Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Офтальмология / Английские материалы / Ocular Pathology_6th edition_Yanoff, Sassani_2009

.pdf
Скачиваний:
0
Добавлен:
28.03.2026
Размер:
98.97 Mб
Скачать

Bibliography 661

Muir KW, Jin J, Freedman SF: Central corneal thickness and its relationship to intraocular pressure in children. Ophthalmology 111:2220,

2004

Mukesh BN, McCarty CA, Rait JL et al.: Five-year incidence of open-angle glaucoma: the visual impairment project. Ophthalmology

109:1047, 2002

Parsa CF, Silva ED, Sundin OH et al.: Redefining papillorenal syndrome: an underdiagnosed cause of ocular and renal morbidity. Oph-

thalmology 108:738, 2001

Racette L, Wilson MR, Zangwill LM et al.: Primary open-angle glau-

coma in blacks: a review. Surv Ophthalmol 48:295, 2003

Schumer RA, Podos SM: T he nerve of glaucoma! Arch Ophthalmol

112:37, 1994

Shih CY, Gra Zivin JS,Trokel SL et al.: Clinical significance of central corneal thickness in the management of glaucoma. Arch Ophthalmol

122:1270, 2004

Sullivan-Mee M, Halverson KD, Saxon GB et al.: T he relationship between central corneal thickness-adjusted intraocular pressure and

glaucomatous visual-field loss. Optometry 76:228, 2005

Tielsch JM, Katz J, Quigley HA et al.: Diabetes, intraocular pressure, and primary open-angle glaucoma in the Baltimore Eye Study. Oph-

thalmology 102:48, 1995

Tielsch JM, Sommer A, Katz J et al.: Racial variations in the prevalence

of primary open-angle glaucoma. JAMA 266:369, 1991

Toda Y, Tang S, Kashiwagi K et al.: Mutations in the optineurin gene in Japanese patients with primary open-angle glaucoma and normal

tension glaucoma. Am J Med Genet A 125:1, 2004

Tonnu PA, Ho T, Newson T et al.: T he influence of central corneal thickness and age on intraocular pressure measured by pneumotonometry, non-contact tonometry, the Tono-Pen XL, and Goldmann appla-

nation tonometry. Br J Ophthalmol 89:851, 2005

Varma R, Ying-Lai M, Francis BA et al.: Prevalence of open-angle glaucoma and ocular hypertension in Latinos: the Los Angeles Latino

Eye Study. Ophthalmology 111:1437, 2004

Walker JH, Buys Y, Trope G et al.: Association between corneal thickness, mean intraocular pressure, disease stability and severity, and cost of treatment in glaucoma: a Canadian analysis. Curr Med Res Opin

21:489, 2005

Whitson JT, Liang C, Godfrey DG et al.: Central corneal thickness in

patients with congenital aniridia. Eye Contact Lens 31:221, 2005 Wilensky J: Racial influences in glaucoma. Ann Ophthalmol 9:1545, 1977

Wolfs RCW, Borger PH, Ramrattan RS et al.: Changing views on open-angle glaucoma: definitions and prevalences: The Rotterdam

study. Invest Ophthalmol Vis Sci 41:3309, 2000

Wolfs RCW, Klaver CCW, Ramrattan RS et al.: Genetic risk of primary open-angle glaucoma: Population-based aggregation study. Arch Oph-

thalmol 116:1640, 1998

Wunderlich K, Golubnitschaja O, Pache M et al.: Increased plasma levels of 20S proteasome alpha-subunit in glaucoma patients: an

observational pilot study. Mol Vis 8:431–5.:431, 2002

Yagci R, Eksioglu U, Midillioglu I et al.: Central corneal thickness in primary open angle glaucoma, pseudoexfoliative glaucoma, ocular

hypertension, and normal population. Eur J Ophthalmol 15:324, 2005 Yamamoto T, Iwase A, Araie M et al.: The Tajimi Study report 2: preva-

lence of primary angle closure and secondary glaucoma in a Japanese

population. Ophthalmology 112:1661, 2005

Zeppieri M, Brusini P, Miglior S: Corneal thickness and functional damage in patients with ocular hypertension. Eur J Ophthalmol 15:196,

2005

Normal Outflow: Hypersecretion

Becker B, Keaky GR, Christensen RE: Hypersecretion glaucoma. Arch Ophthalmol 56:180, 1956

Impaired Outflow: Congenital Glaucoma

Alward WLM, Kwon YH, Kawase K et al.: Evaluation of optineurin sequence variations in 1048 patients with open-angle glaucoma. Am J

Ophthalmol 136:904, 2003

Angius A, De Giola E, Loi A et al.: A novel mutation in the GLCIA gene causes juvenile open-angle glaucoma in 4 families from the Italian region of Puglia. Arch Ophthalmol 116:793, 1998

Barkan O: Pathogenesis of congenital glaucoma: gonioscopic and anatomic observations of the anterior chamber in the normal eye and in

congenital glaucoma. Am J Ophthalmol 40:1, 1955

Bongers EM, Gubler MC, Knoers NV: Nail–patella syndrome. Over-

view on clinical and molecular findings. Pediatr Nephrol 17:703, 2002

Broughton WL, Fine BS, Zimmerman LE: Congenital glaucoma associated with a chromosomal defect: A histologic study. Arch Ophthalmol

99:481, 1981

Broughton WL, Rosenbaum KN, Beauchamp GR: Congenital glaucoma and other abnormalities associated with pericentric inversion of

chromosome 11. Arch Ophthalmol 101:594, 1983

Cibis GW, Tripathi RC: The di erential diagnosis of Descemet’s tears

(Haab’s striae) and posterior polymorphous dystrophy bands: A clini-

copathologic study. Ophthalmology 89:614, 1982

De BI, Walter M, Noel LP: Phenotypic variations in patients with a 1630 A > T point mutation in the PAX6 gene. Can J Ophthalmol

39:272, 2004

Descipio C, Schneider L, Young TL et al.: Subtelomeric deletions of chromosome 6p: molecular and cytogenetic characterization of three new cases with phenotypic overlap with Ritscher–Schinzel (3C) syn-

drome. Am J Med Genet A 134:3, 2005

Edward D, Al RA, Lewis RA et al.: Molecular basis of Peters anomaly

in Saudi Arabia. Ophthalmic Genet 25:257, 2004

Fine BS, Yano M: Ocular Histology: A Text and Atlas, 2nd edn. Hager-

stown, PA, Harper & Row, 1979:251

Hoskins HD, Sha er RN, Hetherington J: Anatomical classification of the developmental glaucomas. Arch Ophthalmol 102:1331, 1984

Hou JW: Long-term follow-up of Marshall–Smith syndrome: report of

one case. Acta Paediatr Taiwan 45:232, 2004

Johnson AT, Richards JE, Boehnke M et al.: Clinical phenotype of juvenile-onset primary open-angle glaucoma linked to chromosome

1q. Ophthalmology 103:808, 1996

Kakiuchi T, Isashiki Y, Nakao K et al.: A novel truncating mutation of cytochrome P4501B1 (CYP1B1) gene in primary infantile glaucoma.

