Aims. This study aims at assessing the relationship between 25 (OH) vitamin D (25-OHD) levels and microvascular complications in patients with type 2 diabetes mellitus (DM2). Methods. 136 patients (59？±？11 years) with DM2 (disease duration 8.6？±？7 years) participated in this cross-sectional study. Anthropometric data, HbA1c, 25-OHD levels, serum creatinine, and urine microalbumin/creatinine ratio were collected. Dilated retinal exam was performed, and diabetic neuropathy was assessed using the United Kingdom Screening Score. Results. Serum 25-OHD correlated negatively with HbA1c ( ？？ ). Mean 25-OHD levels were lower in subjects with diabetic retinopathy compared to those without retinopathy (12.3？±？5.5 versus 21.8？±？13.7, ) and lower in subjects with diabetic neuropathy compared to those without neuropathy (16.4？±？10.4 versus 23.5？±？14.5, ). After adjustment for BMI, diabetes duration, and smoking, 25-OHD was an independent predictor of HbA1c (β？？？0.14; ). After adjustment for HbA1c, age, smoking, BMI and disease duration, 25-OHD were independent predictors for diabetic retinopathy: OR 2.8 [95% CI 2.1–8.0] and neuropathy: OR 4.5 [95% CI 1.6–12] for vitamin D？<？20 versus vitamin D？≥？20？ng/mL. Conclusion. Low serum 25-OHD level was an independent predictor of HbA1c, diabetic neuropathy, and diabetic retinopathy in patients with DM2. 1. Introduction Diabetes affects more than 300 million individuals in the world with significant morbidity and mortality worldwide [1]. In the United States, it has been estimated that the incidence is about 1 million new cases per year [2]. People with diabetes are at high risk of microvascular complications including diabetic retinopathy, diabetic nephropathy, and diabetic neuropathy, which have bad impact on quality of life and are associated with increased mortality [3–5]. Risk factors for the development of diabetic microvascular complications include glycaemic control, age, diabetes duration, and smoking. Additional risk factors are age at onset of diabetes and genetic factors [4, 6]. In parallel to the increase in the prevalence of diabetes mellitus, there has been a resurgence of vitamin D deficiency worldwide [7, 8]. Immigrants to Europe from the Middle East and Asia carry a high risk for vitamin D deficiency [7]. Vitamin D has traditionally been associated with calcemic activities, namely, calcium and phosphorus homeostasis and bone. However, recent evidence from various lines of research suggested nontraditional roles of vitamin D in human health including cancer, autoimmune, infectious, respiratory, and
References
[1]
R. Sherwin and A. M. Jastreboff, “Year in diabetes 2012: the diabetes tsunami,” Journal of Clinical Endocrinology & Metabolism, vol. 97, pp. 4293–4301, 2012.
[2]
A. G. Pittas, J. Lau, F. B. Hu, and B. Dawson-Hughes, “The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis,” Journal of Clinical Endocrinology & Metabolism, vol. 92, no. 6, pp. 2017–2029, 2007.
[3]
R. Raman, A. Gupta, S. Krishna, V. Kulothungan, and T. Sharma, “Prevalence and risk factors for diabetic microvascular complications in newly diagnosed type II diabetes mellitus. Sankara Nethralaya Diabetic Retinopathy Epidemiology And Molecular Genetic Study (SN-DREAMS, report 27),” Journal of Diabetes and Its Complications, vol. 26, pp. 123–128, 2012.
[4]
A. Girach, D. Manner, and M. Porta, “Diabetic microvascular complications: can patients at risk be identified? A review,” International Journal of Clinical Practice, vol. 60, no. 11, pp. 1471–1483, 2006.
[5]
M. Mata-Cases, C. De Prado-Lacueva, V. Salido-Valencia, et al., “Incidence of complications and mortality in a type 2 diabetes patient cohort study followed up from diagnosis in a primary healthcare centre,” International Journal of Clinical Practice, vol. 65, pp. 299–307, 2011.
