Intrascleral intraocular lens fixation with ab interno trabeculotomy in patients with exfoliation glaucoma with lens subluxation.

PURPOSE: To evaluate the surgical outcomes of intrascleral intraocular lens (IOL) fixation using ab interno trabeculotomy (LOT) in patients with exfoliation glaucoma with lens subluxation. STUDY DESIGN: Retrospective case series. METHODS: Twenty eyes of 18 patients with exfoliation glaucoma and lens or IOL subluxations were included. Three success criteria were based on postoperative intraocular pressure (IOP) (A, ≤15 mmHg; B, ≤18 mmHg; C, ≤21 mmHg). The IOP, number of glaucoma medications, and visual acuity were compared before and after surgery. Success probability was analyzed using Kaplan-Meier survival curves. Cox proportional hazards' regression models were used to examine prognostic factors for surgical failure. RESULTS: The mean follow-up period was 23.4 ± 7.8 months. The mean IOP significantly decreased from 23.2 ± 6.8 mmHg preoperatively to 14.0 ± 4.4 mmHg at 1 year postoperative (P<0.001). Postoperative hyphema and vitreous hemorrhage were observed in seven and 15 eyes, respectively, and washout in the anterior chamber or vitreous cavity was performed in four eyes. Postoperative IOP spikes and hypotony were observed in four eyes each. Glaucoma reoperation was performed in two eyes. The success rates at 12 months were 65%, 85%, and 90% using criteria A, B, and C, respectively. The IOP at 1 month after surgery was a significant prognostic factor for surgical failure according to criterion A (hazard ratio: 1.08; P=0.034). CONCLUSION: Intrascleral IOL fixation combined with microhook LOT is a promising option in cases of exfoliation glaucoma with subluxated lens/IOL; however, the high rate of postoperative hyphema and vitreous hemorrhage should be noted.

A novel bleb revision technique: lining with tenon's patch graft for treatment of large, ischemic, leaking blebs with severe conjunctival scarring after trabeculectomy.

PURPOSE: We report a new bleb lining technique with Tenon's patch graft for late-onset leakage from large ischemic bleb with severe conjunctival scarring and impractical conjunctival mobilization after trabeculectomy. STUDY DESIGN: Retrospective case series. METHODS: This study includes six cases with late-onset leakage from large ischemic blebs. Small Tenon's tissue is dissected from the incisional site or a previously made inferior incision for Tenon's anesthesia. A passage is created from the small incision to the leaking area of the bleb using a bleb knife or micro scissors. The Tenon's tissue, stained with indocyanine green, is inserted under the ischemic bleb's conjunctiva. A transconjunctival compression suture is placed across the leaking point to fix the Tenon patch graft positionally. RESULTS: In all cases, bleb leakage was completely sealed immediately after surgery. In 4 cases, the closure of the bleb leakage was maintained after surgery during the follow-up period (6-17 months). In two cases, bleb leakage recurred from different leaking points 7 or 9.5 months after the surgery; however, repeated tenon's patch lining revisions successfully closed these leakages. The intraocular pressure at the final visit was 5-13 mmHg (median, 10 mmHg) without glaucoma medication or additional glaucoma surgery. CONCLUSION: Tenon's patch-lining technique is a promising method for bleb leakage with large ischemic bleb and impractical conjunctival mobilization.

Relationship between Inter-Eye Asymmetries in Corneal Hysteresis and Visual Field Severity in Patients with Primary Open-Angle Glaucoma.

This study investigated the influence of asymmetric corneal hysteresis (CH) on asymmetric visual field impairment between right and left eyes in patients with primary open-angle glaucoma (POAG) without a history of intraocular surgery. CH, corneal resistance factor (CRF), and corneal compensated intraocular pressure (IOPcc) were measured using the Ocular Response Analyzer. Differences between the eyes (right eye-left eye: DIFRL) and CH-based and in target parameters (higher CH eye-lower CH eye: DIFCH) were calculated in the same patient. In 242 phakic eyes of 121 patients, older age (p < 0.001), lower CH (p = 0.001), and lower CRF (p = 0.007) were significantly associated with worse standard automated perimetry (SAP) 24-2 mean deviation (MD). The DIFsRL in axial length (p = 0.003), IOPcc (p = 0.028), and CH (p = 0.001) were significantly associated with the DIFRL in SAP24-2 MD, but not in central corneal thickness (CCT), Goldmann applanation tonometry (GAT) measurement, and CRF. When dividing the patients into two groups based on the median of the CH DIFsCH (0.46), the DIFsCH in CRF (p < 0.001), IOPcc (p < 0.001), CCT (p = 0.004), SAP24-2 MD (p < 0.001), and SAP10-2 MD (p = 0.010) were significantly different between the groups. Large inter-eye asymmetry in CH is an important explanatory factor for disease worsening in patients with POAG.

Gemcitabine induces Parkin-independent mitophagy through mitochondrial-resident E3 ligase MUL1-mediated stabilization of PINK1.

Mitophagy plays an important role in the maintenance of mitochondrial homeostasis. PTEN-induced kinase (PINK1), a key regulator of mitophagy, is degraded constitutively under steady-state conditions. During mitophagy, it becomes stabilized in the outer mitochondrial membrane, particularly under mitochondrial stress conditions, such as in treatment with uncouplers, generation of excessive mitochondrial reactive oxygen species, and formation of protein aggregates in mitochondria. Stabilized PINK1 recruits and activates E3 ligases, such as Parkin and mitochondrial ubiquitin ligase (MUL1), to ubiquitinate mitochondrial proteins and induce ubiquitin-mediated mitophagy. Here, we found that the anticancer drug gemcitabine induces the stabilization of PINK1 and subsequent mitophagy, even in the absence of Parkin. We also found that gemcitabine-induced stabilization of PINK1 was not accompanied by mitochondrial depolarization. Interestingly, the stabilization of PINK1 was mediated by MUL1. These results suggest that gemcitabine induces mitophagy through MUL1-mediated stabilization of PINK1 on the mitochondrial membrane independently of mitochondrial depolarization.