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Chapter 180 – Idiopathic and Other Anterior Uveitis Syndromes

Chapter 180 – Idiopathic and Other Anterior Uveitis Syndromes

ROBERT C. WANG

NARSING A. RAO

DEFINITION

• Inflammation in the anterior uvea not associated with defined clinical syndromes.

KEY FEATURES

• Typically a nongranulomatous inflammation associated with cells and flare in the anterior chamber.

• Small-to-medium–size keratic precipitates.

ASSOCIATED FEATURES

• Pain.

• Photophobia.

• Ciliary “flush.”

• Posterior synechiae.

INTRODUCTION

Idiopathic anterior uveitis is a frequent cause of acute anterior uveitis encountered in clinical practice. Clinical signs and symptoms such as photophobia and anterior segment cell and flare make the diagnosis straightforward. Treatment with topical corticosteroids and cycloplegics are generally rapid and effective, with few bouts of recurrence. However, frequent recurrences or signs of systemic disease warrant further evaluation. Recognition of the lack of these signs and symptoms and elimination of other disease entities strengthen the accurate assessment of idiopathic disease. However, other distinct syndromes can be mistaken for idiopathic anterior uveitis. These include glaucomatocyclitic crisis (Posner–Schlossman syndrome), Fuchs’ heterochromic iridocyclitis (FHI), Schwartz syndrome, and drug-induced anterior uveitis.

IDIOPATHIC ANTERIOR UVEITIS

EPIDEMIOLOGY AND PATHOGENESIS

Idiopathic acute anterior uveitis is the most common cause of uveitis. The prevalence is near 50% (i.e., 50% of uveitis patients have idiopathic uveitis)[1] [2] with an annual incidence of 8–15 cases per 100,000 population.[3] Men and women are affected equally.

Although clinical features of acute or chronic anterior uveitis are well described, including associations of the acute process with the HLA-B27 haplotype, there is a lack of clear understanding about the pathogenesis and etiology of iridocyclitis in the vast majority of cases. Such cases are thought to be mediated by an autoimmune process. The latter could be a response to abnormal immune response consisting of recognition of self-protein, possibly induced by an infectious agent.

Recognition of self-protein involves a breakdown in tolerance and recognition of previously sequestered ocular antigens. In animal models sensitization with the ocular antigen, melanin-associated protein, produced an acute recurrent anterior uveitis with a delayed onset but an extended nature.[4] This model mimics human disease closely, with the underlying mechanism primarily from T cell–mediated delayed hypersensitivity. Recently, herpes simplex virus (HSV) antigens and DNA have been found in the aqueous humor of patients with recurrent anterior uveitis and iris atrophy without keratopathy.[5] These lesions have been attributed previously to varicella zoster virus. However in the younger age group, HSV was recovered in the anterior chamber sample. It is interesting to note that the study was performed on patients who have recurrent disease and that HSV was detected after an average of a 14-year follow-up in some cases.

OCULAR MANIFESTATIONS

Idiopathic anterior uveitis appears with an acute onset of pain, photophobia, and decreased vision. Ocular examination typically exhibits limbal vascular injection (ciliary flush) with occasional chemosis. Intraocular pressure is typically normal. However, severe chronic inflammation can lead to elevated intraocular pressure. Slit-lamp evaluation of the anterior chamber demonstrates variable amounts of cell and flare depending on the severity. Severe inflammation can result in fibrin or hypopyon formation ( Fig. 180-1 ). However, the presence of these two signs is atypical for idiopathic disease and more characteristic of the HLA-B27–associated spondyloarthropathy.[6] Precipitates of inflammatory cells can be seen on the inferior endothelial surface of the cornea (Arlt’s triangle). Small collections of white-appearing keratic precipitates usually represent a nongranulomatous anterior uveitis. Large, greasy, keratic precipitates are not typical of idiopathic anterior uveitis, and their presence should lead to the consideration of other granulomatous processes such as sarcoidosis, lens-induced uveitis, and others.

Chronic or severe inflammation can lead to secondary complications, including cataract formation and glaucoma. In addition, cystoid macular edema can develop decreasing vision out of proportion to the amount of inflammation.

