Discussion
peripheral neuropathy, diabetic, diabetes
DIABETIC RETINOPATHY, PROLIFERATION, DYSFUNCTION, SECONDARY, PERIPHERAL NEUROPATHY, TYPE 2 DIABETES MELLITUS, DIABETES
Numerous researchers have proven the effects of diabetes on tear film and secretion. However, few studies have focused on the impact of diabetes on MG morphology and function [Diagnosis and quantification of MGD involves the evaluation of symptoms (assessed by questionnaires), altered meibomian gland secretions (evaluated by pressing the tarsal plate), changes in lid morphology (assessed by slit-lamp microscopy), and meibomian gland dropout (found by meibography); all of these are characteristics of MGD [The current investigation focuses on meibomian gland morphology and dysfunction in diabetics with DED and provides more convincing evidence for the correlation between MGD and DM. We observed that the meibomian gland loss was significantly higher in both the upper and lower eyelids of diabetics with DED than in nondiabetics with DED. Although the score of either lid margin abnormality or meibum quality was no correspondingly significant higher, but these two variables are just indirectly reflection of MGD. After all, in early or nonobvious MGD, there are no obvious morphological lid margin changes observed by physical examination [Inconsistent with Lin’s study [Thus far, the mechanism of MGD induced by DM is unclear, and further research should be performed to verify some speculations. It has been postulated that type 2 diabetes mellitus might play a key role in MGD through stopping the proliferation of human meibomian gland epithelial cells (IHMGECs) and lipid metabolism. Ding’s study found that insulin stimulates IHMGECs, and that glucose exposure is deleterious to them [Our study found no significant differences in most tear parameters between the diabetic and nondiabetic groups, and only the values of Schirmer I test were significantly decreased, whether comparing the DM-DED group with the nondiabetic DED group or the DM control group with the normal control group. Most published research has reported patients with DM have decreased Schirmer test values [This study also found that the OSDI scores of DM-DED patients were higher than those of the normal controls, but lower than nondiabetic DED patients. Similarly, decreased OSDI scores were shown in the DM control group compared with the normal control group, which was consistent with the study of Lin et al. [The present study had several limitations. First, the small sample size could have affected the results, and the significant correlation between meibomian gland loss of both the upper and lower eyelids and diabetic course should be observed in further studies with a larger sample size. Second, the data of diabetes-related clinical parameters were not perfect. For example, serum glycated hemoglobin (HbA1c), the severity of diabetic retinopathy, and the presence or absence of peripheral neuropathy could all be confounding factors of the results, which should be confirmed in further investigations.In conclusion, in our study, type 2 diabetics with DED worse MGD than nondiabetic DED patients, with significantly higher MG dropout, as well as non-obvious higher levels of lid margin abnormalities and meibum quality. These findings provide concrete evidence for MGD as related to DM-DED. Nevertheless, it is confusing whether MGD is secondary to DM-DED or the latter is caused by the former. Further study must be performed to reveal the causative link between MGD and DM-DED.