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We analyzed OCT biomarkers of 65 eyes with treatment-naive RVO and ME. While none of the factors analyzed predicted successful treatment discontinuation, early improvements in vision and DRIL were associated with long-term visual outcomes.

PURPOSE To identify clinical and anatomic factor-associated vision loss in eyes with treatment-naive diabetic macular edema and good initial visual acuity. METHODS Retrospective cohort study after long-term history of eyes with untreated center-involving diabetic macular edema and baseline visual acuity ≥ 20/25 seen at the University of California, Davis Eye Center between March 2007 and March 2018. We collected characteristics including diabetes type, hemoglobin A1c, presence of visual symptoms, visual acuity, and diabetic retinopathy severity; and spectral-domain optical coherence tomography biomarkers including central subfield thickness, intraretinal cyst size, intraretinal hyperreflective foci, disorganization of retinal inner layers, and outer layer disruptions to determine factors associated with vision loss as defined by DRCR Protocol V as threshold for initiating aflibercept therapy. RESULTS Fifty-six eyes (48 patients) with untreated diabetic macular edema and mean baseline visual acuity of logMAR 0.05 ± 0.05 (Snellen 20/22) were followed for an average of 5.1 ± 3.3 years, with a median time to vision loss of 465 days (15 months). Older age (hazard ratio [HR] 1.04/year, P = 0.0195) and eyes with severe NPDR (HR 3.0, P = 0.0353) or proliferative diabetic retinopathy (HR 7.7, P = 0.0008) had a higher risk of a vision loss event. None of the spectral-domain optical coherence tomography biomarkers were associated with vision loss except central subfield thickness (HR 0.98, P = 0.0470) and cyst diameter (HR 1.0, P = 0.0094). CONCLUSION In eyes with diabetic macular edema and good initial vision, those with older age and worse diabetic retinopathy severity should be monitored closely for prompt treatment initiation when vision loss occurs.

Despite being a common presenting symptom to eye-care clinics, many ophthalmologists have difficulty diagnosing and managing ocular surface pain. The purpose of this review is to discuss potential causes of ocular surface pain, focusing on both nociceptive and neuropathic aetiologies. Specifically, we outline an approach to the diagnosis of ocular surface pain and focus on various management strategies, providing supporting evidence on the efficacy of various treatments.

Metabolic syndrome (MetS) describes a cluster of cardio-metabolic factors that predispose to type 2 diabetes mellitus (T2DM) and atherosclerotic cardiovascular disease (ASCVD). While 35% of Americans suffer from this disorder, the specific pathways related to this disease are largely underexplored. The prevailing consensus is that inflammatory pathways contribute to the pathogenesis of this disease, and therefore new research has uncovered how inflammation plays a critical role in the development and progression of MetS. The purpose of this review is to understand the role of major inflammatory mechanisms and their role in MetS. Our review identifies that adipose tissue (AT) contributes to the inflammatory pathways through the release of pro-inflammatory adipokines such as leptin and chemerin and dysregulation of anti-inflammatory adiponectin. Chemokines and cytokines deriving from monocytes are also altered and promote inflammation and insulin resistance. Circulating inflammatory biomarkers including C-reactive protein (CRP), fibrinogen, Serum amyloid A (SAA), cytokines, and chemokines have also been linked to the pathogenesis of MetS. Researchers have identified the significance of CRP levels in predicting future sequelae of MetS such as ASCVD. Mast cells in subcutaneous adipose tissue (SAT) promote both inflammation and fibrosis. Thus, both AT and phagocyte activity define MetS as an inflammatory disorder.

PURPOSE The aim of this study was to evaluate the prevalence of histopathologically confirmed ocular surface squamous neoplasia (OSSN) in clinically diagnosed pterygium samples at a tertiary center in Northern California, over a 10-year period (2009-2019). METHODS A retrospective chart review of patients older than 18 years with clinically diagnosed benign pterygium requiring excision was conducted. Clinically suspected pterygia were excised using standard techniques and routinely submitted to the University of California Davis for pathologic evaluation. Demographic, clinical, surgical, and pathological information were recorded and analyzed. The prevalence rate of OSSN was calculated. RESULTS A total of 348 consecutive specimens were evaluated. The mean (±SD) age of the patients was 58 ± 12 years, with a near equal sex representation. A total of 57 (16%) pterygia were recurrent at initial presentation. Histopathologic results demonstrated a single case of OSSN. This patient did not have a documented history of carcinoma in other organs or any history of herpes virus, human papilloma virus, or human immunodeficiency virus infection. CONCLUSIONS The prevalence of histopathological OSSN in clinically suspected pterygia within our sample was approximately 0.3%. Because of shared clinical characteristics of pterygia and OSSN, a high index of suspicion and judicious use of anterior segment optical coherence tomography enable for effective preoperative diagnosis of OSSN. However, in the absence of clinical expertise or high-resolution optical coherence tomography, routine tissue pathologic examination may be warranted.

BACKGROUND AND OBJECTIVE: To identify factors associated with successful treatment discontinuation in eyes with retinal vein occlusions (RVOs) and macular edema (ME) in real-world settings. PATIENTS AND METHODS: Retrospective study of 214 eyes with RVO and ME with 24-month follow-up at five academic centers. Regression analyses identified factors associated with (1) successful treatment discontinuation for at least 6 months without fluid recurrence and (2) best-corrected visual acuity (BCVA) at 24 months. RESULTS: Forty percent of eyes with branch RVO and 35% with central RVO (CRVO) / hemi-retinal RVO (HRVO) successfully discontinued therapy without fluid recurrence, with median time to discontinuation of 6 and 7 months, respectively. Lower 6-month central subfield thickness was associated with greater likelihood of treatment discontinuation within 24 months for eyes with CRVO/HRVO ( P = .001), whereas better 6-month BCVA was associated with better 24-month BCVA for all RVO subtypes ( P < .001). CONCLUSION: Early anatomic response at 6 months is associated with greater likelihood of stopping treatments. [ Ophthalmic Surg Lasers Imaging Retina . 2021;52:84–92.]

