In February 2012 the Department of Health released a statement to raise national awareness of vitamin D deficiency in the UK. The statement also gave guidance to health professionals regarding prescribing and recommending vitamin D supplements to groups at risk of vitamin D deficiency.1
We also know from the National Diet and Nutrition Survey that up to a quarter of people in the UK have low levels of vitamin D in their blood, which means they are at risk of the clinical consequences of vitamin D deficiency.1, 2 Vitamin D levels are also modestly associated with risk of stroke. Maintaining adequate vitamin D status may lower the risk of stroke in women.3
Vitamin D deficiency
Vitamin D deficiency impairs the absorption of dietary calcium and phosphorus, which can give rise to bone problems such as rickets in children, and bone pain and tenderness as a result of osteoporosis and osteomalacia in adults.4,5
Possible clinical consequences of vitamin D deficiency are:
• Osteoporosis and osteopenia
• Dull aching bone pain commonly affecting lower spine, hips, pelvis, legs and ribs
• Muscle weakness, decreased muscle tone and wadding gait
• Reduced immune system
• Fatigue and depression.
How do we get vitamin D?
The action of sunlight on the skin, rather than food is the main source of vitamin D. Vitamin D is made under our skin when skin is exposed to day-light, which is the reason vitamin D is sometimes called the “sunshine vitamin.” The amount of vitamin D you make depends on the strength of the sunlight or ultraviolet light. You will make more vitamin D in the middle of the day than early morning or late afternoon. Similarly, you will make more when you are in direct sunlight than in the shade or on a cloudy day. Very few foods contain vitamin D naturally; even a healthy and well balanced diet that provides other vitamins and minerals is unlikely to provide enough vitamin D.
Foods which contain vitamin D include cod liver oil, oily fish, eggs and meat. Some margarine, breakfast cereals and infant formulas have added vitamin D. The commercial food market is acting on increased national awareness of vitamin D deficiency and with certain foods, eg. fortified yoghurts, now being marketed based on the high vitamin D content.6
Normal bone mineralisation depends on adequate calcium and phosphate and this is maintained by vitamin D. Production of metabolically active vitamin D requires hydroxylation, which occurs first in the liver and then in the kidneys to produce 1,25-dihydroxyvitamin D3. The recommended daily intake of vitamin D in the UK is 400 IU (10 micrograms) per day for an adult, 280 IU (7 micrograms) for children aged between six months and three years, and 340 IU (8.5 micrograms) per day for infants under six months. These recommendations only provide sufficient vitamin D to prevent osteomalacia and rickets and, in the absence of skin synthesis, will not provide an optimal level of vitamin D.
Interpreting levels of vitamin D
There is currently no standardised definition “optimal level” of vitamin D. The consensus is that levels of 25-OHD below 25nmol/L indicate deficiency. Some scientists suggest that levels above 50nmol/L are “sufficient” while 70–80nmol/L is “optimal”.3
At risk groups
The Department of Health listed the following patient groups at risk of vitamin D deficiency:
• All pregnant and breast feeding women, especially teenagers and young women
• Infants and children under five years
• Older people aged 65 years and older
• People who have low or no exposure to the sun, for example those who cover their skin for cultural reasons, who are housebound or confined indoors for long periods
• People who have darker skin, for example people of African, African-Caribbean and South Asian origin, because their bodies are not able to make as much vitamin D.1,2
Following the release of the Department of Health statement and raised national awareness of vitamin D deficiency, a clinician discussion took place between the dietetic department and the stroke team at Conquest Hospital, St Leonards-on-Sea, East Sussex. The acute stroke medical team linked with other medical teams and developed new East Sussex Healthcare Trust guidance for interpreting vitamin D levels. They are as follows:
Together the stroke team agreed to audit vitamin D levels in acute thrombotic stroke patients admitted to the acute stroke unit at Conquest Hospital over a six month period (June to November). Exclusion criteria included patients diagnosed with intracranial bleed or non stroke and patients already on vitamin D supplements prior to admission.
An audit form was developed and patient information gathered from medical notes, blood results and patient/carer reported information. Information gathered included stroke diagnosis, past medical history, social history, serum calcium (corrected), serum phosphate, serum 25-hydroxy vitamin D, serum parathyroid hormone and if patient was commenced on vitamin D supplement after identification of low serum level.
A random selection of 100 patients were included in the study—21 patients had a vitamin D above 50nmol/L, meaning that, 79% of patients had a vitamin D level below 50nmol/L. Of the 79/100 patients with a vitamin D level below 50nmol/L, 43% were female and 57%% male. Of the 79/100 patients with vitamin D level less than 50nmol/L, 85% were over 65 years of age and 15% were under 65 years of age.
