Swain Jayshree, Tiwari Shalbha, Pratyush Dd, Dwivedi Awanindra, Gupta Balram, Shukla R C, Singh S K
Department of Endocrinology and Metabolism, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
Indian J Endocrinol Metab. 2012 Dec;16(Suppl 2):S450-2. doi: 10.4103/2230-8210.104128.
Vascular calcification (VC), long thought to result from passive degeneration, involves a complex process of biomineralization resembling osteogenesis, frequently observed in diabetes and is an indicator of diabetic peripheral vascular disease with variable implications.
To study the association between vascular calcification and calcium homeostasis in diabetic patients with foot ulcers without stage 4, 5 chronic kidney disease.
A total of 74 patients with diabetic foot ulcer were enrolled, and VC was detected by X-ray and Doppler methods. Serum calcium, phosphate, alkaline phosphatase (ALKP), fasting and post-prandial glucose levels, and glycosylated hemoglobin (HbA1C) were recorded. Serum iPTH and 25 (OH) vitamin D were estimated by immune radiometric assay and radioimmunoassay, respectively. Data was analyzed by SPSS 16.0.
Vascular calcification was present in 42% of patients. Significant difference in the mean (±SD) of vitamin D, HbA1C, and eGFR was observed in VC +ve compared to VC -ve. There was no significant association of age, duration, BMI, PTH, Ca, PO4, ALKP with that of VC incidence. Severe vitamin D deficiency was more common in VC +ve (51.6%) compared to in VC -ve (18.6%). Sub-group analysis showed that the risk of VC was significantly higher (RR = 2.4, P < 0.05, 95% C.I. = 0.058-2.88) in patients with vitamin D < 10 ng/ml compared to others.
Vitamin D deficiency could be a risk for vascular calcification, which possibly act through receptors on vascular smooth muscle cells or modulates osteoprotegerin/RANKL system like other factors responsible for VC in diabetic foot patients.
