OCCASIONAL REVIEW
A clinician’s guide to
vitamin D and bone health
in children
Ruchi Nadar
Suma Uday
Abstract
Vitamin D and calcium are key determinants of bone health; deficiency
in either or both can cause nutritional rickets in children and osteoma-
lacia in children and adults. Vitamin D is essential for absorption and
supply of calcium and phosphate for bone mineralisation. Individuals
at risk of deficiency in either nutrient can be broadly classed into 2 cat-
egories; healthy at-risk population and those with pre-disposition due
to underlying chronic health conditions. In the former, vitamin D defi-
ciency (VDD) predominantly results from restricted Ultraviolet B, either
due to environmental (high latitude residence), biological (dark skin
pigmentation) or behavioural (sun avoidance, covered clothing) fac-
tors. Calcium deficiency is predominant in individuals with restricted
diet. Only a small fraction of children, during states of high physiolog-
ical demands such as infancy and adolescence, come to medical
attention with symptomatic VDD (hypocalcaemic seizures, dilated car-
diomyopathy, tetany) or rickets. The vast majority of at-risk population
with osteomalacia (including pregnant women) remain unrecognised
due to its non-specific presentation (malaise, tiredness). Clinicians
can play an active role in recognising risk groups and optimising
bone health through promotion of dietary calcium, vitamin D
supplementation at every health care contact and biochemical surveil-
lance in individuals with chronic conditions. Liberal supplementation of
at-risk groups is more effective than biochemical testing; however
large-scale prevention requires political support to implement robust
supplementation and food fortification policies. This article briefly out-
lines what clinicians need to know about vitamin D and bone health in
children and young people.
Keywords alfacalcidol; bone health; cardiomyopathy; cholecalcif-
erol; hypovitaminosis D; nutrition; rickets
Introduction
The first two decades of life provide an opportunity to achieve
maximum bone strength to sustain function for a lifetime. Bone
health, a term that entails integrity of both bone structure and
Ruchi Nadar MBBS, MRCPCH Clinical Fellow in Endocrinology and
Diabetes, Birmingham Women’s and Children’s NHS Foundation
Trust, Birmingham, UK. Conflicts of interest: none declared.
Suma Uday MBBS, MRCPCH, MMedSci Consultant in Paediatric
Endocrinology and Diabetes, Birmingham Women’s and Children’s
NHS Foundation Trust and Institute of Metabolism and Systems
Research, University of Birmingham, Birmingham, UK. Conflicts of
interest: Suma Uday has received research funds and speaker’s
honoraria from Thornton and Ross Pharmaceuticals.
PAEDIATRICS AND CHILD HEALTH 31:9
function, in children encompasses the dynamic changes due to
bone growth from birth to completion of puberty. Peak bone
mass, the maximum bone tissue that an individual can attain,
correlates with the risk of osteoporosis in adult life. Bone mass is
maximally accrued during puberty, and consolidated shortly
after completion of skeletal growth.
Optimizing bone health in the early years is very important.
Although one’s bone health is genetically determined, a large
cohort of children are at risk of poor bone health secondary to
disorders of growth, chronic illness, therapeutic steroid use, non-
ambulatory status due to neuromuscular disorders and poor
nutrition. Physical activity, calcium intake and vitamin D are the
major contributors to bone health for all ages. Both vitamin D
and dietary calcium deficiency can cause rickets, a subacute
disorder of bone and muscle function, but may have catastrophic
presentations with severe hypocalcaemia and cardiomyopathy.
This review will focus on the role of vitamin D and calcium in
growing children and deficiency states leading to nutritional
rickets and osteomalacia, a widely prevalent condition in the UK
and globally. We also emphasize on the key role clinicians can
play in preventing vitamin D and calcium deficiency.
Terminologies in relation to vitamin D physiology and
pharmacology
The vitamin D biosynthetic pathway begins with 7-
dehydrocholesterol present in skin. Ultraviolet B (UVB) radiation
from sunlight breaks the B ring of the steroid molecule, converting
it to cholecalciferol, also referred to as vitamin D or D3. Ergo-
calciferol or vitamin D2, is a plant-derived vitamin D, widely used
in the treatment of vitamin D deficiency (VDD). Ergocalciferol
undergoes further steps of metabolism similar to endogenously
produced cholecalciferol (Figure 1). Both ergo and cholecalciferol
undergo 25-hydroxylation in the liver to form 25-hydroxyvitamin
D (25(OH)D) which is the major circulating form.
Following further 1 hydroxylation in the kidney 1,25 dihy-
droxyvitamin D [1,25(OH)2D or calcitriol], the biologically active
form is synthesized. Calcitriol enhances intestinal calcium and
phosphorus absorption.
Melanin in the skin slows cutaneous production of cholecal-
ciferol. 1-hydroxylation, which is the final step of activation, is
regulated by parathyroid hormone (PTH).
Vitamin D status is usually assessed in the laboratory by
measuring serum 25(OH)D levels as it is the most stable form
and exists at far higher concentrations (typically 1000-fold) than
the biologically active 1,25 (OH)2D form.
The most widely accepted 25(OH)D thresholds suggested by
the National Academy of Medicine (formerly known as the
Institute of Medicine) and ‘Global consensus recommendations
for prevention and treatment of nutritional rickets’1 include:

