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
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Previous responses note the absence of high dose formulations of
either ergocalciferol (calciferol, vitamin D2) or colecalciferol (vitamin
D3). Yet there remains in the BNF the activated forms of vitamin D, namely
Alfacalcidol (1 alpha-Hydroxycholecalciferol) and Calcitriol (1,25-
Dihydroxycholecalciferol). Why can't we use these instead, and given their
greater potency perhaps with a reduced dosage of a single tablet once a
week ? If these still pose a greater risk of hypercalcaemia, would the
reassurance of measuring calcium levels after a month help ?
Competing interests:
None declared
Competing interests: No competing interests
We have noted 7 cases of rickets presenting to our orthopaedic clinic
between 2006 and 2008. This disease, which is primarily caused by a
deficiency in vitamin D, was once referred to as the ‘Englische Krankheit’
(German for the ‘English disease’)(1) due to its prevalence in England in
Victorian times. It has however been noted to be on the increase in the
developed world in recent years(2). Major risk factors include exclusive
breastfeeding, the low use of fortified formulaic milks and foods(3) and
the practice of covering up(4) for cultural or religious reasons.
The 7 cases fell into two distinct groups: males and females under 3
years and female adolescents aged 10 and above. The former presented with
fractures, swollen wrists and limb deformities. The female adolescent
group, comprising 3 members, all presented with valgus knees serious
enough to require corrective osteotomies. 6 of the 7 patients were from
ethnic minority groups.
The presence of rickets in Blackburn seems logical when considering
the demographics of this area: significant social deprivation(5), large
numbers of ethnic minority groups(6) and a sizeable muslim population(7),
in which the practice of ‘covering up’ may be present. The latter issue
was highlighted recently in the national press by the M.P for Blackburn,
Mr. Jack Straw(8). According to met office data, Blackburn also receives a
small number of sunlight hours compared to other areas of England(9).
The ‘Englische Krankheit’ therefore still exists in today’s England
and we would urge practitioners, particularly in deprived urban areas, to
adopt a low threshold of suspicion when faced with the young patient
presenting with vague musculoskeletal symptoms. In addition, testing for
vitamin D levels would be advised in the young adolescent girl presenting
with a valgus knee. Early recognition and treatment of this potentially
reversible condition could prevent the need for future corrective surgery.
(1) The Times. The English disease, David Shepherd, In: Letters to
the editor. 23-1-2010.
Ref Type: Online Source
(2) Holick MF. Resurrection of vitamin D deficiency and rickets. J
Clin Invest 2006; 116(8):2062-2072.
(3) Wharton B, Bishop N. Rickets. Lancet 2003; 362(9393):1389-1400.
(4) Gannage-Yared MH, Chemali R, Yaacoub N, Halaby G. Hypovitaminosis
D in a sunny country: relation to lifestyle and bone markers. J Bone Miner
Res 2000; 15(9):1856-1862.
(5) Communities and Local Government. Indices of Deprivation 2007 (ID
2007). 2010. 21-1-2010.
Ref Type: Online Source
(6) Office of National Statistics. 2001 census: key statistics,
ethnic group (KS06). 9-11-2004. 21-1-2010.
Ref Type: Online Source
(7) Office of National Statistics. 2001 census: key statistics,
religion (KS07). 9-11-2004. 21-1-2010.
Ref Type: Online Source
(8) The Times. "I would prefer women not to wear the veil at all,
says Straw". 7-10-2006. 31-1-2010.
Ref Type: Online Source
(9) Met office. Sunshine duration (hours), Winter average 1973-2000.
2010.
Ref Type: Online Source
Competing interests:
None declared
Competing interests: No competing interests
Approximately 650 000 women give birth in England and Wales each year
(1)
and 2-5% of pregnancies involve women with diabetes (2).
High-risk diabetic pregnant women are prone to a significant risk of
maternal
and fetal morbidity and mortality. If such women are also vitamin D
deficient
during pregnancy should we not strive to detect this and aim to correct
it?
Diabetes in pregnancy is associated with miscarriage, pre-eclampsia
and
pre-term labour. Stillbirth, congenital malformation, macrosomia, birth
injury
and perinatal mortality are more common in babies born to women with
diabetes.
Research has shown that vitamin D deficiency in pregnancy is linked
with
osteoporosis and rickets in offspring. Work carried out in Southampton
showed that 49 (31%) mothers had insufficient and 28 (18%) had deficient
circulating concentrations of 25(OH)-vitamin D during late pregnancy.
