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Vitamin D

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Vitamin D deficiency is widespread and may result in a vast array of health consequences including osteoporosis, falls, increased cancer risk and altered glucose and lipid metabolism – the pathogenesis of diabetes and cardiovascular disease. It plays an essential role in muscle and bone health, immunity and muscle signaling and has been linked with autoimmune disorders such as multiple sclerosis (Cantorna et al. 2006; Cherniak et al. 2008; Ford et al. 2005; Mathieu et al. 2005). Obesity has been associated with decreased bioavailability of vitamin D, and percentage body fat is inversely related to vitamin D levels and directly correlated with parathyroid hormone (PTH) levels (Snijder et al. 2005; Wortsman et al. 2000).

The skeletal effects of hypovitaminosis D are evidenced in progressive stages such as calcium malabsorption with secondary elevation of PTH, increased bone remodeling and osteoporosis and further histologic changes related to continued lack of calcium and poor mineralization (Heaney 1999).

Individuals with SCI have an increased occurrence of vitamin D deficiency, resulting from a number of factors including decreased exposure to sunlight, inadequate dietary intake and the effect of medications (Hummel et al. 2012). In turn, vitamin D deficiency promotes calcium deficiency and secondary hyperparathyroidism, resulting in further bone loss and exacerbating osteoporosis. Myopathy and nonspecific musculoskeletal pain may also develop as a consequence of vitamin D deficiency (Bauman et al. 2005; Holick 2005).

Bauman et al. (1995) reported that 32 of 100 SCI subjects had 25(OH)D levels below normal range and 11 of 32 had elevated serum PTH levels. Zhou et al. (1993) measured the 25(OH)D, serum calcium, magnesium and albumin concentrations of 92 men with SCI, 38 of whom had single or multiple pressure ulcers, and compared these values with those of non-SCI controls. The SCI group had lower serum 25(OH)D, total calcium, and albumin concentrations. Individuals with tetraplegia had lower 25(OH)D levels than those with paraplegia. Additionally, the SCI subgroup with pressure ulcers demonstrated significantly lower serum 25(OH)D, calcium and magnesium levels than the SCI subjects without ulcers.

There is increasing support for vitamin D supplementation beyond present recommendations. Additional studies are needed to establish the best diagnostic and supplementation guidelines for different populations (Cherniak et al. 2008).

Table 7: Vitamin D Supplementation Post SCI

Discussion

Bauman et al. (2005) determined that healthy individuals with chronic SCI living in the community had vitamin D deficiency. Ten subjects with chronic SCI and a diagnosis of absolute vitamin D (25(OH)D) deficiency received 50 ug (2000 IU) of vitamin D3 twice per week for two weeks in addition to 1.5 grams (1500 mg) of elemental calcium daily. Serum 25(OH)D levels significantly increased by day 14; however, levels remained below normal range in eight out of ten subjects. Serum calcium level was not significantly different, urinary calcium significantly increased, and serum PTH levels significantly decreased. In their second study Bauman et al. (2005) gave forty subjects 10 ug (400 IU) of vitamin D3 daily in addition to a multivitamin that contained 10 ug (400 IU) vitamin D3 daily for 12 months. All subjects received this treatment regardless of their initial serum vitamin D status. Subjects were encouraged to have at least 0.8 grams (800 mg) of calcium in their daily diet and were supplemented daily with 0.5 grams (500 mg) elemental calcium. Vitamin D levels significantly increased between baseline and follow-up at 6 and 12 months. There was no significant association between level of injury and baseline 25(OH)D levels.Serum and ionized calcium were not significantly different after 12 months of treatment although serum PTH was significantly reduced at 6 and 12 months. It is important to note that at baseline, 33 of the 40 subjects had 25(OH)D levels that were below the lower limit of normal, and that after 12 months of supplementation at 800 IU, only eight of the 40 subjects had serum 25(OH)D values greater than 30 ng/mL. These levels are not adequate in reversing elevated parathyroid levels and reducing bone turnover, despite significant decreases in PTH at 12 months. In conclusion, vitamin D3 supplementation resulted in significant increases in 25(OH)D levels and reductions in parathyroid hormone; however, suboptimal 25(OH)D levels persisted, suggesting the need for higher doses of vitamin D3 supplementation and/or longer periods of administration.

Conclusion

There is level 4 evidence from 2 pre-post studies (Bauman et al., 2005) that vitamin D3 supplementation raises serum 25(OH) D levels in persons with chronic SCI. However, the dose and duration required to ensure vitamin D3 sufficiency remains unclear.

  • Individuals with SCI should be screened for vitamin D deficiency and, if needed, replacement therapy should be initiated.