Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001

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40 to 80 mg/0.5 mL concentrations. Triamcinolone suspensions are injected periocularly in 10to 40-mg doses. Dexamethasone suspension may be injected with an initial dose of 2 to 4 mg. The blood–ocular barrier limits the intraocular penetration of systemic corticosteroids.73

NONSTEROIDAL ANTIINFLAMMATORY DRUGS

Therapy with NSAIDs is an important adjunct to application of topical, periocular, or systemic steroids. The amount of steroids and thus the rate of side effects can be significantly lessened with topical or oral use of NSAIDs.83

MYDRIATIC AND CYCLOPLEGIC AGENTS

These agents are used to prevent posterior synechiae by dilating the pupil at regular intervals and thus keeping the pupil in motion. They also relieve ocular discomfort by relaxing the ciliary muscle. Homatropine 5% provides good mydriasis and adequate cycloplegia. Its duration of action is much shorter than that of atropine and scopolamine and will therefore keep the pupil much better in motion. Alternatively, a combination of tropicamide 1% and phenylephrine 2.5% can be given.84 Cyclopentolate may be contraindicated in eyes with uveitis because it has been shown to be a chemoattractant to inflammatory cells in vitro.85

AQUEOUS SUPPRESSANTS

Aqueous suppressants such as beta-blockers,86 topical carbonic anhydrase inhibitors, and 2-adrenergics are mainly used to lower the IOP in uveitic glaucoma. Carteolol was found to be effective for the treatment of secondary glaucoma associated with endogenous uveitis.87

What Medications and Procedures Should Be Avoided?

Miotics (parasympathetic drugs) should be avoided because they disrupt the blood–aqueous barrier and thus promote the intraocular inflammation.88 Induced miosis would increase the surface area of the iris coming in contact with the lens, and thus may cause posterior synechiae and iris bombé. Concurrent ciliary body spasm may cause pain and blurred vision.

Prostaglandins such as latanoprost have been shown to cause anterior uveitis and therefore should probably be avoided in the treatment of uveitic glaucoma.89 However, concurrent use of NSAIDs, such as diclofenac, might prevent disruption of the blood–aqueous barrier and maintain the IOP lowering effect.90 Caution should be exercised in patients with a history of glaucoma, previous surgery, or a predilection for uveitis when treated with Nd:YAG laser posterior capsulotomy. These patients may be at risk of developing ciliochoroidal effu-

sions. Symptoms usually resolve after steroid treatment.91

Sympathetic uveitis may develop after filtering procedures on blind, painful eyes. It was the condition of the eye undergoing a filtering procedure that caused the sympathetic uveitis, and not the procedure itself. When glaucoma is

absolute, the risk is much higher. Filtering surgery on blind, painful eyes thus presents increased danger for the fellow eye.92

Is Immunosuppressive Therapy Useful?

Immunosuppression with antimetabolites (azathioprine, methotrexate), alkylators (cyclophosphamide, chlorambucil), and/or CsA is sometimes necessary to treat the ocular inflammation.93,94

What Is the Surgical Therapy?

Surgery should be avoided in an eye with active inflammation.95 But when medical therapy fails, surgery is indicated. Iridoplasty, laser peripheral iridotomy, or peripheral iridectomy is recommended, when mydriatics fail to break posterior synechiae that are causing pupillary block. In cases of uncontrolled openand closed-angle glaucoma, the following surgical options are available:

FILTERING SURGERY

Traditional filtering surgery has a low success rate in eyes with uveitic glaucoma. Failure of trabeculectomy most often results from fibroblast proliferation and subconjunctival fibrosis.96 In patients with uveitis, excessive inflammatory response increases the risk of bleb failure.97 Normal aqueous seems to inhibit subconjunctival fibroblast proliferation,98,99 whereas aqueous100–102 and conjunctiva97 in uveitic eyes contain an increased number of T lymphocytes, which modulate wound healing. Success rates are higher when concurrent antiproliferative agents are used.96,103,104

Trabeculectomy with intraoperative application of mitomycin C for control of uveitic glaucoma achieved an IOP of 21 mm Hg or lower without glaucoma medications in 75%.105

DRAINAGE DEVICES

Use of a drainage implant may be indicated as a primary procedure in glaucoma associated with uveitis.106 Trabeculectomy was successful in four out of five eyes after 1 year, and in three out of four eyes after 2 years. Success rates for Molteno implants were defined as four out of five eyes in the same study and remained stable over 2 years. When significant inflammation is present, aqueous drainage devices are more likely to control IOP.107