Reduced concentration of 25(OH)-vitamin D in mothers during late
pregnancy was associated with reduced whole-body (r=0.21, p=0.0088) and
lumbar-spine (r=0.17, p=0.03) bone-mineral content in children at age 9
years (3).
My research in East London revealed that mean vitamin D levels were
lower in
diabetic compared to non-diabetic pregnant women and decreased by 10.4%
(3.6nmol) as pregnancy advanced. In the eighth month of pregnancy the
mean vitamin D level was 31.6nmol amongst 70 diabetic women. Deficiency
was highest amongst Asian women.
Ask any public health doctor which is the most effective - prevention
or cure
- and the answer will invariably be prevention, regardless of whether they
are
talking about programs to reduce heart disease, cancer or infectious
disease.
Is vitamin D deficiency any different?
1 Office for National Statistics. Key Population and Vital
Statistics 2005.
Local and Health Authority Areas. No. Series VS, No 32. Basingstoke:
Palgrave
Macmillan; 2007
2 CEMACH. Confidential Enquiry into Maternal and Child Health:
Pregnancy in
Women with Type 1 and Type 2 Diabetes in 2002-03, England, Wales and
Northern Ireland. London: CEMACH; 2005
3 Javaid MK, Crozier SR, Harvey NC, Gale CR, Dennison EM, Boucher
BJ,
Arden NK, Godfrey KM, Cooper C; Princess Anne Hospital Study Group.
Maternal vitamin D status during pregnancy and childhood bone mass at 9
years: a longitudinal study. Lancet. 2206 Jan 7: 367 (504):36-43
Competing interests:
None declared
Competing interests: No competing interests
Pearce and Cheetham’s review of the diagnosis and management of
vitamin D deficiency concludes with a claim which attracted considerable
media attention that “rickets and osteomalacia are entirely preventable
diseases that are becoming increasingly common in the UK population”.
Since rickets and osteomalacia are not notifiable diseases and non-fatal,
national incidence data are unavailable. The evidence for the authors’
claim derives from several reports of rickets in ethnic minority children
in the last decade.1-4 However, the absence of publications reporting
clinical cases of nutritional osteomalacia in Asian women in the UK in the
last two decades compared to multiple earlier reports is consistent with a
declining prevalence of severe clinical osteomalacia in this ethnic group.
A survey of the UK incidence of Asian rickets and osteomalacia
commissioned by the Committee on Medical Aspects of Food Policy (COMA)
also found a declining incidence of Asian rickets and a stable incidence
of osteomalacia between 1962 and 1978.5 This survey, based on hospital
inpatient and outpatient activity, has not been repeated.
Glasgow has provided a setting for the study of the epidemiology of
rickets since the beginning of the 20th century when it had the highest
incidence of rickets in the world.6 The city’s northern latitude (56°N)
and cloudy maritime climate ensure that it receives less ultraviolet
radiation (UVR) than England or most European countries.7 Trends in
discharges from the city’s main children’s hospital have been monitored
since the end of the second world war. Discharges of white children with
nutritional rickets declined between 1948 and 1955 with the continuing
availability and widespread uptake of subsidised vitamin D-fortified
welfare foods and supplements. Following a reduction in supplementation
levels with the discovery of infantile hypercalaemia in the nineteen
fifties, there was a subsequent rise in admissions to a 1965 peak,
followed by a progressive decline, with six discharges between 1976 and
1988 and none between 1989 and 1994.8 This decline occurred despite a
progressive fall in supplement uptake from the city’s central pharmacy.
In the 21st century, the absence of hospital discharges of white children
with nutritional rickets has continued despite their negligible uptake of
vitamin D supplements and continuing poverty and deprivation in a
proportion of the city’s children.
Study of the case records of patients with nutritional rickets and
osteomalacia discharged from all hospitals in Scotland (population 5.2
million) during the three year period 1987-89 recorded a single case of
rickets outside Glasgow in a white child with gross malnutrition due to
neglect. There were six discharges with nutritional osteomalacia in white
adults between 16-69 years, in all of whom malnutrition associated with
alcoholism or psychiatric illness was present. In a further 54 patients
over 70 years, malnutrition associated with disorganised vegetarian diets
was identified in 418 (76%). Anecdotally, Scottish consultants in
geriatric medicine report that cases of clinical nutritional osteomalacia
remain rare in the elderly indigenous population, including residents in
long-term institutional care with little or no UVR exposure and very low
levels of vitamin D supplement intake.
