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Zoster pain and vitamine D?
The mechanisms relating to the development of post herpetic neuralgia (PHN) or zoster pain remain uncertain and many different factors are involved. 

Glia, Schwann cells and new targets for neuropathic pain 

Recent attention is focussing on the glia, their receptors and the cytokines they secrete, these all are now known to have a major influence in neuropathic or gliopathic pain. Schwann cells are peripheral glia cells and might also pay an important role in pain states such as postherpetic pain.

Schwann cells become activation in response to infection and trauma and, as central glia, these cells releases a number of neuroexcitatory substances. This goes hand in hand with activation of the nervi nervorum in the peripheral nerves which leads to the release of calcitonin gene related peptide, substance P and nitric oxide.

Therefore Schwann cells and nervi nervorum could be an additional targets for the treatment of postherpetic pain.

Glia modulators in gliopathic pain, topical vitamine D 

The authors then present the drugs potentional useful in the treatment of glial cell activation such as naloxone, naltrexone, minocycline, pentoxifyllline, propentofylline, AV411 (ibudilast) and interleukin 10. All these drugs could be used systemically or even topically.

They state:

High dose topical vitamin D would appear to offer particular promise because vitamin D has the ability to both reduce glial inflammation and reduce nitric oxide production.[1]

Vitamine D and neuropathic pain

Evidence suggests that vitamine D plays a role in glia modulation.[2][3][4][5] In an observational study of diabetic patients type II with neuropathic pain, all 51 patients were 25-hydroxyvitaminD(25D) insufficient, with a mean concentration of 18 ng/mL (insufficient: serum 25D concentration  less than 24 ng/mL).[6] After 3 months of repletion with cholecalciferol (vitamin D3) tablets (mean dose, 2059 IU), Vitamin D repletion resulted in a significant reduction in pain scores on both the VAS and MPQ at −48.5% and −39.4%, respectively. In another study vitamin D deficiency was more prevalent in patients with diabetes type II than the controls.[7]

In our clinic we often treat these intractable pain patients with topical creams, consisting of amitriptyline, ketamine, gabapentine, baclofen and orally with glia modulators such as palmitoylethalonamide. Topical high dose vitamine D might be an interesting treatment option to be explored!

Jan M. Keppel Hesselink, MD, PhD, and David J. Kopsky, MD, November 2010 


Referenties

[1]: Bartley J. | Post herpetic neuralgia, schwann cell activation and vitamin D. | Med Hypotheses. | 2009 Dec;73(6):927-9. Epub 2009 Jul 26.
[2]: Garcion E, Sindji L, Leblondel G, Brachet P, Darcy F. | 1,25-dihydroxyvitamin D3 regulates the synthesis of gamma-glutamyl transpeptidase and glutathione levels in rat primary astrocytes. | J Neurochem. | 1999 Aug;73(2):859-66.
[3]: Kiraly SJ, Kiraly MA, Hawe RD, Makhani N. | Vitamin D as a neuroactive substance: review. | ScientificWorldJournal. | 2006 Jan 26;6:125-39.
[4]: Riaz S, Malcangio M, Miller M, Tomlinson DR. | A vitamin D(3) derivative (CB1093) induces nerve growth factor and prevents neurotrophic deficits in streptozotocin-diabetic rats. | Diabetologia. | 1999 Nov;42(11):1308-13.
[5]: Fukuoka M, Sakurai K, Ohta T, Kiyoki M, Katayama I. | Tacalcitol, an active vitamin D3, induces nerve growth factor production in human epidermal keratinocytes. | Skin Pharmacol Appl Skin Physiol. | 2001 Jul-Aug;14(4):226-33.
[6]: Lee P, Chen R. | Vitamin D as an analgesic for patients with type 2 diabetes and neuropathic pain. | Arch Intern Med. | 2008 Apr 14;168(7):771-2.
[7]: Isaia G, Giorgino R, Adami S. | High prevalence of hypovitaminosis D in female type 2 diabetic population. | Diabetes Care. | 2001 Aug;24(8):1496.
 
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