[Experiences with CO2 laser-assisted sclerectomy surgery]. / CO2-lézerrel végzett mélysclerectomiával szerzett tapasztalatok.

INTRODUCTION: CO2 laser- assisted sclerectomy surgery (CLASS) can be used for the surgical treatment of open-angle glaucoma. AIM: To introduce our results with CLASS. METHOD: We performed 21 CLASS operations using OT-134-IOPtiMate (IOPtima Ltd, Ramat-Gan, Israel). Patients were examined on the 1st day, and in the 1st, 3rd, 6th, 9th and 12th months postoperatively. We evaluated intraocular pressure (IOP), antiglaucomatous medication-use, visual acuity, complications. RESULTS: Mean age was 65.6 yrs. Complete success (no hypotensive medication required to target IOP) was achieved in 61.1% (18 patients) at 6 months, whereas in 50% (10 patients) at 12 months. Qualified success (hypotensive medication required to target IOP) was achieved in 72.2% and in 70%, preoperative mean IOP was 29.2 ± 9.4 Hgmm, which falled to 17.7 ± 4.9 Hgmm and 17.3 ± 4.3 Hgmm, respectively. Antiglaucomatous medication use falled significantly from 2.90 ± 0.83 to 2.05 ± 1.46. Apart from 1 macroperforation, no serious complication occurred. CONCLUSIONS: With CLASS it is possible to effectively lower intraocular pressure in open-angle glaucoma. Orv Hetil. 2017; 158(18): 701-705.

Analysis of complement factor H Y402H, LOC387715, HTRA1 polymorphisms and ApoE alleles with susceptibility to age-related macular degeneration in Hungarian patients.

PURPOSE: Recent studies strongly support the role of genetic factors in the aetiology of age-related macular degeneration (AMD). We investigated the frequency of Tyr402His polymorphism of the complement factor H (CFH) gene, Ser69Ala polymorphism at LOC387715, rs11200638 polymorphism of the HTRA1 gene and different apolipoprotein E (ApoE) alleles in Hungarian patients with AMD in order to determine the disease risk conferred by these factors. METHODS: In a case-control study, we performed clinical and molecular genetic examination of 105 AMD patients (48 patients in the early and 57 in the late subgroup) and 95 unrelated healthy controls. Detailed patient histories were recorded with the use of a questionnaire focusing on known risk factors for AMD. RESULTS: In the early AMD subgroup, homozygous CFH, LOC387715 or HTRA1 polymorphisms conferred a 4.9-fold (95% confidence interval [CI] 1.7-14.2), 7.4-fold (95% CI 2.1-26.2) or 10.1-fold (95% CI 2.5-40.8) risk of disease, respectively. In the late AMD subgroup, carriers of two CFH, LOC387715 or HTRA1 risk alleles were at 10.7-fold (95% CI 3.7-31.0), 11.3-fold (95% CI 3.2-40.4) or 13.5-fold (95% CI 3.3-55.4) greater disease risk, respectively. Two CFH and one LOC387715 risk alleles in combination conferred a 15.0-fold (95% CI 3.2-71.0) increase in risk, whereas two LOC387715 risk alleles combined with one CFH risk allele was associated with a 14.0-fold (95% CI 2.1-95.1) increased risk for late AMD. ApoE alleles neither increased disease risk nor proved to be protective. CONCLUSIONS: The CFH, LOC387715 and HTRA1 polymorphisms are strongly associated with the development of AMD in the Hungarian population. The association is particularly pronounced when homozygous risk alleles are present and in the late stages of the disease.

Bright cyclic rearing protects albino mouse retina against acute light-induced apoptosis.

PURPOSE: Previous studies have shown that albino rats born and raised in bright cyclic light are protected from light-induced apoptosis. The present study was designed to determine if bright cyclic rearing provides protection against retinal degeneration caused by acute light exposure in albino mice. METHODS: BALB/c mice were born in dim cyclic light (5 lux, 12 h ON/OFF). At 1 week of age, half of the litters were moved into 400 lux cyclic light. At 5 weeks of age, mice raised in the dim or bright cyclic conditions were divided into two groups. One group was placed in constant light (3,000 lux for 72 h) and the other was maintained in its original cyclic light environment. Control and constant light-stressed mice were dark-adapted for 24 and 48 h, respectively, after which their eyes were removed immediately for morphologic evaluation or preparation of rod outer segment (ROS) membranes. ROS lipids were extracted and fatty acid methyl esters were analyzed by gas-liquid chromatography. Eyes used for TUNEL (terminal deoxynucleotidyl transferase mediated dUTP nick end labeling) and DNA fragmentation assays were enucleated immediately after the 72 h light exposure. RESULTS: Measurement of outer nuclear layer (ONL) thickness indicated there was no difference in the number of viable photoreceptor cells in the dim-reared controls compared to bright-reared controls. Constant light exposure significantly reduced the ONL thickness in dim- and bright-reared groups, with the largest change occurring in the dim-reared mice. TUNEL assay showed no apoptotic photoreceptor cells in either control group; however, apoptotic nuclei could be detected in both exposed groups, with the largest number found in the dim-reared mice. After light exposure, DNA fragmentation was prominent in dim-reared mice, but was not present in bright-reared animals. There was no significant difference in the fatty acid composition of ROS membranes in the dim- and bright-reared control mice. However, constant light exposure resulted in a greater loss of docosahexaenoic acid (22:6n-3) in the ROS of dim-reared animals. CONCLUSIONS: Mice raised in a bright cyclic light environment are protected against light-induced apoptosis. We suggest that the protection is due to the up-regulation of cell survival pathways or the down-regulation of pathways that are vulnerable to acute cell stress.

L-NAME protects against acute light damage in albino rats, but not against retinal degeneration in P23H and S334ter transgenic rats.

Two previous studies have shown that N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of neuronal nitric oxide synthase, protects retinas of albino rats and mice from damaging levels of light. The aims of the present study were two-fold: (1) to confirm the protective effect of L-NAME on wild type albino rats and (2) to determine if L-NAME protects the retinas of transgenic rats with P23H and S334ter rhodopsin mutations. In the first study, albino rats born and raised in 5-10 lux cyclic light were injected intraperitoneally with either L-NAME or its inactive isomer D-NAME 30 min before being placed in bright light (2700 lux) for 24hr. Electroretinograms (ERGs) were recorded before light treatment and 2 days after cessation of exposure, and eyes were enucleated for morphologic evaluation. L-NAME, but not D-NAME provided structural protection of photoreceptor cells from light damage. The functional rescue was not statistically significant between the drug treated groups. In the second study, albino WT, P23H transgenic, and S334ter transgenic rats were born and raised in 400 lux cyclic light. Three week old animals received daily intraperitoneal injections of L-NAME or D-NAME for 4 weeks, and the same drugs were added to their drinking water. At 7 weeks of age, the ERG sensitivity curves and the outer nuclear layer thickness of both transgenic groups were significantly reduced compared to WT controls. However, administration of L-NAME did not protect against retinal degeneration caused by the rhodopsin mutation in either strain of transgenic (P23H and S334ter) rats. Thus, although photoreceptor cell death in light damage and inherited retinal degenerations share a common apoptotic mechanism, there must be significant 'up-stream' differences that allow selective neuroprotection by L-NAME.