Background Choroidopathy is a rare manifestation of systemic lupus erythematosus (SLE). This entity is associated with active phases of severe SLE and it is frequently accompanied by acute kidney failure, central nervous system involvement and coagulopathy. Purpose To evaluate the choroid thickness of patients with lupus nephritis (LN) without choroidopathy, and to compare this with that of age-matched SLE patients without LN and healthy control subjects. Study design Cross-sectional case control study. Material and methods Fifteen women with LN in remission phase (study group), 15 women with SLE in remission without LN (SLE control group), and 15 healthy women (healthy control group), without ocular diseases or significant refractive error, were recruited. Full ophthalmological examination and a macular optical coherence tomography in enhanced depth imaging mode were performed. The choroid thickness was measured at nine macular points and six lines of mean choroidal thickness were determined. A comparative analysis between the three groups was performed using the one-way ANOVA test and the paired t-test. The choroid thickness of patients under corticotherapy was also compared to that of patients without corticotherapy. Additionally, the correlation between choroid thickness and disease duration was evaluated using the Pearson analysis. Results The mean macular choroidal thickness was 295.73 ± 67.62 μm in the study group, 233.34 ± 41.01 µm in the SLE control group, and 240.98 ± 37.93 μm in the control group ( p = 0.00006 and p = 0.0003, respectively). Additionally, the choroid thickness was significantly thicker than in the SLE and healthy control groups at the foveal ( p = 0.004 and p < 0.000), nasal ( p < 0.000 and p = 0.001), superior ( p = 0.002 and p < 0.000) and inferior ( p < 0.000 and p = 0.001) mean lines. The choroidal thickness in this group was not associated with the duration of the disease. The subgroup of patients with LN under corticotherapy did not reveal a significantly different choroidal thickness. Conclusion This study suggests a relationship between LN and choroidal changes, which may represent an increased risk for choroidopathy in these patients. Choroid thickening was not related with the duration of the disease. This thickening may be correlated with histopathological changes similar to those occurring in kidney glomeruli.

Endophthalmitis is an infection of the vitreous or aqueous humor of the eye. Although it rarely occurs in the neonatal period it has been previously diagnosed in preterm infants.Endogenous endophthalmitis is when eye infection is secondary to septicemia and represent 20% of the cases of endophthalmitis. Pseudomonas aeruginosa is responsible for more than 75% of invasive neonatal eye infections. The course of pseudomonal endophthalmitis is typically fulminant, developing over hours even in early diagnosis. For survivors, the usual result is blindness of the affected eye.We report the case of a preterm infant who developed septicemia and was later diagnosed as having a pseudomonas endophthalmitis.

Cytomegalovirus (CMV) retinitis may occur in profoundly immunocompromised patients and be the initial AIDS-defining infection. The incidence and prevalence of CMV retinitis has declined substantially in the era of highly active antiretroviral therapy (HAART); nevertheless, it remains a leading cause of ocular morbility. We report the case of a 40-year-old man with blurred vision and pain in the right eye, three weeks after the initiation of effective HAART treatment. Ocular examination revealed a panuveitis causing an anterior chamber reaction with hypopyon and a dense vitreous haze. An endogenous endophthalmitis was suspected and treatment was ensued, without improvement. A vitreous tap was performed, and a positive polymerase chain reaction for CMV was found. A diagnosis of immune recovery uveitis (IRU) was made, and the patient responded to treatment with valganciclovir and dexamethasone. IRU is an intraocular inflammation that develops in patients with HAART-induced immune recovery and inactive CMV retinitis, although cases of active CMV retinitis have been described. Presentation with panuveitis and hypopion is rare and may be misleading regarding diagnosis and management.

We report a case of a 74-year-old female, with a mitral heart valve, who presented with pain and blurred vision in the right eye for 2 days. Her visual acuity was light perception (LP) in the right eye and 20/40 in the left eye. Slit lamp examination showed corneal edema and hypopyon, and a view of the right fundus was impossible. Echography showed vitreous condensation. One day after presentation, the patient developed acute lung edema requiring hospitalization, so she was not submitted to vitreous tap and intravitreal treatment. The cardiac and systemic evaluations revealed a mitral endocarditis secondary to Enterococcus faecalis. The patient improved systemically with treatment with gentamicin, vancomycin, and linezolid. Her visual acuity remained as no LP, and her intraocular pressure (IOP) has been controlled with brimonidine bid despite developing a total cataract with 360° posterior synechia. A cardiac source for endogenous endophthalmitis should be considered in the presence of a prosthetic cardiac valve. The treatment and followup must be made in cooperation with a cardiologist specialist, but the ophthalmologist can play a key role in the diagnosis.

PurposeWe aim to report a case of a 15 year‐old patient with severe and rapid bilateral visual impairment due to progressive cone dystrophy and describe the associated mutations.MethodsThis is a case report of a patient with a rare disease who underwent full ophthalmologic evaluations including optical coherence tomography (OCT) of the posterior pole, fundus autofluorescence (FAF) and electroretinography (ERG).ResultsA 15‐year‐old girl was presented at our Department with progressive vision loss and poor colour vision complaints. The patient reported these complaints for a year, despite a full uneventful ophthalmic evaluation at that time. Best‐corrected visual acuity was 6/60 for each eye and Ishihara 24‐plates colour test was altered. Fundoscopic evaluation showed a maculopathy with spotty pigment changes in addition to temporal pallor of the optic disk. Posterior pole OCT showed a reduced outer nuclear layer and retinal pigment epithelium unspecific changes. FAF revealed a central dark area surrounded by a ring of increased autofluorescence. ERG was inconclusive due to poor collaboration, although it was hypothesised to have a slight cone dysfunction. Moreover, genetic analyses of ABCA4 and CDHR1 genes were found to be positive for multiple mutations. The c.6816 + 2T>A (p.Leu2035Pro) mutation was never described and the c.6104T>C (p.Leu2035Pro) mutation was only present in one patient with Stargardt disease. After a period of 2 years of follow‐up visual function and retinal disease remained stable.ConclusionsProgressive cone dystrophy is a rare inherited ocular disorder characterized by the loss of cone cells. This case report emphasizes the need to reach a clear diagnosis when uncommon symptoms appear in an otherwise normal ophthalmic evaluation and also describe newer mutations in ABCA4 gene enhancing our knowledge about this disease.