Am J Ophthalmol 128:370, 1999

Kato R, Kishibayashi J, Shimokawa O et al.: Congenital glaucoma and Silver–Russell phenotype associated with partial trisomy 7q and

monosomy 15q. Am J Med Genet 104:319, 2001

Lee WB, Brandt JD, Mannis MJ et al.: Aniridia and Brachmann–de Lange syndrome: a review of ocular surface and anterior segment

findings. Cornea 22:178, 2003

Lichter PR, Richards JE, Boehnke M et al.: Juvenile glaucoma linked to the GLCIA gene on chromosome 1q in a Panamanian family. Am

J Ophthalmol 123:413, 1997

Mullaney PB, Risco JM, Teichmann K et al.: Congenital hereditary endothelial dystrophy associated with glaucoma. Ophthalmology

102:186, 1995

Payne MS, Nadell JM, Lacassie Y et al.: Congenital glaucoma and neurofibromatosis in a monozygotic twin: case report and review of the

literature. J Child Neurol 18:504, 2003

Rezaie T, Child A, Hitchings R et al.: Adult-onset primary open-agnle glaucoma caused by mutations in optineurin. Science 295:1077,

2002

Richards JE, Lichter PR, Boehnke M et al.: Mapping of a gene for autosomal dominant juvenile-onset open-angle glaucoma to chromosome 1q. Am J Hum Genet 54:62, 1994

662 Ch. 16: Glaucoma

Smith JL, Stowe FR: The Pierre Robin syndrome (glossoptosis, micrognathia, cleft palate): A review of 39 cases with emphasis on associated

ocular lesions. Pediatrics 27:128, 1961

Stambolian D, Quinn G, Emanuel BS et al.: Congenital glaucoma associated with a chromosomal abnormality. Am J Ophthalmol 106:625,

1988

Sweeney E, Fryer A, Mountford R et al.: Nail patella syndrome: a review of the phenotype aided by developmental biology. J Med Genet 40:153,

2003

Taha D, Barbar M, Kanaan H et al.: Neonatal diabetes mellitus, congenital hypothyroidism, hepatic fibrosis, polycystic kidneys, and congenital glaucoma: a new autosomal recessive syndrome? Am J Med

Genet A 122:269, 2003

Toulement PJ, Urvoy M, Coscas G et al.: Association of congenital microcoria with myopia and glaucoma: A study of 23 patients with

congenital microcoria. Ophthalmology 102:186, 1995

Van BI, Alders M, Allanson J et al.: Lymphedema-lymphangiectasia- mental retardation (Hennekam) syndrome: a review. Am J Med Genet

112:412, 2002

Vemuganti GK, Sridhar MS, Edward DP et al.: Subepithelial amyloid deposits in congenital hereditary endothelial dystrophy: a histopatho-

logic study of five cases. Cornea 21:524, 2002

Vidaurri-de la CH, Tamayo-Sanchez L, Duran-McKinster C et al.:

Phakomatosis pigmentovascularis II A and II B: clinical findings in

24 patients. J Dermatol 30:381, 2003

Wiggs J, Auguste J, Allingham RR et al.: Lack of association of mutations in optineurin with disease in patients with adult-onset primary

open-angle glaucoma. Arch Ophthalmol 121:1181, 2003

Wiggs JL, Del Bono EA, Schuman JS et al.: Clinical features of five pedigrees genetically linked to the juvenile glaucoma locus on chromosome 1q21-q31. Ophthalmology 102:1782, 1995

Impaired Outflow: Primary Closed-Angle

Azuara-Blanco A, Spaeth GL, Araujo SV et al.: Plateau iris syndrome associated with multiple ciliary body cysts. Arch Ophthalmol 114:666,

1996

Bruno CA, Alward WL: Gonioscopy in primary angle closure glaucoma.

Semin Ophthalmol 17:59, 2002

Chandler PA: Narrow-angle glaucoma. Arch Ophthalmol 47:695, 1952 Chang BM, Liebmann JM, Ritch R: Angle closure in younger patients.

Trans Am Ophthalmol Soc 100:201, 212, 2002

Dielemans I, deJong PTVM, Stolk R et al.: Primary open-angle glaucoma, intraocular pressure, and diabetes mellitus in the general population: The Rotterdam study. Ophthalmology 103:1271, 1996

Fine BS, Yano M: Ocular Histology: A Text and Atlas, 2nd edn. Hager-

stown, PA, Harper & Row, 1979:251

Frasson M, Calixto N, Cronemberger S et al.: Oculodentodigital dysplasia: study of ophthalmological and clinical manifestations in three boys with probably autosomal recessive inheritance. Ophthalmic Genet

25:227, 2004

Fuchs J, Holm K, Vilhelmsen K et al.: Hereditary high hypermetropia

in the Faroe Islands. Ophthalmic Genet 26:9, 2005

Kerman BM, Christensen RE, Foos RY: Angle-closure glaucoma: A

clinicopathologic correlation. Am J Ophthalmol 76:887, 1973

Leung CK, Chan WM, Ko CY et al.: Visualization of anterior-chamber angle dynamics using optical coherence tomography. Ophthalmology

112:980, 2005

Sha er RN, Hoskins HD Jr: Ciliary block (malignant) glaucoma. Trans

Am Acad Ophthalmol Otolaryngol 85:215, 1978

Sihota R, Lakshmaiah NC, Walia KB et al.: The trabecular meshwork in acute and chronic angle closure glaucoma. Indian J Ophthalmol 49:255, 2001

Vasconcellos JP, Melo MB, Schimiti RB et al.: A novel mutation in the GJA1 gene in a family with oculodentodigital dysplasia. Arch Ophthal-

mol 123:1422, 2005

Wand M, Grant WM, Simmons RJ et al.: Plateau iris syndrome. Trans Am Acad Ophthalmol Otolaryngol 83:122, 1977

Impaired Outflow: Primary Open-Angle

Alvarado JA, Murphy CG: Outflow obstruction in pigmentary and primary open angle glaucoma. Arch Ophthalmol 110:1769,

1992

Alvarado JA, Yun AJ, Murphy CG: Juxtacanalicular tissue in primary open angle glaucoma and in nonglaucomatous normals. Arch Ophthal-

mol 104:1517, 1986

Alward WLM, Fingert JH, Coote MA et al.: Clinical features associated with mutations in the chromosome 1 open-angle glaucoma gene

(GLC1A). N Engl J Med 338:1022, 1998

Anderson DR: Glaucoma:The damage caused by pressure. XLVI Edward

Jackson Memorial Lecture. Am J Ophthalmol 108:485, 1989

Baird PN, Craig JE, Richardson AJ et al.: Analysis of 15 primary open-angle glaucoma families from Australia identifies a founder e ect for the Q368STOP mutation of myocilin. Hum Genet 112:110,

2003

Bhattacharya SK, Rockwood EJ, Smith SD et al.: Proteomics reveal Cochlin deposits associated with glaucomatous trabecular meshwork.