CYCLODESTRUCTIVE PROCEDURES

If medical and surgical therapy fail to control IOP, it may be necessary to ablate parts of the ciliary body to reduce aqueous inflow. Techniques for cyclodestruction that have been tried in the past include diathermy, electrolysis, and beta irradiation. Cyclocryotherapy is also available, although this technique has significant limitations. Newer techniques utilize laser energy (Nd:YAG or diode laser) via a transscleral approach. The disadvantages include the inability to precisely quantify the destruction of the ciliary processes and damage to adjacent

162 Glaucoma Associated with Inflammation

tissue. Transpupillary cyclophotocoagulation minimizes these problems, but is limited to the small number of eyes in which adequate gonioscopic visualization of the ciliary processes can be achieved. An alternative approach for aphakic eyes is intraocular cyclophotocoagulation, utilizing an endophotocoagulator through a pars plana incision. Depending on the status of the eye, visualization for this technique can be accomplished either by the transpupillary route or with an endoscope.108 Cyclodestructive procedures need to be repeated more frequently when compared to drainage device procedures. However, patients with drainage devices are more likely to have other types of adverse ophthalmic events than patients who had a cyclodestructive procedure.109

Cyclodestructive therapy works best if the drainage angle is partially open. Postoperatively, increased inflammation, however, might close the angle further. It can cause phthisis bulbi more often than any other surgical procedure.

How Are Specific Uveitic Syndromes Handled?

FUCHS’ IRIDOCYCLITIS

This is a syndrome that includes stellate keratic precipitates, heterochromia iridis, cataract, and a chronic anterior uveitis without anterior synechiae formation. The condition is typically unilateral. Fine blood vessels, which have a tendency to bleed very easily, but do not represent neovascularization, can be seen in the angle. Rubeosis iridis and rubeosis of the anterior chamber angle have also been reported.110 Chronic anterior segment ischemia seen in Fuchs’ heterochromic iridocyclitis can be possible mechanism predisposing these eyes to neovascularization.111

The prevalence of glaucoma in this condition varies from 6.3 to 59%.57 The IOP is elevated secondary to reduced outflow facility. Glaucoma is usually treated with aqueous suppressants. The iritis does not respond well to corticosteroids, which by itself may induce IOP elevation in steroid responders. Most studies show that surgical intervention is required in approximately half of the patients;112,113 26.2% of patients with Fuchs’ heterochromic uveitis had glaucoma. Half of these patients presented with glaucoma on initial examination. The risk of glaucoma in patients with Fuchs’ heterochromic uveitis is 0.5% per year, decreasing significantly after 15 years. Causes of IOP elevation include inflammation with peripheral anterior synechiae, rubeosis, lens-induced angle closure, and recurrent spontaneous hyphema. Most patients have chronic openangle glaucoma. Cataract surgery may precipitate glaucoma. The failure rate of glaucoma drainage surgery was 55.5%, and antimetabolites are needed for filtering surgery.114

POSNER-SCHLOSSMAN SYNDROME

(GLAUCOMATOCYCLITIC CRISIS)

This condition is usually unilateral.115,116 Recurrent episodes of IOP elevation are usually asymptomatic. The angle remains open. The anterior chamber reaction is minimal. Corneal edema is usually present. Patients with PosnerSchlossman syndrome may have peptic ulcers and other gastrointestinal

disorders.117 Usually individuals 20 to 50 years old are affected. This condition is self-limited and resolves spontaneously regardless of treatment. But aqueous suppressants and topical steroids may be indicated,57 and patients rarely require filtering surgery.

JUVENILE RHEUMATOID ARTHRITIS (JRA)

Juvenile rheumatoid arthritis is a general name for arthritic conditions in children and is relatively rare.118 Secondary glaucoma is the most devastating complication of chronic uveitis65 and can be seen in 14 to 27% of children.119–123 The mechanism of glaucoma in JRA is either a pupillary block95 and/or development of PAS with progressive angle closure.118 Secondary open angle with obstruction of trabecular meshwork has been reported.124 Because steroids are used in the treatment of JRA uveitis, steroid-induced glaucoma may occur. Medical management with topical and systemic aqueous suppressants initially controls IOP in about half of the patients, with only a third controlled later in the course of the disease.125 Traditional filtering surgery is usually not very successful.65,96,120 The use of antimetabolites with filtering surgery or shunting devices can improve the outcome.57,64,105,107,126 In one study trabeculodialysis has been successful in more than half of the eyes after 2 years.127