The initial discovery of infantile and adolescent rickets in Asian
children and osteomalacia in Asian adults in Glasgow in 1962 was
replicated in most other UK Asian communities.9 Case-control surveys of
seven-day weighed dietary intakes and daylight outdoor exposure in Glasgow
Asian women and children subsequently established the significant
independent contributions of variation in UVR exposure, food class and
nutrient intakes to rachitic and osteomalacic relative risk. Multivariate
logistic regression established that low UVR exposure, low available
dietary calcium (resulting from calcium binding by high dietary fibre and
phytate intakes), and absent or low intakes of meat and meat products
(total or near lactovegetarianism) were significant independent risk
factors for nutritional rickets and osteomalacia.10-12 Limited UVR
exposure leading to vitamin D deficiency is necessary but insufficient to
induce clinical rickets and osteomalacia in the absence of the above
nutritional risk factors. Conversely, lactovegetarianism does not
increase rachitic or osteomalacic risk in the presence of adequate UVR
exposure; very low calcium intakes associated with vegan diets may result
in rickets without vitamin D deficiency (“sunshine rickets”).
Multivariate risk-factor models of rickets and osteomalacia have
clarified the significance of long-term trends in the incidence of rickets
and osteomalacia in the indigenous and ethnic minority UK populations.
The decline and virtual disappearance of infantile and toddler rickets
from the Scottish white population from the mid-nineteen sixties onwards
despite falling vitamin D supplementary intakes was accompanied by a major
change in infant feeding practice. Late weaning to a lactovegetarian diet
in which milk intake was supplemented by refined and complex carbohydrate
was replaced by the early introduction of mixed feeding and an omnivore
diet from four to six months of age. This change was facilitated by the
introduction of proprietary tinned baby foods containing a range of meat
and fish products.8
Similarly, a marked decline in the incidence of adolescent Asian
rickets in the Glasgow Asian community in the nineteen eighties resulted
from partial adaptation to a Western dietary pattern, paralleled by a
significant rise in the incidence of acute appendicitis in this age
group.8 This trend has continued until the present while uptake of
vitamin D supplements is negligible.
Past and present preventive strategies for nutritional rickets and
osteomalacia are based on the promotion of vitamin D supplementation by
high-risk groups. The British government’s second world war food policies
led to the widespread introduction of subsidised vitamin D-fortified
welfare foods and supplements with a striking fall in the incidence of
infantile and toddler rickets. Despite this success (offset by the
appearance of infantile hypercalcaemia related to hypersensitivity to
moderately excessive intakes of vitamin D in the nineteen fifties5), the
history of subsequent UK campaigns to encourage vitamin D supplement
uptake by ethnic minorities with a high incidence of rickets and
osteomalacia is not encouraging. The impact of the Stop Rickets campaign
in England and the Glasgow Rickets campaign in Scotland was short-lived,13
and a campaign to promote vitamin D supplement intake by vitamin D
deficient Glasgow Asian women was unsuccessful.14
In relation to current recommended vitamin D intakes, Pearce and
Cheetham’s statement that the Reference Nutrient Intake (RNI) for UK
adults is 10 µg (400 i.u.) daily is incorrect. The Department of Health’s
1998 report on nutrition and bone health states that children and adults
aged 4-65 years generally achieve adequate vitamin D status through the
action of sunlight and suggest continuation of the zero RNI for vitamin D
apart from groups at particular risk of vitamin D deficiency.15 Recent
evidence that optimal serum 25OHD levels should be over 30ng/ml (75nmol/L)
would require oral vitamin D intakes of the order of 100 µg (4000 i.u.)