J Biol Chem 280:6080, 2005

Brubaker RF: Flow of aqueous humor in humans. Invest Ophthalmol Vis

Sci 32:3145, 1991

Caballero M, Borras T: Ine cient processing of an olfactomedindeficient myocilin mutant: potential physiological relevance to glau-

coma. Biochem Biophys Res Commun 282:662, 2001

Charlesworth JC, Dyer TD, Stankovich JM et al.: Linkage to 10q22 for maximum intraocular pressure and 1p32 for maximum cup-to-disc ratio in an extended primary open-angle glaucoma pedigree. Invest

Ophthalmol Vis Sci 46:3723, 2005

Dielemans I, deJong PTVM, Stolk R et al.: Primary open-angle glaucoma, intraocular pressure, and diabetes mellitus in the general population: The Rotterdam study. Ophthalmology 103:1271, 1996

Drance SM: Low-pressure glaucoma: Enigma and opportunity. Arch Ophthalmol 103:1131, 1985

Dunlop AA, Graham SL: Familial amyloidotic polyneuropathy presenting with rubeotic glaucoma. Clin Exp Ophthalmol 30:300, 2002

Fine BS: Observations on the drainage angle in man and rhesus monkey: A concept of the pathogenesis of chronic simple glaucoma. A light and electron microscopic study. Invest Ophthalmol 3:609, 1964

Fine BS, Yano M: Ocular Histology: A Text and Atlas, 2nd edn. Hagerstown, PA, Harper & Row, 1979:251

Fine BS, Yano M, Stone RA: A clinicopathologic study of four cases of primary open-angle glaucoma compared to normal eyes. Am J Oph-

thalmol 91:88, 1981

Fournier AV, Damjl KJ, Epstein DL et al.: Disc elevation in dominant optic atrophy: Di erentiation from normal tension glaucoma. Oph-

thalmology 108:1595, 2002

Fujiwara N, Matsuo T, Ohtsuki H: Protein expression, genomic structure, and polymorphisms of oculomedin. Ophthalmic Genet 24:141,

2003

Graul TA, Kwon YH, Zimmerman MB et al.: A case-control comparison of the clinical characteristics of glaucoma and ocular hypertensive patients with and without the myocilin Gln368Stop mutation. Am J

Ophthalmol 134:884, 2002

Huang EC, Barocas VH: Active iris mechanics and pupillary block: steady-state analysis and comparison with anatomical risk factors. Ann Biomed Eng 32:1276, 2004

Bibliography 663

Ishida K, Yamamoto T, Sugiyama K et al.: Disc hemorrhage is a significantly negative prognostic factor in normal-tension glaucoma. Am J

Ophthalmol 129:707, 2000

Ishikawa K, Funayama T, Ohtake Y et al.: Novel MYOC gene mutation, Phe369Leu, in Japanese patients with primary open-angle glaucoma detected by denaturing high-performance liquid chromatography.

J Glaucoma 13:466, 2004

Izzotti A: DNA damage and alterations of gene expression in chronic-

degenerative diseases. Acta Biochim Pol 50:145, 2003

Izzotti A, Sacca SC, Cartiglia C et al.: Oxidative deoxyribonucleic acid damage in the eyes of glaucoma patients. Am J Med 114:638,

2003

Jansson M, Marknell T, Tomic L et al.: Allelic variants in the MYOC/ TIGR gene in patients with primary open-angle, exfoliative glaucoma

and una ected controls. Ophthalmic Genet 24:103, 2003

Joe MK, Sohn S, Hur W et al.: Accumulation of mutant myocilins in ER leads to ER stress and potential cytotoxicity in human trabecular

meshwork cells. Biochem Biophys Res Commun 19:592, 2003

Jonas JB, Naumann GOH: Parapapillary retinal vessel diameter in normal and glaucoma eyes: 11. Correlations. Invest Ophthalmol Vis Sci 30:1604, 1989

Jonas JB, Xu L: Optic disk hemorrhages in glaucoma. Am J Ophthalmol

118:1, 1994

Jonas JB, Budde WM, Panda-Jones S: Ophthalmoscopic evaluation of

the optic nerve head. Surv Ophthalmol 43:293, 1999

Jonas JB, Nguyen XN, Naumann GOH: Parapapillary retinal vessel diameter in normal and glaucoma eyes: 1. Morphometric data. Invest

Ophthalmol Vis Sci 30:1599, 1989

Kanagavalli J, Krishnadas SR, Pandaranayaka E et al.: Evaluation and understanding of myocilin mutations in Indian primary open angle

glaucoma patients. Mol Vis 9:606, 2003

Kim BS, Savinova OV, Reedy MV et al.: Targeted disruption of the myocilin gene (Myoc) suggests that human glaucoma-causing muta-

tions are gain of function. Mol Cell Biol 21:7707, 2001

Liao SY, Ivanov S, Ivanova A et al.: Expression of cell surface transmembrane carbonic anhydrase genes CA9 and CA12 in the human eye: overexpression of CA12 (CAXII) in glaucoma. J Med Genet

40:257, 2003

Mackey DA, Healey DL, Fingert JH et al.: Glaucoma phenotype in pedigrees with the myocilin Thr377Met mutation. Arch Ophthalmol

121:1172, 2003

Melki R, Belmouden A, Brezin A et al.: Myocilin analysis by DHPLC in French POAG patients: increased prevalence of Q368X mutation.

