Spontaneous hyphaema and acute ocular hypertension associated with severe lens-induced uveitis.

PURPOSE: to report the occurrence of spontaneous hyphaema and acute ocular hypertension in four patients with severe lens-induced anterior uveitis. METHODS: retrospective case series. RESULTS: four patients with mature cataract developed severe acute, unilateral, anterior uveitis associated with spontaneous hyphaema formation and acutely elevated intraocular pressure. None of the patients had a history of trauma or evidence of angle, iris, or retinal neovascularization. Prompt cataract removal led to resolution of the inflammation, clearing of the anterior chamber haemorrhage, and normalization of intraocular pressure in all four affected eyes. CONCLUSIONS: spontaneous hyphaema and acute ocular hypertension can occur in patients with severe lens-induced intraocular inflammation in the absence of trauma or ocular neovascularization.

Unexplained vision loss following removal of epiretinal membrane.

PURPOSE: To report unexplained severe central vision loss accompanied by a dense central scotoma as an uncommon complication following epiretinal membrane removal. METHODS: Retrospective, multicentred, case series. RESULTS: Six patients underwent uncomplicated vitrectomy surgery between 2000 and 2007 at four separate retina practices for removal of an epiretinal membrane. Preoperative vision ranged from 20/60 to 20/100, with a median of 20/70. On the first day postoperatively, all patients noted decreased vision ranging from counting fingers to light perception and were found to have a dense central scotoma. Posterior segment examination revealed a white, oedematous macula in all affected eyes. Vision improved minimally during the follow-up period, which ranged from 2 months to 5 years. The final vision ranged from 20/200 to hand movements. No anatomic or physiologic cause for the decreased vision and central scotoma was identified. CONCLUSIONS: While uncommon, severe, permanent, central vision loss accompanied by a dense central scotoma can occur following epiretinal membrane removal and should be considered when assessing the risks and benefits of such surgery.

Mooren''s ulcer following extracapsular cataract extraction.

PURPOSE: Prior cataract surgery is a recognized risk factor for the development of Mooren''s ulcer, but the demographic and clinical features of a large cohort of such patients have not been described. METHODS: The authors performed a retrospective review of demographic and clinical data from 14 eyes in 13 patients who developed Mooren's ulcer following extracapsular cataract extraction at Aravind Eye Hospital in Madurai, South India. RESULTS: Eight (62%) of the 13 patients were men and 5 (39%) were women. The median age in our population was 65 years, with a range of 45 to 85 years. The median number of months from surgery to the onset of Mooren's ulcer was 19, with a range of 4 to 156 months. Of the 14 eyes with prior cataract surgery, the location of the ulcer was at or contiguous with the wound in 10 eyes (71%), which was 2.5 times more likely than other circumlimbal locations, and only one patient (8%) had bilateral disease. CONCLUSIONS: Mooren''s ulcer may occur following extracapsular cataract extraction and when it does it is most likely to be unilateral and contiguous with the wound. These findings support the notion that exposure of normally concealed corneal antigens may contribute to the pathogenesis of Mooren''s ulcer in some patients.

HLA-DR17 and Mooren's ulcer in South India.

OBJECTIVE: To investigate the association between Mooren's ulcer and human leucocyte antigen (HLA) type DR17(3) in patients from the Tamil Nadu State of South India. METHODS: Blood samples from 38 patients with Mooren's ulcer and 45 age- and sex-matched controls were obtained prospectively. HLA-DR and HLA-DQ typing was performed by PCR using sequence-specific primers. RESULTS: Fifteen (40%) of the patients with Mooren's ulcer tested positive for HLA-DR17(3) compared with seven (16%) of the controls (p = 0.01). Seventeen (45%) of the patients also tested positive for the closely linked HLA-DQ2 compared with 11 (24%) of controls (p = 0.05). When adjusted for multiplicity, the correlation between HLA-DR17(3) and Mooren's ulcer remained significant (p = 0.03). CONCLUSIONS: These data demonstrate an association between HLA-DR17(3) and Mooren's ulcer in South Indian patients, supporting autoimmune theories about the pathogenesis of the disorder.