vitamin D daily for adults living at latitudes where UVR exposure is
limited.16
The persistence of infantile and toddler rickets in ethnic minority
children in the UK in the 21st century reflects a combination of vitamin D
deficiency due to low UVR exposure with delayed weaning, prolonged
breastfeeding and a lactovegetarian diet in keeping with the risk-factor
models for rickets and osteomalacia outlined above. Similar risk factors
are almost invariably present in reports of infantile and toddler rickets
from less developed economies and in ethnic minorities in developed
economies in Europe and North America.17,18
The antirachitic role of meat was first observed by Edward Mellanby
in puppy rickets in 1919.19 Although unacknowledged in Pearce and
Cheetham’s review, meat and meat products provide a significant
contribution to the vitamin D content of an omnivore diet, principally as
the 25(OH)D3 metabolite.20,21 The consumption of animal products in an
omnivore diet, most significantly as meat and meat products, raises serum
25-OHD levels by small increments which provide a safety net for vitamin D
deficient populations. This maintains most children and adults with
severe vitamin D deficiency and adequate calcium intakes above the
threshold for overt clinical rickets and osteomalacia. Despite cultural
and economic constraints, it seems probable that the promotion of early
weaning to an omnivore diet, recapitulating previous similar trends in
developed economies, as noted above, would result in substantial
reductions in the incidence of infantile and toddler rickets in these
settings.
References
1. Shaw NJ, Pal BR. Vitamin D deficiency in UK Asian families:
activating a new concern. Arch Dis Child 2002; 86; 147-49.
2. Ashraf S, Mughal MZ. The prevalence of rickets among non-
Caucasian children. Arch Dis Child 2002; 87, 263-26.
3. Odeka E, Tan J. Nutritional rickets is increasingly diagnosed in
children of ethnic origin. Arch Dis Child 2005; 90: 1203-04.
4. Zipitis CS, Markides GA, Swan IL. Vitamin D deficiency:
prevention or treatment? Arch Dis Child 2006; 91: 1011-14.
5. Department of Health. Rickets and Osteomalacia. Report of the
Working Party on Fortification of Food with Vitamin D. Stationery Office,
1980.
6. Hess AF. Rickets including osteomalacia and tetany. London:
Henry Kimpton, 1930.
7. Gillie O. Scotland’s health deficit: an explanation and a plan.
Health Research Forum Occasional Reports: No. 3, London, 2008.
8. Dunnigan MG, Henderson JB. An epidemiological model of
privational rickets and osteomalacia. Proc Nutr Soc 1997; 56: 939-956.
9. Dunnigan MG, Paton JAJ, Haase S, McNicol GW, Gardner MD, Smith CM.
Late rickets and osteomalacia in the Pakistani community in Glasgow. Scot
Med J 1962; 7: 159-67.
10. Henderson JB, Dunnigan MG, McIntosh WB, Abdul-Motaal A, Gettinby
G, Glekin BM. The importance of limited exposure to ultraviolet radiation
and dietary factors in the aetiology of Asian rickets: a risk factor
model. QJ Med 1987; 63: 413-25.
11. Henderson JB, Glekin BM, McIntosh WB, Dunnigan MG. Asian
osteomalacia is determined by dietary factors when exposure to ultraviolet
radiation is restricted: a risk factor model. QJ Med 1990; 76: 923-33.
12. Dunnigan MG, Henderson JB, Hole DJ, Mawer EB, Berry JL. Meat
consumption reduces the risk of nutritional rickets and osteomalacia. Br
J Nutr 2005; 94: 983-91.
13. 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 1985; 291: 239-42.
14. Henderson JB, Glekin BM, McIntosh WB, Dunnigan MG. A health
education campaign to prevent osteomalacia in Asian women in Glasgow. J
Hum Nutr Diet 1989; 2: 163-77.
15. Department of Health. Nutrition and bone health, report of the
subgroup on bone health, working group on the nutritional status of the
population. Stationery Office, 1998.
16. Vieth R. Critique of the considerations for establishing the
tolerable upper intake level for vitamin D: critical need for revision
upwards. J Nutr 2006; 136: 1117-22.
17. Baldsubramanian S, Ganesh R. Vitamin D deficiency in exclusively
breast-fed infants. Ind J Med Res 2008; 127: 250-55.
18. Weisberg P, Scanlon KS, Li R, Cogswell ME. Nutritional rickets
among children in the United States: review of cases reported between 1986
and 2003. Am J Clin Nutr 2004; 80: 1697S-705S.
19. Mellanby E. An experimental investigation on rickets. 1919; 1:
407-12.
20. Chan W, Brown J, Lee SM, Buss DH. Meat, poultry and game. Fifth
supplement to 6th edition of McCance and Widdowson’s The Composition of
Foods. Cambridge/London: The Royal Society of Chemistry/Ministry of
Agriculture, Fisheries and Food, 1995.
