Endophthalmitis after small-gauge vitrectomy: a retrospective case series from Sweden.

PURPOSE: To investigate the anatomical and functional outcomes of acute-onset endophthalmitis after small-gauge vitrectomy. METHODS: Retrospective case series of patients who underwent 23- or 25-gauge vitrectomy at four centres in Sweden between 2008 and 2012. Postvitrectomy endophthalmitis was identified through the search of the journal records of each institution, and the diagnosis was based on clinical criteria regardless of culture results. RESULTS: Twenty-four patients (24 eyes) were included. The incidence of endophthalmitis following small-gauge vitrectomy was 0.14%. Indications for small-gauge vitrectomy enclosed epiretinal membrane (n = 13), retinal detachment (n = 5) and others (n = 6). Surgical technique included 23- and 25-gauge vitrectomy (23:1). Four eyes had sutured sclerotomies, and two had postoperative hypotony <7 mmHg. Days to endophthalmitis presentation varied between 1 and 21 (mean 6 ± 6). Treatment methods included the following: tap and antibiotic injection (n = 7), tap, antibiotic injection with subsequent vitrectomy (n = 2) and prompt vitrectomy with antibiotics (n = 15). Sixteen eyes (66.7%) were culture positive, whereas the other eight cases were culture negative. Anatomical results included evisceration (n = 1), phthisis (n = 1), and globe intact (n = 22). Presenting best corrected visual acuity (BCVA) were hand motion (n = 14), light perception (n = 7), counting fingers (n = 2), and no data (n = 1). Functionally 19 eyes (79%) had Snellen VA ≥0.1; 11 eyes (46%) had VA ≥0.5 Mean logMar BCVA preoperatively and at the last follow-up were 2.07 ± 0.6 and 0.79 ± 0.99, respectively. CONCLUSIONS: In spite of good anatomical and functional results, this study showed higher rate of endophthalmitis than the latest reports suggesting that small-gauge vitrectomy has reached the safety level of standard 20-gauge vitrectomy when infectious endophthalmitis is concerned.

Enhanced age-related cataract in copper-zinc superoxide dismutase null mice.

BACKGROUND: As the lens is constantly exposed to light and oxygen that generate harmful reactive oxygen species, the importance of the intracellular antioxidant enzyme copper-zinc superoxide dismutase for the protection against age-related cataract development was explored. METHODS: The development of lens opacities and the lens oxidative status were studied in different age groups of mice lacking copper-zinc superoxide dismutase and in wild-type mice. The lens opacities were quantified from lens photographs using digital image analysis. Thereafter, the lenses were homogenized and analysed regarding their contents of reduced glutathione and protein carbonyls suggestive of protein oxidation. RESULTS: The 18-week-old mice of both genotypes had clear lenses. At 1 year of age, the copper-zinc superoxide dismutase null mice had developed cortical lens opacities, whereas the wild-type mice did not show equivalent changes until 2 years of age. The lens contents of glutathione decreased only in the 2-year-old wild-type mice, whereas the carbonyls increased over time without any differences between the two genotypes. CONCLUSIONS: This study indicates that the lack of copper-zinc superoxide dismutase may accelerate age-related lens opacity development and that intracellular superoxide-derived oxidative stress may be damaging to the lens during ageing. Participation of the anti-oxidant enzyme copper-zinc superoxide dismutase in the protection against age-related cataract was thus suggested.

Enhanced diabetes-induced cataract in copper-zinc superoxide dismutase-null mice.

PURPOSE: Oxidative stress is thought to contribute to diabetes-induced cataract, and the authors have previously demonstrated that lenses from mice lacking the antioxidant enzyme copper-zinc superoxide dismutase (SOD1) show elevated levels of superoxide radicals and are more prone in vitro to develop glucose-induced cataract than are wild-type lenses. In the present study the effect of streptozotocin-induced diabetes mellitus on cataract formation in SOD1-null and wild-type mice in vivo was examined. METHODS: Eight weeks after diabetes was established by repeated intraperitoneal streptozotocin injections, the mice were killed and the lenses removed and photographed in retroillumination. The cataract was quantified from the photographs by digital image analysis and the lens contents of glutathione (GSH) as well as the lens protein carbonyl contents suggestive of protein oxidation were analyzed. RESULTS: The streptozotocin-induced diabetic SOD1-null mice developed more cataract than the diabetic wild-type mice. Also, lens GSH levels were lower in the diabetic SOD1-null mice than in the nondiabetic SOD1-null mice. However, the protein carbonyls were equally raised in the diabetic mice of both genotypes. CONCLUSIONS: The increased cataract formation and the compromised antioxidant capacity found in the diabetic SOD1-null lenses thus emphasize the involvement of superoxide radicals in diabetes-induced cataract.

