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BACKGROUND AND OBJECTIVE: To describe the presentation and the authors' evolving management strategy for intraocular dissemination of uveal melanoma cells following radiotherapy during the past decade. PATIENTS AND METHODS: Patients with uveal melanoma who developed intraocular dissemination of pigmented cells following radiotherapy. Histopathology was available in two cases. RESULTS: Four patients underwent treatment for progressive intraocular dissemination of uveal melanoma cells at 9 to 41 months following I-125 plaque radiotherapy (three patients) or proton beam radiotherapy (one patient). Treatments included primary enucleation (one patient), vitrectomy followed later by enucleation (one patient), and vitrectomy followed by intravitreal chemotherapy (two patients). Enucleated eyes demonstrated diffuse invasion of intraocular tissues by viable melanoma cells. No patient has developed systemic metastasis to date. CONCLUSIONS: Intraocular dissemination of pigmented cells following radiotherapy for uveal melanoma should raise suspicion for viable invasive melanoma cells. Prompt vitrectomy with intravitreal chemotherapy can be effective in avoiding enucleation in selected cases. [ Ophthalmic Surg Lasers Imaging Retina . 2019;50:573–579.]

To determine if receiving a prescheduled appointment is associated with an increased likelihood of complying with follow-up eye care among individuals identified as at risk for glaucoma during community-based glaucoma screening in an urban underserved population. This study sampled 362 individuals aged ≥30 years without known glaucoma from low-income, predominantly black/Hispanic neighborhoods in New Haven, Connecticut presenting to one of twelve community-based glaucoma screening events from May 2010 to October 2012. A quasi-experimental design systematically assigned 63 individuals identified as at risk for glaucoma into either intervention or control group with a 1:2 ratio. Individuals in the control group (n = 41) received counseling on glaucoma and a recommendation for obtaining a follow-up appointment at the eye department of a local community health center, which offers affordable health services with income-adjusted fee discounts to uninsured, low-income patients. Those in the intervention group (n = 22) received the same counseling and a prescheduled appointment at the community health center. The overall rate of follow-up compliance within 3 months of screening was 30 % (41 % in the intervention group; 24 % in the control group). Multivariate logistic regression analysis adjusting for sex, age, ethnicity, health insurance status, car access, living situation, and smoking status found that follow-up compliance was significantly associated with intervention (adjusted odds ratio 4.8; 95 % confidence interval 1.1-20.9). Providing prescheduled appointments can improve follow-up compliance after community-based glaucoma screening. This finding may be potentially applicable to community-based health screening for other preventable diseases.

Obstructive sleep apnea (OSA) is a disorder characterized by repeated episodes of partial or complete closure of the upper airway during sleep. Airway closure results in respiratory effort-related arousals and fragmented sleep that cause daytime symptoms such as sleepiness, fatigue, and decreased concentration. During episodes of apnea, patients become hypoxemic and undergo arterial blood pressure surges and increased intracranial pressure.1 Current evidence suggests that inflammatory processes, oxidative stress and endothelial dysfunction may play roles in the pathogenesis of vascular complications in OSA.2 By itself and irrespective of common comorbid conditions like hypertension, OSA has been shown to be an independent risk factor for coronary artery disease, stroke and death.3,4 With the increasing prevalence of OSA and its implications for increased morbidity and mortality further research into ophthalmic associations is important. Several ophthalmic conditions have been thus far linked to OSA including glaucoma, floppy eyelid syndrome, nonarteritic anterior ischemic optic neuropathy (NAION), optic disc edema, and diabetic retinopathy severity.5–8 While no definitive mechanism for ophthalmic associations has been elucidated, the alterations in blood pressure and hypoxemia seen in patients with OSA have been proposed as possible etiologies for glaucoma, NAION, optic disc edema, and the degree of diabetic retinopathy. More recent work by Glacet-Bernard et al. examined the association between OSA and retinal vein occlusion.9 They found a higher than expected prevalence of OSA in patients with vein occlusion proposing the idea that OSA may be a risk factor for vein occlusion. Increased tortuosity of the retinal vasculature has been associated with diabetes, hypoxia, older age, hypertension, and elevated body mass index (BMI).10,11 As all of these aforementioned factors are also associated with OSA we hypothesized that patients with OSA will have alterations in their retinal vascular pattern. Our findings in this pilot study demonstrate increased retinal vascular tortuosity in OSA that appears to be independent of comorbid conditions like hypertension and diabetes.

