Diagnosis and management of vitamin D deficiency
BMJ 2010; 340 doi: https://doi.org/10.1136/bmj.b5664 (Published 11 January 2010) Cite this as: BMJ 2010;340:b5664All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
I wonder if Peter Lewis has considered the costs to the
pharmaceutical industry of measuring Vitamin D levels, diagnosing Vitamin
D deficiency and properly treating it. Has Peter Lewis considered the
impact on sales of biphosphonates, statins and a whole host of anti-
diabetic and other drugs, if there were a wholesale reduction of risk of
such chronic diseases as he attributes to Vitamin D insufficiency? Is it
possible that the huge potential for savings in drug costs is a reason why
it’s so difficult to get levels measured and why only homeopathic doses of
Vitamin D are available to the UK prescriber?
Competing interests:
swine flu escapee and long term daily consumer of 1000iu of Vitamin D (gel caps) acquired from an internet provider.
Competing interests: No competing interests
I first raised this issue back in 2003 having accessed numerous cases
where babies had fractured for no apparent reason excluding abuse, upon
researching the cases in which there was overwhelming evidence of vitamin
D deficiency, I was supported by various experts in nutrition and bone
disorders with whom I had been in contact with.
This is what the now President of the RCPCH Sir Terence Stephenson
said in March 2008 in an interview to Cassandra Jardine, when it was
already clear there was a problem:
"When I suggest that paediatricians, especially those appearing
regularly as expert witnesses, appear to have fixed minds, he counters by
making a derisive comment about Dr Colin Paterson, a pathologist struck
off by the GMC for suggesting for the defence in 30 cases that children
could suffer from temporary brittle bones, resulting in multiple
fractures. Some pathologists believe he had a viable theory, but the wrong
causation. Stephenson says, 'There's no evidence to back up temporary
brittle bones.'
Isn't there? Infants are being diagnosed with rickets resulting from
vitamin D deficiency due to insufficient exposure to sunlight. 'Only in
ethnic minorities.' Not according to research from Birmingham University,
which states that one in eight Caucasian children has rickets." [1]
My concern is, that if the current president of the RCPCH had no idea
how serious the problem is and in fact denied it, it sends out entirely
the wrong message to all doctors who treat children.
If a child were to be born Vit D Deficient and subsequently over a
matter of weeks, having been fed on supplemented baby milk, became vitamin
D replete, but suffered associated bone disorders in the first weeks of
life, then nobody would ever know that the baby, was ever Vit D deplete,
surely the phrase "temporary brittle bone" is the right adjective to
describe the above scenario?
Perhaps Sir Terence would, given his current position, now like to
publicly retract the comments he made?
[1] http://www.telegraph.co.uk/news/uknews/1581407/Has-Sally-Clarks-case-cha...
Competing interests:
I have highlighted my concerns about Vitamin D Deficiency in infants and children in child protection cases having researched the medical records
Competing interests: No competing interests
What is the optimum level of serum 25-hydroxyvitamin-D ?
0-10 ng/mL = Rickets
10-20 ng/mL = Aching bones
20-30 ng/mL = susceptible to illness
30-80 ng/mL = reported as "normal"
200ng/mL = toxicity ?
What should be the target level to achieve significantly better
public health ?
Professor Cedric Garland of University of California has recently
suggested that 60 ng/mL is required to reduce the risk of many illnesses,
including Cancer, Diabetes, Multiple Sclerosis & many other diseases.
If the UK average is typically 20 ng/mL and it takes 1,000IU to raise
the serum level by 10 ng/mL, should most people be taking 4,000IU per day
?
Has anyone looked at the health outcomes of doing this ?
Has anyone looked at the cost savings this would produce ?
.
Competing interests:
None declared
Competing interests: No competing interests
We are grateful to Simon Pearce and Tim Cheetham for raising the
profile of Vitamin D deficiency and highlighting the need to ensure there
are satisfactory public health measures to prevent the problem. We felt it
would be informative to the debate to outline what we have been doing in
Birmingham to address this issue over the past 6 years. In response to an
article published in 2002 [1] highlighting the resurgence of symptomatic
Vitamin D deficiency in children we were witnessing one of the local
directors of public health convened a group of interested health
professionals. We have been working in conjunction with a PCT in central
Birmingham where there is a high level of deprivation with 75% of children
under the age of 4 years being Black or Asian. We started meeting in 2003
and continue to meet on a regular basis with representation from Public
Health, Paediatric Endocrinology, Community Paediatrics, Community
Dietetics, Health Visiting, Midwifery, General Practice, Pharmacy and a
Public and Patient Involvement Manager.