Hum Mutat 22:179, 2003

Mitchell P, Cumming RG, Mackey DA: Inhaled corticosteroids, family history, and risk of glaucoma. Ophthalmology 106:2301, 1

999

Mitchell P, Smith W, Chey T et al.: Open-angle glaucoma and diabetes: The Blue Mountain Eye Study, Australia. Ophthalmology 104:712,

1997

Murphy CG, Johnson M, Alvarado JA: Juxtacanalicular tissue in pigmentary and primary open angle glaucoma. Arch Ophthalmol 110:1779,

1992

Nakabayashi M: Review of the ischemia hypothesis for ocular hypertension other than congenital glaucoma and closed-angle glaucoma. Oph-

thalmologica 218:344, 2004

Puska P, Lemmela S, Kristo P et al.: Penetrance and phenotype of the Thr377Met Myocilin mutation in a large Finnish family with juvenileand adult-onset primary open-angle glaucoma. Ophthalmic Genet

26:17, 2005

Rosman M, Aung T, Ang LP et al.: Chronic angle-closure with glaucomatous damage: long-term clinical course in a North American population and comparison with an Asian population. Ophthalmology 109:2227, 2002

Schulzer M, Drance SM, Carter CJ et al.: Biostatistical evidence for two distinct chronic open angle glaucoma populations. Br J Ophthalmol

74:196, 1990

Stone EM, Fingert JH, Alward WLM et al.: Identification of a gene

that causes primary open angle glaucoma. Science 275:668, 1997

Trifan OC, Traboulsi EI, Stoilova D et al.: A third locus (GLC1D) for adult-onset primary open-angle glaucoma maps to the 8q23 region.

Am J Ophthalmol 126:17, 1998

Trobe GE, Pavlin CJ, Baumal CR et al.: Malignant glaucoma: Clinical and ultrasound biomicroscopic features. Ophthalmology 101:1030,

1994

Wentz-Hunter K, Shen X, Okazaki K et al.: Overexpression of myocilin in cultured human trabecular meshwork cells. Exp Cell Res 297:39,

2004

Wirtz MK, Samples JR, Rust K et al.: GLC1F, a new primary openangle glaucoma locus, maps to 7q35-q36. Arch Ophthalmol 117:237, 1999

Impaired Outflow: Secondary Closed-Angle

Agrawal S, Agrawal J, Agrawal TP: Iridoschisis associated with lens

subluxation. J Cataract Refract Surg 27:2044, 2001

Alvarado JA, Murphy CG, Maglio M et al.: Pathogenesis of Chandler’s syndrome, essential iris atrophy and the Cogan–Reese syndrome: I. Alterations of the corneal endothelium. Invest Ophthalmol Vis Sci

27:853, 1986

Alvarado JA, Murphy CG, Juster RP et al.: Pathogenesis of Chandler’s syndrome, essential iris atrophy and the Cogan–Reese syndrome: II. Estimated age at disease onset. Invest Ophthalmol Vis Sci 27:873,

1986

Arthur SN, Mason J, Roberts B et al.: Secondary acute angle-closure glaucoma associated with vitreous hemorrhage after ruptured retinal

arterial macroaneurysm. Am J Ophthalmol 138:682, 2004

Azuara-Blanco A, Wilson RP, Eagle RC Jr et al.: Pseudocapsulorrhexis in a patient with iridocorneal endothelial syndrome. Arch Ophthalmol

117:397, 1999

Badlani VK, Quinones R, Wilensky JT et al.: Angle-closure glaucoma

in teenagers. J Glaucoma 12:198, 2003

Chandler PA: Atrophy of the stroma of the iris: endothelial dystrophy, corneal edema and glaucoma. Am J Ophthalmol 41:607, 1956

Colosi NJ, Yano M: Reactive corneal endothelialization. Am J Ophthal-

mol 83:219, 1977

Demirci H, Shields CL, Shields JA et al.: Di use iris melanoma: a

report of 25 cases. Ophthalmology 109:1553, 2002

Doe EA, Budnez DL, Gedde SJ et al.: Long-term surgical outcome of patients with glaucoma secondary to the iridocorneal endothelial syn-

drome. Ophthalmology 108:1789, 2001

Drysler RM: Central retinal vein occlusion and chronic simple glau-

coma. Arch Ophthalmol 73:659, 1965

Eagle RC Jr, Shields JA: Iridocorneal endothelial syndrome with contralateral guttate endothelial dystrophy: A light and electron micro-

scopic study. Ophthalmology 94:862, 1987

Eagle RC Jr, Font RL, Yano M et al.: Proliferative endotheliopathy with iris abnormalities: The iridocorneal endothelial syndrome. Arch

Ophthalmol 97:2104, 1979

Escalona-Benz E, Benz MS, Briggs JW et al.: Uveal melanoma presenting as acute glaucoma: report of two cases. Am J Ophthalmol 136:756,

2003

Gogos K, Tyradellis C, Spaulding AG et al.: Iris cyst simulating mela-

noma. J AAPOS 8:502, 2004

Goldberg DE, Freeman WR: Uveitic angle closure glaucoma in a patient with inactive cytomegalovirus retinitis and immune recovery uveitis. Ophthalmic Surg Lasers 33:421, 2002

664 Ch. 16: Glaucoma

Hirst LW, Bancroft J,Tamauchi K et al.: Immunohistochemical pathology of the corneal endothelium in iridocorneal syndrome. Invest Oph-

thalmol Vis Sci 36:820, 1995

Howell DN, Dammas T, Burchette JL Jr et al.: Endothelial metaplasia in the iridocorneal endothelial syndrome. Invest Ophthalmol Vis Sci

38:1896, 1997

Jakobiec FA, Yano M, Mottow L et al.: Solitary iris nevus with peripheral anterior synechias and iris endothelialization: A variant of the iris

nevus syndrome. Am J Ophthalmol 83:884, 1977

Khawly JA, Shields MB: Metastatic carcinoma manifesting as angle-

closure glaucoma. Am J Ophthalmol 118:1161, 1994

Lafaut BA, Loeys B, Leroy BP et al.: Clinical and electrophysiological findings in autosomal dominant vitreoretinochoroidopathy: report of a new pedigree. Graefes Arch Clin Exp Ophthalmol 239:575,

2001

Laganowski HC, Muir MGK, Hitchings RA: Glaucoma and the irido-

corneal endothelial syndrome. Arch Ophthalmol 110:346, 1992

Levy SG, Kirkness CM, Fickler L et al.: On the pathology of the iri- docorneal-endothelial syndrome: The ultrastructural appearances of

“subtotal-ICE.” Eye 9:318, 1995

Levy SG, McCartney ACE, Baghai MH et al.: Pathology of the iridocorneal syndrome: The ICE-cell. Invest Ophthalmol Vis Sci 36:2592,

1995

Lichter PR, Sha er RN: Interstitial keratitis and glaucoma. Am J Oph-

thalmol 68:241, 1969

Lucas-Glass TC, Baratz KH, Nelson LR et al.: The contralateral corneal endothelium in the iridocorneal endothelial syndrome. Arch Ophthal-

mol 115:40, 1997

Makley TA, Kapetansky FM: Iris nevus syndrome. Ann Ophthalmol

20:311, 1988

Naumann GOH: Yano -Syndrom. In Naumann GOH, ed: Pathologie

des Auges. Berlin, Springer, 1997:628

Rodrigues MM, Spaeth GL, Krachmer JH et al.: Iridoschisis associated with glaucoma and bullous keratopathy. Am J Ophthalmol 95:73,

