Overview of Diabetes Mellitus

Diabetes mellitus prevalence worldwide has showed a pronounced rise during the most recent years. According to reports by the International Diabetes Federation reports as of 2015 more than 400 million people were living with diabetes. The Center for Disease Control and Prevention (CDC) also reports that about 90 to 95 percent of all diagnosed cases of diabetes in adults are type 2. The prevalence of diabetes for all age groups worldwide was assessed to be 2.8% during 2000 and is anticipated to rise to 4.4% in of 2030. Diabetes is now considered the leading cause of newly diagnosed blindness in adults, and the WHO anticipates that death rates due to diabetes will double by 2030.

The significance of vascular variations from the norm as well as neuronal anomalies in the pathogenesis of diabetic retinopathy has been as of late indicated. Several studies demonstrated that neuronal degeneration in diabetic retinopathy is expected to mitochondria and caspase-dependent cell demise pathways, and a few neurotrophic components can obstruct the neuronal cell passing initiated by diabetic stress.

Diabetes mellitus most commonly causes ocular complications in the retina, in the form of diabetic retinopathy, retinal vein and arterial occlusions, but may also cause others as anterior ischemic optic neuropathy and cataract. However, not much attention has been drawn to its effect of on the cornea, as it is a less frequent complication. Nevertheless, it is one of the effects that must be studied due to its pronounced effect on vision and its difficulty in management.

It is recognized that neuronal irregularities specifically influence the visual capacity in patients with diabetic retinopathy, however they may likewise be the reason for the corneal changes in diabetic keratopathy. Several processes explain its effect; diabetic neurotrophic keratopathy part of the systemic diabetic polyneuropathy is one. Another is during management of proliferative diabetic retinopathy whether surgical or medical, disruptions may occur. This is due to endothelial decompensation and bullous keratopathy as a consequence diabetic endothelial cell damage. The complications of diabetes are related to the degree of control and the duration of the disease.

The findings of the anterior segment in eyes with diabetic keratopathy are more demanding to identify than those of the posterior segment. In spite of the fact that the corneas may show up illness free in diabetic patients, extreme biochemical and ultra-structural irregularities, which alter its role, can be available. The early diabetic changes of the anterior segment incorporate conjunctival microaneurisms, uveal ectropion and endothelial changes; that include Descemet`s film folds, and pigment deposits in the endothelium. In 1970, Schwartz and Hynduik noticed anabatement in corneal sensitivity in diabetic patients with sterile neurotrophic corneal ulcers. The current utilization of vitrectomy to treat diabetic retinopathy has uncovered that these patients have issues with epithelial cells healing and stromal edema.

Patients with diabetic keratopathy have impairments of the epithelial basement membrane (BM), epithelial wound healing, epithelial–stromal interactions, endothelial function, and corneal nerve functions. The corneal disorders associated with diabetic keratopathy are characterized histologically by sub-epithelial deposits, and altered morphological appearances of the corneal epithelium and endothelium.

The single layered hexagonal corneal endothelium plays a fundamental role in the corneal transparency. They are responsible for maintaining the hydration of the stroma, which is directly related to the corneal transparency. It serves this function by actively removing water from the stroma through the metabolic pump located at its basolateral membrane. These endothelial cells do not possess the capability to proliferate in case of damage, but undergo morphological changes in order to fill the gaps with no clinical consequences. It is thought that the damage of the corneal endothelium in diabetes is mediated through chronic metabolic changes at the cellular level.

Diabetes mellitus causes structural and functional changes in the corneal endothelium and thickness. Numerous studies indicate that diabetes cause abnormalities in the cornea, to mention only a few; greater corneal thickness, lower corneal sensitivity, higher auto-fluorescence, lower endothelial count and increased corneal endothelial permeability. The endothelial cells are less hexagonal and are larger in size. It is also proposed that diabetes reduces the activity of the Na+- K+ ATPase of the corneal endothelium and this causes the morphological and functional changes of the diabetic cornea.