21. Gibson SA, Ashwell MA. New vitamin D values for meat and their
implication for vitamin D intake in British adults. Proc Nutr Soc 1997;
56: 116A.
Competing interests:
None declared
Competing interests: No competing interests
Like Dr McMurtrie, we would appreciate guidance on whether a vitamin
D assay is required in all patients considered at risk of deficiency, or
only in selected cases.
This laboratory received over 3900 requests for 25-OH vitamin D assay
in 2009; demand for this test has increased by 9-fold over the last 4
years. The cost in 2009 was over £54000, a significant impost on the
department’s budget.
We see the same high prevalence of vitamin D deficiency (25-OH
vitamin D < 50 nmol/L) as Drs Hull and Boomla. The conundrum posed by
these data is this: most patients for whom our doctors request vitamin D
assay are deficient; thus if the doctor suspects vitamin D deficiency, he
or she is probably correct - could supplementation be started without
biochemical confirmation? Any risk of toxicity would be low, given the
available vitamin D supplements, periodic monitoring of serum calcium
concentrations and review of patient’s symptoms. Note that this approach
is not advocated in groups of patients, such as children, patients
starting bisphosphonates and those with chronic kidney disease, for whom
the need for 25-OH vitamin D quantitation is more clearly defined.
Alternatively, if vitamin D therapy is to be directed only to those
with basal 25-OH vitamin D concentrations that indicate supplementation,
the funding of vitamin D assays needs to be reviewed by the relevant
bodies so that laboratories can provide this service in an orderly and
efficient manner.
Competing interests:
None declared
Competing interests: No competing interests
I complement Pearce and Cheetham (1) on their review and advice on
vitamin
D deficiency.
However it would have greatly enhanced the article for busy clinicians if
a
brief summary concerning the 3 hormones essential to calcium metabolism:
1, 25 Dihydroxy cholecalciferol (calcitrol), parathyroid hormone and
calcitonin
had been included. (2) Vitamin D by successive hydroxylations in the liver
and kidneys gives rise to calcitriol, a steroid hormone, with the primary
function of increasing calcium absorption form the gut and increasing
serum
calcium and phosphate levels. Parathyroid hormone secreted by the
parathyroid glands primarily mobilizes calcium from the bone and enhances
urinary phosphate excretion, raising the serum calcium and lowering the
phosphate level. Calcitonin is excreted by the C cells in the thyroid
gland and
although overall it appears to have a minor role, it inhibits bone
resorption
and lowers circulating calcium levels and phosphate levels. (2)
These 3 hormones have complex interactions with the net effect of
establishing good bone health by maintaining normal blood levels of
calcium
and phosphate and normal urinary excretion of both minerals.
When a busy clinician decides a patient may have poor bone health and
suspects an abnormality of calcium metabolism it is important they are
aware
that a patient can have both vitamin D deficiency and parathyroid hormone
excess. If vitamin D deficiency is suspected in an adult then analysis of
serum
calcium, phosphate, vitamin D and parathyroid hormone levels as well as
urinary excretion of calcium and phosphate will provide a more
information.
A phone call to the biochemist of the laboratory provider can greatly
assist in
the interpretation of these often, contradictory results.
It is essential when getting on board the 'new epidemic' of vitamin D
deficiency reported in Australia, the USA and Northern Europe that
consideration is given to the value of seeking appropriate sun exposure
when
possible and eating a balanced diet and avoiding inappropriate prescribing
of
vitamin D. The latter point is especially important in patients also
suffering
primary hyperparathyroidism. These patients may have a mild to moderately
elevated calcium, elevated parathyroid hormone and low vitamin D levels.
Vitamin D in this setting can result in dangerously high levels of serum
calcium.
1. Simon Pearce and Tim Cheetham. Clinical review. Diagnosis and
management of vitamin D deficiency. BMJ 2010 vol 340 142 – 147.
2. Review of Medical Physiology. William F Ganong 21st edition 2003
385-
398
Competing interests:
None declared
Competing interests: No competing interests
The comprehensive review by Pearce and Cheetham is yet another timely
reminder of an urgent need to try and improve the VitaminD status of
many sections of the UK population. This was highlighted in this journal
over 10 years ago (1) but no real progress has been made. Although
hypovitaminosis D is increasingly recognized to be a global problem it is
in some of the migrant population in the UK and in other developed
countries that we see severe vitamin D deficiency. We have a large multi-
ethnic population in Leicester comprising nearly 33% of a total of
approximately 280,000 people in the city. In some sections of this
community we continue to see florid clinical vitamin D deficiency (2).
