Hemoglobin, erythropoietin and systemic inflammation in exacerbations of chronic obstructive pulmonary disease
AuthorMarkoulaki, D.; Kostikas, K.; Papatheodorou, G.; Koutsokera, A.; Alchanatis, M.; Bakakos, P.; Gourgoulianis, K. I.; Roussos, C.; Koulouris, N. G.; Loukides, S.
Background: Systemic inflammation may represent a possible cause of anemia. Previous data support that anemic patients with COPD present high erythropoietin (EPO) levels, suggestive of EPO resistance, possibly mediated through inflammatory mechanisms. Objectives: We aimed to determine whether systemic inflammation, which is usually up-regulated during exacerbations of COPD (ECOPD) is associated with low hemoglobin levels expressing erythropoietin resistance. Methods: Hemoglobin (Hb), EPO and serum biomarkers of systemic inflammation [CRP, TNF-alpha, fibrinogen and IL-6] were assessed at three time points (admission, resolution and stable phases) in a selected cohort of 93 COPD patients. Results: Hemoglobin levels were significantly lower on admission compared to resolution and stable phases (median 12.1 g/dl [interquartile ranges 11.2-12.7], vs 13.5 [12.4-14.3] vs 13.4 [12.7-14.08], respectively p = 0.002), whereas EPO was significantly higher on admission compared to resolution and stable phases. A negative association between Hb and IL-6 and a positive association between EPO and IL-6 were observed only during the acute phase of exacerbation. EPO and Hb were negatively associated during the acute phase, whereas they were positively associated during discharge and stable phase. Conclusions: In this observational study we have shown that during admission for ECOPD Hb levels are decreased and EPO levels are increased. We have also identified a negative association between Hb and EPO. The above association is mainly related to increased IL-6 levels, indicating a possible EPO resistance through the mechanism of increased systemic inflammatory process. (C) 2010 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.