi? A clinicopathologic study of 189 lesions. Arch Ophthalmol. 1981;99(12): 2117-2132.

83.Harbour JW, Augsburger JJ, Eagle RC Jr. Initial management and follow-up of melanocytic iris tumors. Ophthalmology. 1995;102(12):1987-1993.

84.Nik NA, Hidayat A, Zimmerman LE, et al. Diffuse iris nevus manifested by unilateral open angle glaucoma. Arch Ophthalmol. 1981;99(1): 125-127.

85.Carlson DW, Alward WL, Folberg R. Aggressive nevus of the iris with secondary glaucoma in a child. Am J Ophthalmol. 1995;119(3):367-368.

86.Scheie HG, Yanoff M. Iris nevus (Cogan-Reese) syndrome. A cause of unilateral glaucoma. Arch Ophthalmol. 1975;93(10):963-970.

87.Cogan DG, Reese AB. A syndrome of iris nodules, ectopic Descemet's membrane, and unilateral glaucoma. Doc Ophthalmol. 1969;26: 424-433.

88.Shields JA, Kline MW, Augsburger JJ. Primary iris cysts: a review of the literature and report of 62 cases. Br J Ophthalmol. 1984;68(3):152-166.

89.Vela A, Rieser JC, Campbell DG. The heredity and treatment of angleclosure glaucoma secondary to iris and ciliary body cysts. Ophthalmology. 1984;91(4):332-337.

90.Alward WL, Ossoinig KC. Pigment dispersion secondary to cysts of the iris pigment epithelium. Arch Ophthalmol. 1995;113(12):1574-1575.

91.Albert DL, Brownstein S, Kattleman BS. Mucogenic glaucoma caused by an epithelial cyst of the iris stroma. Am J Ophthalmol. 1992; 114(2):222-224.

92.Finger PT, McCormick SA, Lombardo J, et al. Epithelial inclusion cyst of the iris. Arch Ophthalmol. 1995;113(6):777-780.

93.Nakazawa M, Tamai M. Iris melanocytoma with secondary glaucoma. Am J Ophthalmol. 1984;97 (6):797-799.

94.Shields JA, Annesley WH Jr, Spaeth GL. Necrotic melanocytoma of iris with secondary glaucoma. Am J Ophthalmol. 1977;84(6):826-829.

95.Traboulsi EI, Maumenee IH. Bilateral melanosis of the iris. Am J Ophthalmol. 1987;103(1):115-

96.Goncalves V, Sandler T, O'Donnell FE Jr. Open angle glaucoma in melanosis oculi: response to laser trabeculoplasty. Ann Ophthalmol. 1985;17(1):33-36.

97.Lieb WE, Shields JA, Eagle RC Jr, et al. Cystic adenoma of the pigmented ciliary epithelium. Clinical, pathologic, and immunohistopathologic findings. Ophthalmology. 1990;97(11):1489-1493.

98.Doro S, Werblin TP, Haas B, et al. Fetal adenoma of the pigmented ciliary epithelium associated with persistent hyperplastic primary vitreous. Ophthalmology. 1986;93(10):1343-1350.

99.Zaidman GW, Johnson BL, Salamon SM, et al. Fuchs' adenoma affecting the peripheral iris. Arch Ophthalmol. 1983;101(5):771-773.

100.Shields CL, Shields JA, Cook GR, et al. Differentiation of adenoma of the iris pigment epithelium from iris cyst and melanoma. Am J Ophthalmol. 1985;100(5):678-681.

101.Shields JA, Augsburger JJ, Sanborn GE, et al. Adenoma of the irispigment epithelium. Ophthalmology. 1983;90(6):735-739.

102.Papale JJ, Akiwama K, Hirose T, et al. Adenocarcinoma of the ciliary body pigment epithelium in a child. Arch Ophthalmol. 1984;102(1):100-103.

103.Van der Hoeve J. Eye symptoms in phakomatoses. Trans Ophthalmol Soc UK. 1932;52:380-401.

104.Sullivan TJ, Clarke MP, Morin JD. The ocular manifestations of the Sturge-Weber syndrome. J Pediatr Ophthalmol Strabismus. 1992; 29(6):349-356.

105.Weiss DI. Dual origin of glaucoma in encephalotrigeminal haemangiomatosis. Trans Ophthalmol Soc UK. 1973;93(0):477-493.

P.328

106.Christensen GR, Records RE. Glaucoma and expulsive hemorrhage mechanisms in the SturgeWeber syndrome. Ophthalmology. 1979; 86(7):1360-1366.

107.Mwinula JH, Sagawa T, Tawara A, et al. Anterior chamber angle vascularization in Sturge-Weber syndrome. Report of a case. Graefes Arch Clin Exp Ophthalmol. 1994;232(7):387-391.

108.Cibis GW, Tripathi RC, Tripathi BJ. Glaucoma in Sturge-Weber syndrome. Ophthalmology. 1984;91(9):1061-1071.

109.Phelps CD. The pathogenesis of glaucoma in Sturge-Weber syndrome. Ophthalmology. 1978;85 (3):276-286.

110.Altuna JC, Greenfield DS, Wand M, et al. Latanoprost in glaucoma associated with Sturge-Weber syndrome: benefits and side-effects. J Glaucoma. 1999;8(3):199-203.

111.Sakai H, Sakima N, Nakamura Y, et al. Ciliochoroidal effusion induced by topical latanoprost in a patient with Sturge-Weber syndrome. Jpn J Ophthalmol. 2002;46(5) 553-555.

112.Ali MA, Fahmy IA, Spaeth GL. Trabeculectomy for glaucoma associated with Sturge-Weber syndrome. Ophthalmic Surg. 1990;21(5):352-355.

113.Iwach AG, Hoskins HD Jr, Hetherington J Jr, et al. Analysis of surgical and medical management of glaucoma in Sturge-Weber syndrome. Ophthalmology. 1990;97(7):904-909.