Inflammatory markers and symptom burden in patients with multiple myeloma undergoing autologous stem cell transplantation.
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9081 Background: We explored the association between activation of inflammatory networks and development of severe symptoms during mobilization and the acute phase of autologous hematopoietic stem cell transplantation (ASCT) for multiple myeloma (MM). Methods: From mobilization through the first 3 months after ASCT, multiple symptoms were measured repeatedly via the myeloma module of the M. D. Anderson Symptom Inventory (MDASI-MM). Serum levels of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-a, soluble TNF receptors 1 and 2 (sTNF-R1, sTNF-R2), IL-1 receptor antagonist (IL-1RA), vascular endothelial growth factor (VEGF), macrophage inflammatory protein-1 (MIP-1a), monocyte chemoattractant protein (MCP)-1 and C-reactive protein (CRP) were collected up to 11 times per patient and assayed by Luminex. Ordinal regression modeling was used to analyze repeated-measures data. Results: Among50 MM patients, the most severe symptoms reported by werefatigue, pain, muscle weakness, disturbed sleep, drowsiness, numbness, poor appetite, and bone aches. Symptoms worsened rapidly from conditioning therapy and peaked at WBC nadir. Over time, controlling for age, sex, and MM stage, increased serum IL-6 (P=.0007) and MCP-1 (P=.0005) were significantly associated with worsening of the most severe symptoms; MIP-1a (P=.005) and VEGF (P=.002) were inversely associated with these symptoms. Increased CRP was significantly associated with worsening pain (P=.01), fatigue (P=.007), and bone aches (P=.006). Conclusions: This longitudinal study indicates a strong association between dynamic changes in circulating inflammatory molecules and the most severe symptoms in MM patients during the acute phase of ASCT. This observation, similar to IL-6-related multisymptom development around WBC nadir of allogeneic SCT (Wang et al, 2008), provides evidence of potential inflammation-induced behavioral changes in humans. Testing of anti-inflammatory interventions is warranted to further confirm the role of inflammation in the development of symptoms and identify effective mechanism-driven symptom management during ASCT.
