Estudo de potenciais marcadores inflamatórios e fator neurotrófico derivado do cerebro na dor neuropática persistente em pacientes oncológicos

Abstract

Introduction: Chemotherapy Induced Peripheral Neurophic Pain (CIPNP) is a serious adverse effect that can persist up to 2 years after discontinuation of antineoplastic treatment. The clinical subordination of the CIPNP involves a loss of the benefits of cancer treatment in addition to a significant impact on quality of life. The pathophysiological mechanisms involved in CIPNP are not yet fully elucidated and generally dependent on the mechanism of action of antineoplastic agents. Neuroinflammation involved the pathophysiology of CIPNP had more and less time discussed. Induction induced by chemotherapy stimulates the infiltration of macrophages and secretion of various cytokines and chemokines. Objective: to evaluate plasma levels of inflammatory markers and brain-derived neurotrophic factor in patients with persistent chemotherapy-induced neuropathy. METHODS: A cross-sectional, analytical and correlational study evaluating 32 cancer patients, 19 of whom had no neuropathic pain and 13 with neuropathic pain, 6 to 9 months after chemotherapy and 23 healthy controls, using a clinical self-report of neuropathic pain symptoms , Short Pain Questionnaires, Questionnaire of Chemotherapy-Induced Neurotoxicity (QNIA), Quality of Life Scale (FACT / GOG-Ntx), Hospital Anxiety and Depression Scale (HAD). Dosages of BDNF, cytokine IL-6 and chemokines CXCL8 / IL-8, CXCL10 / IP-10, CCL2 / MCP-1, CCL5 / RANTES, CXCL9 / MIG and Eotaxin. Results: Cancer patients had a median age of 52.5 years. There was a predominance of women, with a diagnosis of stage II or III breast cancer, in adjuvant treatment mainly with paclitaxel, being the main antineoplastic protocol, Adrianicina, Cycliphosphamide and Paclitaxel (AC-T). 62.5% of the patients presented complaints of pain with moderate to intense intensity. In addition, patients with neuropathic pain had higher rates of sensory and affective pain. In this same group, symptoms of paresthesia and dysesthesia in MMII and MMSS were more present. As well as, higher quality of life scores in subscales physical well-being and neurotoxicity, however, there was no significant difference in the symptoms of depression and anxiety between groups. The presence of neuropathic pain did not differ between the groups without neuropathic pain and control in the concentrations of inflammatory markers and BDNF. However, a reduction in the concentrations of BDNF and CCL2 / MCP1 was found in the group without neuropathic pain compared to the groups with neuropathic pain and control. The CXCL8 / IL8, CCL5 / Rantes and CCL11 / Eotaxin proteins correlated positively with quality of life in the neuropathic pain group. While CCL2 / MCP-1 showed a negative correlation in the group without neuropathic pain. In this same group BDNF correlated negatively with the subscale neurotoxicity. Conclusion: The present study did not show an association between neuropathic pain, inflammatory markers and neurotrophic factor. However, patients with neuropathic pain have higher rates of sensory and affective pain, greater symptoms of paresthesia and dysesthesia in MMII and MMSS, as well as impairment in quality of life