1983

Rodrigues MM, Stulting RD, Waring GO III: Clinical, electron microscopic, and immunohistochemical study of the corneal endothelium and Descemet’s membrane in the iridocorneal endothelial syn-

drome. Am J Ophthalmol 101:16, 1986

Scheie HG, Yano M: Iris nevus (Cogan–Reese) syndrome: A cause of

unilateral glaucoma. Arch Ophthalmol 93:963, 1975

Scheie HG, Yano M, Kellogg WT: Essential iris atrophy: report of a

case. Arch Ophthalmol 94:1315, 1976

Srinivasan R, Kaliaperumal S, Dutta TK: Bilateral angle closure glau-

coma following snake bite. J Assoc Physicians India 53:46, 2005

Teekhasaenee C, Ritch R: Iridocorneal endothelial syndrome in Thai

patients: Clinical variations. Arch Ophthalmol 118:187, 2000

Tester RA, Durcan FJ, Mamalis N et al.: Cogan–Reese syndrome: Progressive growth of endothelium over iris. Arch Ophthalmol 116:1126, 1998

Yano M: Glaucoma mechanisms in ocular malignant melanomas. Am J Ophthalmol 70:898, 1970

Yano M: Iridocorneal endothelial syndrome: Unification of a disease

spectrum (editorial). Surv Ophthalmol 24:1, 1979

Yano M, Scheie HG, Allman MI: Endothelialization of filtering bleb

in iris–nevus syndrome. Arch Ophthalmol 94:1933, 1976

Zografos L, Mirimano RO, Angeletti CA et al.: Systemic melanoma metastatic to the retina and vitreous. Ophthalmologica 218:424, 2004

Impaired Outflow: Secondary Open-Angle

Alvarado JA, Murphy CG: Outflow obstruction in pigmentary and primary open angle glaucoma. Arch Ophthalmol 110:1769, 1992

Anderson MG, Smith RS, Hawes NL et al.: Mutations in genes encoding melanosomal proteins cause pigmentary glaucoma in DBA/2J

mice. Nat Genet 30:81, 2002

Bovell AM, Damji KF, Dohadwala AA et al.: Familial occurrence of

pigment dispersion syndrome. Can J Ophthalmol 36:11, 2001

Breingan PJ, Esaki K, Ishikawa H et al.: Iridolenticular contact decreases following laser iridotomy for pigment dispersion syndrome. Arch Oph-

thalmol 117:325, 1999

Cameron JD, Havener VR: Histologic confirmation of ghost cell glau-

coma by routine light microscopy. Am J Ophthalmol 96:251, 1983

Carlson DW, Alward WLM, Folberg R: Aggressive nevus of the iris with secondary glaucoma in a child. Am J Ophthalmol 119:367,

1995

Clark AF, Steely HT, Dickerson JE Jr et al.: Glucocorticoid induction of the glaucoma gene MYOC in human and monkey trabecular mesh-

work cells and tissues. Invest Ophthalmol Vis Sci 42:1769, 2001

Demirci H, Shields CL, Shields JA et al.: Ring melanoma of the ciliary body: report on twenty-three patients. Retina 22:698, 2002

Farrar SM, Shields MB: Current concepts in pigmentary glaucoma.

Surv Ophthalmol 37:233, 1993

Feibel RM, Perlmutter JC: Anisocoria in the pigmentary dispersion

syndrome. Am J Ophthalmol 110:657, 1990

Fine BS, Yano M, Scheie HG: Pigmentary “glaucoma”: A histologic

study. Trans Am Acad Ophthalmol Otolaryngol 78:314, 1974

Fineman MS, Eagle RC Jr, Shields JA et al.: Melanocytomalytic glaucoma in eyes with necrotic iris melanocytoma. Ophthalmology 105:402, 1998

Foulks GN, Shields MB: Glaucoma in oculodermal melanocytosis. Ann

Ophthalmol 9:1299, 1977

Greenstein VC, Seiple W, Liebmann J et al.: Retinal pigment epithelial dysfunction in patients with pigment dispersion syndrome. Arch Oph-

thalmol 119:1291, 2001

Harris GJ, Rice PR: Angle closure in carotid-cavernous fistula. Ophthalmology 86:1521, 1979

Kozart DM, Yano M: Intraocular pressure status in 100 consecutive

patients with exfoliation syndrome. Ophthalmology 89:214, 1982 Lichter PR, Sha er RN: Interstitial keratitis and glaucoma. Am J Oph-

thalmol 68:241, 1969

Mardein CY, Küchle M, Nguyen NX et al.: Quantification of aqueous melanin granules, intraocular pressure and glaucomatous damage in primary pigment dispersion syndrome. Ophthalmology 107:435, 2000 McMenamin PG, Lee WR: Ultrastructural pathology of melanomalytic

glaucoma. Br J Ophthalmol 70:895, 1986

Micheli T, Cheung LM, Sharma S et al.: Acute haptic-induced pigmentary glaucoma with an AcrySof intraocular lens. J Cataract Refract Surg

28:1869, 2002

Murphy CG, Johnson M, Alvarado JA: Juxtacanalicular tissue in pigmentary and primary open angle glaucoma. Arch Ophthalmol 110:1779,

1992

Pavlin CJ, Harasiewicz K, Foster FS: Posterior iris bowing in pigmentary dispersion syndrome caused by accommodation. Am J Ophthalmol

118:114, 1994

Phelps CD, Watzke RC: Hemolytic glaucoma. Am J Ophthalmol 80:690,

1975

Potash SD, Tello C, Liebmann J et al.: Ultrasound biomicroscopy in pigment dispersion syndrome. Ophthalmology 101:332, 1994

Raitta C, Vannas A: Glaucomatocyclitic crisis. Arch Ophthalmol 95:608,

1977

Rich R, Mudumbai R, Liebman JM: Combined exfoliation and pigment dispersion: Paradigm of an overlap syndrome. Ophthalmology 107:1004,

2000

Richards JE, Lichter PR, Herman S et al.: Probable exclusion of GLC1A as a candidate glaucoma gene in a family with middle-age- onset open-angle glaucoma. Ophthalmology 103:1035, 1996

Bibliography 665

Ritch R: A unification hypothesis of pigment dispersion syndrome. Trans

Am Ophthalmol Soc 94:405, 1996

Ritch R, Steinberger D, Liebmann JM: Prevalence of pigment dispersion syndrome in a population undergoing glaucoma screening. Am J

