Plasma Adiponectin Concentrations in Relation to Chronic Lymphocytic Leukemia and Chronic Myeloproliferative Diseases.

Adiponectin, an adipocyte-secreted hormone, is closely and inversely associated with insulin resistance. Adiponectin suppresses the expression of adhesion molecules in vascular endothelial cells and cytokine production from monocytes/macrophages, thus inhibiting the inflammatory processes. In addition, it is an important negative regulator in immune systems and hematopoiesis that suppressed colony formation from colony forming unit granulocyte and macrophage. For these immunological effects of adiponectin, we hypothesized that decreased adiponectin levels might underlie the association between chronic lymphocytic leukemia (CLL) and chronic myeloproliferative diseases (CMPD), and investigated the levels of adiponectin in patients with 19 CLL and 30 CMPD (14 chronic myelogenous leukemia, 9 polycythemia vera, 4 myelofibrosis, 2 essential thrombocythemia), and compared with age, sex, body mass index match controls. Adiponectin levels in patients with CLL were significantly lower than the controls (4.71±1.33 μg/ml vs. 16.61±3.91 μg/ml; p<0.001). Also, the levels of adiponectin in patients with CMPD were significantly lower than the controls (8.95±2.64μg/ml vs. 17.16±4.77 μg/ml; p<0.001). According to the comparison of interferon (IFN) therapy and non-IFN therapy of the patients with CMPD, plasma adiponectin levels in IFN therapy patients were significantly higher than in non-IFN therapy patients (11.03±1.39μg/ml vs. 6.87±1.79 μg/ml; p<0.001). The results show that adiponectin is lower in patients with both CML and CMPD. These results suggest that lymphopoiesis and myelopoiesis is negatively influence of adiponectin level and its possible role may be related with inflammatory cytokine (eg: TNF, IL-6) release. Also, IFN therapy that suppressed of inflammatory cytokines in patients with CMPD is positively influenced of adiponectin secretion. Future studies are needed to prove causality and provide insight on the mechanism of action of this hormone and its potential role in CML and CMPD.