Metabolic syndrome (MetS) is as a cluster of cardio-metabolic factors that greatly increase the risk of chronic diseases such as type II diabetes mellitus and atherosclerotic cardiovascular disease. In the United States, obesity, physical inactivity, aging, and genetics (to a minor extent) have arisen as risk factors for developing MetS. Although 35% of American adults suffer from MetS, its pathogenesis largely remains unknown. Worse, there is a lack of screening and optimum therapy for this disease. Researchers have consequently turned towards metabolomics to identify biomarkers to better understand MetS. The purpose of this review is to characterize various metabolites and their potential connections to MetS. Numerous studies have also characterized MetS as a disease of increased inflammation, and therefore this review also explores how metabolites play a role in various inflammatory pathways. Our review explores a broad range of metabolites including biogenic amines, branched chain amino acids, aromatic amines, phosphatidylcholines, as well as a variety of other molecules. We will explore their biochemical pathways and their potential role in serving as biomarkers.

Diabetic retinopathy (DR) is the leading cause of vision loss in working-age adults in the developed world. This review discusses the current approach to managing the disease, such as glycemic and blood pressure control, as well as laser photocoagulation, as well as emerging concepts and controversies on novel therapies. In recent years, the rise of intraocular anti-angiogenesis treatments is changing the paradigm of classic laser photocoagulation in the management of DR, but its long-term benefits remain an area of controversy. We also discuss new targets including anti-inflammation, neuroprotection, and novel laser technologies. Finally, we discuss new advances in retinal imaging that has vastly improved the diagnosis and management of DR. Diagnosis and management of diabetic retinopathy is a rapidly progressing field. Emerging concepts in ophthalmic imaging, medical treatments, and surgical approaches provide insights into how DR management will evolve in the near future.

BackgroundMetabolic syndrome (MetS), a cardio-metabolic cluster afflicting 35% of American adults, increases cardiovascular disease (CVD) and type-2 diabetes (T2DM) risk. Increased levels of trimethylamine N-oxide (TMAO), a metabolite derived from choline and L-carnitine, correlates with CVD and T2DM. However, the precise role of TMAO and its precursors in MetS remains unclear. We tested the hypothesis that choline, L-carnitine and TMAO in MetS patients without CVD or T2DM would be altered and correlate with inflammatory markers.Materials and methodsThis was an exploratory study of 30 patients with nascent MetS (without CVD or T2DM) and 20 matched controls. MetS was defined by the Adult Treatment Panel III criteria. TMAO and its precursors were evaluated from each patient’s frozen early morning urine samples and quantified using liquid chromatography/mass spectrometry (LC-MS). These amines were correlated with a detailed repertoire of biomarkers of inflammation and adipokines.ResultsL-carnitine was significantly increased (p = 0.0002) compared to controls. There was a trend for a significant increase in TMAO levels (p = 0.08). Choline was not significantly altered in MetS. L-carnitine correlated significantly with soluble tumor necrosis factor 1 (sTNFR1) and leptin, and inversely to adiponectin. TMAO correlated with IL-6, endotoxin and chemerin. Neither choline, nor L-carnitine significantly correlated with TMAO.ConclusionL-carnitine is directly correlated with markers of inflammation in nascent MetS. Cellular L-carnitine could be a biomediator or marker of inflammation in the pathogenesis of MetS, and the sequelae of CVD and T2DM.

Background: Low testosterone and obesity are independent risk factors for dysfunction of the nervous system including neurodegenerative disorders such as Alzheimer’s disease (AD). In this study, we investigate the independent and cooperative interactions of testosterone and diet-induced obesity on metabolic, inflammatory, and neural health indices in the central and peripheral nervous systems. Methods: Male C57B6/J mice were maintained on normal or high-fat diet under varying testosterone conditions for a four-month treatment period, after which metabolic indices were measured and RNA isolated from cerebral cortex and sciatic nerve. Cortices were used to generate mixed glial cultures, upon which embryonic cerebrocortical neurons were co-cultured for assessment of neuron survival and neurite outgrowth. Peripheral nerve damage was determined using paw-withdrawal assay, myelin sheath protein expression levels, and Na + ,K + -ATPase activity levels. Results: Our results demonstrate that detrimental effects on both metabolic (blood glucose, insulin sensitivity) and proinflammatory (cytokine expression) responses caused by diet-induced obesity are exacerbated by testosterone depletion. Mixed glial cultures generated from obese mice retain elevated cytokine expression, although low testosterone effects do not persist ex vivo. Primary neurons co-cultured with glial cultures generated from high-fat fed animals exhibit reduced survival and poorer neurite outgrowth. In addition, low testosterone and diet-induced obesity combine to increase inflammation and evidence of nerve damage in the peripheral nervous system. Conclusions: Testosterone and diet-induced obesity independently and cooperatively regulate neuroinflammation in central and peripheral nervous systems, which may contribute to observed impairments in neural health. Together, our findings suggest that low testosterone and obesity are interactive regulators of neuroinflammation that, in combination with adipose-derived inflammatory pathways and other factors, increase the risk of downstream disorders including type 2 diabetes and Alzheimer’s disease.