Vitamin D sufficiency >50 nmol/L

Vitamin D insufficiency at 30e50 nmol/L

Vitamin D deficiency (VDD) < 30 nmol/L
The UK Scientific advisory committee on nutrition (SACN) do
not set sufficiency thresholds, however suggest that the risk of
poor musculoskeletal health is increased at 25(OH)D levels
below 25 nmol/L.
In clinical practice Vitamin D is often used as a generic term to
describe various vitamin D metabolites including cholecalciferol
364 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW

Figure 1 Key steps and metabolites in vitamin D synthesis and their significance for investigations and treatment. Arrows indicate steps at which
various pharmacologic preparations of vitamin D and it’s analogues enter the biosynthesis pathway.

synthesized in the skin, 25-hydroxycholecalciferol, ergocalciferol
derived from plant sources and pharmaceutically produced
cholecalciferol, alfacalcidol and calcitriol. It is important to
clearly delineate these terms (Figure 1) to avoid errors in
requesting the right investigations and prescribing the appro-
priate medications.
calcium deficiency; where low enteral calcium availability causes
secondary hyperparathyroidism, phosphate loss and rickets.
The diagnostic terminologies relating to the pathophysiolog-
ical stage of VDD are clarified in Box 1.

Vitamin D deficiency: an evolving pathophysiological state Terminologies related to VDD