Interleukin-1alpha downregulates extracellular-superoxide dismutase in human corneal keratoconus stromal cells.

PURPOSE: The purpose of this investigation was to elucidate the regulation of corneal extracellular superoxide dismutase (SOD3) synthesis in keratoconus. We compared the basal and cytokine-regulated SOD3 synthesis in cultured human stromal cells from keratoconus corneas to stromal cells from normal and bullous keratopathy corneas. METHODS: Keratocyte cultures were obtained from patients undergoing corneal transplantation for keratoconus and bullous keratopathy, and from healthy donor corneas. The cell lines obtained were cultured until near confluence and interleukin-1alpha, interleukin-6, transforming growth factor beta, or platelet derived growth factor were added to the media. The phenotypes of the cultured cells were assessed by immunocytochemical expression of alpha-smooth muscle actin and CD34. SOD3 protein contents were determined in the culture media with ELISA after 24, 48, 72, and 96 h. RESULTS: Interleukin-1alpha had an inhibitory effect on SOD3 synthesis exclusively in the keratoconus cultures (p<0.01). Platelet derived growth factor induced a reduction in SOD3 synthesis in all groups (p<0.05). CONCLUSIONS: Here, we demonstrate that cultured keratoconus stromal cells respond with a reduced SOD3 synthesis to interleukin-1alpha, which is not the case in corresponding normal or bullous keratopathy cells. Since interleukin-1alpha is upregulated in corneal trauma and inflammation, keratoconus corneas may muster an insufficient oxidative defense under such conditions.

Glucose-induced cataract in CuZn-SOD null lenses: an effect of nitric oxide?

Lenses from mice lacking the antioxidant enzyme copper-zinc superoxide dismutase (SOD1) show elevated levels of superoxide radicals and are prone to developing cataract when exposed to high levels of glucose in vitro. As superoxide may react further with nitric oxide, generating cytotoxic reactive nitrogen species, we attempted to evaluate the involvement of nitric oxide in glucose-induced cataract. Lenses from SOD1-null and wild-type mice were incubated with high or normal levels of glucose (55.6 and 5.56 mM). A nitric oxide synthase inhibitor (L-NAME) or a nitric oxide donor (DETA/NO) was added to the culture medium. Cataract development was assessed using digital image analysis of lens photographs and cell damage by analyzing the leakage of lactate dehydrogenase. The levels of superoxide radicals in the lenses were also measured. L-NAME was found to reduce cataract development and cell damage in the SOD1-null lenses exposed to high glucose. On the other hand, DETA/NO accelerated cataract development, especially in the SOD1-null lenses. These lenses also showed a higher leakage of lactate dehydrogenase than wild-type controls. We conclude that a combination of high glucose and absence of SOD1 increases the formation of cataract and that nitric oxide probably contributes to this process.

In vitro glucose-induced cataract in copper-zinc superoxide dismutase null mice.

The purpose of this study was to evaluate the involvement of the superoxide radical in glucose-induced cataract using lenses from mice lacking the cytosolic copper-zinc superoxide dismutase (SOD1). Lenses from wild-type mice and SOD1 null mice were kept in organ culture with either 5.6 or 55.6 mM glucose for 6 days. The cataract formation was followed with digital image analysis and ocular staging. The lens damage was further quantified by analysis of the leakage of lactate dehydrogenase into the medium by the uptake of 86Rb and by determining the water content of the lenses. The formation of superoxide radicals in the lenses was assessed with lucigenin-derived chemiluminescence. Immunohistochemical staining for SOD1 was also performed on murine lenses. The SOD1 null lenses exposed to high glucose developed more cataract showed an increased leakage of lactate dehydrogenase and developed more oedema compared to the control lenses. At 5.6 mM glucose there was no difference between the SOD1 null and wild-type lenses. Staining for SOD1 was seen primarily in the cortex of the wild-type lens. This in vitro model suggests an involvement of the superoxide radical and a protective effect of SOD1 in glucose-induced cataract formation.