Clinical profile and long term outcomes of eyes with choroidal detachment following trabeculectomy

Purpose:To assess the long-term outcomes of choroidal detachments (CDs) in eyes following trabeculectomy.Methods:Retrospective comparative case series. Data of patients with CDs following trabeculectomy (5-year period) with or without cataract surgery with a minimum of 3 months of follow-up were included.Results:In total, 45 patients with CDs following trabeculectomy were included. The mean age was 63.27 ± 8.68 years, (M:F = 2:1); 29 of 45 eyes (64.4%) had a baseline IOP of >24 mm Hg. Patients had a median follow-up of 22.2 (IQR: 16.2–30.5) months. Further, 10 of 45 eyes (22.2%) had CDs following suture lysis. The median onset of choroidal detachment from the time of surgery was 16.0 (IQR: 11–36) days. The mean BCVA improved from 0.62 ± 0.28 to 0.24 ± 0.27 (P < 0.001) and mean IOP increased from 4.07 ± 2.66 to 11.20 ± 5.31 (P < 0.001) at last visit. The cumulative success rates were 76.4% (95% CI: 48.4–90.5) in POAG eyes and 79.3% (95% CI: 62.8–89.1) in PACG eyes (P = 0.547). Medical management was the mainstay in all patients. Four of 45 (8.88%) patients underwent subsequent choroidal drainage.Conclusion:Choroidal detachment following modern-day trabeculectomy has favorable long-term visual acuity and IOP outcomes. There was no difference in the long-term surgical success of trabeculectomy with choroidal detachments in primary angle-closure and open-angle glaucoma eyes. Long-term follow-up is essential to prevent chronic hypotony and trabeculectomy failure.     

Assessing the Temporality Between Transitions onto Opioid Agonist Therapy and Engagement with Antiretroviral Therapy in a Cohort of HIV-Positive People Who Use Opioids Daily

AIDS and Behavior - A robust evidence-base describes the beneficial association between opioid agonist therapy (OAT) and HIV-related outcomes among people living with HIV and opioid use disorder....     

Hyperhomocysteinemia, endothelial dysfunction, and cardiovascular risk: the potential role of ADMA

Hyperhomocysteinemia is an emerging risk factor for cardiovascular disease and stroke. The mechanisms underlying the pathophysiology of hyperhomocysteinemia are not completely defined, but endothelial dysfunction resulting from impaired bioavailability of nitric oxide is a consistent finding in experimental models. One potential mechanism for decreased nitric oxide bioavailability is inhibition of endothelial nitric oxide synthase by its endogenous inhibitor, asymmetric dimethylarginine (ADMA). Elevated plasma levels of ADMA have been found in association with hyperhomocysteinemia and endothelial dysfunction in both animals and humans. Additional studies are required to determine the mechanisms by which ADMA accumulates in hyperhomocysteinemia and to define the importance of ADMA in the endothelial dysfunction of hyperhomocysteinemia in vivo.     

Potential neuroprotective role of astroglial exosomes against smoking-induced oxidative stress and HIV-1 replication in the central nervous system

Introduction: HIV-1-infected smokers are at risk of oxidative damage to neuronal cells in the central nervous system by both HIV-1 and cigarette smoke. Since neurons have a weak antioxidant defense system, they mostly depend on glial cells, particularly astrocytes, for protection against oxidative damage and neurotoxicity. Astrocytes augment the neuronal antioxidant system by supplying cysteine-containing products for glutathione synthesis, antioxidant enzymes such as SOD and catalase, glucose for antioxidant regeneration via the pentose-phosphate pathway, and by recycling of ascorbic acid.

Areas covered: The transport of antioxidants and energy substrates from astrocytes to neurons could possibly occur via extracellular nanovesicles called exosomes. This review highlights the neuroprotective potential of exosomes derived from astrocytes against smoking-induced oxidative stress, HIV-1 replication, and subsequent neurotoxicity observed in HIV-1-positive smokers.

Expert opinion: During stress conditions, the antioxidants released from astrocytes either via extracellular fluid or exosomes to neurons may not be sufficient to provide neuroprotection. Therefore, we put forward a novel strategy to combat oxidative stress in the central nervous system, using synthetically developed exosomes loaded with antioxidants such as glutathione and the anti-aging protein Klotho.