Vitamin D insufficiency and deficiency are terms used to indicate low
VDD of any aetiology results in reduced intestinal calcium and
levels of 25(OH)D. It does not indicate the presence or absence of
phosphate absorption. Reduced serum calcium levels trigger the
rickets (can be termed as simple vitamin D insufficiency/
release of PTH which improves calcium absorption from the gut
deficiency).
through increased 1 hydroxylation of calcidiol to calcitriol. PTH
Rickets, a disorder of defective mineralization of the growth plate
also promotes calcium resorption in the kidney but this comes at
cartilage and adjacent primary and secondary spongiosa in the
the expense of renal phosphate loss which impairs bone mineral-
metaphysis (“new bone”) occurs in children with open epiphyses.
ization. Hypophosphataemia causes impairment of chondrocyte
Rickets is a radiological diagnosis.
apoptosis (a process essential for normal mineralization) leading to
Osteomalacia represents defective mineralization of pre-formed
accumulation of hypertrophic chondrocytes in the growth plate.
osteoid (“old bone”) during remodeling occurring in children and
These pathologic processes contribute to the classic radiological
adults. It is a histological diagnosis manifesting as bowing limb
features of rickets, such as widening of the growth plates, splaying
deformities in children or Looser zone fractures on X-rays in
and fraying of metaphysis. Raised PTH also mobilises stored cal-
adults.
cium from bones through its action on osteoclasts. Hence, elevated
Osteoporosis relates to reduced bone mass and structural quality,
PTH and alkaline phosphatase (ALP) are early indicators of
not directly associated with reduced bone mineralization or VDD.
compensatory mechanisms in action. Serum calcium levels do not
Although bone mineral density may be reduced in an individual
always reflect the calcium status in the body. Only with prolonged
with severe rickets and osteomalacia, it is not classed as osteo-
VDD, serum calcium levels ultimately drop.
porosis, as the latter refers specifically to a pathology due to
Just as vitamin D sufficiency is a pre-requisite to prevent
excessive bone resorption or from reduced bone mass accrual.
rickets, adequate dietary intake of calcium (calcium intake in
Osteogenesis imperfecta (primary) and steroid induced (second-
mg/day as per age: 0e6 months ¼ 200 mg, 6e12 months ¼
ary) osteoporosis are examples in children.
260 mg and >12 months ¼ 500 mg) is also essential. A similar
pathophysiological process as VDD occurs in prolonged dietary Box 1

PAEDIATRICS AND CHILD HEALTH 31:9 365 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW

Children at risk of vitamin D deficiency

A. Apparently healthy at-risk children Maternal factors: Infants born to mothers with VDD
Feeding practices: Exclusively breast-fed infants (especially if there is maternal VDD),
prolonged breast feedinga, infants with delayed introduction of complementary fooda
Dietary factorsa: Vegan diet, children with restricted diet for various reasons including
dairy intolerance
Dark skin pigmentation: Children from Black, Asian and Minority Ethnic (BAME) groups
Factors limiting UVB exposure:
i. Individuals with photosensitivity
ii. Covered cultural clothing
iii. Excessive sunscreen use (therapeutic or non-therapeutic)
iv. High latitude residence (such as UK)
Children with previous VDD unless risk factors are mitigated
B. Children with underlying medical Malabsorptiona syndromes such as coeliac disease, cystic fibrosis, intestinal failure or
conditions short gut syndrome
Chronic liver disease
Chronic renal disease
Medications e.g. prednisolone, sevelamer, antiepileptics: phenytoin, carbamazepine,
valproic acid and Phenobarbitone
Malnutritiona due to poor intake or chronic systemic illness
Conditions predisposing to secondary osteoporosis: chronic steroid use, chronic
inflammatory conditions.
Children with restricted mobility who spend very little time outdoors.
a
Conditions where dietary calcium intake could also be restricted.

