Volume 4, Issue 1

  • 2020, April

    observational study

    Micropulse Transscleral Cyclophotocoagulation: Our ExperienceOpen Access

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    Abstract [+]

    Introduction

    Traditionally, ciliary body destruction has been used to treat uncontrolled intraocular pressure (IOP) following maximally tolerable medical therapy. This is due to the large number of complications seen with this procedure. However, recently a new technique of sub-threshold laser or micropulse laser, is able to provide selective destruction of the ciliary body in a controlled manner. This avoids most of the complications seen with other modalities. We have performed a small case descriptive pilot study to assess the effectiveness of micropulse transscleral cyclophotocoagulation (MP-TSCPC) in lowering IOP.

    Methods

    This pilot study was conducted on four patients in the age range 55-70-years with intractable glaucoma. Two patients had primary angle closure glaucoma, one-each had steroid-induced glaucoma and neovascular glaucoma. Mean baseline IOP was 32±2.4 mmHg. Mean number of glaucoma medications were 2.5±1.5. All patients underwent 180° MP-TSCPC. Absolute success was defined as IOP<20 mmHg without acetazolamide.

    Results

    Following the procedure the patients were followed-up at days 1,7,30 and 90. At the last follow-up of the study, mean IOP was 18.2±1.2 mmHg in all four patients. Mild anterior chamber inflammation was the only complication noted. Mean number of glaucoma medications reduced to 1.5±1.0 following the procedure. Thus, absolute success was achieved in all patients.

    Conclusion

    This small pilot study validates other studies which show effectiveness of MP-TSCPC as an efficient and safe procedure to lower IOP. This procedure can be used over a wide variety of cases, though the indications for such procedures are still evolving. More extensive and long-term studies will clarify the position of this procedure in our glaucoma management practices.

    Keywords

    Glaucoma; Micropulse laser; Cyclophotocoagulation.


  • 2020, December

    brief research report

    Anti-Platelet-Derived Growth Factor Receptor-Beta Therapy Does Not Trigger Retinal Endothelial Cell ToxicityOpen Access

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    Abstract [+]

    Background

    Retinoblastoma (Rb) is a highly angiogenic tumor, for which anti-vascular endothelial growth factor (VEGF) therapies have shown limited success in clinical setting. Recent investigations demonstrated upregulation of ancillary axis including the platelet-derived growth factor (PDGF) when VEGF is inhibited. This illustrates the need for novel therapeutics. Previous work from our lab showed inhibition of the platelet-derived growth factor receptor-beta (PDGFR-β) by imatinibmesylate (IM), inhibited Rb cells proliferation in vitro. Novel therapies ideally are tumor-specific, leaving normal non-cancerous cells a stroma to perform their homeostatic functions. Rb treatments induce apoptosis of the retinal endothelial cells, causing the release of pro-inflammatory cytokines and chemokines to the microenvironment.

    Aims

    We investigated the role of the PDGFR-β in the tumor microenvironment and how inhibition of this signaling pathway, as a potential targeted therapy, impacts angiogenesis in human retinal microvascular endothelial cells (hRECs), specialized neurons arborizing the retinal microvasculature.

    Results

    Our results demonstrated that inhibition of the PDGFR-β signaling pathway by IM affects the proliferation of the Rb cells, but not hRECs. PDGFR-β signaling is not required for hRECs angiogenic activity, although it reduces the percentage of VEGF-Aproducing cells.

    Conclusion

    These results illustrate a lack of functional activity PDGFR-β signaling in hRECs and points to a more tumor-specific therapeutic option. This is of critical importance as success of treatment also depends on the ability of the normal tissues to remain healthy after sensitization and/or killing of the Rb tumor.

    Keywords

    Retinoblastoma; Retinal endothelial cells; Ocular oncology; Imatinib mesylate.