Does diabetes affect paraneoplastic thrombocytosis in colorectal cancer?

Abstract

Background A large variety of factors can affect colorectal cancer (CRC) survival, including type 2 diabetes mellitus (T2DM) and paraneoplastic thrombocytosis. Although several common factors play a role in their development and platelets are damaged in both diseases, the combined relationship of the three conditions was never investigated previously. Methods A prospective, real-life observational cohort study was conducted with the inclusion of 108 CRC patients and 166 voluntary non-CRC subjects. Plasma interleukin-6 and thrombopoietin levels were measured. Results Study participants were divided into cohorts based on the presence of T2DM. Platelet count (p < 0.0500) and interleukin-6 (p < 0.0100) level were significantly higher in the CRC groups. Thrombopoietin level was higher in the T2DM, CRC, and CRC + T2DM groups (p < 0.0500). Analysis of parameter changes over time and survival models revealed that neither platelet count, interleukin-6, nor thrombopoietin levels were affected by T2DM. Death of patients was associated with higher baseline platelet count (p = 0.0042) and interleukin-6 level (p < 0.0001). Conclusion Although the independent, disease-worsening effect of paraneoplastic thrombocytosis and T2DM is known, the coexistence of the two did not further impair the survival of CRC patients, suggesting that T2DM has no significant effect over paraneoplastic thrombocytosis.

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“… 79 This increase can develop for several reasons, such as bleeding from the tumor-reactive thrombocytosis or metabolic changes caused by the tumor itself, called paraneoplastic thrombocytosis. 80 …”

“…79 This increase can develop for several reasons, such as bleeding from the tumor-reactive thrombocytosis or metabolic changes caused by the tumor itself, called paraneoplastic thrombocytosis. 80 The way platelets interact with tumor cells is complex. In the tumor microenvironment, platelets promote angiogenesis and, consequently, the formation of metastatic foci, eg, by releasing vascular endothelial growth factor (VEGF) and transforming growth factor beta (TGF-β).…”