East Sussex has higher proportions of people over 65 years than England overall and proportions are expected to grow faster than England overall over 2010–2020.6 The Department of Health highlighted that people over 65 years are at risk of vitamin D deficiency, therefore the stroke team believe it likely that East Sussex will have a higher prevalence of vitamin D deficiency compared to other counties in England.
Following these results the stroke medical team liased with pharmacy and other medical teams to develop the new clinical guidelines for use within acute hospitals in East Sussex to replace low vitamin D level (<50nmol/L) in patients with normal calcium level and eGFR >30 ml as below.
Indications for checking vitamin D include:
• Recurrent fallers
• Fragility fractures
• Chronic kidney disease stage 4 patients
• Suspected osteomalacia (unexplained elevated ALP, muscle weakness, non-specific aches and pains)
• Malabsorption (coeliac, small bowel resection etc.)
• On bone modifying drugs: steroids, antiepileptic, antiaromatase, antiretrovirals
• Risk of osteoporosis: inflammatory disease: rheumatoid arthritis; chronic obstructive pulmonary disease, immobilisation, liver or kidney disease.
Active treatment in the audit
If eGFR >30, one of the following options was started:
• 1-Adcal D3 one tablet BD long-term and vitamin D3 (cholecalciferol), 60,000 units once weekly after the main meal of the day for eight weeks. Check bone profile and vitamin D levels after eight weeks, to achieve and maintain 25-hydroxy vitamin D levels of >75nmol/L.
• 2-Adcal D3 one tablet BD long-term and vitamin D3 (cholecalciferol), 40,000 units, daily after the main meal of the day for seven days. Check bone profile and vitamin D levels after eight weeks, to achieve and maintain 25-hydroxy vitamin D levels of >75nmol/L.
• In patients with non-compliance/intolerance of oral colecalciferol or with extensive small bowel resection treat with ergocalciferol (vitamin D2) 300,00 IU IM injections; load with two injections three months apart, maintenance with six monthly injections. Check bone profile, vitamin D level and 25-hydroxy vitamin D level six weeks after the injection to achieve and maintain 25-hydroxy vitamin D levels of >75nmol/L.
Other treatments for vitamin D deficiency
Adcal is used as an example but other effective treatments for vitamin D deficiency include: Accrete D3, Cacit Tablets, Calceos, Calcichew, Calcium 500, Calcium-Sandoz, Calfovit D3, Kalcipos-D, Natecal D3, Sandocal 1000, Desunin and Fultium-D3.
Vitamin D tablets are often required long-term, to prevent further deficiency in the future, as it is unlikely that any risk factor for vitamin D deficiency in the first place would have completely resolved.
A further review after six months is advised with bone profile, vitamin D level and 25-hydroxy vitamin D level.
This audit has led to interesting findings in the limited area of UK vitamin D deficiency. We recognise that the audit was carried out on a small patient group and recommend that further studies take place in the UK. The aim of the audit was achieved and the stroke team have raised local and national awareness of vitamin D deficiency.
Audit findings were presented at the consultant clinical audit meeting in the Conquest Hospital. The questions below were left unanswered and clinicians are left hoping for further national studies and research into the field of vitamin D deficiency:
• What is the optimal level of 25-OHD for various health outcomes?
• How much sun exposure is needed to ensure optimal levels of vitamin D in people of different skin types and under different environmental conditions?
• Can higher levels of 25-OHD directly reduce the risk of cancer or other chronic diseases, and can supplementation achieve the same effects?
• Could we use over the counter vitamin D supplements rather than prescription supplements?
• Does body fat act as a sink or source of vitamin D in winter?
Conflict of interest: none declared
1. Department of Health, (2012). Vitamin D – Advice on supplements for at risk groups
3. Department of Health, (2011). The National Diet and Nutrition Survey. http://www.noo.org.uk/data_sources/Nutrition/NDNS
4. National Osteoporosis Society, British Association of Dermatologists, Diabetes UK, (2010). Consensus Vitamin D position statement Cancer Research UK
5. AU, Visser M, Deeg DJ, Lips P (2003). Journal of Endocrinology and Metabolism - Low vitamin D and high parathyroid hormone levels as determinants of loss of muscle strength and muscle mass (sarcopenia): the Longitudinal Aging Study Amsterdam
6. British Dietetic Association (2008). Vitamin D food fact sheet
7. Dr Armstrong (2012). Proactively caring for the elderly and those with complex need in Sussex. Access via internet http://www2.westsussex.gov.uk/ds/cttee/hasc/hasc040712i6a.pdf