Necrotising retinopathies simulating acute retinal necrosis syndrome.

AIM: To determine an aetiological diagnosis in patients presenting with necrotising retinopathies that simulate acute retinal necrosis (ARN). METHODS: Retrospective non-comparative case series. The charts of 16 patients presenting with a clinical impression of ARN at Pitie-Salpetriere Hospital, Paris, France, between 1994 and 1999, who required initial antiviral therapy were reviewed. All of the patients had extensive laboratory tests. Anterior chamber paracentesis was performed on 14 patients and evaluated by polymerase chain reaction (PCR) and/or the Witmer-Goldmann coefficient to determine the cause of retinitis. Three of the 14 cases also had diagnostic vitrectomy. Responses to specific treatment, initiated based on laboratory results, and the final outcome were evaluated. RESULTS: Seven of the 16 patients were female and nine were male. The retinitis was bilateral in five patients and unilateral in 11 patients. The average age of the patients at presentation was 53.6 years. 13 patients were immune deficient for various reasons. Upon initial presentation, the patients' visual acuities were less than 20/200 in 68% of the affected eyes. The final diagnoses, based on laboratory data and therapeutic response were toxoplasmic retinochoroiditis (62.5%), syphilitic retinitis (12.5%), aspergillus endophthalmitis (12.5%), Behcet's disease (6.2%), and intraocular lymphoma (6.2%). Visual acuity was stabilised or improved in 12 patients (75%). Two patients with aspergillosis died despite antifungal therapy. CONCLUSIONS: Toxoplasmic retinochoroiditis is the major cause of retinal necrosis that simulates ARN, and PCR analysis of the aqueous humour is helpful in establishing the diagnosis. Such atypical toxoplasma retinochoroiditis may be associated with poor visual outcome.

[Ocular metastasis of cutaneous melanoma]. / Métastase oculaire d'un mélanome cutané.

We report a case of vitreal metastases from cutaneous melanoma. We describe the clinical findings and the histological aspects of the lesions, which allows us to discuss the diagnosis of masquerade syndrome and highlight the diagnostic importance of vitreous biopsy.

Caterpillar setae-induced acute anterior uveitis: a case report.

PURPOSE: To report uveitis secondary to ocular penetration of caterpillar hairs (setae). METHODS: Case report. A documented attack of acute anterior uveitis was caused by initially overlooked penetration of caterpillar setae. RESULTS: A 66-year-old man presenting with unilateral hypertensive keratouveitis was treated with antiherpes simplex medication (along with local anti-inflammatory and cycloplegic agents) after anterior chamber paracentesis and serologic testing. Laboratory testing was negative. Resolution occurred after 5 days, and corneal clearing showed a predescemetic caterpillar seta. CONCLUSION: Patient history taken in an anterior uveitis setting should include gardening habits and searching for possible exposure to insects or arachnids.

Cognitive decline is associated with systemic oxidative stress: the EVA study. Etude du Vieillissement Artériel.

OBJECTIVE: To determine whether systemic oxidative stress status is associated with cognitive decline. DESIGN: A longitudinal population-based study. SETTING: A cohort study of older subjects in Nantes, France. PARTICIPANTS: A total of 1166 high cognitive functioning subjects aged 60 to 70 in the Etude du Vieillissement Arteriel (EVA) cohort with a 4 year follow-up. MEASUREMENTS: Subjects completed a baseline interview and a global cognitive test (Mini-Mental Status Examination (MMSE)). Blood samples were obtained at baseline to determine plasma levels of selenium, carotenoids, thiobarbituric acid reactant substances (TBARS), an indicator of lipoperoxidation, and red blood cell vitamin E. Risk of cognitive decline, defined as a loss of 3 points in MMSE score between baseline and the 4 year follow-up, was assessed by oxidative stress level. RESULTS: Subjects with the highest levels of TBARS show an increased risk of cognitive decline (adjusted odds ratio (OR) = 2.25; confidence interval (CI) 95% = 1.26-4.02). This result is reinforced in the lower antioxidant status subgroup. Subjects with low levels of selenium have an increased risk of cognitive decline (OR = 1.58; CI 95% = 1.08-2.31) after adjustment for various confounding factors. CONCLUSIONS: These results suggest that increased levels of oxidative stress and/or antioxidant deficiencies may pose risk factors for cognitive decline. The direct implication of oxidative stress in vascular and neurodegenerative mechanisms that lead to cognitive impairment should be further explored.