Table 1

Population groups at risk of vitamin D deficiency Black children, was 5 to 10-fold higher, respectively, when
compared to the general population and 90 to 166-fold higher,
Worldwide, solar VDD and dietary calcium deficiency are the
respectively, when compared to white children. The groups who
commonest causes of nutritional rickets. The condition is re-
would benefit most from testing are listed in Box 2.
emerging in higher income, Western countries like the UK, due
There are no specific recommendations for the frequency of
to immigration of “at- risk” groups from low and middle income
testing, however six to twelve monthly testing based on indi-
countries. Several factors affect availability of solar UVB: envi-
vidual circumstances is reasonable. In children with chronic
ronmental factors like areas of higher latitude, cloud cover, air
renal or liver diseases, more frequent monitoring may be needed.
pollution level and personal factors like skin pigmentation,
Children with hypocalcaemic or hypophosphataemic symp-
clothing and time spent outdoors. Children with underlying
toms (detailed later) and those with suspected VDD or rickets
health conditions are predisposed to deficiency in the setting of
malabsorption and/or altered vitamin D metabolism in chronic
liver or renal disease. Use of antiepileptic medications may
contribute to deficiency by inducing mitochondrial P450 en-
zymes enhancing vitamin D breakdown. Indications for measuring 25(OH)D levels
We have categorized the risk groups as healthy children who Children presenting with symptomatic VDD.
are predisposed to deficiency due to dietary, ethnicity or social Children with suspected VDD or rickets based on clinical,
factors and those with underlying health conditions (Table 1) so biochemical or radiological features (which only occur in late
as to consider these groups separately from a testing, supple- stages of the disease process)
mentation and prevention perspective. Children with underlying health conditions predisposing them to
VDD (Table 1, part B).
Who should undergo testing for vitamin D deficiency? Children presenting with features of primary osteoporosis such as
low trauma fractures or back pain (due to vertebral compression
Routine measurement of 25(OH)D levels is not indicated in
fractures).
asymptomatic healthy or at-risk children, instead vigorous pro-
Children with underlying bone disorders.
motion of supplementation should be prioritized here. Despite
Family members of at-risk (Table 1, part A) children with symp-
the rise in 25(OH)D testing in the UK over the last few decades,
tomatic VDD (as they share common risk factors).
hospitalization due to rickets has not reduced.
Mothers of breast-fed infants with VDD.
The British Paediatric Surveillance Unit, in 2017, reported an
All cases of infantile dilated cardiomyopathy.
overall incidence of nutritional rickets of 0.48 per 100,000 chil-
dren aged 0e16 years. Unsurprisingly, the incidence in Asian and Box 2

PAEDIATRICS AND CHILD HEALTH 31:9 366 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW
should have the following investigations in addition to serum
25(OH)D levels:

Bone profile (adjusted calcium, phosphate, alkaline phos-
phatase levels)

Urea and creatinine levels

Serum parathyroid hormone levels

X-ray of the knee and/or wrist antero-posterior view to look
for rickets

Additionally, symptomatic infants should have cardiac
assessment including electrocardiogram and echocardiogram.
Clinical features of vitamin D and/or calcium deficiency
The spectrum of presentation is broad and can be considered
under calcipaenic or phosphopaenic features. Calcipaenic
symptoms of rickets such as hypocalcaemic seizures are common
during periods of rapid growth such as infancy and adolescence.
Infants may also present with catastrophic heart failure due to
hypocalcaemic dilated cardiomyopathy,2 but bony deformities,
delayed motor development and muscle weakness are more
common.
Musculoskeletal symptoms are predominantly phospho-
paenic. Wide-open anterior fontanelle, costochondral beading,
wide wrist, varus deformity of knees and spontaneous fractures
are classical skeletal features of rickets. Adolescents present
predominantly with carpopedal spams, crampy muscle pain
and seizures due to hypocalcaemia. Examination may reveal a
Figure 2 Flowchart illustrating a clinician’s role in promotion of bone health and prevention and treatment of rickets.
*D3 (Cholecalciferol) or D2 (ergocalciferol) can be used for supplementation and treatment. 25(OH)D: 25 hydroxyvitamin D; VDD: vitamin D defi-
ciency; PTH: parathyroid hormone; ALP: Alkaline phosphatase.
PAEDIATRICS AND CHILD HEALTH 31:9
positive Chvostek’s (ipsilateral facial contractions on tapping
the facial nerve just anterior to the tragus) or Trousseau’s sign
(carpal spasms elicited by maintaining occlusive pressure for
3 minutes in the arm using a sphygmomanometer).
A wide cohort of affected children may however be completely
asymptomatic with osteomalacia, similar to adults. Osteomalacia
manifests with non-specific symptoms of tiredness, malaise,
chronic joint and muscle pains. Some children may come to
attention following incidental finding of typical biochemical ab-
normalities during evaluation for unrelated conditions. The ma-
jority of children however will have one of the risk factors outlined
in Table 1 making them amenable to prevention.
Management of vitamin D deficiency and nutritional
rickets
Rickets is suspected based on clinical and biochemical features
and confirmed on radiographs. Initial management (Figure 2)
and follow up is based on whether there is:

