Open AccessChronic inflammatory demyelinating polyradiculoneuropathy induced by paclitaxel
Author(s) -
Isabella Sabião Borges,
João Victor Aguiar Moreira,
Eustaquio Costa Damasceno,
Alencar Pereira dos Santos,
Gabriela Tomás Alves,
Leonardo Peixoto Garcia,
Maria Fernanda Prado Rosa,
Gabriel Nunes Melo Assunção,
Pedro Otávio Rego de Aguiar,
Thaciany Soares Ferreira,
Glauber Mota Pacheco,
Clarice Pereira Sales Oliveira,
Pedro Henrique Pereira Maciel,
João Paulo Moreira Fernandes,
Mateus Barros Bueno,
Rafael Lopes de Souza,
Leonardo Rivelli Silvestre,
Diogo Fernandes dos Santos
Publication year - 2021
Language(s) - English
Resource type - Conference proceedings
DOI - 10.5327/1516-3180.413
Subject(s) - medicine , polyradiculoneuropathy , peripheral neuropathy , paclitaxel , chemotherapy , neuroinflammation , pathology , breast cancer , immunology , cancer , inflammation , endocrinology , guillain barre syndrome , diabetes mellitus
Background: Peripheral neuropathies in cancer are most often due to neurotoxic chemotherapeutic agents. Approximately 30% of patients receiving neurotoxic chemotherapy (CTX) will suffer from chemotherapy-induced peripheral neuropathy (CIPN). Paclitaxel is an extremely effective chemotherapeutic agent for the treatment of breast, ovarian, and lung cancer. However, paclitaxel-induced peripheral neuropathy occurs in 59-87% of patients who receive this drug. Paclitaxel is an anti-tubulin drug that causes microtubule stabilization, resulting in distal axonal degeneration, secondary demyelination and nerve fiber loss. Case: We present a case of a 68-year-old female patient with history of breast cancer who presented sensorial ataxia and progressive muscle weakness two months after starting CTX with paclitaxel. The physical examination showed tetraparesis with proximal predominance, areflexia, severe hypopalesthesia and postural instability. Electroneuromyography showed the existence of asymmetric demyelinating polyradiculoneuropathy, with conduction block and temporal dispersion in practically all evaluated nerves. The cerebrospinal fluid confirmed the albumin-cytological dissociation. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was confirmed and patient underwent monthly treatment with methylprednisolone with good response. Discussion: Evidences has implicated neuroinflammation in the development of PIPN. While most CTX drugs do not cross the blood-brain-barrier, they readily penetrate the blood-nerve-barrier and bind to and accumulate in dorsal root ganglia and peripheral axons. CTX can induce neuroinflammation through activation of immune and immune- like glial cells. In fact, immune cells (e.g., macrophages, lymphocytes) and glial cells (e.g., Schwann cells) in the peripheral nervous system play important role in the induction and maintenance of neuropathy. Conclusion: CIDP should be included in the spectrum of CIPN.