Title

Relationship of cytokines to symptom distress and symptom clusters among non-small-cell lung cancer patients receiving gefitinib treatment: A pilot study

Document Type

Article

Publication Date

1-1-2014

Abstract

Purpose: Several cytokines involved in the development of sickness behaviors are considered to be related to the development of cancer symptoms. However, the mechanism of cytokines' involvement in symptom relief with gefitinib treatment remains unknown. This study analyzed the relationships between single symptoms/symptom clusters and cytokines in patients with advanced non-small-cell lung cancer (NSCLC) at pretreatment and at 1 month, 3 months, and 6 months after gefitinib treatment. Methods: Fifty-seven patients with NSCLC were recruited via convenience sampling from a group of thoracic oncology patients in Northern Taiwan. Research measures included the use of the M.D. Anderson Symptom Inventory-Taiwan form and enzyme-linked immunosorbent assays. Statistical analyses included descriptive statistics and generalized estimating equation analysis. Results: Positive relationships were observed between interleukin (IL)-2 and nausea (p<0.01), distress (p< 0.05), drowsiness (p<0.01), lack of appetite (p=0.01), sum of symptom severity scores (p<0.01), and a gastrointestinal symptom cluster (p<0.01). Positive relationships between IL-6 and sadness (p<0.05), lack of appetite (p<0.05), and pain (p=0.014), and a negative relationship between IL-6 and difficulty remembering (p<0.05) were also observed. In addition, positive relationships were observed between IL-10 and fatigue (p<0.01), lack of appetite (p<0.01), drowsiness (p<0.01), sadness (p< 0.05), sum of symptom severity scores (p< 0.01), and a general symptom cluster (p<0.01). Conclusion: These results may provide a basis for understanding possible mechanisms of symptom distress in patients with NSCLC; this may possibly lead to the identification of a target for effective symptom management, i.e., focusing on the inflammation pathway for the treatment of detrimental effects of cytokine-induced inflammatory responses. © 2014.

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