Purpose To apply a previously published scleral fixation technique to secure one-piece acrylic intraocular lenses (IOLs) to the sclera. Methods Retrospective, consecutive, noncomparative case series. Results All patients (16 eyes of 15 patients) who underwent scleral fixation of 1-piece acrylic IOLs using the loop method from 2014 to 2016 were included. The mean follow-up was 8.1 months. Repositioning of dislocated 1-piece acrylic IOLs was performed in 8 eyes, a primary implantation in 5 eyes, and IOL exchange in 3 eyes. All IOLs remained well-centered postoperatively. The vision improved from an initial best-corrected visual acuity of 0.97 ± 0.74 logMAR (Snellen equivalent ≈20/190) to 0.47 ± 0.49 logMAR (≈20/60, P = 0.031) at the last follow-up. The postoperative complications were self-limited. Conclusion The previously reported scleral suture fixation technique can be readily applied to one-piece acrylic IOLs.

Hypertension, carotid occlusive disease, diabetes, cardiac valvular disease, stroke, and peripheral vascular disease are common causes of ocular ischemic syndrome.

CRAO: Central retinal artery occlusion causes diffuse superficial retinal whitening leading to appearance of a cherry-red spot in the macula due to arteriolar constriction.

Idiopathic juxtafoveal telangiectasis (IJT) refers to a heterogeneous group of rare clinical conditions that entail telangiectatic changes of the juxtafoveal or parafoveal capillary network in one or both eyes.

Retinal arterial macroaneurysm (RAM) is the outpouching of the wall within the first three orders of the arterial tree. Leakage may occur from the aneurysm or from the surrounding capillaries. If the aneurysm ruptures, then hemorrhage at all levels is possible.

BRAO: Branch retinal artery occlusion causes superficial retinal whitening and edema along the distribution of ischemic branch of the retinal artery.

CRVO: central retinal vein occlusion causes diffuse retinal hemorrhages (blood and thunder) associated with tortuous retinal venous vasculature.

CLRAO: cilioretinal artery occlusion can be isolated in collagen vascular disorders, may occur secondary to the increased hydrostatic pressure associated with CRVO or with anterior ischemic optic neuropathy.

BRVO: branch retinal vein occlusion causes sectoral retinal hemorrhages with associated venous dilation/tortuosity.

Mutations in the β-globin gene result in erythrocytes that undergo sickling in response to hypoxic, acidotic, and hyperosmolar conditions. Sickled erythrocytes are not pliable thereby resulting in mechanical occlusion of arterioles. Arteriolar occlusion is at the core of sickle cell retinopathy as it causes both nonproliferative and proliferative disease.

Adenosine has been implicated in the pathogenesis of chronic lung diseases such as asthma and chronic obstructive pulmonary disease. In vitro studies suggest that activation of the A2B adenosine receptor (A2BAR) results in proinflammatory and profibrotic effects relevant to the progression of lung diseases; however, in vivo data supporting these observations are lacking. Adenosine deaminase-deficient (ADA-deficient) mice develop pulmonary inflammation and injury that are dependent on increased lung adenosine levels. To investigate the role of the A2BAR in vivo, ADA-deficient mice were treated with the selective A2BAR antagonist CVT-6883, and pulmonary inflammation, fibrosis, and airspace integrity were assessed. Untreated and vehicle-treated ADA-deficient mice developed pulmonary inflammation, fibrosis, and enlargement of alveolar airspaces; conversely, CVT-6883-treated ADA-deficient mice showed less pulmonary inflammation, fibrosis, and alveolar airspace enlargement. A2BAR antagonism significantly reduced elevations in proinflammatory cytokines and chemokines as well as mediators of fibrosis and airway destruction. In addition, treatment with CVT-6883 attenuated pulmonary inflammation and fibrosis in wild-type mice subjected to bleomycin-induced lung injury. These findings suggest that A2BAR signaling influences pathways critical for pulmonary inflammation and injury in vivo. Thus in chronic lung diseases associated with increased adenosine, antagonism of A2BAR-mediated responses may prove to be a beneficial therapy.

