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ALL autoimmune peripheral neuropathy patients had low vitamin D levels – Oct 2014

Vitamin D deficiency in patients with primary immune-mediated peripheral neuropathies

Journal of the Neurological Sciences, Volume 345, Issues 1–2, 15 October 2014, Pages 184–188 DOI: 10.1016/j.jns.2014.07.040
Kristin Elfa, Håkan Askmarkb, Ingela Nygrenb, Anna Rostedt Pungaa

VitaminDWiki

Vitamin D appears to both prevent and treat diabetes

  • Appears that >2,000 IU will Prevent
  • Appears that >4,000 IU will Treat , but not cure
  • Appears that Calcium and Magnesium are needed for both Prevention and Treatment
    • which are just some of the vitamin D cofactors

Number of articles in both categories of Diabetes and:

  • Dark Skin 22;   Intervention 49;   Meta-analysis 28;   Obesity 26;  Pregnancy 39;   T1 (child) 34;  Omega-3 10;  Vitamin D Receptor 18;  Genetics 10;  Magnesium 18    Click here to see details

Highlights

  • ALL patients with autoimmune peripheral neuropathies (PNP) had vitamin D deficiency.
  • Vitamin D levels were lower in patients with PNP than in healthy controls.
  • Motor neuron disease patients had comparable vitamin D status to healthy controls.
  • We suggest monitoring of vitamin D status in PNP patients.

Purpose
T cells are important in the immunopathology of immune-mediated peripheral neuropathies (PNP) and activated vitamin D regulates the immune response through increasing the amount of regulatory T cells. An association between vitamin D deficiency and polyneuropathy has been stipulated; hence we assessed whether patients with primary immune-mediated PNP have low vitamin D [25(OH)D] levels.

Methods
Plasma levels of 25(OH)D were analyzed in 26 patients with primary immune-mediated PNP, 50 healthy matched blood donors and 24 patients with motor neuron disease (MND). INCAT score was assessed in patients with Guillain–Barré syndrome and chronic inflammatory demyelinating polyneuropathy. ALSFRS-R score was applied to MND patients and the modified Rankin (mRankin) scale compared disability among patient groups.

Results
Mean 25(OH)D value in PNP patients was 40 ± 16 nmol/l, compared to 69 ± 21 nmol/l in healthy blood donors (p < 0.001). MND patients had a higher mean 25(OH)D than PNP patients (59 ± 26 nmol/L; p = 0.006) and comparable levels to healthy blood donors (p = 0.15). Mean 25(OH)D value was not higher in PNP patients with pre-existing vitamin D3 supplementation of 800 IU/day (N = 6; 35 ± 18 nmol/L) than in unsupplemented PNP patients (42 ± 16 nmol). INCAT score ranged from 0 to 10 (mean 3.5) and ALSFRS-R ranged from 11 to 44 (mean 31). mRankin score was more severe in MND patients (mean 3.5) compared to PNP patients (mean 2.1).

Conclusions
All patients with primary immune-mediated PNP were diagnosed with vitamin D deficiency and they had significantly lower 25(OH)D values than healthy control persons and MND patients. We suggest monitoring of vitamin D status in patients with autoimmune PNP, since immune cells are responsive to the ameliorative effects of vitamin D.

Keywords
Guillain–Barre syndrome; Chronic inflammatory demyelinating polyneuropathy; CIDP; GBS; Vitamin D; Autoimmune

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