Our previous work has suggested impaired DNA repair efficiency in multiple sclerosis (MS), a central demyelinating disease. We examined if a similar pathomechanism is present in CIDP, a demyelinating disease of the peripheral nervous system.

We found increased oxidative DNA damage in CIDP and MS patients compared to the controls and observed statistically higher PMBC sensitivity to TBH (MS-25.3%, CIDP-19.57% vs 10.6% in controls, p<0,05). We observed elevated levels of endogenous DNA lesions in CIDP patients that we did not notice in MS patients and controls (CIDP-11.27%, MS- 2.3% vs 2.81% in controls, p<0.05). Examination of the repair kinetics between groups revealed that the DNA lesions induced by TBH were more efficiently repaired in controls than in CIDP and MS patients (p<0.05).

The preliminary data suggest an elevated level of endogenous oxidative DNA lesions in PBMCs that occurs in CIDP but not in the clinical course of MS. We observed increased susceptibility to oxidative factors and delayed repair efficiency in both of these demyelinating conditions. Further studies are needed to understand the role of DNA damage and repair in peripheral nerve demyelination in CIDP.