Year : 2021 | Volume
: 14 | Issue : 2 | Page : 160--161
Dry eye disease in patients with diabetes mellitus: An overview
Department of Ocular Inflammation and Immunology, Singapore National Eye Centre; Department of Ocular Inflammation & Immunology, Singapore Eye Research Institute, Singapore
Department of Ocular Inflammation and Immunology, Singapore National Eye Centre; Department of Ocular Inflammation & Immunology, Singapore Eye Research Institute
|How to cite this article:|
Waduthantri S. Dry eye disease in patients with diabetes mellitus: An overview.Med J DY Patil Vidyapeeth 2021;14:160-161
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Waduthantri S. Dry eye disease in patients with diabetes mellitus: An overview. Med J DY Patil Vidyapeeth [serial online] 2021 [cited 2021 May 12 ];14:160-161
Available from: https://www.mjdrdypv.org/text.asp?2021/14/2/160/309338
Dry eye disease (DED) is a global public health issue with significant socioeconomic implications, such as increased health-care costs and negative impact on quality of life., Diabetes mellitus (DM) has been identified as an important systemic risk factor of DED, with a reported prevalence of 20.6%–54.3% worldwide.,,, Poor glycemic control, long duration of diabetes, diabetic peripheral neuropathy (DPN), and diabetic retinopathy (DR) have been reported as risk factors for DED.,,
The secretion and stability of the tear film are diminished in patients with DM compared to age- and gender-matched controls.,,, Chronic hyperglycemia can lead to formation and accumulation of advanced glycation end products, which promote inflammation and oxidative stress contributing to structural damage and dysfunction of the lacrimal gland. Impaired lacrimal innervation due to diabetic autonomic neuropathy may further contribute to diminished tear production in these patients. DPN can lead to decreased corneal nerve fiber density and impaired corneal sensitivity, resulting in decreased reflex tearing., In addition, reduced blinking increases the evaporation of tears., Recent studies show that insulin resistance or deficiency and chronic hyperglycemia can cause loss of meibomian gland epithelial cells and goblet cells, resulting in an altered tear film., Increased tear evaporation and decreased tear production can result in increased tear osmolarity, activating a series of inflammatory responses. Inflammatory cytokines, such as tumor necrosis factor-alpha and matrix metalloproteinase (MMP)-9, have been implicated in the pathogenesis of DED.
Chronic tear secretion deficiency, DPN, and hyperglycemia can cause corneal epitheliopathy.,, The concentration of lactoferrin and tear-specific prealbumin is decreased in patients with DM. Superficial punctate keratitis, recurrent corneal erosions, persistent epithelial defects, neurotrophic keratopathy, delayed wound healing, and alterations in tear proteins increase the risk of developing microbial keratitis in these patients. Therefore, early diagnosis and intervention of diabetic-associated DED is important to prevent long-term complications.
Clinicians should be aware that patients with DM-associated DED can be asymptomatic due to corneal hypoesthesia caused by chronic hyperglycemia, despite having severe DED. Therefore, it is important to examine the ocular surface and tear film of these patients in addition to DR assessment during routine checkups as emphasized by the authors.
Currently, there are no specific guidelines on treatment of DM-associated DED. Systemic glycemic control and local therapy with topical preservative-free artificial tears, topical antibiotics, autologous serum, bandage contact lenses, amniotic membrane transplantation, and tarsorrhaphy remain the mainstay of treatment of DM-associated DED and persistent epitheliopathy. Topical steroids, cyclosporine eye drops, and bandage/scleral contact lenses should be used with caution in patients with poor glycemic control due to increased risk of infection. Prolonged use of topical nonsteroidal anti-inflammatory eye drops may lead to corneal epithelial breakdown, corneal erosion, ulceration, and perforation. Recent preclinical and clinical studies have shown that growth factors and cytokines significantly enhance corneal re-epithelialization and reverse corneal nerve degeneration in diabetics.,, Topical administration of thymosin beta-4, insulin, naltrexone (opioid antagonist), nicergoline (ergoline derivative), substance P (11-amino-acid polypeptide), aldose reductase inhibitors (ARIs) such as sorbinil and CT-112, and epalrestat (an ARI)-loaded silicone hydrogel contact lenses was effective in treating diabetic keratopathy.,, Oral administration of enalapril, ilepatril, and resolvin-D1was reported to reverse diabetic corneal neuropathy. The limbal epithelial stem cells in diabetic corneas appear to be dysfunctional due to reduced expression of putative markers. Emerging therapies such as adenoviral gene therapy inducing overexpression of c-Met proto-oncogene and/or silencing MMP-10 and cathepsin F genes and inhibition of microRNA-146a using antagomir have been shown to normalize epithelial wound healing and stem cell marker expression in human organ-cultured diabetic corneas. Further research is needed to evaluate the efficacy and safety of these novel therapies, which can potentially halt or reverse the progression of the disease.
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