Mechanistic Involvement of Inflammation in Bortezomib-induced Peripheral Neuropathy.

AIM

The aim of the study was to establish the role of inflammation in bortezomibinduced peripheral neuropathy (BIPN).

BACKGROUND

Peripheral neuropathy is the dose-limiting toxicity of bortezomib that can lead to discontinuation of the treatment. There are multiple mechanisms involved in the disposition of BIPN. However, the role of inflammatory mediators is still under investigation. A complete understanding of inflammatory markers in relation to BIPN can lead to the development of effective therapy for prophylaxis and treatment of peripheral neuropathy.

OBJECTIVE

Based on the available data, the role of inflammatory mediators in the development of peripheral neuropathy due to bortezomib has been postulated.

METHODS

The "Pubmed" and "Google Scholar" were used as the search engines with terms like "peripheral neuropathy", "bortezomib-induced peripheral neuropathy" and "inflammation". Original research, case reports and review articles were considered.

RESULTS

Bortezomib use is associated with the development of peripheral neuropathy. This effect is due to the damage to Schwann cells and dorsal root ganglion neurons, mitochondrial damage, increased ion channel susceptibility, and higher infiltration of macrophages in the spinal cord. All these factors collectively increase the secretion of inflammatory mediators and lead to the development of neuropathic pain.

CONCLUSION

Targeting inflammatory mediators may be helpful in the treatment of bortezomibinduced peripheral neuropathy.