More than 30 million Americans (about 10%) have diabetes, and 90% to 95% of these have type 2 diabetes. Type 2 diabetes most often develops in people over the age of 45, but it is becoming more prevalent in children, teens, and young adults. In type 2 diabetes, insulin resistance results in high blood sugar that is damaging to the body and causes other health problems, including heart disease, diabetic retinopathy, and kidney disease (www.cdc.gov/diabetes/basics/type2.html ).
Diabetes and the Meibomian Glands
The ocular complications of diabetes can decrease quality of life and can create a significant economic burden. In addition to diabetic retinopathy, numerous studies have indicated that patients who have diabetes are more likely to have ocular surface disorders such as dysfunction of lacrimal gland secretion, superficial punctate keratitis, persistent epithelial defects, and decreased corneal sensitivity (Yu et al, 2019).
It has been demonstrated that compared with non-diabetic patients, there is more meibomian gland (MG) dropout in patients who have diabetes; and, the longer that patients have diabetes, the higher the dropout score (Yu et al, 2019). Laser scanning confocal microscopy shows that cytological alterations in the acinar cells of MGs—such as expansion, atrophy, or fibrosis of MG acinar units; decreased density of MG acinar units; deposition of lipid substances; infiltration of inflammatory cells; and proliferation of fibrous tissues—progress with the duration of diabetes. The openings of the glandular ducts of the MGs of diabetic patients become narrowed, blocked, and/or fibrotic (Yu et al, 2019). These changes may result in the dysfunction of the MGs, tear film instability, and dry eye symptoms in patients who have type 2 diabetes. An in vitro report suggests that insulin stimulates, and that high glucose is toxic for, immortalized human MG epithelial cells, offering an explanation for type 2 diabetes as a risk factor for MG dysfunction (MGD) (Ding et al, 2015).
The secretion and distribution of MGs are mainly dependent on the blink movements (Knop et al, 2011; Yu et al, 2019). Lipid is delivered to the tear film as the eyelid opens after a blink. Delivery of lipid to the marginal reservoirs mainly results from continuous secretion under neural and hormonal control, which is supplemented by lid action. However, diabetic patients generally exhibit decreased corneal sensitivity and blink movement (Yu et al, 2019), so less lipid is excreted and the ducts become blocked, further resulting in MGD.
Finally, type 2 diabetes patients have more severe MGD compared with non-diabetic patients; the longer that patients have diabetes, the greater the MG symptoms and changes (Parra et al, 2019). In a prospective study of 76 males who had a mean age of 59 ± 8 years, 37 of whom had type 2 diabetes (average duration between 7 ± 5 years) and a control group of 36 males, 71% of participants presented with MGD (76% diabetics and 67% controls). Ocular Surface Disease Index (OSDI) scores were significantly higher in the diabetes group. There was a positive correlation between glycemia (the presence of glucose in the blood) and symptoms, and there was a strong correlation between HbA1c and OSDI scores. The diabetes group also exhibited changes in lid architecture (Marx’s line changes and keratinization of meibomian gland orifices) and tear function, contributing to evaporative dry eye and correlating with MG inflammation and obstruction (Parra et al, 2019).
Look for Ocular Surface Disease in Diabetic Patients
As clinicians, assessing for diabetic retinopathy is top-of-mind for our patients who have diabetes. Monitoring for signs and symptoms of ocular surface disease should be as well. CLS
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