DIAGNOSIS

Diagnosis of idiopathic disease is generally straightforward. Clinical history is typical, with an acute onset of pain and photophobia in a healthy individual without systemic disease. Examination demonstrates small keratic precipitates, anterior chamber cells, and flare. Usually the inflammation responds rapidly to therapy. However, frequent recurrences, slowly resolving inflammation, systemic symptoms, or granulomatous keratic precipitates should indicate the possibility of an alternative diagnosis.

DIFFERENTIAL DIAGNOSIS

Critical to the diagnosis of idiopathic disease is a thorough and complete history and review of systems. Importantly, review of systems can differentiate HLA-B27–associated disease, which is among the common causes of anterior uveitis. These diseases include Reiter’s syndrome, ankylosing spondylitis, psoriatic arthritis, ulcerative colitis, and Crohn’s disease. Other possibilities include

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Figure 180-1 Severe idiopathic anterior uveitis with fibrinoid reaction in a patient with HLA-B27. Extensive anterior segment reaction with posterior synechiae is present. Note large amount of fibrin in the anterior chamber. Typical limbal injection is seen.

TABLE 180-1 — DIFFERENTIAL DIAGNOSIS OF ENTITIES WITH ANTERIOR UVEITIS

ANTERIOR SEGMENT SIGNS

Granulomatous keratic precipitates

Sarcoid, sympathetic ophthalmia, VKH, tuberculosis, toxoplasmosis, infectious etiologies

Hypopyon

HLA-B27, Behçet’s, intraocular lymphoma, endophthalmitis

Diffuse keratic precipitates

Fuchs’ heterochromic iridocyclitis, herpes simplex virus, cytomegalovirus retinitis

SYSTEMIC DISEASE

Autoimmune

HLA-B27 (ankylosing spondylitis, Reiter’s, psoriasis, ulcerative colitis, Crohn’s disease), sarcoid, Behçet’s disease, VKH, TINU

Infectious

Syphilis, tuberculosis, herpes simplex virus, Whipple’s, fungal, Propionibacterium acnes, and others

HLA-B27, Human lymphocyte antigen B27; TINU, tubulointerstitial nephritis and uveitis; VKH, Vogt-Koyanagi-Harada syndrome.

infectious and noninfectious causes. In addition, diagnosis can be refined in the presence of a granulomatous keratic precipitates. Dilated fundal examination should be performed to eliminate other pathology with secondary anterior uveitis ( Table 180-1 ).

PATHOLOGY

Histologically the inflammatory infiltrate consists of lymphocytes admixed with monocytes.[4] They are seen primarily in the anterior uvea, with spillover of cells into the anterior chamber and vitreous cavity. Monocytes are seen as the earliest cellular infiltrate marginating in the iris vasculature. Chemotactic factors are found in the aqueous humor and contribute to migration of leukocytes. Accumulating evidence suggests that cytokines produced by the uveal macrophages initiate the uveitis.[7]

TREATMENT

Topical corticosteroids remain the mainstay of therapy for idiopathic anterior uveitis. Frequent administration of topical corticosteroids rapidly resolves the inflammation. Although studies noted differences in efficacy between phosphate and acetate formulations, most have not noticed a difference in treatment outcomes. [8] Addition of a mydriatic agent reduces pain associated with the uveitis, prevents the likelihood of posterior synechiae formation, and attempts to break those that have formed already. Rarely, idiopathic inflammation fails to respond to topical therapy. In these recalcitrant cases, sub-Tenon’s injection of corticosteroids delivers a relatively high concentration in a sustained release fashion, resulting in rapid resolution. Additionally, sub-Tenon’s injection of corticosteroids is effective in the treatment of cystoid macular edema.[9] Different formulations of injectable corticosteroids are available. In particular, triamcinolone appears to have a better safety profile causing less local fibrosis than other injectable corticosteroid formulations.

Occasionally, topical treatment with corticosteroids produces a rise in intraocular pressure not associated with anterior segment inflammation. Newer formulations of corticosteroids, such as loteprednol, have reduced the steroid-response effect.[10] [11] Though both standard topical corticosteroid therapy and corticosteroid-sparing therapy reduced intraocular inflammation, the latter appears less efficacious in reducing inflammation.[12] [13]

FUCHS’ HETEROCHROMIC IRIDOCYCLITIS

FHI is a rare form of anterior uveitis that accounts for approximately 1.5% of all anterior uveitis.[14] [15] Most patients are diagnosed between 35–40 years of age with equal male-to-female predominance. The intraocular inflammation is typically unilateral. However, bilateral involvement is seen in 15% of cases.[16] Ocular toxoplasmosis and herpes simplex virus (HSV) infection have been implicated. [17] [18] [19] However, the underlying etiology remains unknown.