Ophthalmol 115:707, 1993

Santos C: Herpes simplex uveitis. Bol Asoc Med P R 96:71, 2004 Scheie HG, Cameron JD: Pigment dispersion syndrome: A clinical

study. Br J Ophthalmol 65:264, 1981

Semple HC, Ball SF: Pigmentary glaucoma in the black population. Am

J Ophthalmol 109:518, 1990

Siegner SW, Netland PA: Optic disc hemorrhages and progression of

glaucoma. Ophthalmology 103:1014, 1996

Sokol J, Stegman Z, Liebmann JM et al.: Location of the iris insertion

in pigment dispersion syndrome. Ophthalmology 103:289, 1996 Teichmann KD, Karcioglu ZA: Melanocytoma of the iris with rapidly

developing secondary glaucoma. Surv Ophthalmol 40:136, 1995 Wentz-Hunter K, Shen X, Yue BY: Distribution of myocilin, a glaucoma

gene product, in human corneal fibroblasts. Mol Vis 9:308–14:308,

2003

Yamamoto S, Pavan-Langston D, Yamamoto R et al.: Possible role of herpes simplex virus in the origin of Posner–Schlossman syndrome.

Am J Ophthalmol 119:796, 1995

Yano M: Glaucoma mechanisms in ocular malignant melanomas. Am J Ophthalmol 70:898, 1970

Yano M: In discussion of Ritch R: A unification hypothesis of pigment

dispersion syndrome. Trans Am Ophthalmol Soc 94:405, 1996

Yano M, Scheie HG: Cytology of human lens aspirate and its relationship to phacolytic glaucoma and phacoanaphylactic endophthalmitis.

Arch Ophthalmol 80:166, 1968

Yano M, Scheie HG: Melanomalytic glaucoma: Report of patient. Arch Ophthalmol 84:471, 1970

Tissue Changes Caused by Elevated

Intraocular Pressure

Agapova OA, Ricard CS, Salvador-Silva M et al.: Expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in

human optic nerve head astrocytes. Glia 33:205, 2001

Agapova OA, Yang P, Wang WH et al.: Altered expression of 3 alphahydroxysteroid dehydrogenases in human glaucomatous optic nerve

head astrocytes. Neurobiol Dis 14:63, 2003

Albert DM, Gangnon RE, Zimbric ML et al.: A study of iridectomy histopathologic features of latanoprostand non-latanoprost-treated

patients. Arch Ophthalmol 122:1680, 2004

Aung T, Okada K, Poinoosawmy D et al.: T he phenotype of normal tension glaucoma patients with and without OPA1 polymorphisms.

Br J Ophthalmol 87:149, 2003

Beck RW, Messner DK, Musch DC et al.: Is there a racial di erence in

physiologic cup size? Ophthalmology 92:873, 1985

Brownstein S, Font RL, Zimmerman LE et al.: Nonglaucomatous cavernous degeneration of the optic nerve: Report of two cases. Arch

Ophthalmol 98:354, 1980

Caprioli J, Ortiz-Colberg R, Miller JM et al.: Measurements of peripapillary nerve fiber layer contour in glaucoma. Am J Ophthalmol

108:404, 1989

Carelli V, Ross-Cisneros FN, Sadun AA: Mitochondrial dysfunction as a cause of optic neuropathies. Prog Retin Eye Res 23:53, 2004

Colosi NJ, Yano M: Reactive corneal endothelialization. Am J Ophthal-

mol 83:219, 1977

Farkas RH, Chowers I, Hackam AS et al.: Increased expression of ironregulating genes in monkey and human glaucoma. Invest Ophthalmol Vis Sci 45:1410, 2004

Giovannini A, Amato G, Mariotti C: The macular thickness and volume in glaucoma: an analysis in normal and glaucomatous eyes using OCT.

Acta Ophthalmol Scand Suppl 236:34, 2002

Guo L, Moss SE, Alexander RA et al.: Retinal ganglion cell apoptosis in glaucoma is related to intraocular pressure and IOP-induced e ects

on extracellular matrix. Invest Ophthalmol Vis Sci 46:175, 2005 Healey PR, Mitchell P: Visibility of lamina cribrosa pores and open-

angle glaucoma. Am J Ophthalmol 138:871, 2004

Hernandez MR, Agapova OA, Yang P et al.: Di erential gene expression in astrocytes from human normal and glaucomatous optic nerve

head analyzed by cDNA microarray. Glia 38:45, 2002

Hernandez MR, Andrzejewska WM, Neufeld AH: Changes in the extracellular matrix of the human optic nerve head in primary open-

angle glaucoma. Am J Ophthalmol 109:180, 1990

Jonas JB, Fernàndez MC, Naumann GOH: Glaucomatous parapapillary atrophy. Arch Ophthalmol 110:214, 1992

Jonas JB, Naumann GOH: Parapapillary chorioretinal atrophy in

normal and glaucoma eyes. Invest Ophthalmol Vis Sci 30:919, 1989

Jonas JB, Fernàndez MC, Naumann GOH: Parapapillary atrophy and retinal vessel diameter in nonglaucomatous optic nerve damage. Invest

Ophthalmol Vis Sci 32:2942, 1991

Jonas JB, Nguyen NX, Gusek GC et al.: Parapapillary chorioretinal atrophy in normal and glaucoma eyes. Invest Ophthalmol Vis Sci 30:908,

1989

Jonas JB, Nguyen NX, Naumann GOH: The retinal nerve fiber layer in

normal eyes. Ophthalmology 96:627, 1989

Jonas JB, Schmidt AM, Müller-Bergh JA et al.: Human optic nerve fiber count and optic disc size. Invest Ophthalmol Vis Sci 33:2012,

1992

Kendell KR, Quigley HA, Kerrigan LA et al.: Primary open-angle glaucoma is not associated with photoreceptor loss. Invest Ophthalmol Vis

Sci 36:200, 1995

Kubota T, Naumann GOH: Reduction in number of corpora amylacea with advancing histological changes of glaucoma. Graefes Arch Clin

Exp Ophthalmol 231:249, 1993

Kubota T, Holbach LM, Naumann GOH: Corpora amylacea in glaucomatous and non-glaucomatous optic nerve and retina. Graefes Arch

Clin Exp Ophthalmol 231:7, 1993

Kuehn MH, Fingert JH, Kwon YH: Retinal ganglion cell death in glaucoma: mechanisms and neuroprotective strategies. Ophthalmol

Clin North Am 18:383, 2005

Lin HJ, Chen WC, Tsai FJ et al.: Distributions of p53 codon 72 polymorphism in primary open angle glaucoma. Br J Ophthalmol 86:767,