[6]
C. R. L. Cardoso and G. F. Salles, “Predictors of development and progression of microvascular complications in a cohort of Brazilian type 2 diabetic patients,” Journal of Diabetes and Its Complications, vol. 22, no. 3, pp. 164–170, 2008.
[7]
P. Lips, “Vitamin D status and nutrition in Europe and Asia,” Journal of Steroid Biochemistry and Molecular Biology, vol. 103, no. 3–5, pp. 620–625, 2007.
[8]
M.-H. Gannage-Yared, R. Chemali, N. Yaacoub, and G. Halaby, “Hypovitaminosis D in a sunny country: relation to lifestyle and bone markers,” Journal of Bone and Mineral Research, vol. 15, no. 9, pp. 1856–1862, 2000.
[9]
S. B. Mohr, “A brief history of vitamin D and cancer prevention,” Annals of Epidemiology, vol. 19, no. 2, pp. 79–83, 2009.
[10]
J. M. Lappe, D. Travers-Gustafson, K. M. Davies, R. R. Recker, and R. P. Heaney, “Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial,” The American Journal of Clinical Nutrition, vol. 85, pp. 1586–1591, 2007.
[11]
R. Staud, “Vitamin D: more than just affecting calcium and bone,” Current Rheumatology Reports, vol. 7, no. 5, pp. 356–364, 2005.
[12]
S. Nagpal, S. Na, and R. Rathnachalam, “Noncalcemic actions of vitamin D receptor ligands,” Endocrine Reviews, vol. 26, no. 5, pp. 662–687, 2005.
[13]
W. Janssens, A. Lehouck, C. Carremans, R. Bouillon, C. Mathieu, and M. Decramer, “Vitamin d beyond bones in chronic obstructive pulmonary disease; time to act,” American Journal of Respiratory and Critical Care Medicine, vol. 179, no. 8, pp. 630–636, 2009.
[14]
K. B. Gibney, L. MacGregor, K. Leder et al., “Vitamin D deficiency is associated with tuberculosis and latent tuberculosis infection in immigrants from sub-Saharan Africa,” Clinical Infectious Diseases, vol. 46, no. 3, pp. 443–446, 2008.
[15]
G. Karatekin, A. Kaya, O. Salihoglu, H. Balci, and A. Nuhoglu, “Association of subclinical vitamin D deficiency in newborns with acute lower respiratory infection and their mothers,” European Journal of Clinical Nutrition, vol. 63, pp. 473–477, 2007.
[16]
J. Kendrick, G. Targher, G. Smits, and M. Chonchol, “25-Hydroxyvitamin D deficiency is independently associated with cardiovascular disease in the Third National Health and Nutrition Examination Survey,” Atherosclerosis, vol. 205, no. 1, pp. 255–260, 2009.
[17]
M. T. Cantorna, “Vitamin D and multiple sclerosis: an update,” Nutrition Reviews, vol. 66, supplement 2, pp. S135–S138, 2008.
[18]
L. Adorini and G. Penna, “Control of autoimmune diseases by the vitamin D endocrine system,” Nature Clinical Practice Rheumatology, vol. 4, no. 8, pp. 404–412, 2008.
[19]
G. Isaia, R. Giorgino, and S. Adami, “High prevalence of hypovitaminosis D in female type 2 diabetic population,” Diabetes Care, vol. 24, no. 8, p. 1496, 2001.
[20]
A. G. Need, P. D. O'Loughlin, M. Horowitz, and B. E. C. Nordin, “Relationship between fasting serum glucose, age, body mass index and serum 25 hydroxyvitamin D in postmenopausal women,” Clinical Endocrinology, vol. 62, no. 6, pp. 738–741, 2005.
[21]
R. Scragg, M. Sowers, and C. Bell, “Serum 25-hydroxyvitamin D, diabetes, and ethnicity in the Third National Health and Nutrition Examination Survey,” Diabetes Care, vol. 27, no. 12, pp. 2813–2818, 2004.