Acute symptomatic hypocalcaemia

Simple vitamin D deficiency

Evidence of rickets

Additional morbidity including muscle weakness or bowing
deformities
Acute symptomatic hypocalcaemia is managed along standard
guidelines using calcium gluconate bolus followed by infusion. It
is important to administer oral cholecalciferol as soon as possible
367 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW
to enable rapid recovery, reducing morbidity from ongoing
hypocalcaemia.
Treatment of VDD includes:
1. Daily cholecalciferol/ergocalciferol for a minimum of twelve
weeks. Recommended doses are:

Birth to 12 months: 2000 IU/day

12 months to 12 years: 3000e6000 IU/day

12 years: 6000 IU/day
In some circumstances, single dose oral therapy may be
necessary to ensure compliance, in which case, Cholecalciferol is
the preferred drug at the dose of: 50,000 IU for age 3e12 months,
150,000 IU for 12 months to 12 years and 300,000 IU for over 12
years of age.
2. Optimizing calcium intake to a minimum of 500 mg/day in all
age groups, which can easily be achieved through diet. Sup-
plementation, with higher doses, may be necessary in the
acute setting.
The use of activated vitamin D analogues such as alfacalcidol
should be restricted to short term use in severe hypocalcaemia
and to conditions with malabsorption such as chronic liver dis-
ease. These preparations have no place as replacement therapy
in VDD. Phosphate supplements should not be used in the
management of VDD or calcipaenic rickets. Low phosphate levels
in VDD correct with cholecalciferol treatment. As calcium ab-
sorption improves, PTH normalises, reducing renal phosphate
loss.
Evaluation of treatment response
Routine re-testing in simple VDD without rickets or additional
morbidity is not warranted. 25(OH)D levels should be re-tested
after 3 months of treatment in severe VDD, to assess the dura-
tion of treatment course. Surveillance of 25(OH)D levels at reg-
ular intervals is indicated in conditions where ongoing
monitoring of vitamin D status is required (Table 1, part B). In
children with rickets, a lack of clinical and/or biochemical
response to treatment (normalization of calcium, phosphate, ALP
or PTH) warrants earlier re-testing and consideration of alter-
native/additional diagnoses and specialist referral.
Long term supplementation following treatment completion is
essential in high-risk groups where risk factors cannot be
eliminated.
Prevention of nutritional rickets: dietary calcium and
vitamin D supplementation
Twin nutrient deficiencies, in calcium and vitamin D, co-exist in
various degrees in at-risk groups. Prevention should therefore
target both nutrients. The recommended calcium intake to pre-
vent rickets, is 200e260 mg/day for infants and >300 mg/day for
older children. These requirements can easily be met through
consumption of calcium rich foods such as milk, yogurt, cheese
or fortified food. Parents should be provided with information
and guidance regarding appropriate and timely weaning prac-
tices. Sufficiency of dietary calcium intakes should be screened
by health care professionals3 in at-risk children.
In contrast, daily requirements of vitamin D in at-risk groups,
in the absence of mandatory food fortification, can only be met
PAEDIATRICS AND CHILD HEALTH 31:9
Children who warrant vitamin D supplements
All infants less than 12 months of age
All children <4 years of age
All children in the at-risk group for VDD (Table 1)
Lifelong supplementation for children found to have VDD after
completion of treatment course, unless the underlying risk factors
can be mitigated.
Box 3
by supplementation. Very few food sources are rich in vitamin D
and include egg yolks, mushrooms, oily fish (e.g. sardines,
mackerel, salmon), liver, and red meat.
Restricted UVB, particularly in the winter months, is the
predominant cause of VDD in the UK, hence supplementation,
especially in the at-risk population, is the cornerstone of
prevention.
Unfortunately, the uptake of infant vitamin D supplements in
the UK remains low (<20%)4 due to inadequate policy features
(lack of universal supplementation of breast and formula fed
infants) which are also poorly implemented (lack of national
