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The New Zealand Medical Journal

 Journal of the New Zealand Medical Association, 28-November-2008, Vol 121 No 1286

Prevalence of vitamin D deficiency among patients attending a multidisciplinary tertiary pain clinic
Jim Bartley
Abstract
Aim To estimate the prevalence of vitamin D deficiency in a tertiary multidisciplinary pain clinic.
Methods From 14 July 2006 to 30 November 2007, the author requested vitamin D status from all patients with chronic persistent pain presenting to The Auckland Regional Pain Service (a tertiary multidisciplinary pain service). Serum 25-hydroxyvitamin D levels were determined by radioassay.
Results Of 177 patients, 3% had 25-hydroxyvitamin D levels ≤17.5 nmol/L—a level associated with osteomalacia, 32% had 25-hydroxyvitamin D levels ≤50 nmol/L—a level associated with vitamin D deficiency, and 73% had 25-hydroxyvitamin D levels ≤80 nmol/L.
Conclusions The prevalence of vitamin D deficiency in patients attending a multidisciplinary pain clinic is similar to if not less than that of the normal New Zealand population. Recent African immigrants and south Asian females are two patient groups that are frequently vitamin D deficient. The identification and treatment of vitamin D deficiency has the theoretical potential to help a number of chronic pain patients. Only a limited number of interventional clinical trials have looked at this.

Vitamin D deficiency has been increasingly implicated in a number of pain syndromes. Pain refractory to narcotics is well recognised in severe vitamin D deficiency.1 Plotnikoff and Quigley have documented that vitamin D deficiency is common in patients presenting with persistent non-specific musculoskeletal pain in a primary care setting.2
In New Zealand, Chiu has reported that vitamin D deficiency is common in a private rheumatology practice.3 Similarly vitamin D deficiency has been reported in pain syndromes such as low back pain,4 migraine,5 and diabetic peripheral neuropathy.6 Because of these observations, a survey was conducted to determine the prevalence of vitamin D deficiency among patients attending a tertiary multidisciplinary pain clinic.

Methods

All new patients presenting to the author as part of their initial evaluation had their 25-hydroxyvitamin D level requested. Pathology forms were given to patients and the assay was performed by the Auckland District Health Board laboratories. The laboratory uses the Diasorin assay kit, which has a coefficient of variation of 6% between tests which approximates to ±12% for confidence limits. Those patients already taking colecalciferol were excluded from the survey.
Because 25-hydroxyvitamin D measurement is an expensive test, if 25-hydroxyvitamin D levels had been measured in the previous 3 months, the test was not repeated. These patients were still included in the survey if they had not been treated.
Within the pain clinic, a number of doctors have specific pain interests. While a broad range of pain conditions were seen, the population assessed reflected the author’s particular interest in facial pain.

Results

From 14 July 2006 to 30 November 2007, the author saw 187 patients. Two patients did not have their 25-hydroxyvitamin D levels measured. Three patients did not have their 25-hydroxyvitamin D levels done because they were already taking colecalciferol.
Patients taking multivitamin supplements, which can include low doses of vitamin D, were included in the survey. Another patient with a previous vitamin D level consistent with osteomalacia (13 nmol/L) had stopped her medication 6 months earlier. Four additional patients taking colecalciferol 1.25 mg monthly, where there were still concerns about their vitamin D status, had their 25-hydroxyvitamin D levels checked. One of these patients despite taking replacement therapy had a 25-hydroxyvitamin D level of 33 nmol/L. These ten patients were not included in the survey. Two patients who had had their 25-hydroxyvitamin D levels done in the 3 months prior to being seen at the pain clinic were included.
Female patients comprised 66% of the patients seen. Of the 177 eligible patients who had 25-hydroxyvitamin D levels performed 3% had levels ≤17.5nmol/L—a level associated with osteomalacia, 32% had levels ≤ 50nmol/L—a level associated with vitamin D deficiency, and 73% had levels ≤80nmol/L. No seasonal variation was observed.
The majority of the patients seen were European. Four patients were of African ethnicity (average 25-hydroxyvitamin D level—25 nmol/L); 14 patients were South East Asian (average vitamin D level—54 nmol/L); 17 patients were South Asian (average vitamin D— 65 nmol/L; 80% of the females had levels less than 50 nmol/L); 7 patients were from the Middle East (average vitamin D level—47 nmol/L); 6 patients were from the Pacific Islands (average vitamin D level—40 nmol/L); and 10 patients identified themselves as Māori (average vitamin D level—54 nmol/L).
The average 25-hydroxyvitamin D level of those referred specifically with low back pain (20 patients) was 54 nmol/L. Of those patients with vitamin D levels ≤17.5nmol/L, a level typically associated with osteomalacia, all were female with a wide range of age ranges being represented (Table 1). Vitamin D deficiency was observed in all age groups with a slight female predominance (Figure 1).

