Ocular surface disease in glaucomatous patients

Th is review presents an exhaustive analysis of the current literature on ocular surface disease (OSD) in glaucoma. OSD in this population mainly manifests in the cornea and conjunctiva as superfi cial punctate keratitis and tear fi lm instability, aggravated by the chronic use of intraocular pressure–lowering medications; this could account for poor treatment adherence and worsening of the patient’s quality of life. A large body of literature has found increasing evidence implicating preservatives as the main factor, through both in vitro and clinical studies, especially in regard to benzalkonium chloride. However, the impact of preservatives on clinical practice varies in diff erent studies. Th e decision to use preservative-free medication or alternative preservatives should therefore be assessed on an individual basis, whereby some subpopulations with abnormal tearing, decreased tear break-up time (TBUT) or corneal staining could benefi t. Clinical assessment with validated quality of life questionnaires, corneal and conjunctival staining, TBUT and Schirmer’s test is mandatory in these populations. J Emmetropia 2016; 2: 111-117 Glaucoma is a chronic, progressive optic neuropathy in which increased intraocular pressure (IOP) is the most signifi cant risk factor1,2. IOP reduction in the treatment of glaucoma has already been confi rmed to be benefi cial in large prospective randomised clinical trials3-7, and can decelerate or halt disease progression. Topical IOP-lowering drugs remain the fi rst line therapy and, considering that IOP is the only controllable risk factor, the majority of patients receive medical treatment throughout their lifetime. Ocular surface disease (OSD) is a general term to describe a wide spectrum of diseases such as dry eye syndrome (DES), eyelid disease, conjunctivitis and keratitis8. OSD is a wellknown comorbidity in glaucomatous patients that has been found to be aggravated by the chronic use of IOP-lowering medications9,10, thus accounting for poor treatment adherence and concordance11 and a decline in the patient’s quality of life (QoL)12,13. Nonetheless, both OSD and glaucoma are age-related diseases14-18 that can occur as separate entities. Th us, the role of each component —whether age or medical treatment— must be assessed on an individual basis for each patient to optimise the treatment outcome. OSD induced by hypotensive therapy can result from the eff ect of the active ingredients of the medical treatment or the preservative agents, particularly benzalkonium chloride BAK9,19. Of these two factors, the preservative element of IOP-lowering drugs is one of the most relevant features in OSD9,20. Th e role of active ingredients Th e main topical hypotensive eye drops are timolol (non-selective adrenergic beta-blocker), carteolol (non-selective adrenergic beta-blocker with intrinsic sympathomimetic activity), carbonic anhydrase inhibitors such as dorzolamide or brinzolamide, brimonidine (adrenergic agonist alpha-2 selective) and prostaglandin analogues (latanoprost, bimatoprost, travoprost, tafl uprost)15. Among these, prostaglandin analogues and beta-blockers are considered fi rstline therapies15,21,22. Common symptoms of OSD in glaucomatous patients include redness, dryness, irritation, tearing, burning and foreign body sensation, 1 Department of Ophthalmology. Hospital Clínico San Carlos, Madrid, Spain. 2 Department of Opthalmology. St Th omas Hospital, London, UK. Financial Disclosure: None of the authors have any fi nancial interest in any of the products mentioned herein Corresponding Author: Francisco Pérez Bartolomé Department of Ophthalmology, Hospital Clínico San Carlos Calle del Prof. Martín Lagos, s/n, 28040 Madrid. E-mail: [email protected]