This is manifest in adults by myopathy, occasionally progressing to
paraperesis, bone pain, pseudofractures and sometimes hypocalcaemic
paresthesia. Children present with infantile and adolescent clinical
rickets, very rarely a child has required corrective orthopedic surgery.
Neonates present with hypocalcaemic fits due to maternal Vitamin D
deficiency (3). With increasing recognition and earlier treatment by GPs
there has been some decline in such severe cases presenting to hospital.
Nevertheless in recent times this profound vitamin D deficiency seems
almost exclusively to be a feature of the migrant population including
Hindu vegetarian women and men,fully covered Muslim women, from East
Africa, India, Pakistan,Middle East and more recently from Somalia
together with other sections of this population. Afro-Caribbean men seem
not to have presented to hospital with such severe deficiency.
Serum parathyroid hormone (PTH) levels are now routinely measured in
the assessment of vitamin D status and can be raised with any level of
hypovitaminosis D but levels may change quite quickly with evolving and
resolving disease. PTH measurement is now accessible to GPs using EDTA
sample tubes. Very occasionally in vitamin D deficiency with hypocalcaemia
PTH levels can be inappropriately low reminiscent of a hypoparathyroid
picture, but correcting the 25(OH) Vitamin D and serum magnesium levels
normalizes PTH levels (3)(4). With modern biochemistry and bone
densitometry, bone biopsy is very rarely used in diagnosis of osteomalacia
due to Vitamin D deficiency. Osteomalacia is a categorical histological
diagnosis. With different levels of vitamin D deficiency there is likely
to be a gradient of bone mineral deficit so probably we should move to a
terminology of mineralisation defect rather than osteomalacia as evidence
by low bone density with simultaneous abnormal vitamin D related
biochemical measures. In adults with appropriate symptoms X-rays
especially of the pelvis and femora are sometimes warranted to exclude
pseudofractures as they may rarely progress to complete fractures.
The unusual physiology of vitamin D with sunshine being its major
determinant and the implications this has for the UK where we well know
how variable but generally poor sunshine is and its poor uptake in this
vulnerable group; it is hardly surprising then that we frequently find
abysmally low vitamin D levels in this population. In the UK the vitamin
D content of ordinary widely consumed food such as milk is very low so we
have found that dietary modification is a waste of time and will remain so
until wider fortification of food is introduced. In terms of primary
prevention as suggested before (1) and outlined by Pearce and Cheetham
together with other measures some form of supplementation will be
required. The recent recommendations; by the Royal college of
Obstetricians and Gynecologists, a reiteration of the bone health COMA
group recommendation in 1998 (5), to supplement all pregnant women and
by the Department of Health to supply vitamin D drops to infants and pre
-school children is a welcome move in that direction. The city of Glasgow
reported a successful rickets campgain by providing free vitamin D
supplements to children (6). It is very unlikely that single uniform
regimen for primary prevention will be suitable for the diverse UK
population each with its own clinical, social and cultural circumstance
however a move towards achieving improved vitamin D status with all its
health related implications has been long overdue for sometime and is now
mandatory.
References
1. Compston J E. Vitamin D deficiency; Time for Action. BMJ 1998; 31:
1466-7.
2. Iqbal S, Kaddam I, Wassif W, Nichol F, Walls J. Continuing
clinically severe vitamin D deficiency in Asians in the UK (Leicester).
Post Grad Med J 1994; 70: 708-714.
3. Shenoy S D, Swift P, Cody D, Iqbal S J. Maternal Vitamin D
deficiency, refractory neonatal hypocalcaemia and nutritional rickets.
Arch Dis Child 2005;90;437-438
4. Iqbal SJ. Impaired parathyroid levels in vitamin D deficiency. In
Abstracts of 13th Vitamin D Workshop Victoria BC. P81, 2006.
5. Department of Health. Nutrition and bone health with particular
reference to calcium and Vitamin D. Report on health and social subjects
49. London HMSO.1998
6. Dunnigan M G, Geikin BM , Henderson J B, McIntosh W B , Summer
D ,Sutherland G R. Prevention of rickets in Asian children assessment of
the Glasgow campaign. Br Med J. 1985. 291 ; 239-242.
