The Analysis Of Correlation Between Type 2 Diabetes Mellitus And Dry Eye

Objective To investigate tear film function and prevalence rate of dryeye in type 2 diabetes mellitus.Methods The primary research carried through in 55 Type 2 Diabeticcases(110 eyes) and 40 non-diabetic controls(80 eyes). The Type 2Diabetic patients were divided into three groups by diabetic retinopathy,duration of diabetes mellitus and metabolic control. All patients wereinquired about dry eye syndrome and examined on tear film function,Schirmer I test(SIt), tear break-up time(BUT) and corneal fluoresceinstaining(FL).Results The diabetic group showed higher prevalence rate of dry eyesyndrome (50.91%,) than that of the control group(15.00%), whichpresented obvious difference (P<0.01). Type 2 diabetes mellitus showedlesser SIt(diabetics 9.48±4.02mm, control 11.73±3.79mm, P<0.05) ,faster BUT(diabetics 6.64±3.18s, control 12.30±2.78s, P<0.01), andhigher rate of FL(diabetics 20%, control 5%, P<0.01). Tear film functionhad a good correlation with diabetic retinopathy and metabolic control,but was poorly correlated with duration of diabetes mellitus.Conclusions1,Type 2 diabetics tend to develop tear film dysfunction, so they aresusceptible persons of dry eye. Among the type 2 diabetic patients abroad,70% of them were confirmed to have dry eye syndrome, while 57% ofpatients with type 1 diabetes suffered from this. In our cases, there were110 eyes of 55 patients with type 2 diabetes mellitus (26 males, 29famales) whose age distribution ranged from 39 to 78 years (mean, 54.52±9.24 years ), and their prevalence rate of dry eye was 50.91%, whichwas lower than the study abroad.2,Diabetes mellitus leaded to many changes in the surface of eye.(1) The changes in tear film. Diabetes mellitus could lead to changes intear quantity and quality. Diabetics tended to develop tear filmdysfunction and make the stability of tear film lower, so they weresusceptible persons suffering from dry eye. Most scholars thought thatBUT and SIt were significantly reduced, and found increased rate ofstaining with fluorescein sodium on the cornea and abnormal conjunctivalepithelium in the diabetic patients. Our study indicated that type 2diabetes mellitus showed lesser SIt(diabetics 9.48±4.02mm, control11.73±3.79mm, P<0.05) and had a good correlation with diabeticretinopathy, but was poorly correlated with metabolic control. BUT intype 2 diabetes mellitus was faster than control(diabetics 6.64±3.18s,control 12.30±2.78s, P<0.01)and had a good correlation with diabeticretinopathy and metabolic control. The two prior indexes were poorlycorrelated with duration of diabetes mellitus.(2) The changes in corneal epithelium. Diabetes mellitus could lead tochanges in corneal epithelium and made the stability of tear film lower.Ultrastructural changes in corneas of diabetic patients: less cellmultiplication, occasional focal epithelial cell degeneration, accumulationof glycogen granules, irregular thickening and multilamination of theepithelial basement membrane, and the aggregates of wide-spacedcollagen fibrils. The poor adhesion of epithelial cells may contribute tosome of the clinical manifestations of diabetic keratopathy. Our studyindicated that there was obvious difference (P<0.01) in FL between thediabetic group and control. Moreover, FL had a correlation with diabeticretinopathy and metabolic control.(3) The changes in corneal nerves. Diabetes mellitus could make cornealsensitivity lower so as to diminish times of wink and lead to tear filmvaporizing quickly. Meanwhile, lower corneal sensitivity could bringabout the dull dry sensation of corneal surface and the lower stimulationto lacrimal gland so as to influence the tear secretion. The study showedthat the corneal nerve fibers myelin in diabetes mellitus degenerated, andtheir nerve conduction velocity and corneal sensitivity decreased. Inrecent years,more and more clinic studies and animal experiments provedthat decreased corneal sensitivity in diabetes mellitus had a correlationwith diabetic retinopathy, peripheral neuropathy and metabolic control.The change was an important manifestation of diabetic polyneuropathy.3,The pathogenesis inducing the changes in tear film and corneal epitheliumin diabetes mellitus includes advanced glycation end products(AGEs),aldose reductase(AR) iter, matrix metalloproteinases(MMPs) action,proteinkinase C(PKC) iter, corneal neurotransmitter abnormality, et al.4,With the the number of diabetics increasing, people pay more attentionto the ocular surface disease of diabetic patients. Schirmer Ⅰ test, thetear film break-up time and staining with fluorescein sodium on thecornea should become routine tests of ophthalmology in diabetes mellitus.The occurrence of the ocular surface disease should be considered,patients are taking routine tests in diabetes mellitus;Once symptomsappear, doctors must accord the proper treatment in time.