[22]
R. Scragg, “Vitamin D and type 2 diabetes: are we ready for a prevention trial?” Diabetes, vol. 57, no. 10, pp. 2565–2566, 2008.
[23]
L. Danescu, S. Levy, and J. Levy, “Vitamin D and diabetes mellitus,” Endocrine, vol. 35, pp. 11–17, 2008.
[24]
C. Mattila, P. Knekt, S. M？nnist？ et al., “Serum 25-hydroxyvitamin D concentration and subsequent risk of type 2 diabetes,” Diabetes Care, vol. 30, no. 10, pp. 2569–2570, 2007.
[25]
C. Dalg？rd, M. S. Petersen, P. Weihe, and P. Grandjean, “Vitamin D status in relation to glucose metabolism and type 2 diabetes in septuagenarians,” Diabetes Care, vol. 34, no. 6, pp. 1284–1288, 2011.
[26]
P. Pietschmann, G. Schernthaner, and W. Woloszczuk, “Serum osteocalcin levels in diabetes mellitus: analysis of the type of diabetes and microvascular complications,” Diabetologia, vol. 31, no. 12, pp. 892–895, 1988.
[27]
A. Suzuki, M. Kotake, Y. Ono et al., “Hypovitaminosis D in type 2 diabetes mellitus: association with microvascular complications and type of treatment,” Endocrine Journal, vol. 53, no. 4, pp. 503–510, 2006.
[28]
T. Inukai, Y. Fujiwara, K. Tayama, Y. Aso, and Y. Takemura, “Alterations in serum levels of 1α,25(OH)2 D3 and osteocalcin in patients with early diabetic nephropathy,” Diabetes Research and Clinical Practice, vol. 38, no. 1, pp. 53–59, 1997.
[29]
P. Naveilhan, I. Neveu, D. Wion, and P. Brachet, “1,25-Dihydroxyvitamin D3, an inducer of glial cell line-derived neurotrophic factor,” NeuroReport, vol. 7, no. 13, pp. 2171–2175, 1996.
[30]
P. Lee and R. Chen, “Vitamin D as an analgesic for patients with type 2 diabetes and neuropathic pain,” Archives of Internal Medicine, vol. 168, no. 7, pp. 771–772, 2008.
[31]
M. J. Young, A. J. M. Boulton, A. F. Macleod, D. R. R. Williams, and P. H. Sonksen, “A multicentre study of the prevalence of diabetic peripheral neuropathy in the United Kingdom hospital clinic population,” Diabetologia, vol. 36, no. 2, pp. 150–154, 1993.
[32]
M. S. Hutchinson, Y. Figenschau, I. Nj？lstad, H. Schirmer, and R. Jorde, “Serum 25-hydroxyvitamin D levels are inversely associated with glycated haemoglobin (HbA1c). The Troms？ Study,” Scandinavian Journal of Clinical and Laboratory Investigation, vol. 71, no. 5, pp. 399–406, 2011.
[33]
L. A. Plum and J. B. Zella, “Vitamin D compounds and diabetic nephropathy,” Archives of Biochemistry and Biophysics, vol. 523, pp. 87–94, 2012.
[34]
P. A. Patrick, P. F. Visintainer, Q. Shi, I. A. Weiss, and D. A. Brand, “Vitamin d and retinopathy in adults with diabetes mellitus,” Archives of Ophthalmology, vol. 1, pp. 756–760, 2012.
[35]
D. M. Albert, E. A. Scheef, S. Wang et al., “Calcitriol is a potent inhibitor of retinal neovascularization,” Investigative Ophthalmology and Visual Science, vol. 48, no. 5, pp. 2327–2334, 2007.
[36]
K. Bu？an, M. Ivanisevi？, T. Zemunik et al., “Retinopathy and nephropathy in type 1 diabetic patients–association with polymorphysms of vitamin D-receptor, TNF, Neuro-D and IL-1 receptor 1 genes,” Collegium Antropologicum, vol. 33, supplement 2, pp. 99–105, 2009.
