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BACKGROUND
The term vitamin D encompasses two compounds. Ergocalciferol (vitamin D2) is formed following ultraviolet (UV) irradiation of the plant
steroid ergosterol1,2,12 which is obtained from dietary
sources.2,13 Cholecalciferol (vitamin D3) is both synthesized in the skin, from the cholesterol precursor
7-dehydrocholesterol,1,2,12 and ingested from foods
such as oily fish, liver, eggs, and fortified foods (eg,
margarine).2,13 Both forms of vitamin D are hydroxylated in the liver to form calcidiol (25(OH)D), which
is the major circulating form of the vitamin and is
commonly used to determine vitamin D levels.1,12,14
Calcidiol undergoes hydroxylation in the kidneys to
form the hormone calcitriol (1,25(OH)2D), which is
the biologically active form of vitamin D responsible
for its metabolic effects.1,2
The majority of vitamin D is synthesized in the
skin, catalyzed by exposure to UV light, and provides
731
732 Schumann et al
METHODS
A literature search was conducted using Medline,
the Cochrane central register of controlled trials,
and EMBASE to identify any trials of vitamin D deficiency in burn patients. Key medical subject headings
search terms used included burn, vitaminD,
and deficiency. Reference lists of identified articles
were also reviewed to assist identification of related
articles not identified in the literature search.
RESULTS
Six published studies regarding vitamin D status in
burn patients were found (Table 3). Five of these
were conducted in pediatric populations. In 2002,
a group of 24 pediatric patients with burns greater
than 40% TBSA were followed up at 2 years (12
patients) and at 7 years (12 patients). They found
that in the 2-year group, 10 had low calcidiol levels
and 0 had low calcitriol levels. In the 7-year group,
they found that 10 had low calcidiol levels and 5 had
low calcitriol levels.10 In 2002, a prospective study of
41 pediatric patients with a mean burn size of 52.1%
TBSA showed that in the initial week after injury,
calcidiol and calcitriol levels were low.47 In 2002, a
study of 30 adult burn patients with a mean burn
size of 21.1% TBSA examined the endocrine changes
after burn injury, in particular looking at bone density. Although not assessing vitamin D levels as a
major endpoint, they found that calcidiol levels were
usually low or low-normal in their population.48 In
2003, a retrospective review of 104 pediatric patients
with burns greater than 40% TBSA was conducted
looking for long-bone fractures that developed during the course of healing. Six patients were identified with fractures, and of these four were shown to
have low levels of both calcidiol and calcitriol.11 In
2004, a study conducted on 69 pediatric patients
with burns greater than 25% TBSA found that 62.3%
of all patients had low calcidiol or calcitriol at some
point during their admission.8 Another study in
2004, on small numbers of pediatric patients with
burns greater than 40% TBSA, looked at skin biopsy
samples for vitamin D precursors after exposure to
Table 1. Standardized vitamin D (25-OHD) deficiency levels for the United Kingdom, United States of America, and
Australia/New Zealand1921
Deficiency Level
UK Reference
Range
USA Reference
Range
Severe deficiency
Deficient
Mild deficiency
Adequate
Optimal
Upper limit associated with adverse effects
<25 nmol/L
2550 nmol/L
5075 nmol/L
>75 nmol/L
<30 nmol/L
3050 nmol/L
>50 nmol/L
>125 nmol/L
<12.5 nmol/L
12.525 nmol/L
2550 nmol/L
>50 nmol/L (75100 nmol/L if >65 yr of age)
Schumann et al 733
Table 2. Vitamin D intake recommendations for the United Kingdom, United States of America, and Australia/New
Zealand2224
Age Group
(yr)
UK
(Reference Nutrient Intake)
USA
(Recommended Dietary Allowance)
600 IU
600 IU
600 IU/800 IU
1950
5065
>65/>70
DISCUSSION
Vitamin D deficiency affects pediatric burn populations, with one study demonstrating that 62.3% had
low calcidiol or calcitriol during the acute admission.8
Other studies assessing vitamin D deficiency in pediatric burn populations also revealed its existence,
albeit in smaller study groups or retrospectively.