monitoring of supplement uptake or provision of information to
parents at discharge from neonatal units).4 The Royal College of
Paediatrics and Child Health recommend supplementation with
340e400 IU in infants less than a year who consume <500ml
formula feed/day and 400 IU in all children <4 years. Most Eu-
ropean countries recommend supplementation of both breast
and formula fed infants which enhances adherence.4
Global Consensus recommendations for the prevention of
nutritional rickets1 suggest supplementing all infants with 400
IU/day irrespective of the mode of feeding, and children over 1
year are recommended 600 IU/day through diet or supplements.
Maternal supplementation in pregnancy (minimum of 600 IU/
day) is promoted to protect the fetus.
Vitamin D supplements provided either as freely available
preparations from local authorities, or purchased by parents over
the counter, should be ensured in the groups detailed in Box 3.
Case vignettes
Case 1
An eighteen-month-old male Asian child presented with acute
lower respiratory tract infection. A routine blood gas showed low
ionized calcium levels of 0.9 mmol/L, normal range (NR) 1.1
e1.4 mmol/L. History revealed vegan diet in the mother and lack
of supplement use. The child was established on a dairy free
vegan diet on weaning. He had delayed gross motor milestones,
did not pull to stand or walk. On examination there was marked
frontal bossing, wide open anterior fontanelle and wide wrists.
Investigations revealed low adjusted calcium 1.8 mmol/L (NR
2.2e2.7 nmol/L), low phosphate, 0.6 mmol/L (NR 1.2
e1.8 mmol/L), elevated ALP 2350 IU/L, (NR 52e230 IU/L) and
PTH 412 ng/L, (NR 35e69 ng/L) levels. VDD was confirmed with
low 25(OH)D levels (18 nmol/L). Rickets was confirmed on wrist
radiograph. Mother and two other siblings also had VDD.
368 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW
He was treated with ergocalciferol 3000 IU/day along with
500 mg/day of oral calcium supplements. Expected biochemical
and radiological response was noted. At 10-week follow up
appointment he was able to pull to stand and cruise along
furniture. Mother and siblings also received ergocalciferol treat-
ment followed by recommendation for lifelong supplementation.
Discussion: The multiple risk factors for nutritional rickets in
this child included BAME ethnicity, maternal VDD, lack of sup-
plement use and calcium restricted diet. Testing family members
who share common risk factors is crucial. Parental education is
important to ensure compliance with lifelong supplementation.
Case 2
A 20-week-old African breast-fed infant was brought to the
Emergency Department (ED) following an unresponsive episode,
thought to be due to a seizure. He was noted to have significant
tachycardia and tachypnoea. He had been experiencing breathing
difficulties intermittently during feeds and had presented to ED
on two occasions in the last 3 weeks and was discharged with a
diagnosis of bronchiolitis. He was exclusively breast fed and had
not received any vitamin D supplements. He was up to date with
his immunisations. The mother was treated for VDD in
pregnancy.
Investigations showed severe hypocalcaemia, adjusted calcium
1.4 mmol/L (NR 2.2e2.7 mmol/L), low phosphate 0.6 mmol/L
(NR 0.9e1.8 mmol/L), 25(OH)D <7.5 nmol/L (deficiency) with
markedly elevated ALP and PTH levels. Rickets was confirmed on
a wrist X-ray. An enlarged heart on chest X-ray triggered further
cardiac evaluation uncovering congestive cardiac failure second-
ary to dilated cardiomyopathy with profound left ventricular
dysfunction [ejection fraction of 35% (normal 55e70%)].
He was treated with 3000 IU/day of ergocalciferol and IV
calcium. He required invasive ventilation and cardiac failure was
managed with diuretics and ACE inhibitors. He had extensive
investigations to exclude other causes of dilated cardiomyopathy
and an MRI brain to exclude other causes of seizures.
Discussion: Infantile hypocalcaemic cardiomyopathy is a dreaded
complication of VDD which is entirely preventable. These children
often have extensive investigations due to the drastic presentation
and under-recognition of nutritional rickets as a cause of seizures
and cardiomyopathy. This child suffered severe morbidity and