2002

Ljubimov AV, Burgeson RE, Butkowski RJ et al.: Extracellular matrix alterations in human corneas with bullous keratopathy. Invest Ophthal-

mol Vis Sci 37:997, 1996

May CA, Lutjen-Drecoll E: Choroidal ganglion cell changes in human

glaucomatous eyes. J Glaucoma 13:389, 2004

McKinnon SJ, Lehman DM,Tahzib NG et al.: Baculoviral IAP repeat- containing-4 protects optic nerve axons in a rat glaucoma model. Mol

Ther 5:780, 2002

Miller KM, Quigley HA: The clinical appearance of the lamina cribrosa as a function of the extent of glaucomatous optic nerve damage. Oph-

thalmology 95:135, 1988

Radius RL: Anatomy of the optic nerve head and glaucomatous optic

neuropathy. Surv Ophthalmol 32:35, 1987

Ricard CS, Agapova OA, Salvador-Silva M et al.: Expression of myocilin/TIGR in normal and glaucomatous primate optic nerves. Exp Eye Res 73:433, 2001

Schnabel J: Die Entwicklungsgeschichte der glaukomatosen Exkavation.

Z Augenheilkd 14:1, 1905

Shin DH, Bielik M, Hong YJ et al.: Reversal of glaucomatous optic disc cupping in adult patients. Arch Ophthalmol 107:1599, 1989

666 Ch. 16: Glaucoma

Tan JC, Hitchings RA: Reversal of disc cupping after intraocular pres-

sure reduction in topographic image series. J Glaucoma 13:351, 2004

Votruba M, Thiselton D, Bhattacharya SS: Optic disc morphology of patients with OPA1 autosomal dominant optic atrophy. Br J Ophthalmol 87:48, 2003

Wax MB, Tezel G: Neurobiology of glaucomatous optic neuropathy: diverse cellular events in neurodegeneration and neuroprotection. Mol Neurobiol 26:45, 2002

Wax MB, Tezel G, Edward PD: Clinical and ocular histopathologic findings in a patient with normal-pressure glaucoma. Arch Ophthalmol

116:993, 1998

Wu SC, Huang SC, Kuo CL et al.: Reversal of optic disc cupping after trabeculotomy in primary congenital glaucoma. Can J Ophthalmol

37:337, 2002

Yang P, Agapova O, Parker A et al.: DNA microarray analysis of gene expression in human optic nerve head astrocytes in response to hydrostatic pressure. Physiol Genomics 17:157, 2004

17

Ocular Melanocytic Tumors

NORMAL ANATOMY

Ocular Melanocytes

I.Conjunctival and uveal melanocytes (Fig. 17.1; see also Fig.

17.29D, top) are derived from the neural crest; pigment epithelial cells (PE) are derived from neuroepithelium or

the layers of the optic cup.

II. Dermal and conjunctival melanocytes are solitary dendritic cells.

III.Uveal melanocytes are also solitary and dendritic, and their cytoplasm contains fine, dustlike, ovoid melanin granules of a size bordering on the limits of resolution of the light microscope.

Cultured human melanocytes from different-colored eyes can produce melanin in vivo. The color of the iris is determined by the density of melanocytes in the most anterior portion of the iris.

IV. Pigment epithelium is neither solitary nor dendritic, but is epithelial, and exists as a sheet of cuboidal cells containing large, easily visualized pigment granules.

The cytoplasm of PE cells contains two basic types of pigment granules: melanin granules, which are either ovoid or spherical, and lipofuscin granules, which are usually somewhat spherical.

V.Dermal, conjunctival, and uveal melanocytes tend to vary in size, number, and melanin content among the races.

VI. Normal PE tends to vary little, if at all, among the races, and always appears heavily pigmented.

VII. Dermal, conjunctival, and uveal melanocytes almost never undergo reactive (nonneoplastic) proliferation under

normal circumstances. Neoplastic proliferation, however, does occur.

VIII. The PE readily undergoes reactive proliferation, but rarely becomes neoplastic.

IX. Dysplastic nevus syndrome is associated with an increased prevalence of conjunctival nevi, iris nevi, iris freckles, and choroidal nevi. It has been postulated that such individuals may have overstimulation of the melanocytic system not only in the skin, but also in ocular tissues, possibly increasing the risk for melanocytic malignancies.

MELANOTIC TUMORS OF EYELIDS

Ephelis (Freckle)

I.An ephelis (freckle) is a brown, circumscribed macule normally only found on areas of skin exposed to sunlight.

II.The color is due to increased pigmentation in the basal cell layer of the epidermis. The pigment (melanin) is derived

from hyperactive melanocytes that “secrete” their pigment into epidermal basal cells.

III.The melanocytes are fewer in number, but larger and more functionally active than those in adjacent, surrounding, paler epidermis.

Lentigo

I.Lentigo

A.Lentigo is similar clinically to an ephelis but is somewhat larger.

B.In addition to hyperpigmentation of the basal cell layer of epithelium, increased numbers of melanocytes are

668 Ch. 17: Ocular Melanocytic Tumors

A B

C D

Fig. 17.1 Ocular melanocytes. Normally, the epidermal melanocytes appear in hematoxylin and eosin-stained sections as clear cells wedged between basal epithelial cells. Melanin is transferred by the dendritic processes of the melanocytes to the basal keratocytes, where it is stored and later degraded. A, In this tangential section of “reactive” epidermis, the usually clear melanocytes contain pigment around their nuclei and in their dendritic processes, making them easily visible (see Fig. 1.26C). B, A flat preparation of retinal pigment epithelium (RPE) of owl monkey shows the epithelial sheet configuration. RPE cells have a basement membrane (inner or cuticular portion of Bruch’s membrane) and are attached to one another near their apexes by terminal bars that contain “tight junctions.” C, Cross-section of the retina and choroid compares the epithelial nature of RPE with the nonepithelial individual and solitary choroidal melanocytes. The RPE cells have larger pigment granules than the choroidal melanocytes (see Fig. 9.2C). D, Thin section shows RPE pigment granules are considerably larger than those in choroidal melanocytes. Large nonpigmented cells in choroid (center toward bottom) are probably ganglion cells.

present. It may also be found on nonexposed skin in older people.

C.Multiple lentigines syndrome

1.Multiple lentigines syndrome also goes by the acronym LEOPARD (lentigines, multiple; electrocardiographic conduction defects; ocular hypertelorism; pulmonary stenosis; abnormal genitalia;

retardation of growth; and deafness, sensorineural).

2. In addition to ocular hypertelorism (occurring in 40% of patients), other ocular findings include ptosis; microcornea; cortical punctate lenticular opacities and anterior subcapsular and zonular cataracts; patches of myelinated nerve fibers; flat pigmented spots of the iris; and glaucoma.