Unlike idiopathic anterior uveitis, patients with FHI have minimal symptoms. Typically patients have a noninjected, “quiet-appearing” eye, with decreased vision due to the development of cataract. Slit-lamp evaluation typically demonstrates fine, “stellate” keratic precipitates (KP). Unlike idiopathic uveitis, these KP generally cover the entire corneal endothelium. There is usually a mild anterior chamber cellular reaction with minimal flare, without iris synechiae. [16]

Gonioscopy demonstrates fine vessels crossing the trabecular meshwork in 20–30% of patients. These vessels do not tend to cause neovascular glaucoma. However, they are friable and may cause minute hemorrhages into the anterior chamber. Historically, surgical intervention into the anterior chamber produces hemorrhages from these vessels, termed Amsler’s sign.[20]

The classic description of FHI includes diffuse, stellate keratic precipitates with iris heterochromia. Unilateral inflammation causes the involved iris to appear lighter compared with the fellow eye. In lighter color eyes, extensive iris atrophy may produce a paradoxical heterochromia. Bilateral disease is subtle and can be discerned by signs of blurring of the iris stroma and loss of detail of the iris surface. Bilateral, diffuse stellate keratic precipitates are a more specific sign.[16]

Complications of FHI include elevated intraocular pressure, which is seen in 25–60% of the patients.[16] Additionally, cataract formation, most commonly posterior subcapsular cataracts, develops in over 80% of patients.[21] Patients tend to tolerate cataract extraction well. However, glaucoma develops in 6.3–59% of eyes, and 25–60% of these eyes require filtering surgery.[22]

Despite these complications there is currently no indication that treatment with anti-inflammatory agents alters the course or the outcome of the disease. Up to 50% of eyes retain 20/40 or better vision.[16] [23] Occasional use of glucocorticoids may be indicated if an exacerbation of inflammation is symptomatic. Periocular glucocorticoids may help to decrease symptomatic vitreous inflammation.

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GLAUCOMATOCYCLITIC CRISIS

Glaucomatocyclitic crisis, also known as Posner–Schlossman syndrome, is an entity associated with an acute uniocular elevation of intraocular pressure. Glaucomatocyclitic crisis is rare and reported in 0.5% of cases of uveitis.[1] Studies demonstrate a stronger male predilection, with onset from the third through sixth decade of life.[24] Although recurrent, it rarely occurs later in life. However, in recurrent cases in patients who have the disease for longer than a 10-year period, there is an increased risk of developing glaucoma.[25] The pathogenesis has been suggested to be both immunological and infectious in nature. Association with both HLA-Bw54 and Borrelia burgdorferi have been shown.[26] [27] Recently DNA fragments of HSV have been recovered in the aqueous humor of patients with acute episodes.[28] However, it is still unclear whether these observations are related directly to the underlying pathogenesis.

Patients typically seek treatment for a blurring of vision and periorbital discomfort. Examination reveals a noninjected eye with a slightly mydriatic pupil. Slit-lamp examination reveals a paucity of anterior chamber cells with occasional, small, nonpigmented keratic precipitates on the corneal endothelium. The intraocular pressure is elevated to 40–60?mm Hg, usually despite an open angle. [24]

Diagnosis generally is based on clinical findings. However, herpetic uveitis can mimic this disease. Unlike glaucomatocyclitic crisis, herpetic anterior uveitis typically reveals a heavier anterior chamber reaction with signs of posterior synechiae and iris atrophy.

Therapy of glaucomatocyclitic crises is directed primarily at control of the elevated intraocular pressure. Apraclonidine appears to be especially effective in the reduction of intraocular pressure in glaucomatocyclitic crises; it has been shown in one study to reduce intraocular pressure by 50% over a 4-hour period.[29] However, use of other pressure-lowering agents such as ß-blockers and topical carbonic anhydrase inhibitors also may be used. The prostaglandin analog, latanoprost, was associated with an increase in intraocular pressure and worsening of uveitis in a small case series. [30] [31] [32] Due to the inflammatory component, anecdotal evidence suggests that therapy with topical glucocorticoids may shorten the duration of the intraocular pressure rise.