INTERMEDIATE UVEITIS (PARS PLANITIS)

Intermediate uveitis is defined as a clinical condition with usually bilateral inflammation of the peripheral retina (“snow banking”) and vitritis.128 It has been associated with sarcoidosis, multiple sclerosis, Lyme disease, and tuberculosis, but often remains idiopathic. Glaucoma occurs in 7 to 8% of adult patients with intermediate uveitis60,129,130 and in 15% of children.131,132 The IOP is elevated probably due to synechiae formation, rubeosis, and cortico- steroid-induced glaucoma.133

Management includes topical aqueous suppressants. Cyclocryotherapy131,134,135 has been used. Implantation of a drainage device might be necessary for uncontrolled glaucoma.

BEHÇET’S DISEASE

This disorder presents with acute hypopyon, iritis, aphthous and genital ulcers, and erythema nodosum in young adults.136,137 Ocular involvement is found in 83 to 95% in males and 67 to 73% in females; the male to female ratio is 1.78:1.138 Glaucoma usually occurs from obstruction of the trabecular meshwork by inflammatory cells and synechiae formation,136 and sometimes neovasculariza- tion.139–143 All patients initially respond to steroids, but steroids appear to be deleterious to visual prognosis and the patients eventually require cytotoxicimmunosuppressive drugs such as chlorambucil and cyclophosphamide after “resistance” to steroids develops. Glaucoma is treated with aqueous suppressants, filtration surgery, or drainage implants. The prognosis is poor. Only one

of four patients had useful visual acuity after 10 years.138,144

164 Glaucoma Associated with Inflammation

VOGT-KOYANAGI-HARADA (VKH) SYNDROME

Patients with VKH usually present with bilateral decreased vision and general symptoms such as headache, nausea, vomiting, and hearing loss. Bilateral panuveitis with serous retinal detachments and underlying choroidal infiltrates are seen. Perilimbal vitiligo is common.145 Typically, affected individuals are 20 to 50 years of age and of Asian or Native-American descent. Uveitic glaucoma occurs in almost every third patient with VKH syndrome.146–148 The IOP is usually elevated due to secondary open-angle glaucoma. Pupillary block due to posterior synechiae is also encountered frequently.146–148 Rarely, angle closure secondary to choroidal effusion with anterior rotation of the ciliary body can be seen.149 The main treatment consists of systemic corticosteroids. In severe cases or in patients who cannot tolerate high doses of steroids, cytotoxic agents or immunosuppressives such as CsA might be indicated.147,150 The possibility of steroid-induced glaucoma must always be kept in mind. Glaucoma is treated medically with aqueous suppressants. If surgery is necessary, drainage devices offer a greater degree of success than trabeculectomies even with antiproliferative agents.147,148

SYMPATHETIC OPHTHALMIA

This entity consists of bilateral granulomatous panuveitis after injury to one eye. Uveitic glaucoma develops in 43% of the eyes with sympathetic ophthalmia.151 Filtering procedure on blind painful uveitic glaucoma eyes may provoke sympathetic ophthalmia in the fellow eye.92 Mechanisms of uveitic glaucoma in sympathetic ophthalmia include angle closure secondary to pupillary block and iris bombé,152 angle closure due to a thickening of the iris and ciliary body by cellular infiltration,153 PAS and infiltration of the outflow pathway by inflammatory cells.151 The main treatment for sympathetic ophthalmia consists of administration of topical and systemic corticosteroids and occasionally cytotoxic or immunosuppressive agents. Filtering surgery or implantation of a drainage device might be necessary.

SARCOIDOSIS

Ocular manifestations of sarcoidosis most commonly include bilateral chronic granulomatous uveitis with mutton fat keratic precipitates, iris nodules, and synechiae.154 Ocular manifestations in systemic sarcoidosis occur in 38% of patients.154 Granulomatous uveitis occurs in 52154 to 74% of patients with ocular sarcoidosis. Glaucoma develops in 10.9 to 25.5% of patients with sarcoidosis uveitis.154,155 Blacks with sarcoid uveitis have a higher risk than whites of developing glaucoma and blindness.154

Impairment to outflow in sarcoid uveitis arises from posterior and anterior synechiae, neovascularization of the angle and the iris, steroid-induced ocular hypertension,156 and inflammatory precipitates and changes in the trabecular meshwork.66 The aqueous level of angiotensin-converting enzyme (ACE) may be elevated in patients with uveitis suspected to have sarcoidosis and may need to be measured when serum ACE level and other laboratory and radiologic findings are negative.157 Association of elevated serum levels of ACE in

166 Glaucoma Associated with Inflammation

steroid-sparing agent, which can be used to treat ocular inflammatory disease. In a recent study mycophenolate mofetil was given 1 g twice daily in conjunction with steroids, as a steroid-sparing agent, or as an additional agent with CsA, or instead of CsA or azathioprine.164 The addition of MMF to immunosuppressive regimens improved symptoms and allowed reducing the dose of prednisone in most patients. MMF may become a useful immunosuppressive drug for controlling ocular inflammation without significant side effects.