This report describes a unique case of coexisting necrobiotic xanthogranuloma and chronic lymphocytic leukemia in a patient presenting with scleritis and uveitis. A 53-year-old Caucasian man diagnosed with anterior uveitis and scleritis for the prior year was referred to our uveitis clinic for further evaluation. Prior uveitis/scleritis workup performed by the referring ophthalmologist was negative. Examination demonstrated unilateral uveitis and posterior scleritis along with bilateral conjunctival lesions. Incisional biopsy of the conjunctiva was carried out. The excised tissue was sent fresh for histopathologic studies. Slit-lamp examination revealed bilateral yellow-white bulbar conjunctival lesions, 1+ conjunctival injection OU, stellate keratic precipitates OS with 25 cells per high-powered field. Funduscopic examination was significant for subretinal fluid OS. Conjunctival biopsy revealed necrobiotic xanthogranuloma and chronic lymphocytic leukemia. Systemic workup demonstrated paraproteinemia consistent with necrobiotic xanthogranuloma and a complete blood count consistent with leukemia. This case demonstrates an atypical presentation of necrobiotic xanthogranuloma and concomitant chronic lymphocytic leukemia presenting in the form of uveitis, scleritis, and conjunctival infiltration. Masquerade syndromes, such as necrobiotic xanthogranuloma and leukemia, must be kept in mind when treating patients with uveitis or scleritis with negative workups.

Advances in the diagnosis and treatment of retinoblastoma have vastly improved patient outcomes. In developed countries, the most common cause of death in patients with heritable retinoblastoma is now a second primary tumor occurring in retinoblastoma survivors; many of these second primaries can be avoided by the reduced use of radiation. Mesenchymal tumors including primitive neuroectodermal tumors, bone and soft tissue sarcomas, leiomyomas, lipomas, cutaneous melanomas, and gliomas are the most common types of the second primary tumors in retinoblastoma survivors. Osteogenic sarcoma is the most common type of second primary tumor particularly in younger patients.

Angiogenesis is a feature of chronic lung diseases such as asthma and pulmonary fibrosis; however, the pathways controlling pathological angiogenesis during lung disease are not completely understood. Adenosine is a signaling molecule that has been implicated in the exacerbation of chronic lung disease and in the regulation of angiogenesis; however, the relationship between these factors has not been investigated. The current study utilized adenosine deaminase (ADA)-deficient mice to determine whether chronic elevations in adenosine in vivo result in pulmonary angiogenesis. Results demonstrate substantial angiogenesis in the tracheas of ADA-deficient mice in association with adenosine elevations. ADA replacement enzyme therapy resulted in a lowering of adenosine levels and reversal of tracheal angiogenesis, indicating that the increases in vessel number are dependent on adenosine elevations. Levels of the angiogenic chemokine CXCL1 (mouse functional homologue of human IL-8) were found to be elevated in an adenosine-dependent manner in the lungs of ADA-deficient mice. Neutralization of CXCL1 and its receptor, CXCR2, resulted in the inhibition of angiogenic activity, which suggests that CXCL1 signaling through the CXCR2 receptor mediated the observed increases in angiogenesis. Our findings suggest that adenosine plays an important role, via CXCL1, in the induction of pulmonary angiogenesis.

Purpose of review The chronic lung diseases, asthma and chronic obstructive pulmonary disease, are pulmonary disorders in which persistent inflammation and alterations in lung structure contribute to a progressive loss of lung function. Although the exact type of inflammation and damage in each disease is distinct, they share the common feature that they are chronic in nature. Despite efforts, little is known about the cellular and molecular mechanisms that drive the chronicity of these two diseases. This review will summarize important findings regarding the role of adenosine, a signaling nucleoside implicated in the pathogenesis of these two disorders. Recent findings Aerosolized adenosine induces bronchoconstriction in patients with asthma and chronic obstructive pulmonary disease primarily through the release of mast cell mediators. In this setting it can not only be used to aid in diagnosis but also to monitor patient responses to steroid therapy. Adenosine levels are elevated in the lungs of asthma patients, indicating greater flux through adenosine receptor signaling pathways. In-vitro studies have shown adenosine to access pathways leading to the genesis of chronic inflammation via the release of proinflammatory cytokines and chemokines. Animal studies demonstrate that merely elevating adenosine levels in the mouse is sufficient to induce a pulmonary phenotype with features of asthma and chronic obstructive pulmonary disease. Summary Identifying mediators regulating the chronic nature of asthma and chronic obstructive pulmonary disease is critical towards advancements in treatment options. Adenosine has been implicated in promoting the inflammation and airway remodeling seen in chronic lung disease and thus makes an attractive therapeutic target.