Two studies looked at supplementation of vitamin
Australia/NZ
(Adequate Intake, No Recommended
Dietary Intake Available)
5 g/d (200 IU)
10 g/d (400 IU)
10 g/d (400 IU)/15 g/d (600 IU)
D-deficient patients. One study supplemented ergocalciferol for 2 weeks at 800 IU daily for children
younger than 3 years and 1600 IU daily for those
older.8 The supplemental dose was doubled every 2
weeks up to a maximum dose of 4000 IU daily if
vitamin D levels failed to respond. They found that
patients having vitamin D supplementation had consistently lower levels of calcidiol and calcitriol compared with patients not having supplementation and
concluded the presence of a malabsorptive defect
or an inability to hydroxylate vitamin D. The other
study assessing supplementation in pediatric patients
Study
Study
Design
Klein
et al10
Prospective
cohort
Wray
et al47
Prospective
cohort
Population Size
24 pediatric
patients
(12 patients
assessed at
2 yr postburn,
12 patients at
7 yr postburn)
41 pediatric
patients
% TBSA of
Population
>40%
Related
Outcome
Measures
Calcidiol and
calcitriol in
blood
Mean 53.1%
Calcidiol and
calcitriol in
blood
Prospective
30 adult patients
cohort
Retrospective 104 pediatric
review
patients of which
6 had sustained
long-bone
fractures
Gottschlich Prospective
69 pediatric
et al24
cohort
patients
Mean 21.1%
Calcidiol levels
Klein
et al9
Mean TBSA
52%
Dolecek
et al48
Mayes
et al11
Prospective
cohort
11 pediatric
patients
>40%
>25%
Calcidiol and
calcitriol
levels in
blood
Results
2-yr group: 83.3% had
low calcidiol, 0.0%
had low calcitriol;
7-yr group: 90.9%
had low calcidiol,
45.5% had low
calcitriol.
In the initial week,
mean calcidiol was
low at 29 nmol/L,
and mean calcitriol
was low at 33
pmol/L
Calcidiol levels were
low or low-normal
66.7% of those with a
long-bone fracture
had low calcidiol and
calcitriol
Vitamin D Deficiency
Level Used
Calcidiol < 37 nmol/L,
calcitriol < 36 pmol/L
Unknown
734 Schumann et al
with vitamin D deficiency employed 400 IU of ergocalciferol daily.49 This similarly demonstrated that
this dose failed to correct the deficiency. Both these
studies may have been limited by their choice of
vitamin D supplementation, as ergocalciferol is less
effective than cholecalciferol on raising serum levels.
No studies on isolated vitamin D deficiency in adult
burn patients have been conducted; however, the one
study of adult burn patients reported that the patients
in their population had low or low-normal levels of
calcidiol. There are a number of mechanisms by which
these patients could become deficient in vitamin D
and possibly compounded by deficiency on admission. They receive limited UV radiation during prolonged institutionalisation in the acute burn period
and are advised to avoid sun exposure on discharge
to prevent or minimise scar hyperpigmentation. Furthermore, the use of pressure garments and wound
dressings limit the area of skin available for sun exposure and hence vitamin D production.50 The biosynthetic functions of skin are known to be impaired after
burn injury; in both burn skin and adjacent normal
skin, levels of 7-dehydrocholesterol are decreased,
as well as its subsequent conversion to cholecalciferol following exposure to UV light.9 Abnormalities
in the calcium-parathyroid hormone (Ca-PTH) axis
postburn are also thought to lead to decreased levels
of vitamin D.51 The proinflammatory state induced
by burn injury leads to upregulation of PTH calcium
receptor52 which in turn leads to inappropriately low
levels of circulating PTH and decreased action of 1-
hydroxylase in the kidney. This results in a deficiency
of metabolically active vitamin D.51,52
A recent review suggests that replenishment of
vitamin D levels can be considered in two phases,
restoration and maintenance.53 Restoration of vitamin D levels requires larger doses to be given than
for maintenance, because the body stores have a large
volume of distribution. However, recent research
suggests that giving large doses of vitamin D may
itself cause adverse effects.54 Treatment of vitamin D
deficiency may also improve common symptoms suffered by burn patients, such as pruritis. A retrospective case series of patients with idiopathic pruritis,
rashes, and angioedema treated with vitamin D led
to complete resolution of symptoms in a significant
proportion of the cohort.55 This has the potential
to improve patient quality of life, in addition to the
prevention of deficiency-related complications.
CONCLUSION
Further investigation is required into the prevalence of vitamin D deficiency in adult burn patients.
Schumann et al 735