long-term cardiac dysfunction which was reversed over 6 months
with vitamin D replacement. There were missed opportunities to
prevent this; the child having had several contacts with healthcare
professionals during vaccination and hospital visits.
Case 3
A 15-year-old male child with severe autism and epilepsy was
reported to have increased seizure activity which persisted
despite optimization of antiepileptic medications. He was sub-
sequently hospitalized with ongoing seizures and carpopedal
spams. He had a restricted diet due to severe autism and had not
received vitamin D supplements.
Investigations revealed adjusted calcium of 1.2 mmol/L (NR
2.2e2.7 mmol/L), elevated PTH 340 ng/L (NR 11e35 ng/L) and
ALP 550 IU/L (NR 65e240 IU/L) and normal phosphate levels
PAEDIATRICS AND CHILD HEALTH 31:9
Four steps for clinicians to incorporate bone health
assessment at every clinical contact
1. Ascertain: Vitamin D supplement use in all at-risk groups
(Table 1), feeding practices including appropriate weaning and
dietary calcium intake.3
2. Examine: In suspected cases of deficiency examine for signs of
hypocalcaemia (heart failure with dilated cardiomyopathy, carpo-
pedal spasms, Chovstek’s or Trousseau’s sign) and/or hypo-
phosphataemia (bowing, swollen joints, soft skull, large
fontanelle).
3. Manage: Investigate based on clinical symptoms and initiate
appropriate treatment followed by lifelong vitamin D supplemen-
tation in at-risk groups.
4. Prevent: Recommend vitamin D supplements to all healthy at-risk
children and their family members at any healthcare contact,
ensure surveillance in children with underlying health conditions
predisposing them to VDD or calcium deficiency
Box 4
(1.7 mmol/L). 25(OH)D levels were 12.5 nmol/L. There was no
evidence of rickets on radiographs due to closure of growth plates.
Complex medical and social situation pre-disposed the child
to non-compliance which led to administration of a single high
oral dose of 300,000 IU cholecalciferol, (Stoss therapy) followed
by recommendation of weekly supplementation.
Discussion: This child developed severe hypocalcaemia during
his adolescent growth phase. Of note, he had not had vitamin D
supplementation or monitoring of 25(OH)D levels in spite of risk
factors such as anti-epileptic medication use, restricted dietary
calcium intake and outdoor time.
Incorporating children’s bone health assessment in
everyday practice: a clinician’s role in making a difference
Assessment and management of bone health in children is often
perceived as being within the remits of the paediatric endocri-
nologist. However, if a preventive approach is adopted in pri-
mary and secondary care, fewer children are likely to need
specialist support that represents the very tip of the hidden
iceberg of the burden of nutritional rickets as demonstrated in the
case vignettes.
Clinicians should incorporate bone health assessment in
routine history taking and examination of every child who has a
healthcare contact for any indication; such as immunization visits,
contact with the General Practitioner or other clinicians in acute
assessment units or clinics. Box 4 demonstrates a simple guide for
clinicians to ascertain risk factors, evaluate clinical signs, manage
deficiency and most importantly engage in prevention of VDD.
In summary, suboptimal bone health mostly due to vitamin D
deficiency is widely prevalent but often under recognized.
Knowledge of risk factors predisposing to vitamin D and also
calcium deficiency will enable clinicians to recognize early signs,
initiate appropriate testing and adopt preventive strategies. In the
absence of mandatory food fortification, liberal supplementation
of at-risk groups is more effective than testing. Clinicians can
369 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW
play an active role in promoting bone health and supplementa-
tion in children with chronic health conditions and in children
who have any contact with the health care system. However,
improving the vitamin D status of the wider population requires
political support to implement robust supplementation and food
fortification policies. A
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370 Ó 2021 Elsevier Ltd. All rights reserved.