References

1.Macri FJ, Cevario SJ: The formation and inhibition of aqueous humor production. A proposed mechanism of action. Arch Ophthalmol 1978;96:1664–1667.

2.Howes ELJ, Cruse VK: The structural basis of altered vascular permeability following intraocular inflammation. Arch Ophthalmol 1978;96:1668–1676.

3.Mandelbaum S: Glaucoma associated with corneal disorders. In: Tasman W, Jaeger EA (eds): Duane’s Clinical Ophthalmology. Philadelphia: Lippincott Williams & Wilkins, 1998:1–13.

4.Paterson CA, Eakins KE, Paterson E, et al: The ocular hypertensive response following experimental acid burns in the rabbit eye. Invest Ophthalmol Vis Sci 1979;18:67–74.

5.Paterson CA, Pfister RR: Intraocular pressure changes after alkali burns. Arch Ophthalmol 1974;91:211–218.

6.Falcon MG, Williams HP: Herpes simplex kerato-uveitis and glaucoma. Trans Ophthalmol Soc UK 1978;98:101–104.

7.Tavs LE: Syphilis. Major Probl Clin Pediatr 1978;19:222–256.

8.Grant WM: Late glaucoma after interstitial keratitis. Am J Ophthalmol 1975;79:87–91.

9.Tsukahara S: Secondary glaucoma due to inactive congenital syphilitic interstitial keratitis. Ophthalmologica 1977;174:188–194.

10.Lichter PR, Shaffer RN: Interstitial keratitis and glaucoma. Am J Ophthalmol 1969;68:241–248.

11.Kuriakose T, Thomas PA: Keratomycotic malignant glaucoma. Indian J Ophthalmol 1991;39:118–121.

12.Naumann G, Green WR, Zimmerman LE: Mycotic keratitis: a histopathologic study of 73 cases. Am J Ophthalmol 1967;64:668.

13.Townsend WM, Kaufman HE: Pathogenesis of glaucoma and endothelial changes in herpetic kerato-uveitis in rabbits. Am J Ophthalmol 1971;71:904–910.

14.Salvador F, Linares F, Merita I, et al: Unilateral iridoschisis associated with syphilitic interstitial keratitis and glaucoma. Ann Ophthalmol 1993;25:328–329.

15.Sundmacher R, Neumann-Haefelin D: [Herpes simplex virus isolations from the aqueous humor of patients suffering from focal iritis, endotheliitis, and prolonged disciform keratitis with glaucoma (author’s transl)]. Klin Monatsbl Augenheilkd 1979;175:488–501.

16.Hara J, Ishibashi T, Fujimoto F, et al: Adenovirus type 10 keratoconjunctivitis with increased intraocular pressure. Am J Ophthalmol 1980;90:481–484.

17.Womack LW, Liesegang TJ: Complications of herpes zoster ophthalmicus. Arch Ophthalmol 1983;101:42–45.

18.Reijo A, Antti V, Jukka M: Endothelial cell loss in herpes zoster keratouveitis. Br J Ophthalmol 1983;67:751–754.

19.Schwartz SD, Borchert M, Oberman A: Hypopyon keratouveitis in acute angle-closure glaucoma. Am J Ophthalmol 1987;104:430–431.

20.Zhang MY: Hypopyon and iris necrosis in acute-closure glaucoma. Report of two cases. Chin Med J (Engl) 1984;97:583–586.

21.Friedman Ah, Bloch R, Henkind P: Hypopyon and iris necrosis in angle-closure glaucoma. Report of two cases. Br J Ophthalmol 1974;56:632–635.

22.Rhee DJ, Pyfer MF: Corneal abrasion. In: Rhee DJ, Pyfer MF (eds): The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. Philadelphia: Lippincott Williams & Wilkins, 1999:23–24.

23.Rhee DJ, Pyfer MF: Recurrent corneal Erosin. In: Rhee DJ, Pyfer MD (eds): The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. Philadelphia: Lippincott Williams & Wilkins, 1999:62–64.

