Background: To evaluate efficacy and safety of combined pars plana vitrectomy (PPV) and scleral fixated intraocular lens (SFIOL) surgery as a single procedure.

Methods: Retrospective interventional case series done at a tertiary eye care center in Northern India. Eleven patients who underwent combined PPV and SFIOL surgery were included and analyzed retrospectively.

Results: Mean age of the patients was 43.36±15.12 years (range, 22–64 years). Eight were male. Mean baseline best corrected visual acuity (BCVA) was 0.78±0.63 logMAR units while the mean post-operative BCVA at 6 months follow-up was 0.37±0.29 logMAR units, the visual gain being statistically significant (P=0.021). None of the patients had a drop in BCVA with nine patients having final BCVA better than 0.48 logMAR units. Choroidal detachment (CD) was the only notable complication, seen in three patients. Other complications included two cases of intraoperative retinal breaks, a case each of reversible corneal edema, ocular hypertension and cystoid macular edema.

Conclusions: Combined PPV and SFIOL is an efficacious procedure for managing IOL/lens dislocation and aphakia in a single surgery. There may be short-term reversible complications with no impact on final visual gain.

Abstract: Myopia and astigmatism, two common refractive errors frequently co-exist, are degrading vision at all working distances in populations worldwide. Eyeballs having high degrees of myopia and astigmatism are known to exhibit abnormal eye shape at the anterior and posterior eye segments, but whether the outer coats of these abnormal eyeballs, cornea anteriorly and sclera posteriorly, are regulated by region-specific molecular mechanism remains unclear. Here we presented the changes in eye shape and mRNA expression levels of three genes (MMP2, TIMP2, and TGFB2), all known to participate in extracellular matrix organization, at five regions of the cornea and sclera in chickens developing high myopia and astigmatism induced by form deprivation. Our results showed that, compared to normal chicks, the highly myopic-astigmatic chicks had significantly astigmatic cornea, deeper anterior chamber, longer axial length, and higher expressions of all three genes in the superior sclera. These results imply that local molecular mechanism may manipulate the eye’s structural remodeling across the globe during refractive eye growth.

Abstract: Dopamine is known as a key molecule in retinal signaling pathways regulating visually guided eye growth, as evidenced by reduced retinal dopamine levels in various species when experimental myopia is generated. However, in C57BL/6 mice our recent work demonstrated that neither retinal dopamine levels, retinal tyrosine hydroxylase (rate-limiting enzyme in dopamine synthesis) levels, nor dopaminergic amacrine cell density/morphology, were altered during the development of form-deprivation myopia (FDM). These results suggest that retinal dopamine is unlikely associated with FDM development in this mouse strain. The role of dopamine in refractive development was further explored in this mouse strain when retinal dopamine levels were reduced by intravitreal injections of 6-OHDA, a neurotoxin that specifically destroys dopaminergic neurons. The dose was so chosen that retinal dopamine levels were reduced, but no significant changes in electroretinographic responses were detected. 6-OHDA induced significant myopic shifts in refraction in a dose-dependent manner, suggesting the involvement of dopamine in normal refractive development. Biometric measurements of ocular dimensions revealed that 6-OHDA resulted in a shorter axial length and a steeper cornea, while form-deprivation led to a longer axial length without changing the corneal radius of curvature. These results strongly suggest that in addition to the dopamine-independent mechanism, a dopamine-dependent mechanism works for refractive development. We have obtained evidence, suggesting that the dopamine-independent mechanism might be related to intrinsically photosensitive retinal ganglion cells (ipRGCs). Firstly, selective ablation of ipRGCs with an immunotoxin resulted in myopic shifts in refraction. Secondly, form-deprivation induced less myopic shifts in animals with ipRGC ablation.

Abstract: Corneal injuries and infections are the leading cause of blindness worldwide. Thus, understanding the mechanisms that control healing of the damaged cornea is critical for the development of new therapies to promptly restore vision. Innate lymphoid cells (ILCs) are a recently identified heterogeneous cell population that has been reported to orchestrate immunity and promote tissue repair in the lungs and skin after injury. However, whether ILCs can modulate the repair process in the cornea remains poorly understood. We identified a population of cornea-resident group 2 ILCs (ILC2s) in mice that express CD127, T1/ST2, CD90, and cKit. This cell population was relatively rare in corneas at a steady state but increased after corneal epithelial abrasion. Moreover, ILC2s were maintained and expanded locally at a steady state and after wounding. Depletion of this cell population caused a delay in corneal wound healing, whereas supplementation of ILC2s through adoptive transfer partially restored the healing process. Further investigation revealed that IL-25, IL-33, and thymic stromal lymphopoietin had critical roles in corneal ILC2 responses and that CCR2- corneal macrophages were an important producer of IL-33 in the cornea. Together, these results reveal the critical role of cornea-resident ILC2s in the restoration of corneal epithelial integrity after acute injury and suggest that ILC2 responses depend on local induction of IL-25, IL-33, and thymic stromal lymphopoietin.