Surgery, anticancer drugs (chemotherapy, hormonal medicines, and targeted treatments), and/or radiation are common treatment strategies for neoplastic diseases. Anticancer drugs eliminate malignant cells through the inhibition of specific pathways that contribute to the formation and development of cancer. Given the ability of such pharmacological medications to combat cancerous cells, their role in the management of neoplastic diseases has become essential. However, these drugs may also lead to undesirable systemic and ocular adverse effects due to cyto/neuro-toxicity and inflammatory reactions. Ocular surface side effects are recognized to significantly impact patient’s quality of life and quality of vision. Blepharoconjunctivitis is known to be a common side effect caused by oxaliplatin, cyclophosphamide, cytarabine, and docetaxel, while anastrozole, methotrexate, and 5-fluorouracil can all determine dry eye disease. However, the potential processes involved in the development of these alterations are yet not fully understood, especially for novel drugs currently available for cancer treatment. This review aims at analyzing the potential ocular surface and adnexal side effects of novel anticancer medications, trying to provide a better understanding of the underlying pharmacological processes and useful insights on the choice of proper management.

In recent years, researchers have been interested in neuroprotective therapies as a cutting-edge therapeutic strategy to treat neurodegenerative disorders by shielding the brain system from harmful events. Millions of individuals worldwide suffer from glaucoma, an ocular neurodegenerative disease characterized by gradual excavation of the optic nerve head, retinal axonal damage, and consequent visual loss. The pathology’s molecular cause is still mostly unknown, and the current treatments are not able to alter the disease’s natural progression. Thus, the modern approach to treating glaucoma consists of prescribing medications with neuroprotective properties, in line with the treatment strategy suggested for other neurodegenerative diseases. For this reason, several naturally derived compounds, including nicotinamide and citicoline, have been studied throughout time to try to improve glaucoma management by exploiting their neuroprotective properties. The purpose of this review is to examine the naturally derived compounds that are currently utilized in clinical practice for neuroprotection in glaucomatous patients based on scientific data, emphasizing these compounds’ pivotal mechanism of action as well as their proven therapeutic and neuroprotective benefits.

Among working-age people, diabetic retinopathy and diabetic macular edema are currently considered the main causes of blindness. Nowadays, intravitreal injections are widely acknowledged as a significant milestone in ophthalmology, especially for the treatment of several retinal diseases, including diabetic macular edema. In particular, anti-vascular endothelial growth factor (VEGF) agents are typically the first line of treatment; however, monthly injections are required, at least, during the loading dosage. Notably, an intravitreal 0.7 mg dexamethasone (DEX) implant (Ozurdex^®, AbbVie Inc., North Chicago, IL, USA) is considered a legitimate substitute treatment for diabetic eyes that have not responded to anti-VEGF treatment. In fact, clinical trials and real-life studies have demonstrated the effectiveness and safety of an intravitreal DEX implant in treating such conditions over a period of three to six months. For this reason, wisely selecting diabetic patients might be crucial to decreasing the load of injections in clinics and hospitals. The purpose of this review is to analyze the available scientific literature to highlight the benefits, efficacy, and clinical criteria for choosing whether to switch from intravitreal anti-VEGF therapy to an intravitreal DEX implant in diabetic macular edema.

Purpose: To report a case of non-arteritic ischemic optic neuropathy (NAION) in an otherwise healthy patient treated with Glucagon-Like Peptide-1 (GLP-1) receptor agonists (RAs) liraglutide and semaglutide. Observations: A 47-year-old Caucasian female with a Body Mass Index (BMI) of 27.92, and no known history of diabetes, hypertension, or ischemic heart disease, developed a progressive decline in visual acuity in the right eye one month after initiating liraglutide therapy for weight loss. Upon symptom presentation, ophthalmic examination performed elsewhere revealed a best-corrected visual acuity (BCVA) of 20/40, optic nerve head (ONH) swelling, and inferior hemifield scotoma on Humphrey Visual Field testing. Oral corticosteroids were prescribed and discontinued because of poor glycemic control. Liraglutide therapy was continued for further three months and then switched to semaglutide owing to poor clinical results. Eight months later, the patient discontinued weight loss therapy because of progressive visual deterioration and presented to our clinic for a second opinion. Upon examination, BCVA was limited to 20/400, ONH edema was evident and confirmed on optical coherence tomography (OCT), and further worsening of the visual field defects was detected. Given the absence of anatomical and/or systemic risk factors, NAION secondary to GLP-1 RAs was diagnosed. Conclusion and Importance: In our patient, liraglutide likely served as the initial trigger for the NAION, with semaglutide acting as an additional contributing factor in the progression of the disease. This case adds to the complex puzzle regarding the association between GLP-1 RAs therapy and NAION. Given the increasing use of these drugs for both obesity and diabetes and the close temporal correlations between GLP-1 RAs use and NAION, healthcare providers should be aware of the possible risk of serious ocular complications. Upon onset of visual symptoms, early ophthalmologic diagnosis and treatment interruption are essential to prevent or limit severe visual morbidities.

Nowadays, retinal vein occlusion (RVO) is the second most prevalent cause of vision loss associated with retinal vascular disease. Intravitreal injections are currently known as a major advancement in ophthalmology, particularly in the treatment of RVO and other retinal disorders. Particularly, the first line of therapy is usually anti-vascular endothelial growth factor (VEGF) drugs. Notably, for RVO eyes that have not responded to anti-VEGF therapy, an intravitreal dexamethasone (DEX) implant 0.7 mg (Ozurdex^®, AbbVie Inc., North Chicago, IL, USA) is considered a suitable therapeutical substitute. Actually, investigations carried out in the real world and clinical trials have shown the safety and the efficacy of intravitreal DEX implants for treating this retinal disease. For this reason, choosing patients carefully may thus be essential to reduce the number of injections that clinics and hospitals have to do to manage RVO and its complications. The primary aim of this review is to summarize the pathophysiology of this retinal vascular disease, as well as the clinical and ocular imaging features that may support a switch from prior anti-VEGF treatment to intravitreal DEX implant, to provide the RVO patients with the best possible treatment to ensure maximum visual recovery.

Globally, diabetic retinopathy (DR) and diabetic macular edema (DME) are the leading causes of visual loss in working people. Current treatment approaches mostly target proliferative DR and DME, such as intravitreal injections of antivascular endothelial growth factor agents and laser photocoagulation. Before DR progresses into the more severe, sight‐threatening proliferative stage, patients with early stages of the disease must get early and appropriate care. It has been suggested that nutraceuticals, which are natural functional foods with minimal adverse effects, may help diabetic patients with DR and DME. Several in vitro and in vivo studies were carried out over the last years, showing the potential benefits of several nutraceuticals in DR due to their neuroprotective, vasoprotective, anti‐inflammatory, and antioxidant properties. Although most of the research is restricted to animal models and many nutraceuticals have low bioavailability, these compounds may adjuvate and implement conventional DR therapies. The purpose of this review is (i) to summarize the complex pathophysiology underlying DR and DME and (ii) to examine the main natural‐derived molecules and dietary habits that can assist conventional therapies for the clinical management of DR and DME.