24.Messmer EM, Raizman MB, Foster CS: Lepromatous uveitis diagnosed by iris biopsy. Graefes Arch Clin Exp Ophthalmol 1998;236:717–719.

25.Heiligenhaus A, Steuhl KP: Treatment of HSV-1 stromal keratitis with topical cyclosporin A: a pilot study [in process citation]. Graefes Arch Clin Exp Ophthalmol 1999;237:435–438.

26.Watson PG, Hayreh SS: Scleritis and episcleritis. Br J Ophthalmol 1976;60:163–191.

27.McGavin DD, Williamson J, Forrester JV, et al: Episcleritis and scleritis. A study of their clinical manifestations and association with rheumatoid arthritis. Br J Ophthalmol 1976;60:192–226.

28.Harbin TSJ, Pollack IP: Glaucoma in episcleritis. Arch Ophthalmol 1975;93:948–950.

29.Sainz dlM, Jabbur NS, Foster CS: Severity of scleritis and episcleritis. Ophthalmology 1994;101:389–396.

30.Akpek EK, Uy HS, Christen W, et al: Severity of episcleritis and systemic disease association. Ophthalmology 1999;106:729–731.

31.Leo RJ, Palmer DJ: Episcleritis and secondary glaucoma after transscleral fixation of a posterior chamber intraocular lens [letter]. Arch Ophthalmol 1991;109:617.

32.Watson PG: Diseases of the sclera and episclera. In: Tasman W, Jaeger EA (eds): Duane’s Clinical Ophthalmology. Philadelphia: Lippincott Williams & Wilkins, 1998;1–45.

33.Rhee DJ, Pyfer MF: Episcleritis. In: Rhee DJ, Pyfer MF (eds): The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. Philadelphia: Lippincott Williams & Wilkins, 1999;133–134.

34.Lyons CJ, Hakin KN, Watson PG: Topical flurbiprofen: an effective treatment for episcleritis? Eye 1990;4:521–525.

35.Bonne C, Latour E, Muller A, et al: 2-(2-hydroxy-4-methylphenyl)aminothiazole hydrochloride as a dual inhibitor of cyclooxygenase/lipoxygenase and a free radical scavenger. 2nd communication: anti-inflammatory activity. Arzneimittelforschung 1989;39:1264–1250.

36.Bonne C, Muller A, Latour E, et al: 2-(2-hydroxy-4-methylphenyl)aminothiazole hydrochloride as a dual inhibitor of cyclooxygenase/lipoxygenase and a free radical scavenger. 1st communication: in vitro studies. Arzneimittelforschung 1989;39:1242–1245.

37.Liu CS, Ramirez-Florez S, Watson PG: A randomised double blind trial comparing the treatment of episcleritis with topical 2-(2-hydroxy-4-methylphenyl) aminothiazole hydrochloride 0.1% (CBS 113A) and placebo. Eye 1992;5:678–685.

38.Lloyd-Jones D, Tokarewicz A, Watson PG: Clinical evaluation of clobetasone butyrate eye drops in episcleritis. Br J Ophthalmol 1981;65:641–643.

39.Watson PG, McKay DA, Clemett RS, et al: Treatment of episcleritis. A double-blind trial comparing betamethasone 0.1 percent, oxyphenbutazone 10 percent, and placebo eye ointments. Br J Ophthalmol 1973;57:866–870.

40.Watson PG: Management of scleral disease. Trans Ophthalmol Soc UK 1966;86:151–167.

41.Watson PG: Glaucoma associated with keratitis, episcleritis, and scleritis. In: Ritch R, Shields MB, Krupin T (eds): The Glaucomas. St. Louis: Mosby-Year Book, 1996;1207–1223.

42.Becker B, Mills DW: Corticosteroids and intraocular pressure. Arch Ophthalmol 1963;70:500.

43.Armaly MF: Effect of corticosteroids on intraocular pressure and fluid dynamics. II. The effects of dexamthasone in the glaucomatous eyes. Arch Ophthalmol 1963;70:492–499.

44.Rhee DJ, Pyfer MF: Scleritis. In: Rhee DJ, Pyfer MD (eds): The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. Philadelphia: Lippincott Williams & Wilkins, 1999;135–137.

45.Wilhelmus KR, Grierson I, Watson PG: Histopathologic and clinical associations of scleritis and glaucoma. Am J Ophthalmol 1981;91:697–705.