We initially identified and tackled a number of problems including:
1)Confusing and conflicting national guidelines regarding Vitamin D supplementation
2) Lack of availability and short shelf life of the existing Department of Health preparations
3) a NICE antenatal guideline in 2003 stating that “there was no evidence to support supplementing breast feeding women”
4) a low level of health professional awareness of existing national guidelines.
We were successful in persuading the PCT to fund a policy of free
provision of Vitamin D supplements to all children up to the age of 4
years from two weeks of age whether breast or bottle fed and all pregnant
or breastfeeding women regardless of ethnic group. In July 2006 this
policy was launched with a public health campaign entitled “ My little ray
of sunshine”. The campaign has been publicised by posters in places which
issue the supplements; leaflets in eight languages given out by health
visitors, midwives and other staff; and via adverts on buses, press
releases and radio interviews on local radio stations and those targeting
ethnic minority populations. During early 2008, a shopkeeper’s campaign
was carried out with shopkeepers being supplied with free Vitamin D
campaign carrier bags in exchange for the provision of a Vitamin D
leaflet to all shoppers for a 6 week period with 13,000 leaflets and
20,000 carrier bags being distributed.
Access and availability of the supplements is now excellent, but depends
on continuous access via NHS Supplies, funding to pay for deliveries, and
the support and efficiency of frontline staff at Children’s Centres,
Health Centres, and participating pharmacies and GP practices. Regular
education of key health professional occurs through Protected Learning
Time events. A qualitative study by students in summer 2007 undertaken at
health centres revealed a low public awareness of vitamin D. This was
repeated in early 2009 with the proportion knowing correct information
about vitamin D increasing from 27% to 41%. The preliminary findings of an
ongoing survey of children admitted to hospitals in Birmingham with
symptomatic Vitamin D deficiency indicates that more cases are being seen
in children living in areas represented by the other two PCT’s within the
city who currently do not have a Vitamin D supplementation policy.
We need to remember that we have been here before in the UK with a
nationwide Stop Rickets campaign being successful in reducing the numbers
of children with rickets admitted to hospitals in Glasgow which was
documented in the BMJ some 25 years ago[2]. We wish to highlight the
challenges in implementing a local public health policy with the need for
continued engagement of relevant professional and patient groups until the
need for Vitamin D supplementation becomes embedded in health care
practice. Whilst we support the suggestion of Pearce and Cheetham of
extending the scope of food fortification with Vitamin D we have some
reservations that milk may not be the most appropriate food as it is often
not consumed in significant quantities by the groups who are most
vulnerable to Vitamin D deficiency such as infants.
1. Shaw NJ & Pal BR. Vitamin D deficiency in UK Asian families – activating a new concern. Arch Dis Child 2002 ;86:147-149
2. Dunnigan MG, Glekin BM, Henderson JB, McIntosh WB, Sumner D, Sutherland GR. Prevention of rickets in Asian children: assessment
of the Glasgow campaign Br Med J (Clin Res Ed) 1985;291:239-42
Competing interests:
None declared
Competing interests: No competing interests
In response to concerns expressed about the cost of measuring 25OHD
levels, it is likely that the cost of failing to diagnose and treat
vitamin D deficiency by not measuring vitamin D levels would greatly
exceed the cost of measuring them!
Measurement of vitamin D levels is firstly necessary to diagnose
deficiency (<100 nmol/L); secondly, to determine an appropriate
supplemental dosage of vitamin D (1,000 IU of cholecalciferol per day will
generally raise a patient’s 25OHD level by approximately 10 nmol/L over 3
months); and thirdly to monitor response to treatment and ensure that
optimal levels (100-200 nmol/L) are attained and maintained.
Diagnosis and appropriate treatment of vitamin D deficiency would, in
the long run, likely result in huge savings in healthcare costs due to the
reduced risk of bone diseases, cardiovascular disease, stroke, diabetes,
cancer and many other serious diseases.
Furthermore, there are also the medico-legal consequences to consider
in failing to diagnose and treat vitamin D deficiency, especially when a
serious, perhaps fatal, condition results.
Competing interests:
None declared
Competing interests: No competing interests
We have been encouraged to prescribe Sterogyl to get decent doses of
Vitamin D into our deficient patients. It has to be imported from France,
costs a lot, and some pharmacies don't want to get involved.
Apart from that I have found nothing else for deficiency.
For people I think just need a supplement, but who cannot stand the pills
with calcium I sometimes give Vitamins caps (3 daily should be enough).