Table 1. Race, sex and age of those patients whose 25-hydroxyvitamin D levels were less than 17.5 nmol/L (n=6)

Ethnicity
Sex
Age
25-hydroxyvitamin D level (nmol/L)
Middle East
South Asian
European
African
Māori
South Asian
Female
Female
Female
Female
Female
Female
35
48
80
39
51
32
13
13
11
12
16
16

Figure 1. Vitamin D level (nmol/L) by age, sex, and ethnicity (European/non-European) in patients with vitamin D deficiency (25-hydroxyvitamin ≤50 nmol/L)


Discussion

This survey has shown that vitamin D deficiency is common in patients attending a multidisciplinary pain clinic, however the prevalence of vitamin D deficiency is similar if not less than that seen in the general New Zealand population.
In a recent national sample of 2946 New Zealanders aged 15 years and over, 84% of people had a mean serum 25-hydroxyvitamin D concentration of ≤80 nmol/L, 48% had levels of ≤50 nmol/L, and 3% had levels of ≤17.5 nmol/L. Mean serum 25-hydroxyvitamin D levels were 5 nmol/L lower in females and were lower in the South Island. Mean serum 25-hydroxyvitamin D levels were also lower in Maori (42 nmol/L) and Pacific Island people (37 nmol/L) compared to people of other ethnicities (51 nmol/L).7
An Auckland survey in women ≥55 years of predominantly Caucasian/European women found a high prevalence of vitamin D deficiency even in summer.8 In a similar Auckland survey in predominantly European men, 9% of men had vitamin D levels <50 nmol/L.9 A substantial seasonal variation was demonstrated in both studies.
Many of the patients with vitamin D levels ≤17.5 nmol/L, a level indicative of osteomalacia, could be predicted on the basis of age, sex, and ethnicity. One African patient receiving vitamin D supplementation remained vitamin D deficient. Increasing his vitamin D dosage led to a significant reduction in his pain.
Heaney et al showed in men that 1 microgram of colecalciferol/ day raises serum vitamin D levels 0.7 nmol/L.10 Bacon et al showed that 1.25mg of colecalciferol/month raised serum vitamin D levels on average 20 nmol/L. Because it can take up to 5 months for vitamin D levels to plateau, they recommended a loading dose of 12.5 mg.11
In some patients, current dosage regimes may be inadequate. Another South Asian lady with a vitamin D level of 13 nmol/L diagnosed in the previous year had stopped taking her medication. Some patients remain unaware that they may need to continue taking vitamin D on a long-term basis.
Previous surveys have shown that patients presenting with non-specific musculoskeletal pain have a high incidence of vitamin D deficiency.2,3 The incidence of vitamin D deficiency in this tertiary pain clinic population, while high, reflects that of the normal New Zealand population.
One of the limitations of this survey and other previous observational studies is the lack of an adequate control group.
While a large percentage of the New Zealand population is vitamin D deficient, many people in the New Zealand population also suffer from diffuse musculoskeletal pain.
In New Zealand, 15% of general practice consultations between 1996 and 1999 were for musculoskeletal disorders.12 A pilot postal survey of 540 adults in New Zealand randomly selected from the electoral roll for the lower North Island, found that almost half of the 289 responders reported musculoskeletal pain, defined as muscle or joint pain, swelling, or stiffness that lasted more than 1 week during the last month.13 Vitamin D deficiency could be a factor in the pain experienced by some of these people.
While Vitamin D deficiency has been increasingly implicated in several pain syndromes, the benefits of vitamin D supplementation in these syndromes has not been well documented in clinical trials. Theoretically vitamin D deficiency may have a role in a number of pain states.
Vitamin D inhibits inducible nitric oxide synthesis (NOS) and increases glutathione levels in astrocyte detoxification processes.14 Glial hypersensitivity has been implicated in a number of pain syndromes.15 Nitric oxide has an important role in pain transmission and administration of NOS inhibitors results in reduced pain and reduced hyperalgesia.16