Inflammatory ocular hypertension syndrome (IOHS) in patients with syphilitic uveitis.

AIM: To determine the prevalence and clinical characteristics of the inflammatory ocular hypertension syndrome (IOHS) in patients with uveitis and serological evidence of syphilis. METHODS: A retrospective, observational case review of 39 consecutive patients with uveitis and serological evidence of syphilis was carried out between January 1977 and December 2001. Other causes of uveitis were excluded. The prevalence and clinical characteristics of IOHS among patients with uveitis and serological evidence of syphilis were documented. IOHS was defined as an increase in intraocular pressure (IOP) of more than 21 mm Hg that began at the onset of acute, recurrent, or chronic anterior chamber inflammation and reversed promptly with appropriate anti-inflammatory or antimicrobial treatment. RESULTS: Of the 39 patients with uveitis and serological evidence of syphilis, eight eyes from seven patients (18%) presented with IOHS, a significantly higher prevalence than in the uveitis population at large (2.3%; p<0.001). Best-corrected visual acuity varied from 20/20 to 20/200, with a median of 20/40, and three of the eight eyes (37.5%) had granulomatous features, including large keratic precipitates and, in two eyes, Koeppe nodules. Intraocular pressure varied from 23 to 51 mm Hg, with a mean of 36 and a median of 34. One patient had bilateral IOHS. CONCLUSIONS: Syphilitic uveitis should be included in the differential diagnosis of IOHS along with more commonly recognised causes.

Year 2 efficacy results of 2 randomized controlled clinical trials of pegaptanib for neovascular age-related macular degeneration.

OBJECTIVE: To evaluate the efficacy of a second year of pegaptanib sodium therapy in patients with neovascular age-related macular degeneration (AMD). DESIGN: Two concurrent, multicenter, randomized, double-masked, sham-controlled studies (V.I.S.I.O.N. [Vascular Endothelial Growth Factor Inhibition Study in Ocular Neovascularization] trials). PARTICIPANTS: Patients with all angiographic neovascular lesion compositions of AMD were enrolled. In combined analyses, 88% (1053/1190) were re-randomized at week 54, and 89% (941/1053) were assessed at week 102. INTERVENTIONS: At week 54, those initially assigned to pegaptanib were re-randomized (1:1) to continue or discontinue therapy for 48 more weeks (8 injections). Those initially assigned to sham were re-randomized to continue sham, discontinue sham, or receive 1 of 3 pegaptanib doses. MAIN OUTCOME MEASURES: Mean change in visual acuity (VA) over time and mean change in the standardized area under the curve of VA and proportions of patients experiencing a loss of > or =15 letters from week 54 to week 102; losing <15 letters (responders) from baseline to week 102; gaining > or =0, > or =1, > or =2, and > or =3 lines of VA; and progressing to legal blindness (20/200 or worse). RESULTS: In combined analysis, mean VA was maintained in patients continuing with 0.3-mg pegaptanib compared with those discontinuing therapy or receiving usual care. In patients who continued pegaptanib, the proportion who lost >15 letters from baseline in the period from week 54 to week 102 was half (7%) that of patients who discontinued pegaptanib or remained on usual care (14% for each). Kaplan-Meier analysis showed that patients continuing 0.3-mg pegaptanib for a second year were less likely to lose > or =15 letters than those re-randomized to discontinue after 1 year (P<0.05). The proportion of patients gaining vision was higher for those assigned to 2 years of 0.3-mg pegaptanib than receiving usual care. Progression to legal blindness was reduced for patients continuing 0.3-mg pegaptanib for 2 years. CONCLUSIONS: Continuing visual benefit was observed in patients who were randomized to receive therapy with pegaptanib in year 2 of the V.I.S.I.O.N. trials when compared with 2 years' usual care or cessation of therapy at year 1.