Competing interests:
None declared
Competing interests: No competing interests
It was mentioned in an earlier rapid response that some
doctors have expressed concern about the cost of measuring 25-
OH-vitamin D levels in large numbers of patients. Could the
authors give some more detail of the cost of 25-OHD
measurement? Would the authors recommend that GPs should
measure 25-OHD levels in all patients prior to prescription if
we clinically suspect them to be deficient or only in certain
scenarios?
Competing interests:
None declared
Competing interests: No competing interests
The call for a change in UK public health policy on vitamin D is welcome. Pearce and Cheetham (1) point to the growing problem of vitamin D deficiency in the UK.
In east London 50% of the population is from Black and ethnic minority groups. A survey of routine clinical tests for vitamin D by general practitioners in Tower Hamlets during 2009 demonstrates that 80% of tests from South Asian and Black groups show deficiency or insufficiency, and over 50% of those among the White population (Table 1). 58% of those with deficient levels and 39% of those with insufficiency had prescriptions for vitamin D supplements.
These results draw attention to the high burden of deficiency in a socially deprived, ethnically diverse inner city population, with insufficiency rates considerably higher than the 50% quoted as the UK average (1,2).
These are populations which are already burdened by a high prevalence of CVD and diabetes, only some of the chronic disorders now associated with vitamin D deficiency.
Treatment of dietary deficiency and insufficiency remains problematic. Compliance with available oral medication is low due to the unpalatable nature of vitamin D in combination with calcium (3) and the poor availability of calcium free preparations. Having a range of oral preparations to suit all requirements (taste, diet and religion) is essential. In view of the size of the problem we need to avoid resorting to parenteral administration with the consequence of blood monitoring requirements, over medicalisation, and workload implications for general practices, wherever possible.
For such a common and preventable condition, with a health burden which falls disproportionately on inner urban deprived populations, the NHS needs to make a coherent public health response. This should include the re-introduction of freely available vitamin drops for children and mothers, food supplementation and the production of suitable, and palatable, vitamin D preparations. What about a new 1,000 IU ergocalciferol tablet without calcium, safe for daily use without blood monitoring? Extrapolation from our audit suggests a large and growing market for such preparations, which should be commissioned from drug companies by the NHS.
Table 1. Vitamin D values for 13,183 tests performed during 2009 in Tower Hamlets (population 250,692), stratified by ethnicity and age.
References
1. Pearce S, Cheetham T. BMJ 2010;340:b5664.
2. Drugs and Therapeutics Bulletin. Primary vitamin D deficiency in adults. 2006; Vol 44: No 4
3. Lambert J. Vitamin D deficiency. Br J Gen Pract. (letter) 2007; 57(541) 6
Sally Hull
Senior Clinical Lecturer,
Institute of Health Sciences,
Queen Mary University of London
Kambiz Boomla
Senior Clinical Lecturer
Institute of Health Sciences,
Queen Mary University of London
Competing interests:
None declared
Competing interests: No competing interests
We are gratified by the interest in our review article and by the
fact that there
appears to be a general consensus amongst doctors at the ‘coal-face’ that
the current UK situation with regards vitamin D is unsatisfactory. Like
several
other correspondents, we have also been frustrated by lack of suitable
compounds. The potent colecalciferol preparation (20,000 units per
capsule;
‘Dekristol’) is available to high street chemists from the import house
“IDIS
World Medicines”, although as Dr. Livingstone points out, these capsules
have
a gelatine coating.
Nagaraj and Howe generate at least one new myth and perpetuate
others.
-•Firstly they raise the phantom that “chronic toxicity has also been
documented” (unreferenced). Nephrocalcinosis/ nephrolithiasis are
toxicities
specific for the chronic use of activated vitamin D analogues (calcitriol/
alfacalcidol), usually with additional calcium intake in management of
hypoparathyroidism, in which urine calcium excretion is additionally
increased by lack of parathyroid hormone. We are not aware of any ‘chronic
toxicity’ from supplementary doses of calciferol.
-•They state that ‘supermarket cereals which has 100% of RDA’. Few
supermarket cereals contain any vitamin D. Popular brands with no vitamin
D
include Kellogs cornflakes and rice crispies, Weetabix, Shredded wheat,
Alpen, Cheerios and Quaker oat products. Some supermarket own brand
cereals (mainly rice pops or corn flakes) are supplemented with 4 or
5μg
(160-200 U) vitamin D per 100g of cereal; however, a portion of cereal is
25-
35g, so to get ‘100% RDA’ (400 U) you would have to eat 5 to 8 bowls of
such
cereals daily. Branded cereals containing some vitamin D (3-8μg/100g)
are
Special K, bran flakes and all bran, and several sorts of wheat
‘Shreddies’, the
latter being the only ones specifically targeted at children. In short,
the
population can’t rely on breakfast cereal consumption for adequate vitamin
D
intake.
