Association of serum vitamin D levels with clinical spectrum of central serous chorioretinopathy patients of Indian origin

Vitamin D, a fat-soluble prohormone has been implicated in various ophthalmological diseases such as ocular inflammation, glaucoma, diabetic retinopathy and ocular angiogenesis. Many studies have shown effect of vitamin D on oxidative stress, angiogenesis and retinal circulation. However, there is definitive lack in published literature on effect of vitamin D on central serous chorioretinopathy especially in view of various epidemiological studies reporting risk of vitamin deficiency in up to 40% adult population.To determine serum vitamin D levels in various clinical profiles of central serous chorioretinopathy and their effect on its pathophysiology in Indian population.Case control observational study METHODS: Study included 42 patients (group P) of central serous chorioretinopathy (CSCR) diagnosed with optic coherence tomography (OCT), fundus fluorescein angiography (FFA) which were further sub-grouped into acute(P1), chronic (P2) and recurrent (P3). A total of 44 age & sex-matched healthy control subjects (group C) were also included. The vitamin D levels of both groups were examined and analyzed.No significant difference between the groups P and C in respect of age, gender or baseline best corrected visual acuity (P = 0.153, P = 0.123 and P = 0.08, respectively) was noted. Vitamin D levels were determined as 16.473 ± 7.307 ng/mL in group P and 34.940 ± 8.348 ng/mL in group C and difference was statistically significant(P = 0.001). There were statistically significantly more no of patient in group P (78.57%) with deficient vitamin D levels as compared to normal serum levels (4.76%) (P = 0.04). Patients in group P1(acute CSCR) and P2(Chronic CSCR) also had significant more no of subjects with deficient vitamin D levels as compared to normal serum levels (P = 0.01 and P = 0.03).The low serum vitamin D levels were determined in all clinical sub-types of central serous chorioretinopathy patients which point to its possible role in the pathophysiology of the disease. There is a need for further studies to determine the changes that could occur with vitamin replacement therapy in CSCR.