The normal mean level of 25(OH)D is considered to be 30 ng/mL, but the minimum bodily requirement for 25(OH)D is still controversial (
10). In the present study, the mean 25(OH)D level was 14.58 ng/mL (SD = 6.96), and 114 (96.61%) of the patients had levels of < 30 ng/mL.
The main site for endogenous synthesis of 25(OH)D is the skin, which provides the majority of vitamin D precursor, with a small amount being absorbed through dietary intake (
11). In burn patients, this source is impaired; however, other factors also contribute to 25(OH)D deficiency in these patients, including electrolyte disturbances, malabsorption, reduced albumin levels, post-burn hypermetabolism, and immobilization ( 12).
Klein et al. showed that vitamin D deficiency occurs in children suffering from burn injuries. Moreover, they found that the conversion of 7-dehydrocholesterol into previtamin D3 was impaired in biopsies from both the scar tissue and adjacent healthy skin. This finding indicates that the burden of the inability of the skin to synthesize vitamin D goes beyond the TBSA and involves a larger area (
Serum albumin is the main protein that binds to D1,25. Serum albumin concentrations are reduced following thermal damage, and can remain low for a long period of time (
13). A significant correlation was observed between the 25(OH)D levels and albumin in the present study, which is in concordance with this finding.
It has been shown that many growth factors and cytokines play active roles in inflammatory and immunological responses after injury. These factors are also effective in bone remodeling and pathological destruction. The associations of 25(OH)D metabolism with these new factors and cytokines have recently been studied, but their impact on 25(OH)D levels after burn injury is unclear (
14). Bone metabolism is a complex and multifactorial process that is regulated by systemic hormones. Since the consumption of corticosteroids is associated with bone loss and bone fractures, increasing endogenous glucocorticoid production, which occurs after a burn, can be associated with vitamin D abnormalities ( 6, 15).
Several studies have looked at supplementation for vitamin D-deficient patients. A study by Gottschlich et al. used ergocalciferol in children younger than three years at a dose of 800 IU daily, and for patients older than three years, they used 1600 IU daily for two weeks. They doubled the supplemental dose every two weeks, up to a maximum dose of ten times the recommended dietary allowance (RDA), or 4000 IU daily, if there was no improvement in the serum levels of vitamin D in these patients. It was found that patients receiving vitamin D supplementation had consistently lower levels of 25(OH)D and D1,25. It was presumed that there might be a malabsorptive defect or an inability to hydroxylate vitamin D (
16). In another study, Klein et al. assessed supplementation with ergocalciferol in eight burned children suffering from vitamin D deficiency (D2). Vitamin D2 400 IU (10 ug) was administered daily for six months in order to raise serum levels of 25(OH)D back to normal. The 25(OH)D levels were raised in these patients, but not enough to compensate for the deficiency; the increase was also not statistically meaningful in comparison to the control group, who had not received the supplementation ( 17). Both of these studies may have been limited by their choice of vitamin D supplementation, as ergocalciferol is less effective than cholecalciferol in raising serum levels of vitamin D.
On the other hand, several additional studies have indicated the benefits of vitamin D supplementation in burn patients. Mayes et al. followed 39 burn patients for fractures after discharge while giving them vitamin D2 and D3 supplementation for one year. The results showed that vitamin D3 may have been beneficial in reducing the fracture risk in these patients (
18). In a randomized clinical trial by Rousseau et al. on 15 burn patients followed for one year, the patients were divided into two groups. One group received intramuscular injection of cholecalciferol (200000 IU) every three months with oral daily calcium, and the other group received normal saline every three months with oral daily lactose as a placebo. The results indicated that calcidiol (25(OH)D) levels increased significantly in the experimental group that received vitamin D supplementation and calcium. However, there was no significant change in bone health in either of the groups. Quadriceps strength did improve in the case group ( 19). Table 5 shows the results of some previous studies.
Table 5. Summary of Previous Studies
Researcher/Year Sample Size 25-Hydroxyvitamin D Klein GL/2002 ( 7 ) 11 low in 90% (7 year follow up) Gottschlich MM/2004 ( 16 ) 69 low in 26.2%, very low in 11% Klein GL/2009 ( 17 ) 8 16 ng/mL Rousseau AF/2015 ( 19 ) 26 21.5 ng/mL
Although there is controversy with regard to administering vitamin D supplementation to patients after acute burn injuries, some studies strongly suggest that vitamin D is beneficial in these patients. We also began administering vitamin D to our burn patients as a part of their treatment protocol; however, the follow-up is still ongoing, and the results are not yet ready to be published. Whatever the results indicate, it is obvious that patients with acute burn injuries will need essential vitamins and minerals more than normal individuals will. Therefore, we recommend administering vitamins and minerals to this group of patients, beyond the usual and common RDA.
Based on the results of this study, we can conclude that 25-hydroxyvitamin D levels are low in children after acute burns, and these patients should be given vitamin D supplementation at 2 - 3 times the physiologic range (800 - 1200 IU/day). The present study also showed a higher frequency of vitamin D deficiency compared with other studies; vitamin D levels were lower than recommended levels in 96.61% of patients, while 81.35% had deficiencies and 16.10% had insufficiencies.