DRUG-INDUCED ANTERIOR UVEITIS: RIFABUTIN AND CIDOFOVIR

Rifabutin is used in the treatment or prophylaxis of Mycobacterium avium complex (MAC) infections in acquired immunodeficiency syndrome. [33] [34] Patients who have human immunodeficiency virus (HIV) at risk of MAC infection tend to have a low CD4 cell count and high viral load. With the advent of highly active antiretroviral therapy (HAART), the incidence of MAC infection has decreased.[35] However, use of rifabutin in doses of 300–1800?mg has been associated with the development of a severe hypopyon anterior uveitis in 16% of patients receiving therapy. Rifabutin levels have been demonstrated to increase with the addition of clarithromycin, a macrolide, which inhibits the cytochrome P450 enzymatic pathway, increasing the concentration of rifabutin.[36] The concomitant use of clarithromycin and ethambutol was not associated with increased risk of uveitis.[37] Recently rifabutin-associated anterior uveitis has been observed in immunocompetent individuals, thus making the association between the anterior uveitis and immune status less likely.[38] The exact pathogenesis of the rifabutin-associated uveitis is still unknown.

Patients typically experience an acute onset of uniocular blurring of vision and ocular injection. Examination demonstrates a marked fibrinoid anterior chamber reaction and hypopyon that mimic infectious endophthalmitis ( Fig. 180-2 ). Anterior vitreous

Figure 180-2 Rifabutin-associated anterior uveitis. Severe inflammation with evidence of hypopyon and fibrin formation.

cells are typically present, rarely with diffuse vitreitis. Occasionally, bilateral involvement can occur.[39] [40]

Diagnosis is based on clinical findings, history of recent rifabutin treatment, and clinical suspicion. Differential diagnosis includes infectious causes causing endophthalmitis. Differentiation can be especially challenging in an immunocompromised HIV-infected individual, occasionally requiring diagnostic vitrectomy to eliminate an infectious etiology.

Patients typically respond to withdrawal of the rifabutin.[39] Clinical improvement has been seen after reduction of the dosage. In addition, adjunctive use of frequently applied topical steroids and mydriatic agents resolve most of the anterior segment inflammation. Occasionally regional or oral administration of steroids is required for recalcitrant inflammation or vitreitis.

Cidofovir is a nucleotide analog used primarily for the treatment of cytomegalovirus (CMV) retinitis in patients who have HIV.[41] [42] Use of cidofovir has been associated with the development of anterior uveitis and hypotony.[43] Cidofovir seems to contribute directly to the development of anterior uveitis.[44]

Cidofovir-associated anterior uveitis typically occurs unilaterally. Patients exhibit signs of anterior uveitis with decreased vision, photophobia, and limbal injection. Anterior segment examination reveals a mild cellular reaction with fibrinous response. Posterior synechiae is occasionally present. Mild amounts of anterior vitreous humor reaction can be seen in 50% of cases.[45]

Diagnosis requires a high clinical suspicion and a recent history of cidofovir treatment. The differential diagnosis includes the entity of immune recovery uveitis (IRU). IRU occurs following immune reconstitution with HAART therapy with CD4 counts of 100 cells/µl or more. In contrast to cidofovir uveitis, IRU typically is associated with a prominent vitreitis.[46] In addition, IRU typically occurs following immune reconstitution with quiescence of the CMV lesion, whereas cidofovir uveitis can occur during an early phase of the infection.

Treatment consists of removal of the drug, if possible, with substitution of ganciclovir or other anti-CMV agents. Ocular hypotony tends to return to normal after cessation of the drug. However, prolonged use can result in ciliary body atrophy and permanent hypotony.[47] The intraocular inflammation tends to clear rapidly and seems to be sensitive to topical glucocorticoid therapy.

SCHWARTZ SYNDROME

Schwartz syndrome was initially described as increased intraocular pressure with an open chamber angle, anterior uveitis, and

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rhegmatogenous retinal detachment.[48] However, unlike with idiopathic uveitis, patients have a quiet eye and fine anterior chamber reaction. Additionally, retinal examination reveals peripheral retinal detachment.

Predisposition to Schwartz syndrome was found in patients with small oral dialysis with detachments that were flat in height, involved a large area including the macula, and were of long duration. [49] [50] [51]

Management is best accomplished by surgical repair of retinal detachment. Topical pressure-lowering agents can control acute IOP rises prior to the surgery.