46.Sainz dlM, Foster CS, Jabbur NS: Scleritis-associated uveitis [see comments: Ophthalmology 1997 Aug;104(8):1207–1208]. Ophthalmology 1997;104:58–63.

47.Benson WE: Posterior scleritis. Surv Ophthalmol 1998;32:297–316.

48.Litwak AB: Posterior scleritis with secondary ciliochoroidal effusion. J Am Optom Assoc 1989;60:300–306.

49.Quinlan MP, Hitchings RA: Angle-clsoure glaucoma secondary to posterior scleritis. Br J Ophthalmol 1978;62:330–335.

50.Mangouritsas G, Ulbig M: [Secondary angle-block glaucoma in posterior scleritis]. Klin Monatsbl Augenheilkd 1997;199:40–44.

51.Fourman S: Angle-closure glaucoma complicating ciliochoroidal detachment. Ophthalmology 1989;96:646–653.

52.Foster CS, Sainz DLM: Clinical considerations of episcleritis and scleritis. In: The Sclera. New York: Springer Verlag, 1994;95–136.

53.Chen CJ, Harisdangkul V, Parker L: Transient glaucoma associated with anterior diffuse scleritis in relapsing polychondritis. Glaucoma 1982;109–111.

54.Denk PO, Thiel HJ, Zierhut M: [Episcleritis and scleritis. An overview of modern diagnostic and therapeutic concepts]. Klin Monatsbl Augenheilkd 1997;211:140–150.

55.Michelson PE: Red eye unresponsive to treatment. West J Med 1997;166:145–147.

56.Ortiz JM, Kamerling JM, Fischer D, et al: Scleritis, uveitis, and glaucoma in a patient with rheumatic fever. Am J Ophthalmol 1995;120:538–539.

57.Moorthy RS, Mermoud A, Baerveldt G, et al: Glaucoma associated with uveitis. Surv Ophthalmol 1997;41:361–394.

58.Ritch R: Pathophysiology of glaucoma in uveitis. Trans Ophthalmol Soc UK 1981;101:321–324.

168 Glaucoma Associated with Inflammation

59.Beardsley TL, Brown SV, Sydnor CF, et al: Eleven cases of sarcoidosis of the optic nerve. Am J Ophthalmol 1984;97:62–77.

60.Henderly DE, Genstler AJ, Smith RE, et al: Changing patterns of uveitis. Am J Ophthalmol 1987;103:131–136.

61.Weiner A, BenEzra D: Clinical patterns and associated conditions in chronic uveitis. Am J Ophthalmol 1991;112:151–158.

62.Linssen A, Rothova A, Valkenburg HA, et al: The lifetime cumulative incidence of acute anterior uveitis in a normal population and its relation to ankylosing spondylitis and histocompatibility antigen HLA-B27. Invest Ophthalmol Vis Sci 1991;32:2568–2578.

63.Rothova A, van Veenedaal WG, Linssen A, et al: Clinical features of acute anterior uveitis. Am J Ophthalmol 1987;103:137–145.

64.Panek WC, Holland GN, Lee DA, et al: Glaucoma in patients with uveitis Br J Ophthalmol 1990;74:223–227.

65.Kanski JJ, Shun-Shin GA: Systemic uveitis syndromes in childhood: an analysis of 340 cases. Ophthalmology 1984;91:1247–1252.

66.Roth M, Simmons RJ: Glaucoma associated with precipitates on the trabecular meshwork. Ophthalmology 1979;86:1613–1619.

67.Cohen RG, Wu HK, Schuman JS: Glaucoma with inflammatory precipitates on the trabecular meshwork: a report of Grant’s syndrome with ultrasound biomicroscopy of precipitates. J Glaucoma 1966;5:266–270.

68.Epstein DL, Hashimoto JM, Grant WM: Serum obstruction of aqueous outflow in enucleated eyes. Am J Ophthalmol 1978;86:101–105.

69.Mapstone R: Vascular factors involved in aetiology of secondary glaucoma. Trans Ophthalmol Soc UK 1971;91:741–748.

70.O’Connor GR: Recurrent herpes simplex uveitis in humans. Surv Ophthalmol 1976;21:165–170.

71.Teitelbaum CS, Streeten BW, Dawson CR: Histopathology of herpes simplex virus keratouveitis. Curr Eye Res 1987;6:189–194.

72.Schlaegel TFJ: Complications of uveitis. Int Ophthalmol Clin 1977;17:65–74.

