Increased of Serum IL-1β and MDA in Diabetic and Hypertensive Retinopathies

Retinopathy (RP) is a microvascular complication induced by diabetes and hypertension. Its onset and progression are associated with chronic hyperglycemia and dysregulated arterial hypertension. In microvascular abnormality, it is observed increased oxidative stress and elevated inflammatory cytokines in the eyes. Diabetic retinopathy is triggered by hyperglycemia of diabetes, however, while in nondiabetic individuals, retinopathy can be triggered by chronic arterial hypertension inducing abnormality in arteriolar retina circulation leading to hypertensive retinopathy. Chronic and noncontrolled hypertension leads to a pathological hypertensive retinopathy and microalbuminuria [1]. Both, diabetic and hypertensive retinopathies constitute inflammatory processes and culminating with blindness. Some biomarkers of inflammation are altered in aqueous humor and serum. It is reported that in type 2 diabetes mellitus (T2DM) patients with retinopathy, VEGF and IL-6 were similar in plasma but increased in aqueous humor [2]. Superoxide is high in the retinas of diabetic rats and retinal cells incubated in high-glucose media [3,4]. Reports have been suggested that oxidative stress mediate several diabetic complications, including retinopathy. Chan & Zhu et al. [5,6] in a review and meta-analysis study observed a significant association between gestational hypertensive disorders and development of retinopathy of prematurity. High serum level of uric acid correlated with the presence of hypertensive retinopathy [7], stroke, diastolic dysfunction and renal abnormality [8-11]. In spite of several studies on diabetic retinopathy, there are few reports in the literature comparing diabetic and hypertensive retinopathy. We aimed to study the level of a biomarker of oxidative stress (malondialdehyde) and to evaluate cytokines from inflammasome (IL-1β) or activation of NF-κB (IL-6) in T2DM with either hypertensive or diabetic.