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3. 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;32:2568–78.

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8. Musson DG, Bidgood AM, Olejnik O. An in vitro comparison of the permeability of prednisolone, prednisolone sodium phosphate, and prednisolone acetate across the NZW rabbit cornea. J Ocul Pharmacol. 1992;8:139–50.

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10. Whitcup SM, Ferris FL III. New corticosteroids for the treatment of ocular inflammation. Am J Ophthalmol. 1999;127:597–9.

11. Bartlett JD, Horwitz B, Laibovitz R, et al. Intraocular pressure response to loteprednol etabonate in known steroid responders. J Ocul Pharmacol. 1993; 9:157–65.

12. Howes JF. Loteprednol etabonate: a review of ophthalmic clinical studies. Pharmazie. 2000;55:178–83.

13. Controlled evaluation of loteprednol etabonate and prednisolone acetate in the treatment of acute anterior uveitis. Loteprednol Etabonate US Uveitis Study Group. Am J Ophthalmol. 1999;127:537–44.

14. La Hey E, de Jong PT, Kijlstra A. Fuchs’ heterochromic cyclitis: review of the literature on the pathogenetic mechanisms. Br J Ophthalmol. 1994;78:307–12.

15. Paivonsalo-Hietanen T, Tuominen J, Vaahtoranta-Lehtonen H, et al. Incidence and prevalence of different uveitis entities in Finland. Acta Ophthalmol Scand. 1997;75:76–81.

16. Fearnley IR, Rosenthal AR. Fuchs’ heterochromic iridocyclitis revisited. Acta Ophthalmol Scand. 1995;73:166–70.

17. Schwab IR. The epidemiologic association of Fuchs’ heterochromic iridocyclitis and ocular toxoplasmosis. Am J Ophthalmol. 1991;111:356–62.

18. La Hey E, Rothova A, Baarsma GS, et al. Fuchs’ heterochromic iridocyclitis is not associated with ocular toxoplasmosis. Arch Ophthalmol. 1992;110:806–11.

19. Barequet IS, Li Q, Wang Y, et al. Herpes simplex virus DNA identification from aqueous fluid in Fuchs’ heterochromic iridocyclitis. Am J Ophthalmol. 2000;129:672–3.

20. Bloch-Michel E, Frau E, Chhor S, Tounsi Y. Amsler’s sign associated significantly with Fuch’s heterochromic cyclitis (FHC). Int Ophthalmol. 1995;19:169–71.

21. Jones NP. Cataract surgery in Fuchs’ heterochromic uveitis: past, present, and future. J Cataract Refract Surg. 1996;22:261–8.

22. La Hey E, de Vries J, Langerhorst CT, et al. Treatment and prognosis of secondary glaucoma in Fuchs’ heterochromic iridocyclitis. Am J Ophthalmol. 1993; 116:327–40.

23. Liesegang TJ. Clinical features and prognosis in Fuchs’ uveitis syndrome. Arch Ophthalmol. 1982;100:1622–6.

24. Camras CD, Schlossman A, Posner A. Posner–Schlossman syndrome. Ocular infection and immunity. St Louis: Mosby; 1996:529–36.

25. Jap A, Sivakumar M, Chee SP. Is Posner–Schlossman syndrome benign? Ophthalmology. 2001;108:913–8.

26. Isogai E, Isogai H, Kotake S, et al. Detection of antibodies against Borrelia burgdorferi in patients with uveitis. Am J Ophthalmol. 1991;112:23–30.

27. Hirose S, Ohno S, Matsuda H. HLA-Bw54 and glaucomatocyclitic crisis. Arch Ophthalmol. 1985;103:1837–9.

28. Yamamoto S, Pavan-Langston D, Tada R, et al. Possible role of herpes simplex virus in the origin of Posner–Schlossman syndrome. Am J Ophthalmol. 1995;119:796–8.

29. Hong C, Song KY. Effect of apraclonidine hydrochloride on the attack of Posner–Schlossman syndrome. Korean J Ophthalmol. 1993;7:28–33.

30. Warwar RE, Bullock JD. Latanoprost-induced uveitis. Surv Ophthalmol. 1999;43:466–8.

31. Smith SL, Pruitt CA, Sine CS, et al. Latanoprost 0.005% and anterior segment uveitis. Acta Ophthalmol Scand. 1999;77:668–72.