73.Vitale A, Foster CS: Pharmacology of medical therapy for uveitis. In: Zimmerman TJ, Kooner KS, Sharir M, et al (eds): Textbook of Ocular Pharmacology. Philadelphia: Lippincott-Raven, 1997;683–701.

74.Biswas J, Neelakantan A, Rao BS: Adenoma of nonpigmented epithelium of the ciliary body presenting as anterior uveitis and glaucoma: a case report. Indian J Ophthalmol 1995;43: 137–140.

75.Asaria RH, Salmon JF, Skinner AR, et al: Electron microscopy findings on an intraocular lens in the uveitis glaucoma, hyphaema syndrome. Eye 1997;11:827–829.

76.Cates CA, Newman DK: Transient monocular visual loss due to uveitis-glaucoma-hyphaema (UGH) syndrome. J Neurol Neurosurg Psychiatry 1998;65:131–132.

77.Filipe JC, Palmares J, Delgado L, et al: Phacolytic glaucoma and lens-induced uveitis. Int Ophthalmol 1993;17:289–293.

78.Rodgin SG: Neovascular glaucoma associated with uveitis. J Am Optom Assoc 1987;58:499–503.

79.Yamada K, Hayasaka S, Setogawa T: Nonpenetrating trauma in the right eye induces anterior uveitis and secondary glaucoma in the contralateral eye. Ann Ophthalmol 1993;25:277–278.

80.Baratz KH, Hattenhauer MG: Indiscriminate use of corticosteroid-containing eyedrops. Mayo Clin Proc 1999;74:362–366.

81.Novack GD, Howes J, Crockett RS, et al: Change in intraocular pressure during long-term use of loteprednol etabonate. J Glaucoma 1998;7:266–269.

82.Leibowitz HM, Bartlett JD, Rich R, et al: Intraocular pressure-raising potential of 1.0% rimexolone in patients responding to corticosteroids [see comments]. Arch Ophthalmol 1996;114:933–937.

83.Vitale A, Foster CS: Nonsteroidal antiinflammatory drugs. In: Zimmerman TJ, Kooner KS, Sharir M, et al (eds): Textbook of Ocular Pharmacology. Philadelphia: Lippincott-Raven, 1977;713–722.

84.Vitale A, Foster CS; Mydriatic and cycloplegic agnets. In: Zimmerman TJ, Kooner KS, Sharir M, et al (eds): Textbook of Ocular Pharmacology. Philadelphia: Lippincott-Raven, 1997;703–711.

85.Tsai E, Till Go, Marak GEJ: Effects of mydriatic agents on neutrophil migration. Ophthalmic Res 1988;20:14–19.

86.Saari KM, Airaksinen PJ, Jaanio EA: Hypotensive effect of timolol on secondary glaucoma in chronic uveitis [letter]. Lancet 1978;1:442.

87.Ohno S, Ichiishi A, Matsuda H: Hypotensive effect of carteolol on intraocular pressure elevation and secondary glaucoma associated with endogenous uveitis. Ophthalmologica 1989;199:41–45.

88.Kaufman PL, Gabelt BT: Direct, indirect, and dual-action parasympathetic drugs. In: Zimmerman TJ, Kooner KS, Sharir M, et al (eds): Textbook of Ocular Pharmacology. Philadelphia: Lippincott-Raven, 1997;221–238.

89.Fechtner RD, Khouri As, Zimmerman TJ, et al: Anterior uveitis associated with latanoprost. Am J Ophthalmol 1998;126:37–41.

90.Miyake K, Ota I, Maekubo K, et al: Latanoprost accelerates disruption of the blood-aqueous barrier and the incidence of angiographic cystoid macular edema in early postoperative pseudophakias. Arch Ophthalmol 1999;117:34–40.

91.Schaeffer AR, Ryll DL, O’Donnell FEJ: Ciliochoroidal effusions after neodymium: YAG posterior capsulotomy: association with pre-existing glaucoma and uveitis. J Cataract Refract Surg 1989;15:567–569.

92.Shammas HF, Zubyk NA, Stanfield TF: Sympathetic uveitis following glaucoma surgery. Arch Ophthalmol 1977;95:638–641.

93.Vitale A, Foster CS: Immunosuppressive chemotherapy. In: Zimmerman TJ, Kooner KS, Sharir M, et al (eds): Textbook of Ocular Pharmacology. Philadelphia: Lippincott-Raven, 1997;723–761.