Pegaptanib sodium for neovascular age-related macular degeneration: two-year safety results of the two prospective, multicenter, controlled clinical trials.

OBJECTIVE: To evaluate the safety of pegaptanib sodium injection, a specific vascular endothelial growth factor (VEGF) antagonist, in the treatment of neovascular age-related macular degeneration (AMD) during 2 years of therapy. DESIGN: Two concurrent, prospective, randomized, multicenter, double-masked, sham-controlled studies. METHODS: Patients with all angiographic choroidal neovascularization lesion compositions of AMD received either intravitreous pegaptanib sodium (0.3 mg, 1 mg, 3 mg) or sham injections every 6 weeks for 54 weeks. Those initially assigned to pegaptanib were re-randomized (1:1) to continue or discontinue therapy for 48 more weeks; sham-treated patients were re-randomized (1:1:1:1:1) to continue sham, discontinue, or receive one of the pegaptanib doses. MAIN OUTCOME MEASURES: All reported adverse events, serious adverse events, and deaths. PARTICIPANTS: In year 1, 1190 subjects received at least one study treatment (0.3 mg, n = 295; 1 mg, n = 301; 3 mg, n = 296; sham, n = 298); 7545 intravitreous injections of pegaptanib were administered. In year 2, 425 subjects (0.3 mg, n = 128; 1 mg, n = 126; 3 mg, n = 120; sham, n = 51) continued the same masked treatment as in year 1 and received at least one study treatment in year 2; 2663 intravitreous injections of pegaptanib were administered in these subjects. RESULTS: All doses of pegaptanib were well tolerated. The most common ocular adverse events were transient, mild to moderate in intensity, and attributed to the injection preparation and procedure. There was no evidence of an increase in deaths, in events associated with systemic VEGF inhibition (e.g., hypertension, thromboembolic events, serious hemorrhagic events), or in severe ocular inflammation, cataract progression, or glaucoma in pegaptanib-treated patients relative to sham-treated patients. In year 1, serious injection-related complications included endophthalmitis (12 events, 0.16%/injection), retinal detachment (RD) (6 events [4 rhegmatogenous, 2 exudative], 0.08%/injection), and traumatic cataract (5 events, 0.07%/injection). Most cases of endophthalmitis followed violations of the injection preparation protocol. In patients receiving pegaptanib for >1 year, there were no reports of endophthalmitis or traumatic cataract in year 2; RD was reported in 4 patients (all rhegmatogenous, 0.15%/injection). CONCLUSION: The 2-year safety profile of pegaptanib sodium is favorable in patients with exudative AMD.

[Approach to the patient with acute anterior uveitis]. / Manejo del paciente con uveítis anterior aguda.

Uveitis refers to inflammation of the uveal tract, which includes the iris, ciliary body, and choroid. Common usage has expanded this definition, however, to include intraocular inflammation of any type. Hence, retinitis, retinal vasculitis, and papillitis are also grouped under uveitis, even in the absence of significant uveal tract inflammation. Uveitis can also be secondary to corneal, scleral, or orbital inflammation. Experience has shown that identifying the primary focus of intraocular inflammation is important, both for establishing a diagnosis and as a predictor of natural history and response to therapy. A number of ocular and systemic syndromes are recognized to cause anterior uveitis. Clues to the diagnosis of the more commonly encountered anterior uveitis syndromes are outlined below. It is important to pay particular attention to the severity of the anterior chamber inflammation, and to note the presence of anterior granulomatous findings since the intensity and character of the inflammation can sometimes suggest a diagnosis.

Biotypes and serotypes of Haemophilus influenzae ocular isolates.

