brief research report
Since the emergence of coronavirus disease-2019 (COVID-19) and its declaration as a global pandemic, multiple ophthalmic manifestations secondary to this infection have been reported, ranging from conjunctivitis to more serious and vision impairing manifestations. In this case report, we present a case of transient myopic shift observed after COVID-19 infection, in an ophthalmology specialty hospital in Beirut, Lebanon, with a discussion of the possible causes based on literature review.
COVID-19; SARS-COV-2; Pandemic.
To evaluate the density of conjunctival goblet cells (GCs) from in vivo confocal microscopy (IVCM) and impression cytology (IC) and mucin expression in ten glaucomatous patients treated with preservative-free latanoprost (Monoprost®)
Ten glaucomatous patients (10 eyes) were enrolled. Conjunctiva was examined clinically and morphologically by IVCM and IC. Both IVCM and IC were performed at baseline, and after the 1st and 4th month of Monoprost® therapy. GC density (GCD) in cells⁄mm2 was the main outcome measurement.
At baseline, mean GCD was 147+/-78 cells/mm2 for IVCM and 114+/-62 cells/mm2 for IC GCD. At month one, mean GCD was 149+/-69 and 120+/-56 measured with IVCM and IC, respectively (p=0.31 for IVCM and p=0.40 for IC). At month four, GCD increased to 162+/-81 and 134+/-61 measured with IVCM and IC, respectively (p=0.02 for IVCM and p=0.02 for IC).
Treatment with preservative-free (PF) latanoprost was associated with an increase in conjunctival GCD in glaucomatous eyes. Further studies are mandatory to verify this finding because its validation may have important consequences in the medical management of glaucoma.
In vivo confocal microscopy; Conjunctiva; Goblet cell; Prostaglandin; Cytology impression; Polymerase chain reaction (PCR).
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.
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.
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.
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.
Glaucoma; Micropulse laser; Cyclophotocoagulation.
brief research report
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.
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.
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.
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.
Retinoblastoma; Retinal endothelial cells; Ocular oncology; Imatinib mesylate.
Nowadays intravitreal drug injection is the most frequent treatment for retinal diseases. Despite widely use endophthalmitis is already most feared complication of every intravitreal injection in each patient. In clinical setting topical antibiotics have been widely used as a precaution to prevent endophthalmitis however recent published evidence showed it to be unnecessary. Furthermore repeated use of topical antibiotics might give rise to antibiotic resistance in conjunctival flora and thus more aggressive endophthalmitis. Strict asepsis has been awarded as the main rule for endophthalmitis prophylaxis intravitreal injection.
Intravitreal injection; Steroid; Anti-vascular endothelial growth factor (VEGF); Topical antibiotic; Enodphthalmitis; Antibiotic resistance.
To make an account of published implant-related complications (IRC) by a systematic review of the literature.
A systematic search of Pubmed and Scopus databases and Google Scholar engine was performed with selection criteria to detect papers on IRC. We excluded unrelated papers and reviewed selected ones. We considered papers that did not explicitly state about occurrence or not occurrence of IRC as non-IRC reporting. Main outcome measures were the number of papers reporting on complications, IRC, and types of IRC.
After the search, selection, and addition, we studied 109 papers. Incidence of IRC was 4.5%, half required explantation. While 26 implant studies found IRCs (23%), 13 case reports on surgical complications, 8 (61.5%) of them reported IRC. Frequent complications were conjunctival erosion, blockage of the tube, migration to anterior chamber or damage to surrounding tissues.
Most papers did not report on IRC. Length or nature of studies may skew finding IRC. The incidence of IRC was 4.5%. Hard and sharp implants carry a greater risk of IRC and explantation.
Implant-related complications (IRC); Glaucoma surgery; Anterior bleb forming.
The liver is the most common site of uveal melanoma (UM) metastasis with approximately 50% of UM patients being affected. With no proven therapies that mitigate metastases the mortality rate is 85% within the first year after detection of the liver disease. In this study, we provide a mechanistic understanding of the de-regulation of the TP53-MDM2 pathway in UM, which plays a central role in tumor biology.
We investigated the TP53-MDM2 signaling pathway in the microenvironment of liver metastases taken from both a murine orthotopic xenograft and post-mortem metastatic UM human liver. These findings were studied in-depth using both primary and metastatic UM cell lines treated with the MDM2 antagonist Nutlin-3a and the sirtuin inhibitor and transcriptional activator of TP53, Tenovin-6.
De-regulation of the TP53-MDM2 signaling pathway is specific to the liver microenvironment, providing a survival mechanism for UM metastases. Tenovin-6, not Nutlin-3a, reduced UM cell survival by increasing the percentage of cell death and reducing the percentage of proliferating cells. Tenovin-6 increased acetylation of p53, reduced ubiquitination of the protein, and acted as a cell cycle regulator.
Our findings suggest that in patients with metastatic UM de-regulation of TP53-MDM2 signaling pathway promotes growth of the liver metastases and provides pre-clinical information on the potential of targeting of the TP53-MDM2 signaling pathway via Tenovin-6.
Uveal melanoma; Ocular tumors; Nutlin-3a; Tenovin-6; TP53; MDM2.
2591 Compass Rd. Ste 115 Glenview, IL 60026, USA andAssistant Professor of OphthalmologySection Director of Oculoplastic and Reconstructive SurgeryRush University School of Medicine Chicago, IL 60026, USA
Medicine Practitioner Hôpital ophtalmique Jules-Gonin Lausanne, Switzerland
Ophthalmology Specialist Department of Ophthalmology Queen Elizabeth Hospital Kota Kinabalu, Malaysia
Faculty Department of Vitreous-RetinaZhongshan Ophthalmic Center Sun Ya-Sen University Guangdong, China