94.Cheung KL, Rosenbaum JT: Immunosuppressive therapy for uveitis. In: Zimmerman TJ, Kooner KS, Sharir M, et al (eds): Textbook of Ocular Pharmacology. Philadelphia: LippincottRaven, 1997;95–118.

95.Shields MB: Glaucomas associated with ocular inflammation. In: Shields MB (ed): Textbook of Glaucoma. Baltimore, MD: Williams & Wilkins, 1998;308–322.

96.Skuta GL, Parrish RK: Wound healing in glaucoma filtering surgery. Surv Ophthalmol 1987;32:149–170.

97.Broadway DC, Bates AK, Lightman SL, et al: The importance of cellular changes in the conjunctiva of patients with uveitic glaucoma undergoing trabeculectomy. Eye 1993;7:495–501.

98.Herschler J: The inhibitory factor in aqueous humor. Vision Res 1981;21:163.

99.Herschler J, Claflin AJ, Fiorentino G: The effect of aqueous humor on the growth of subconjunctival fibroblasts in tissue culture and its implications for glaucoma surgery. Am J Ophthalmol 1980;89:245–249.

100.Deschenes J, Char DH, Freeman W, et al: Uveitis: lymphocyte subpopulation studies. Trans Ophthalmol Soc UK 1986;105:246–251.

101.Deschenes J, Char DH, Kaleta S: Activated T lymphocytes in uveitis Br J Ophthalmol 1988;72:83–87.

102.Deschenes J, Freeman WR, Char DH, et al: Lymphocyte subpopulations in uveitis. Arch Ophthalmol 1986;104:233–236.

103.Skuta GL, Beeson CC, Higginbotham EJ, et al: Intraoperative mitomycin versus postoperative 5-fluorouracil in high-risk glaucoma filtering surgery. Ophthalmology 1992;99:438–444.

104.The Fluorouracil Filtering Surgery Study Group: Five-year follow-up of the Fluorouracil Filtering Surgery Study. The Fluorouracil Filtering Surgery Study Group [see comments]. Am J Ophthalmol 1996;121:349–366.

105.Prata JAJ, Neves RA, Minckler DS, et al: Trabeculectomy with mitomycin C in glaucoma associated with uveitis. Ophthalmic Surg 1994;25:616–620.

106.Bartholomew RS: Glaucoma implants. Their use in difficult cases of glaucoma. Trans Ophthalmol Soc UK 1978;98:482–485.

107.Hill RA, Nguyen QH, Baerveldt G, et al: Trabeculectomy and Molteno implantation for glaucomas associated with uveitis. Ophthalmology 1993;100:903–908.

108.Shields MB: Cyclodestructive surgery for glaucoma: past, present, and future. Trans Am Ophthalmol Soc 1985;83:285–303.

109.Topouzis F, Yu F, Coleman AL: Factors associated with elevated rates of adverse outcomes after cyclodestructive procedures versus drainage device procedures. Ophthalmology 1998; 105:2276–2281.

110.Perry HD, Yanoff M, Scheie HG: Rubeosis in Fuchs’ heterochromic iridocyclitis. Arch Ophthalmol 1975;93:337–339.

111.Berger BB, Tessler HH, Kottow MH: Anterior segment ischemia in Fuchs’ heterochromic cyclitis. Arch Ophthalmol 1980;98:499–501.

112.Liesegang TJ: Clinical features and prognosis in Fuchs’ uveitis syndrome. Arch Ophthalmol 1982;100:1622–1626.

113.Jones NP: Fuchs’ heterochromic uveitis: a reapprasial of the clinical spectrum. Eye 1991; 5:649–661.

114.Jones NP: Glaucoma in Fuchs’ heterochromic uveitis: aetiology, management and outcome. Eye 1991;5:662–667.

115.Posner A, Schlossman A: Further observations on the syndrome of glaucomatocyclitic crises. Trans Am Acad Ophthalmol Otolaryngol 1953;57:531–536.

116.Posner A, Schlossman A: Syndrome of unilateral recurrent attacks of glaucoma with cyclitic symptoms. Arch Ophthalmol 1948;39:517–535.

117.Knox DL: Glaucomatocyclitic crises and systemic disease: peptic ulcer, other gastrointestinal disorders, allergy and stress. Trans Am Ophthalmol Soc 1988;86:473–495.

118.Kanski JJ: Uveitis in juvenile chronic arthritis: incidence, clinical features and prognosis. Eye 1988;2:641–645.

119.Key SN, Kimura SJ: Iridocyclitis associated with juvenile rheumatoid arthritis. Am J Ophthalmol 1975;80:425–429.