Multiple lentigines also occur in Carney’s syndrome (complex; see p. 244 in Chapter 7). Carney’s syndrome has

an autosomal-dominant inheritance pattern and consists of bilateral, primary, pigmented, nodular adrenocortical hyperplasia; multiple lentigines, especially of the head and neck, and blue nevi; cutaneous myxomata; large cell, calcifying Sertoli’s cell tumor of testes; cardiac myxoma; myxoid fibroadenomas of breast; pituitary tumors (which may lead to Cushing’s syndrome); and melanotic schwannomas.

D.Lentigo maligna (melanotic freckle of Hutchinson; circumscribed precancerous melanosis of Dubreuilh; Fig. 17.2)

1.Lentigo maligna occurs as an acquired pigmented lesion, mostly in adults older than 50 years of age.

2.It appears as a brown or black flat lesion, usually on the face, sometimes with involvement of the eyelids and conjunctiva (see subsection Primary Acquired

Melanosis in section Melanotic Tumors of Conjunc-

Melanotic tumors of eyelids 669

Fig. 17.2 Lentigo maligna (Hutchinson’s freckle). A, Clinical appearance of acquired pigmented lesion of the left lower lid. B, Histologic section shows nevus cells in the junctional location, indistinguishable from a junctional nevus. (Case presented by Dr. VB Bernardino, Jr to the meeting of the

Eastern Ophthalmic Pathology Society, 1975.)

tiva, later), enlarging slowly in an irregular manner.

3.Approximately one-third of all lentigo maligna eventuates in malignant melanoma, noted clinically by a thickening or infiltration that elevates into a papule or nodule.

Lentigo maligna melanoma is the most common type of melanoma of the eyelid.

4.Histologically, lentigo maligna is indistinguishable from a junctional nevus. An underlying, chronic, nongranulomatous inflammatory infiltrate is common.

Nevus*

I.General information

A.A nevus is a congenital, hamartomatous tumor, a flat or elevated, usually well-circumscribed lesion.

1.It may be pigmented early in life, or not until puberty or even early adulthood.

2.The nevus is composed of nevus cells that are atypical but benign-appearing dermal melanocytes.

Congenital melanocytic nevus has occurred in association with ankyloblepharon. This lesion may be explained by a failure of eyelid separation, which should occur near the 20th week of gestation..

B.Five types:

1.Junctional

2.Intradermal

*A nevus is any congenital lesion composed of one of several types of cells found in the skin. A melanocytic nevus is composed of atypical but benign-appearing melanocytes (nevus cells). In this chapter (and elsewhere in the book), the term nevus always refers to the melanocytic nevus.

3.Compound (Fig. 17.3)

4.Blue (Fig. 17.5)

5.Congenital oculodermal melanocytosis (nevus of Ota) (Fig. 17.6)

C.The familial atypical mole and melanoma (FAM-M) syndrome (dysplastic nevus syndrome; B-K mole syndrome)

1.The FAM-M syndrome consists of multiple, large, typical and atypical cutaneous nevi of the upper part of the trunk, buttocks, and extremities.

2.The nevi appear at an early age (usually during adolescence) and increase in number throughout life.

3.Familial cases are inherited in an autosomal-domi- nant pattern; sporadic cases also occur.

4.Patients who have the syndrome definitely carry an increased risk for development of cutaneous melanomas; melanomas develop in them at an earlier age than in the general population.

Unlike cutaneous melanomas, ocular (conjunctival and uveal) melanocytic lesions rarely occur, and may be no more common in patients with FAM-M syndrome than in the general population.

II.Junctional nevus

A.A junctional nevus is flat, well circumscribed, and a uniform brown color.

B.The nevus cells are located at the “junction” of the epidermis and dermis (Fig. 17.3C).

C.The nevus has a low malignant potential.

III.Intradermal nevus (common mole; Fig. 17.4)

A.Intradermal nevus is usually elevated, frequently is papillomatous, and is the most common type of nevus.

B.It has a brown to black color when pigmented; often, however, it is almost flesh-colored.

C.The nevus cells are entirely in the dermis.

1.The nuclei of the nevus cells tend to become “mature” (i.e., smaller, thinner or spindle-shaped,

670 Ch. 17: Ocular Melanocytic Tumors

A

C

and darker) as they go deeper into the dermis. This orderly progression in structural change from superficial to deep layers is termed the normal polarity of the nevus.

2.No inflammatory cells are present unless the nevus is inflamed secondarily.

D.The nevus may be seen with proliferated Schwann elements (i.e., a neural nevus).

E.An unusual intradermal (or subepithelial) nevus is the peripunctal melanocytic nevus.

1.These involve the lower punctum, are dome-shaped and benign, and circumferentially surround the punctum, creating swollen punctal lips that result in a slitlike punctal orifice

2.The nevus cells are subepithelial and also infiltrate the orbicularis muscle fibers.

F.Intradermal nevus probably has no malignant potential.

IV. Compound nevus (see Fig. 17.3)

A.It combines junctional and dermal components, and is usually brown.

B.The dermal component shows a normal polarity (see

Fig. 17.4C; i.e., cells closest to the epidermis are larger, plumper, rounder, and paler than the deeper cells).

C.The spindle cell nevus (juvenile “melanoma,” Spitz nevus) is a special form of compound nevus that occurs predominantly in children, often as a solitary lesion on the face.

B

Fig. 17.3 Compound nevus. A, Moderately pigmented nevus at lid margin. B, Histologic section shows nevus cells at junction of epidermis and dermis as well as in dermis. C, Increased magnification demonstrates nevus cells in junctional and dermal locations.

1.Histologically, it superficially resembles a malignant melanoma, but biologically it is benign.

2.It may contain spindle cells, “epithelioid” cells, and single-nucleus and multinucleated giant cells that contain abundant basophilic cytoplasm.

D.The compound nevus has a low malignant potential.

The malignant melanoma arises from the junctional component.

V.Blue nevus

A.The blue nevus is usually flat and is almost always pigmented from birth; it appears blue to slate-gray.

Congenital pigmented (melanocytic) nevi are arbitrarily divided into small (<3 to 4 cm), large (up to 10 cm), and giant (>10 cm). The large and giant melanocytic nevi have an approximately 8.5% chance of undergoing malignant transformation during the first 15 years of life. Most primary orbital melanomas occur in white patients and are associated with blue nevi.

B.Nevus cells are present deep in the dermis in interlacing fasciculi.

1.The cells are located deeper than junctional, dermal, or compound nevus cells.

2.The nevus cells are more spindle-shaped, more elongated, and contain larger branching processes than other types of nevus cells. They more closely resemble uveal nevus cells than do other skin nevus cells.

Соседние файлы в папке Английские материалы