Vitamin D An Effective Analgesic for Type 2?s With Neuropathic Pain*

April 24, 2008

Vitamin D An Effective Analgesic for Type 2ï¿½s With Neuropathic Pain*

Vitamin D insufficiency is under recognized and may be a significant contributor

to neuropathic pain in type 2 diabetes. Vitamin D supplementation may be

an effective " analgesic " in relieving neuropathic pain.

Treatment of neuropathic pain is generally unsatisfying for patients with type 2

diabetes mellitus, and patients with debilitating residual symptoms may

be given nonspecific diagnoses such as " chronic pain syndrome. " Although

hypovitaminosis D is highly prevalent in patients with type 2 diabetes, to our

knowledge, its impact on neuropathic pain has not been previously evaluated. Our

objective was to evaluate the impact of vitamin D repletion on neuropathic

pain in patients with type 2 diabetes and vitamin D insufficiency.

A total of 51 patients with type 2 diabetes with typical neuropathic pain,

including burning, tingling, numbness, and throbbing sensations, and physical

examination findings of reduced sensation to monofilament, were included.

Severity of pain was evaluated by the short form of the McGill pain

questionnaire

Serum 25-hydroxyvitamin D (25D) concentration was measured by radioimmunoassay

and intact parathyroid hormone (iPTH) concentration by automated immunoassay.

Vitamin Dâ€“insufficient patients (serum 25D concentration <24 ng/mL), were

supplemented with cholecalciferol (vitamin D3) tablets (mean dose, 2059 IU).

Patients

were reevaluated in 3 months with repeated biochemistry tests and reevaluation

of pain by the questionnaires used at baseline.

All patients were vitamin D insufficient, with mean serum 25D concentration of

18 ng/mL. The mean VAS score for pain at baseline was 3.3 ( " distressing " ).

Pain scores for both the VAS correlated negatively with serum 25D concentration

but not with serum iPTH concentration. Vitamin D repletion resulted in

a significant reduction in pain scores on both the VAS and MPQ at â€“48.5% and

â€“39.4%, respectively.

Severe vitamin D deficiency leads to osteomalacic myopathy, as characterized in

a case series demonstrating severe muscle weakness and pain in patients

with serum 25D concentrations lower than 12 ng/mL, with prompt resolution of

symptoms following vitamin D replacement. Vitamin D insufficiency (serum 25D

concentration, 12-24 ng/mL), on the other hand, has not been reported to cause

significant pain in patients.

To our knowledge, this is the first prospective observational study addressing

the impact of vitamin D repletion on neuropathic pain in patients with type

2 diabetes mellitus. The mean serum 25D concentration in our patients was higher

than " osteomalacic myalgic patients " reported in the literature (18 ng/mL

vs <12 ng/mL). There is both in vitro and in vivo evidence that vitamin D is a

neurotrophic substance and modulates neuromuscular function and neuronal

growth and differentiation. Its role in diabetic neuropathic pain is uncertain.

Vitamin D insufficiency may potentiate diabetic nerve damage and may impair

nociceptor function, resulting in pain at a threshold of serum 25D concentration

higher than that in the nondiabetic population.

While primary hyperparathyroidism has been associated with nonspecific

musculoskeletal symptoms, the improvement of pain in our subjects following

vitamin

D repletion could not be attributed to a decrease in parathyroid hormone level.

There was no evidence of secondary hyperparathyroidism at baseline, and

the decrease in parathyroid hormone level following vitamin D repletion was not

statistically significant, indicating that the improvement in symptoms

was independent of parathyroid status.

The definition of vitamin D sufficiency is an ongoing debate in the literature.

While vitamin D insufficiency is generally defined as a serum 25D concentration

of less than 20 ng/mL, the optimal level of vitamin D most beneficial to bone

health is not known. From the point of view of osteoporosis prevention, there

is an argument in aiming at a serum 25D concentration of above 24 ng/mL, since

bone resorption markers have been shown to be significantly higher in

individuals

below this threshold. The mean (SD) serum 25D concentration at 3 months in our

study was 30 (5) ng/mL, which correlated with significant pain reduction.

Achieving adequate serum 25D concentration (>24 ng/mL) may not only help to

prevent osteoporosis in patients with type 2 diabetes but may also relieve

neuropathic pain.

Our study was neither blinded nor randomized, resulting in the possibility of

treatment bias. However, vitamin D has definite proven benefit in the prevention

of osteoporosis, which is prevalent in the diabetic population. Vitamin D has

been increasingly recognized for its pleiotropic effect, including improvement

in glycemic control. It is also free of adverse effects. Because the treatment

of diabetic neuropathic pain is generally unsatisfying for patients and

is associated with significant adverse effects, we advocate a trial of vitamin D

supplementation in vitamin Dâ€“insufficient patients with neuropathic pain.

It is unlikely to have any harmful effects and may offer not only pain relief

but also beneficial effects on bone health and glycemic control.

In conclusion, vitamin D insufficiency is underrecognized and may be a

significant contributor to neuropathic pain in type 2 diabetes. Vitamin D

supplementation

may be an effective " analgesic " in relieving neuropathic pain.

Arch Intern Med. 2008;168(7):771-772.

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