Dry Eye Syndrome in Patients with Diabetes Mellitus: Prevalence, Etiology, and Clinical Characteristics

Abstract

There has been substantial progress in our understanding of the ocular surface system/lacrimal function unit in the past 15 years. Keratoconjunctivitis sicca, more commonly referred to as dry eye syndrome (DES), is the most frequently encountered condition and diabetes mellitus (DM) has been identified as one of the leading causes of DES. Poor glycemic control affects both the anterior and the posterior segments of the eye and increasing prevalence of diabetes-associated DES (DMDES) has been reported in recent years. The pathogenesis and specific features of DMDES remain uncertain and interventions are limited to those used in DES. This review outlines the pathogenesis, clinical manifestations, and the current preventive and treatment strategies for diabetes-related DES.

Figure 1

Lacrimal function unit (LFU) is composed of the “cornea, conjunctiva, lacrimal gland, meibomian gland, lids, and the sensory and motor nerves that connect them,” which protect and maintain the tear film and normal function of the ocular surface. LFU plays a regulatory role in tear secretion and tear film formation to maintain the normal physiology of the ocular surface; damage to any component of LFU leads to tear-deficient or evaporative diabetes mellitus associated dry eye syndrome.

Figure 2

Etiology and pathogenesis of diabetes mellitus associated dry eye syndrome. Chronic hyperglycemia, diabetic periphery neuropathy, decreased insulin hormone, microvasculopathy, and systemic hyperosmotic disturbances are risk factors for diabetes-associated dry eye syndrome, which subsequently induce lacrimal function unit and tear film dysfunction and abnormal tear dynamics. Several proteins have been identified to be the contributor to diabetes mellitus associated dry eye syndrome.