AIM: To determine which subtypes of Haemophilus influenzae are most commonly associated with ocular disease, and whether the site of ocular H influenzae infection is correlated with specific subtypes of the organism. METHODS: The biotypes and serotypes of ocular H influenzae isolates collected at the Francis I Proctor Foundation between March 1989 and January 2000 were examined. A total of 62 ocular isolates were retrieved from frozen storage and plated on chocolate agar. Biotypes were assigned based upon the ability of the isolates to produce indole, urease, and ornithine decarboxylase. Capsular subtypes a-f were determined by slide agglutination using commercially available subtype specific antisera. Identified biotypes and serotypes were then analysed with regard to site of infection. RESULTS: Patient age ranged from 1 to 92 years with a median age of 45 years. 38 (61%) of the isolates were biotype II, 23 (37%) were biotype III, and one (2%) was biotype VII. All of the isolates were non-encapsulated and thus serologically non-typable. H influenzae biotype II was found in 28 of 48 (58%) conjunctivitis cases, five of eight (63%) keratitis cases, and two of two (100%) endophthalmitis cases. Biotype III was found in 20 of 48 (42%) conjunctivitis cases, two of eight (25%) keratitis cases, and a single case of dacryocystitis. Biotype VII was associated with one of eight (13%) keratitis cases. CONCLUSION: Most ocular H influenzae isolates appear to be serologically non-typable strains from biotypes II and III, less virulent subtypes that frequently colonise the nasopharynx. In addition, the site of ocular H influenzae infections appears to be largely independent of species subtype.

Ocular syphilis.

Although the annual incidence of primary and secondary syphilis has dropped to the lowest rate recorded, syphilis remains an important cause of ocular disease. Uveitis is the most common ocular manifestation of syphilis in both HIV-positive and HIV-negative patients, and the diagnosis should prompt an analysis of the cerebrospinal fluid to exclude associated neurosyphilis. Newer modalities such as enzyme immunoassays and genomic amplification using the polymerase chain reaction may prove to be useful techniques to detect Treponema pallidum in intraocular specimens. The preferred treatment for all stages of syphilis remains parenteral penicillin G, although the preparation, dose, route of administration, and duration of therapy are dictated by the stage of disease and various host factors. All patients diagnosed with ocular syphilis should be tested for HIV, because the presence of a primary genital chancre increases the risk of acquiring or transmitting HIV, and because risk factors for the two diseases are similar.

Ischemic maculopathy in patients with acquired immunodeficiency syndrome.

PURPOSE: To describe the characteristics of ischemic maculopathy in patients with human immunodeficiency virus (HIV) infection, as a means of understanding this uncommon disorder more fully. METHODS: This is a multicenter, retrospective review of clinical data available for five HIV-infected patients who were given the diagnosis of ischemic maculopathy. RESULTS: All cases had been diagnosed on the basis of fluorescein angiograms obtained after patients complained of vision loss. Four of the five patients had bilateral macular disease. Visual acuity at presentation in the nine affected eyes ranged from 20/20 to count fingers. Vision loss was gradual in both eyes of one patient and was abrupt in onset in seven eyes. Each of the seven eyes with abrupt vision loss had opacification of the superficial retina and/or intraretinal hemorrhages near the fovea. Fluorescein angiography revealed enlargement of the foveal avascular zone and mild staining of the juxtafoveal vessels in affected eyes. Six eyes had active or clinically inactive cytomegalovirus retinitis at presentation, and a seventh eye developed cytomegalovirus retinitis 2 weeks later. All patients were receiving anticytomegalovirus drugs when they developed visual symptoms. Visual acuity remained stable in five eyes, became worse in two eyes, and improved in two eyes; final visual acuity ranged from 20/25 to count fingers. CONCLUSIONS: Ischemic maculopathy may cause profound and permanent vision loss in HIV-infected individuals. Fluorescein angiography should be considered in all HIV-infected patients with unexplained loss of vision. The pathogenesis of ischemic maculopathy remains unknown.