Competing interests:
nil
Competing interests: No competing interests
--Simon Pearce and Tim Cheetham [1] are to be congratulated for
highlighting the problems associated with vitamin D deficiency and
stimulating discussion. Over the last few years hypovitaminosis D has been
linked with a multitude of problems such as type 1 diabetes mellitus,
cardiovascular morbidity and mortality, certain cancers and multiple
sclerosis [2]. Supplementation with vitamin D in children has been shown
to be cost-effective even when considering acute treatment costs incurred
to deal with rickets alone [3].
--It is widely accepted that effective Public Health measures are
needed to combat the problems arising from vitamin D deficiency.
Unfortunately, in the 2003 antenatal guideline, NICE did not see vitamin D
supplementation as a recommended component of routine antenatal care.
However, this has been rectified in the latest version of the guideline in
2008 [4] which suggests that all women should be informed at the booking
appointment about the importance, for their own and their baby’s health,
of maintaining adequate vitamin D stores during pregnancy and the
breastfeeding period. Further, women from low-income households, those
with a low intake of vitamin D in their diets, South-Asian and Black
women, those with limited skin exposure to sun, those aged 19-24, and
obese women are identified as high-risk for vitamin D deficiency.
--This latest guideline from NICE [4] has been adopted in our
institution (Central Manchester Foundation Trust). There is also guidance
from the DoH recommending supplementation of children to the age of 5 [5].
We undertook a prospective audit over 1 week in January 2010, in St.
Mary’s Hospital, Manchester, aiming to assess maternity team awareness of
the guidelines. Approval from the Trust’s Audit Department was obtained.
We collected information on specifically designed proformas from 50 new
mothers and 52 midwives selected at random. 36/50 (72%) of the mothers we
approached had at least one factor putting them in the high-risk category
(12/50 (24%) were in the high-risk age group; 7/50 (14%) had a pre-
pregnancy BMI>30; 24/50 (48%) had dark skin; 16/50 (32%) dressed
conservatively).
--8/50 (16%) of the mothers had been informed about vitamin D
supplements and/or Healthy Start multivitamins. 19/50 (38%) had been
taking vitamin D supplements. Interestingly, only 3 of these got their
vitamins from their GP; the rest got them over the counter. Although the
majority (14/19; 74%) started their supplementation in the first
trimester, there was a significant number who started in the second (3/19;
16%) and even third (2/19; 10%) trimester.
--The midwives we interviewed worked in the community (20/52; 38%),
postnatal wards (18/52; 35%), and antenatal clinics (9/52; 17%) or were in
rotation between all sites (5/52; 10%). Only 22/52 (42%) were aware of the
guidelines and these midwives were giving advice on vitamin D
supplementation to expectant women. There was some confusion among the
interviewed midwives as to who prescribes the supplements with the
majority replying that it was the GP (15/22; 68%), whilst some thought it
was the obstetrician (4/22; 18%), or were not sure (3/22; 14%). Of the 22
midwives aware of the local guideline, 16 knew that supplements should be
started in the first trimester whereas the rest did not know when they
should be started.
--It was good to see that the majority 34/52 (65%) of the midwives
interviewed were aware of who is considered high risk. When asked whether
they might want to check vitamin D levels on these women, 11 of these
midwives (34%) said that they would. For this, some would have referred to
the obstetrician (5/11; 45%), others to the GP (5/11; 45%) and there was 1
midwife (10%) who would have checked vitamin D levels with the booking
bloods.
--When asked about supplementation of babies, only 15 of the 52
interviewed midwives (29%) were aware of the DoH guideline.
--It is obvious that despite the release of guidelines from respected
bodies such as NICE, there is, still, limited awareness of the guidelines
and absence of clear pathways of how to deal with this growing problem.
Campaigns to raise awareness among both healthcare staff and the general
public are mandatory. Further, all women should be provided with written
information about vitamin D at their booking appointment and those
identified as high-risk (perhaps combining 2-3 risk factors) need to have
their vitamin D levels measured as supplementation at the recommended
amounts will not treat deficiency. Clear and funded referral pathways need
to be in place in every area so that those with deficiencies are
appropriately investigated and treated. All pregnant and breastfeeding
mothers, and babies need to be offered vitamin D supplements. Perhaps, the
Birmingham model of Public Health interventions [6] should be followed
more widely in order to curtail vitamin D deficiency and decrease ill
health. We are currently looking to bring in a similar arrangement in
Manchester.