Vitamin D would also appear to have an important role in neural repair being a potent up-regulator of nerve growth factor. Thus vitamin D has a potential pharmacological role in the treatment of neural disorders, as well as in nerve repair.14
Vitamin D also has an important role in musculoskeletal health with improved muscle strength seen up to 80 nmol/L.17 Vitamin D supplementation has been recommended as part of pain rehabilitation,18 however only a limited number of clinical studies looking at the benefits of vitamin D supplementation in the pain population have been performed.1-6,18,19 The significance of vitamin D deficiency in chronic pain patients may have been over emphasised.
This study confirms a high prevalence of vitamin D deficiency within a tertiary pain clinic. The levels of vitamin D deficiency were similar, if not less, than that seen in the normal New Zealand population.
Recent African immigrants and south Asian females are two high-risk patient groups that would benefit from routine vitamin D supplementation. The identification and treatment of vitamin D deficiency has the theoretical potential to help a number of chronic pain patients. Only a limited number of interventional clinical trials have looked at this.
Competing interests: None known.
Author information: Jim Bartley, Otolaryngologist/Pain Medicine Physician, The Auckland Regional Pain Service, Green Lane Clinical Centre, Auckland
Correspondence: Mr J. Bartley, 10 Owens Rd, Epsom, Auckland, New Zealand. Fax: +64 (0)9 6310478; email: jbartley@ihug.co.nz
References:
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  2. Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, non-specific muscle pain. Mayo Clin Proc. 2003;78(12):1463–70.
  3. Chiu G. Vitamin D deficiency among patients attending a central New Zealand rheumatology outpatient clinic. N Z Med J. 2005;118(1225). http://www.nzma.org.nz/journal/118-1225/1727
  4. Al Faraj S, Al Mutairi K. Vitamin D deficiency and chronic low back pain in Saudi Arabia. Spine. 2003;28(2):177–9.
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  7. Rockell JEP, Skeaff CM, Williams SM, Green TJ. Serum 25-hydroxyvitamin D concentrations of New Zealanders aged 15 and over. Osteoporos Int. 2006;17(9):1382–9.
  8. Lucas JA, Bolland MJ, Grey AB et al. Determinants of vitamin D status in older women living in a subtropical climate. Osteoporos Int 2005; 16: 1641–8.
  9. Bolland MJ, Grey AB, Ames RW et al. Determinants of vitamin D status in older men living in a subtropical climate. Osteoporos Int 2006; 17: 1742–8.
  10. Heaney RP, Davies KM, Chen TC et al. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr. 2003;77(1): 204–10.
  11. Bacon CJ, Gamble GD, Horne AM et al. A comparison of three high dose oral vitamin D3 supplementation regimes. Twenty-Ninth Annual Meeting of the American Society for Bone and Mineral Research. 2007; S126–7.
  12. Taylor W, Smeets L, Hall J, McPherson K. The burden of rheumatic disorders in general practice: consultation rates for rheumatic disease and the relationship to age, ethnicity and small area deprivation. N Z Med J. 2004;117(1203). http://www.nzma.org.nz/journal/117-1203/1098
  13. Taylor W. Musculoskeletal pain in the adult New Zealand population: prevalence and impact. N Z Med J. 2005;118(1221). http://www.nzma.org.nz/journal/118-1221/1629
  14. Kiraly SJ, Kiraly MA, Hawe RD, Makhani N. Vitamin D as a neuroactive substance: review. Scientific World Journal. 2006;6:125–39.
  15. Hutchinson MR, Bland ST, Johnson KW et al. Opioid-induced glial activation: mechanisms of activation and implications for opioid analgesia, dependence and reward. Scientific World Journal. 2007;7:98–111.
  16. Wu J, Lin Q, McAdoo DJ, Willis WD. Nitric oxide contributes to central sensitization following intradermal injection of capsaicin. Neuroreport. 1998;9(4):589–592.
  17. Bischoff-Ferrari HA. Optimal serum 25-hydroxyvitamin D levels for multiple health outcomes. Adv Exp Med Biol. 2008;624:55–71.
  18. Heath KM, Elovic EP. Vitamin D deficiency: implications in the rehabilitation centre. Am J Phys Med Rehabil. 2006;85(11):916–23.
  19. Warner AE, Arnspiger SA. Diffuse musculoskeletal pain is not associated with low vitamin D levels or improved by treatment with vitamin D. J Clin Rheumatol. 2008;14(1):12–16.
     
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