PurposeThere is a limited understanding of factors that influence the efficacy of topical glaucoma medication. Our study is a long-term, case–control analysis of how systemic antihypertensive (anti-HTN) medications influence the change in IOP after initiating prostaglandin (PG) drop therapy.Materials and methodsA retrospective chart review of 3,781 patients was performed on patients with a diagnosis of glaucoma suspect that progressed to primary open-angle glaucoma (POAG) by ICD-9 codes over a 10-year period. Inclusion criteria consisted of the following: 1) progression from preglaucoma to glaucoma diagnosis in a time span of ≥6 months; 2) two visual fields recorded between these dates; 3) initial average IOP of both eyes of ≥21 mmHg; and 4) initiation of topical PG therapy alone. IOP (in mmHg) was measured at initiation of PG drops and at next visit.ResultsOne hundred eleven patients were qualified for analysis. Patients not on anti-HTN agents had an average IOP decrease of 6.38±0.56 mmHg. Comparatively, patients on anti-HTN agents had an average IOP decrease of 6.66±0.48 mmHg (P=0.61). In addition, there was no statistical difference between IOP decrease between patients on single vs multiple systemic anti-HTN agents (P=0.85). There were eight nonresponders to PGs on no anti-HTN medications and 12 nonresponders on anti-HTN medication (P=0.55).ConclusionSystemic anti-HTN medication use did not significantly impact IOP reduction after topical PG initiation for POAG. Additionally, nonresponse to PG therapy was not correlated to systemic anti-HTN use.

Vesicular stomatitis virus (VSV) applied intranasally produces a well-characterized encephalitis. However, mice that experienced controllable stress via an escapable foot-shock (ES) demonstrated an enhanced immune response relative to mice that experienced uncontrollable stress (inescapable foot shock, IS) or non-stressed control mice (NS). These differences began as early as 1 day post-infection, where IS mice show a more robust cytokine response than ES or NS mice. By 3 days post-infection, however, ES mice showed enhanced inflammatory cytokine responses in the olfactory bulb. We used the Ingenuity Pathways Analysis (IPA) platform to identify regulatory genes responsible for the differences. IPA identified miRNA146a as an upstream regulator of the antiviral response and qPCR found elevated levels (~5-fold) of miRNA146a in the olfactory bulb from ES versus IS mice. miRNA levels in the non-stressed group were below detectable limits. These results suggested increased inflammation in the brains of ES mice, which were supported by more aggressive weight loss in ES mice compared to IS or NS mice as the encephalitis progressed. By 28 days post-infection, surviving mice subjected to ES continue to show increased immune activation as evidenced by increased leukocyte infiltration and enhanced production or infiltration of CD103+ (memory phenotype) T cells relative to IS or NS mice.

Background and Objective: Sustained-release dexamethasone intravitreal implant is an effective treatment for macular edema secondary to retinal vein occlusion (RVO) but ocular hypertension is a side effect. This study evaluated whether the addition of a single combination IOP-lowering medication will reliably control intraocular pressure (IOP) for those patients.   Study Design/Patients and Methods: Retrospective chart review of 62 patients that underwent multiple injections of combination anti-VEGF and sustained-release dexamethasone intravitreal implant for macular edema secondary to RVO. IOP spikes were treated with brimonidine 0.2% - timolol 0.5%. IRB approval was obtained.   Results: The average elevated IOP requiring treatment was 28.6 mmHg. The average IOP after adding brimonidine 0.2% - timolol 0.5% was 16.7 mmHg. 100 percent of treatment cycles had an IOP< 30 mmHg after starting treatment.   Conclusions: Using one combination IOP-lowering drop can reliably control the ocular hypertension that occurs secondary to combination therapy for macular edema in RVO.