Endocrine Abstracts

Introduction: Carcinoid heart disease (CHD) develops in patients with small bowel NETs with carcinoid syndrome. Currently NT-proBNP (NTP) is suggested as the best current biomarker to screen for CHD and monitor heart failure. A number of other markers have been investigated for heart failure, however, none of these have been explored in NET patients with CHD or carcinoid syndrome. Galectin-3 (GAL3) promotes fibroblast proliferation and correlates with worse outcomes in heart failure. Adrenomedullin is elevated in heart failure and Calprotectin is an inflammatory protein increased in heart failure. ST-2 is an interleukin-1 receptor that signals for severity of cardiac remodelling and tissue fibrosis. In this study we have assessed these markers in three cohorts of NET patients to determine how they compared with NTP.

Methods: About 3 groups of sbNET patients (n=37) were identified with blood released from the King’s College Hospital Institute of Liver Studies biobank; CHD (Group A, n=10), non-functional (Groups B, n=12, normal CgA, 5HIAA, BNP), functional (Group C, n=15, elevated chromogranin A (CgA) & urine 5HIAA, normal BNP). Analysis was performed using NTP, GAL3, ST2, calprotectin and adrenomedullin assays. Statistical analysis was performed with SPSS.

Results: The median values for NTP in the CHD cohort was above the 260 pg/ml cut off. Median values for calprotectin were elevated across all three groups. ST2, GAL3 and adrenomedullin were not elevated. The Kruskal–Wallis test across the 3 patient groups was significant for NTP (P=<0.001) but not for ST2, GAL3, adrenomedullin and calprotectin. The Mann-Whitney U-test was significant (P<0.05) between the CHD and both other groups but was not significant (P=0.12) between the functional and non-functional groups. There was significant correlation between GAL3 and calprotectin.

Discussion: The results corroborate the role of NTP in CHD for NET patients. ST2 may play a role in combination with NTP for risk stratification in CHD and heart failure. GAL3 requires further evaluation given its possible role in the development of cardiac fibrosis. Its value may be for screening at an earlier stage of CHD.