-•They state that ‘there is no national data at population level to
support’
the fact that vitamin D deficiency is common in the UK. We would again
draw
their attention to the MRC 1958 birth cohort study (citation 5 in our
review
paper) that measured serum 25-OHD in 7437 people aged 45 from all over
the UK, including Harrow (1). Fifty percent were vitamin D insufficient in
winter/spring and 16% frankly deficient. However, this study represents
the
most optimistic assessment, as only ‘whites’ were included and vitamin D
status is certainly worse in children and elderly individuals than in 45
year
olds.
We agree entirely with Danczak’s sentiments and the comparison with
smoking bears additional consideration. Government health warnings on
tobacco products were introduced at a time when there was excellent
laboratory data to link tobacco tar to carcinogenesis and a clear
epidemiological association between lung cancer and smoking, but no
double-blinded RCT to demonstrate that smoking cessation lowered cancer
incidence. We are in a similar situation today with vitamin D. While there
are
numerous laboratory studies showing anti-inflammatory and anti-neoplastic
effects of vitamin D, the epidemiological association studies with disease
do
have the capacity to be misleading (ill people stay indoors) and need to
be
cautiously interpreted. Nevertheless, the numerous studies in which
supplementation has been studied are more robust and lend substantial
weight to the detrimental effect of vitamin D insufficiency on many
important
health outcomes (2). However, there are 2 key issues with many
supplementation studies: firstly, calcium is often supplemented along with
vitamin D; secondly, that the dose of vitamin D used (generally 400 -800
units daily) is not sufficient to raise serum 25-OHD into the optimal
range.
For instance, a regular daily dose of 800 units calciferol daily might be
expected to raise serum 25-OHD by 20 nmol/l, which given the baseline
values of many populations may not be sufficient to make marked
improvements in major outcomes over short periods of observation. Data
from supplementation studies using 1600 units or more daily are urgently
needed. Irrespective of these non-skeletal effect of vitamin D, the reason
we
urge a change in policy over milk supplementation is primarily to reduce
symptomatic rickets and osteomalacia, as this is an important and
achievable
goal in itself.
1. Hyppönen E, Power C. Hypovitaminosis D in British adults at age
45 y:
nationwide cohort study of dietary and lifestyle predictors. Am J Clin
Nutr
2007;85:860–8.
2. Autier P, Gandini S. Vitamin D supplementation and total
mortality: a
meta-analysis of randomized controlled trials. Arch Intern Med
2007;167:1730-7.
Competing interests:
None declared
Competing interests: No competing interests
Neonatal hypocalcaemia and Rickets in South Asians – Case for vitamin D supplementation in pregnancy
Pearce and Chatham inform that, at northern latitudes, there is a
high prevalence of vitamin D deficiency in dark skinned immigrant children
or first generation children of dark-skinned immigrant parents.1 This is
especially relevant to the UK, since UK born South Asian children,
compared to White children, are at increased risk of neonatal
hypocalcaemia, rickets and poor growth due to vitamin D deficiency.2 We
have recently reported that South Asian newborn babies have marked
hypovitaminosis D compared to White newborn babies born in Wolverhampton,
UK during the summer months.3 Maternal vitamin D is the only source of
foetal and newborn vitamin D4 and vitamin D is known to be lower in South
Asian compared to white pregnant women.5 We, therefore, suggest there is a
strong case for recommending vitamin D supplementation in pregnancy of
South Asians (and other at risk groups) to reduce the increased risk of
neonatal hypocalcaemia and rickets in their offspring.
References
1. Pearce SHS, Cheetham TD. Diagnosis and management of vitamin D
deficiency. BMJ 2010;340:142-7.
2. Ladhani S, Srinivasan L, Buchanan C, AllgroveJ. Presentation of vitamin
D deficiency. Arch Dis Child 2004; 89:781-4.
3. Sulaiman RA, Sharratt CL, Lee P, SkinnerA, Griffith MJ, Webster C et
al. Ethnic differences in umbilical cord blood vitamin D and parathyroid
hormone- South Asians compared to Whites born in the UK. J Matern Fetal
Neonatal Med (accepted for publication).
4. Salle BL, Delvin E, Bishop NJ, Lapillonne A, Bishop NJ, Glorieux FH.
Perinatal metabolism of vitamin D Am J Clin Nutr 2000;71 (suppl):1317S-
24S.
5. Dent CE, Gupta MM. Plasma 25 Hydroxyvitamin D levels during pregnancy
in Caucasians and in vegetarian and nonvegetarian Asians. Lancet
1975;306:1057-60.
Competing interests:
None declared
Competing interests: No competing interests