32. Sacca S, Pascotto A, Siniscalchi C, et al. Ocular complications of latanoprost in uveitic glaucoma: three case reports. J Ocul Pharmacol Ther. 2001;17:107–13.

33. Schouten JT, Whittemore S. Recent development in the treatment and prevention of disseminated Mycobacterium avium complex (MAC). STEP Perspect. 1996;8:5–6.

34. MAC management. PI Perspect. 1996:16–7.

35. Tumbarello M, Tacconelli E, de Donati KG, et al. Changes in incidence and risk factors of Mycobacterium avium complex infections in patients with AIDS in the era of new antiretroviral therapies. Eur J Clin Microbiol Infect Dis. 2001; 20:498–501.

36. Kuper JI, D’Aprile M. Drug–drug interactions of clinical significance in the treatment of patients with Mycobacterium avium complex disease. Clin Pharmacokinet. 2000;39:203–14.

37. Shafran SD, Singer J, Zarowny DP, et al. Determinants of rifabutin-associated uveitis in patients treated with rifabutin, clarithromycin, and ethambutol for Mycobacterium avium complex bacteremia: a multivariate analysis. Canadian HIV Trials Network Protocol 010 Study Group. J Infect Dis. 1998;177:252–5.

38. Bhagat N, Read RW, Rao NA, et al. Rifabutin-associated hypopyon uveitis in human immunodeficiency virus–negative immunocompetent individuals. Ophthalmology. 2001;108:750–2.

39. Tseng AL, Walmsley SL. Rifabutin-associated uveitis. Ann Pharmacother. 1995;29:1149–55.

40. Cunningham ET Jr. Uveitis in HIV positive patients. Br J Ophthalmol. 2000;84:233–5.

41. Rougier MB, Neau D, Viallard JF, et al. Anterior uveitis and cidofovir. J Fr Ophthalmol. 2001;24:491–5.

42. The ganciclovir implant plus oral ganciclovir versus parenteral cidofovir for the treatment of cytomegalovirus retinitis in patients with acquired immunodeficiency syndrome: the Ganciclovir Cidofovir Cytomegalovirus Retinitis Trial. Am J Ophthalmol. 2001;131:457–67.

43. Long-term follow-up of patients with AIDS treated with parenteral cidofovir for cytomegalovirus retinitis: the HPMPC Peripheral Cytomegalovirus Retinitis Trial. The Studies of Ocular Complications of AIDS Research Group in collaboration with the AIDS Clinical Trials Group. AIDS. 2000;14:1571–81.

44. Scott RA, Pavesio C. Ocular side-effects from systemic HPMPC (cidofovir) for a non-ocular cytomegalovirus infection. Am J Ophthalmol. 2000;130:126–7.

45. Cochereau I, Doan S, Diraison MC, et al. Uveitis in patients treated with intravenous cidofovir. Ocul Immunol Inflamm. 1999;7:223–9.

46. Karavellas MP, Azen SP, MacDonald JC, et al. Immune recovery vitreitis and uveitis in AIDS: clinical predictors, sequelae, and treatment outcomes. Retina. 2001;21:1–9.

47. Taskintuna I, Rahhal FM, Rao NA, et al. Adverse events and autopsy findings after intravitreous cidofovir (HPMPC) therapy in patients with acquired immune deficiency syndrome (AIDS). Ophthalmology. 1997;104:1827–36; discussion 1836–7.

48. Netland PA, Mukai S, Covington HI. Elevated intraocular pressure secondary to rhegmatogenous retinal detachment. Surv Ophthalmol. 1994;39:234–40.

49. Matsuo N, Takabatake M, Ueno H, et al. Photoreceptor outer segments in the aqueous humor in rhegmatogenous retinal detachment. Am J Ophthalmol. 1986;101:673–9.

50. Lambrou FH, Vela MA, Woods W. Obstruction of the trabecular meshwork by retinal rod outer segments. Arch Ophthalmol. 1989;107:742–5.

51. Matsushita M, Matsuo T, Matsuo N. Retinal detachment with oral dialysis: differences in clinical features between cases with and without photoreceptor outer segments in aqueous humor. Jpn J Ophthalmol. 1990;34:338–4.

One comment on “Chapter 180 – Idiopathic and Other Anterior Uveitis Syndromes

  1. Thanks for posting this. This information really helps people that are suffering on arthritis.

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