Levels of NT‑proBNP in patients with cancer

Oncol Lett. 2023 May 16;26(1):280. doi: 10.3892/ol.2023.13866. eCollection 2023 Jul.

Abstract

At present, it is well known that natriuretic peptides may be produced by cancer cells. Stimulation of N-terminal pro B-type natriuretic peptide (NT-proBNP) synthesis may be a reaction to activity of several proinflammatory cytokines. NT-proBNP is also a marker of myocardial damage during cardiotoxic chemotherapy by anthracyclines. The present study aimed to analyze the association between NT-proBNP and patient/disease characteristics in patients without cardiac symptoms. The present clinical study included 112 patients with cancer who were undergoing anticancer therapy between December 2017 and December 2021. From each patient, peripheral blood was obtained for detection of NT-proBNP before any therapy, after therapy and 1 year after the first sample. NT-proBNP was examined using an immunochemical method. The mean ± SEM value of NT-pro-BNP in the first, second and third sample was 561.0±75.1, 1,565.4±461.1 and 1,940.7±581.1 ng/l. A total of 15 (13.4%), 27 (24.1%) and 25 (30.1%) patients had elevated levels of NT-pro-BNP in the first, second and third sample above the normal value adjusted to age. It was observed that NT-proBNP was increased in older patients and in patients with progressive metastatic disease with poor prognosis. Patients with non-elevated NT-proBNP in the second and third sample had significantly improved OS compared with patients with elevated NT-proBNP [hazard ratio (HR), 0.47; 95% CI, 0.26-0.85; P=0.002 for the second sample; and HR, 0.29; 95% CI, 0.14-0.60; P=0.0000007, for the third sample]. The baseline NT-proBNP value was not prognostic for OS (HR, 0.98; 95% CI, 0.50-1.92; P=0.96). The present results suggest that the level of NT-proBNP was associated with the extent of oncologic disease. Higher levels were associated with progression of metastatic disease and shorter overall survival.

Keywords: N-terminal pro B-type natriuretic peptide; biomarker; cancer; inflammation; progression.

Grants and funding

The present study was supported by Slovak Research and Development Agency (contract no. APVV-15-14-0086 and APVV-19-0411 and VEGA 1/0327/19).