Chronic immune-mediated diseases of the peripheral nervous system, such as chronic inflammatory
demyelinating polyradiculoneuropathy (CIDP), are primarily characterized by demyelination. To
attenuate persistent inflammation, early, continuous, synergistic vitamin D supplementation, which
reduces immune tolerance, is a standard treatment option for effective treatment. The misguided
autoimmune mechanisms persist for a lifelong. Calcitriol influences the players involved in CIDP, such
as CD4+ helper T cells, CD8+ T cells, B cells, macrophages, T regulatory cells, complement activation,
NLRP3 inflammasomes, and a dysfunctional blood-nerve barrier. 1,25-dihydroxyvitamin D3 is also a
target of the immune-activating, pro-inflammatory cytokines and chemokines involved, such as TNFalpha,
INF-gamma, IL-2, and IL-6. It promotes the formation of the anti-inflammatory cytokine IL-10.
Immunological mechanisms indicate the potentiation of IVIG and glucocorticoid therapy by calcitriol.
The protective effect of vitamin D, added to standard therapy, may offer promise for a more effective
treatment of chronic immune-mediated neuropathies. The use of serum neurofilament light chain (NfL)
and serum glial fibrillary acidic protein (GFAP) determination will reflect the dynamics of the disease
progression and determine the intensity of treatment. The effect of vitamin D supplementation depends
on the individual vitamin D response and the achieved serum 25-hydroxyvitamin D level. All therapeutic
options must be used to slow chronic inflammation, demyelination, and progressive neurological
deterioration in immune-mediated neuropathies.
