Systemic supplemental oxygen therapy during accelerated corneal crosslinking for progressive keratoconus: randomized clinical trial.

PURPOSE: To investigate the potential additive effect of systemic supplemental oxygen administered during accelerated corneal crosslinking (CXL) for progressive keratoconus (KC). SETTING: Academic center. DESIGN: Randomized clinical trial. METHODS: Eyes with progressive KC randomized to 3 different CXL protocols were included. The first group (OA-CXL) included 19 eyes that underwent an accelerated CXL protocol (9 mW/cm2 for 10 minutes) while receiving systemic oxygen at a rate of 5 L/min for 10 minutes. The second group consisted of 14 eyes undergoing the same accelerated CXL protocol without supplemental oxygen therapy (A-CXL). The third group (C-CXL) comprised 14 eyes undergoing conventional CXL according to the Dresden protocol. All subjects were followed up for at least 6 months. Visual acuity, keratometry and corneal biomechanical parameters including corneal hysteresis and corneal resistance factor (CRF) were measured preoperatively and 6 months postoperatively. RESULTS: Reduction in maximum keratometry (Kmax) was significantly greater in the OA-CXL group (P = .01). At baseline, the mean Kmax was 54.31 ± 3.64 diopters (D) in the OA-CXL group, 54.66 ± 4.99 D in the A-CXL group, and 56.03 ± 5.28 D in the C-CXL group (P = .58), which reached 53.58 ± 3.24 D, 54.59 ± 4.65 D, and 55.87 ± 4.73 D at 6 months in the 3 study groups, respectively (P = .115). The mean CRF increased significantly only in the OA-CXL group from a baseline value of 6.32 ± 2.12 mm Hg to 7.38 ± 1.88 mm Hg at 6 months (P = .009). CONCLUSIONS: This study suggests superior efficacy of an accelerated CXL protocol coupled with systemic oxygen supplementation when compared with the accelerated CXL protocol and the conventional protocol in eyes with progressive KC. In addition to greater reduction in Kmax as the primary outcome, improvement in corneal biomechanics was also observed at 6 months.

The ocular hypotensive effect of saffron extract in primary open angle glaucoma: a pilot study.

BACKGROUND: The progressive nature of glaucoma and its growing incidence make its therapy an important target for research. The role of oxidative damage in the pathogenesis of glaucoma makes antioxidants such as saffron extract an attractive target for potential clinical use. Herein, we evaluate the effect of aqueous saffron extract on intraocular pressure (IOP) in eyes with primary open-angle glaucoma (POAG). METHODS: Thirty-four eyes of 34 clinically stable POAG patients receiving treatment with timolol and dorzolamide eye drops were enrolled in this prospective, comparative, randomized interventional pilot study. Eligible subjects were randomized to receive 30 mg/day aqueous saffron extract orally (17 subjects, 17 eyes) or placebo (17 subjects, 17 eyes) for one month as an adjunct to timolol and dorzolamide. Following treatment, both study groups entered a one-month wash-out period. The main outcome measure was IOP during treatment and after the wash-out period. RESULTS: Mean baseline IOP was 12.9 ± 3.7 versus 14.0 ± 2.5 mmHg in the saffron and control groups, respectively (p = 0.31). After three weeks of treatment, IOP was significantly decreased to 10.9 ± 3.3 mmHg in the saffron group as compared to 13.5 ± 2.3 mmHg in the control group (p = 0.013). At four weeks, IOP was still significantly lower in the saffron group (10.6 ± 3.0 versus 13.8 ± 2.2 mmHg, p = 0.001). At the end of the wash-out period, IOP was 12.9 ± 3.0 in the saffron group versus 14.2 ± 2.0 mmHg in the control group (p = 0.175). None of the patients experienced side effects during the study and wash-out period. CONCLUSIONS: Oral aqueous saffron extract seems to exert an ocular hypotensive effect in primary open-angle glaucoma. This effect became evident after three weeks of therapy.The current study was registered at the International Clinical Trials Registry Platform (ICTRP) as IRCT201201278832N1.

Pregabalin and gabapentin for post-photorefractive keratectomy pain: a randomized controlled trial.

PURPOSE: To evaluate the efficacy of pregabalin and gabapentin for reducing post-photorefractive keratectomy (PRK) pain. METHODS: In this randomized clinical trial, 150 subjects undergoing PRK were allocated into 3 groups. In addition to the routine regimen, pregabalin 75 mg, gabapentin 300 mg, and placebo were administered 3 times daily for 3 days, in groups 1, 2, and 3, respectively. Subjects could take acetaminophen-codeine 300/10 mg tablets every 4 hours as needed. Patients completed a pain assessment survey (visual analogue scale ranging from 0 = no pain to 10 = most severe pain) 7 times in the first 3 days following PRK and also recorded the number of consumed acetaminophen-codeine tablets. RESULTS: Age, sex, refractive error, ablation depth, and mitomycin-C (MMC) application were similar in the 3 study groups (all p values>0.05). Overall pain scores in the placebo group were 0.9 and 1 unit higher than the pregabalin (p=0.029) and gabapentin (p=0.023) groups, respectively. Severe pain (score >7) was more frequent in the placebo group on the morning of the first postoperative day (p=0.043). The difference in the number of consumed acetaminophen-codeine tablets was statistically borderline (p=0.061) and less in the pregabalin (7.9 ± 5.2) and gabapentin (9.0 ± 4.1) groups in comparison to the placebo group (10.3 ± 5.6). CONCLUSIONS: Pregabalin and gabapentin seem to be helpful in alleviating post-PRK pain when combined with other measures. Depending on availability, either compound can be used as an adjuvant for pain control in this setting.

Loss of function mutations in the gene encoding latent transforming growth factor beta binding protein 2, LTBP2, cause primary congenital glaucoma.

Glaucoma is a heterogeneous group of optic neuropathies that manifests by optic nerve head cupping or degeneration of the optic nerve, resulting in a specific pattern of visual field loss. Glaucoma leads to blindness if left untreated, and is considered the second leading cause of blindness worldwide. The subgroup primary congenital glaucoma (PCG) is characterized by an anatomical defect in the trabecular meshwork, and age at onset in the neonatal or infantile period. It is the most severe form of glaucoma. CYP1B1 was the first gene genetically linked to PCG, and CYP1B1 mutations are the cause of disease in 20-100% of patients in different populations. Here, we report that LTBP2 encoding latent transforming growth factor beta binding protein 2 is a PCG causing gene, confirming results recently reported. A disease-associated locus on chromosome 14 was identified by performing whole genome autozygosity mapping in Iranian PCG families using high density single nucleotide polymorphism chips, and two disease-segregating loss of function mutations in LTBP2, p.Ser472fsX3 and p.Tyr1793fsX55, were observed in two families while sequencing candidate genes in the locus. The p.Tyr1793fsX55 mutation affects an amino acid close to the C-terminal of the encoded protein. Subsequently, LTBP2 expression was shown in human eyes, including the trabecular meshwork and ciliary processes that are thought to be relevant to the etiology of PCG.