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Cherfan C.G.,American University of Beirut | Traboulsi E.I.,Cole Eye Institute
Canadian Journal of Ophthalmology

Slipped, severed, torn and lost extraocular muscles (EOM) are infrequently encountered in clinical practice but constitute significant complications of strabismus and other eye surgery and of orbital injuries. Knowledge of the clinical aspects of these various disease entities and their anatomical underpinnings are of utmost importance in providing effective recognition and treatment. These conditions share some common presenting signs, symptoms and clinical findings that are discussed in this review. The literature will be reviewed and management strategies will be presented. ©2011 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. Source

Traboulsi E.I.,Cole Eye Institute
Current Opinion in Ophthalmology

PURPOSE OF REVIEW: Pigmented and depigmented ocular fundus lesions (de-POFLs) can be isolated and clinically insignificant, or they may be the hallmark of associated serious systemic disorders such as familial polyposis. The ophthalmologist is often called upon to look for these retinal lesions, or may encounter them in the course of routine examination when appropriate medical referral becomes essential. RECENT FINDINGS: The ophthalmoscopic and location differences between grouped pigmentation of the retinal pigment epithelium (bear tracks) and multiple POFLs associated with familial adenomatous polyposis is reviewed. The differential diagnosis, morphology and associations of de-POFLs are also listed and some of the associated genetic conditions are reviewed. SUMMARY: Familiarity with the morphologic and ophthalmoscopic features of pigmented and de-POFLs is essential for the ophthalmologist so that an exact diagnosis is made and the appropriate workup and referrals initiated. © 2012 Wolters Kluwer Health. Source

Stohr H.,University of Regensburg | Anand-Apte B.,Cole Eye Institute
Advances in Experimental Medicine and Biology

Sorsby fundus dystrophy (SFD) is a rare autosomal dominant macular degeneration characterized by abnormal thickening of Bruch's membrane (BM) leading to macular atrophy and choroidal neovascularization (CNV). SFD is caused by mutations in the gene encoding the tissue inhibitor of metalloproteinase-3 (TIMP3), a multifunctional protein component of BM. Disturbed homeostasis in extracellular matrix (ECM) remodeling is likely involved in SFD pathology. Here, we summarize the current findings on the mechanism(s) by which mutant TIMP3 causes the phenotypical expression of SFD. In addition, the association between SFD and complex age-related macular degeneration (AMD) is discussed. © 2012 Springer Science+Business Media, LLC. Source

Englander M.,Cole Eye Institute | Kaiser P.K.,Cole Eye Institute
Current Opinion in Ophthalmology

Using combination treatments that target other pathways involved in angiogenesis will hopefully improve on the results of current anti-VEGF agents and may result in greater visual improvement and more convenient dosing regimens. © 2013 Wolters Kluwer Health. Source

Xu D.,Cole Eye Institute | Kaiser P.K.,Cole Eye Institute

Neovascular age-related macular degeneration (AMD) is the leading cause of legal blindness in patients over the age of 50 in the western world. Intravitreally administered anti-VEGF drugs have been developed to halt neovascular growth in AMD. Randomized trials have demonstrated the excellent safety profile and significant benefit of anti-VEGF therapy in maintaining vision. Aflibercept (Eylea®; Regeneron, NY, USA) is a soluble decoy receptor against VEGF that offers greater potency and binding affinity than other anti-VEGF drugs. Having received US FDA approval for neovascular AMD in November 2011, aflibercept given every 8 weeks after a loading dose was 'clinically equivalent' and statistically noninferior to the current FDA-approved therapy ranibizumab (Lucentis®; Genentech, CA, USA), given every 4 weeks. This article discusses the clinical background of AMD, development of aflibercept, results of the clinical trials and the future role of aflibercept in ocular neovascular diseases. © 2013 Future Medicine Ltd. Source

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