References:
1. Pearce SHS, Cheetham TD. Diagnosis and management of vitamin D
deficiency. BMJ 2010; 340: b5664
2. Zipitis CS, Akobeng AK. Vitamin D supplementation in early childhood
and risk of type 1 diabetes: a systematic review and meta-analysis. Arch
Dis Child. 2008 Jun;93(6):512-7
3. Zipitis CS, Markides GA, Swann IL. Vitamin D deficiency: prevention or
treatment? Arch Dis Child. 2006 Dec;91(12):1011-4.
4. National Institute for Clinical Excellence. Antenatal care. Routine
care for the healthy pregnant woman. London, NICE, 2008 (available at
http://www.nice.org.uk/nicemedia/
pdf/CG62FullGuidelineCorrectedJune2008July2009.pdf)
5. Chief Medical Officer. Meeting the need for vitamin D. CMO Update
2005;42:6 (available at
http://www.dh.gov.uk/assetRoot/04/11/56/64/04115664.pdf
6. Nick J Shaw, et al. Vitamin D supplementation-Easier said than done.
BMJ (available at
http://www.bmj.com/cgi/eletters/340/jan11_1/b5664#230270)
Competing interests:
None declared
Competing interests: No competing interests
Dear Sir/Madam,
The cover page of BMJ January 16, is the most appropriate and
symbolic in recent times. It takes me back a little over three years when
I gave a presentation under the title ‘Statins and Sunlight’ at a local
academic meeting, which is available on our public medical information
website viz.www.pubmedinfo.com since 2007. (1).
I would like to share with your readers, through the columns of the BMJ,
three significant points that I had presented in my talk.
a) The seminal work of David S.Grimes (2) and his hypothesis that statins
are but analogues of Vitamin D.
b) that ‘sunlight cuts the risk of death by 50%’ – published recently (3)
but known to the ancient Hindu vedic scriptures for several millennia the
beneficial effects of the electromagnetic energy of the sun on the
humanbody (including the bones) through the daily practice of Surya
namaskar (Sun worship). And
c) my observation for the past 10 years on the pavement of the street
where I live, of an elderly destitute lady sitting and
living on the alms of the passers- by daily, day-in and day-out, obviously
under-nourished, exposed to the elements (including the SUN), surely
inhaling or consuming all possible varieties of pollutants (including
deadly tropical bacteria, viruses and other micro organisms), but carrying
on without falling sick or absent even for a day during these long years
of her soujourn under the SUN, up till date!!
Surely there is a lot be learned, researched and knowledge &
wisdom gained, on the positive benefits on human immune system and tissue
healing, from sunlight and chronic suboptimal nutrition (4) and ‘The
wisdom of the Human Body’ (5).
Yours,
C.V.Krishnaswami.
Reference:
1. Krishnaswami C.V. (2007).http://www.pubmedinfo.com/pdf/statins.pdf
2. David S.Grimes. ‘Are Statins Analogues of Vitamin D’ ? Lancet 2006; -
368: 83-86 (July,1).
3. ‘Sunlight can cut your risk of death to half’, Arch.of Intern-Med,
2008; - 168(12):1340-1349.
4. Subba Rao K, Ayyagiri S, Raji N.S, Murthy K.J.R. ‘Under nutrition, and
aging; effects on DNA repair in human peripheral lymphocytes’. Current
Science 1996; 71:464-469.
5. Hegde B.M.(2009) http://www.pubmedinfo.com/wisdomhuman.aspx
Competing interests:
None declared
Competing interests: No competing interests
Re: Alfacalcidol ?
My understanding is that Alfacalcidol is much too prone to causing
high calcium levels, as well as being costly. Colecalciferol ( D3) IS
available..eg as Dekristol imported from Germany. It works well, costs
about 16 pounds per year and is easy to swallow. The only difficulty is
that it is unlicensed in the UK although licensed in Europe and used
widely there. GPs can prescribe colecalciferol ( D3) 20 000iu capsules
with confidence as we are able to use unlicensed products where we make an
appropriate professional judgement to do so. Why doesnt the DOH license
this product as there is such a need for it? Why is there no UK
manufacture/licensed product?
Competing interests:
None declared
Competing interests: No competing interests