1155P - Niacin (vitamin B3) suppletion in patients with serotonin producing neuroendocrine tumors

Date 27 September 2014
Event ESMO 2014
Session Poster Display session
Topics Neuroendocrine Cancers
Supportive measures
Presenter Grietje Bouma
Citation Annals of Oncology (2014) 25 (suppl_4): iv394-iv405. 10.1093/annonc/mdu345
Authors G. Bouma1, M. van Faassen2, E. De Vries1, I. Kema2, A. Walenkamp1
  • 1Medical Oncology, University Medical Center Groningen, 9713 GZ - Groningen/NL
  • 2Clinical Chemistry, University Medical Center Groningen, 9713 GZ - Groningen/NL



Serotonin is derived from the essential amino acid tryptophan. Tryptophan is also a precursor of niacin (vitamin B3) which is critical for normal cellular metabolism. In case of excessive serotonin production by neuroendocrine tumors (NETs), tryptophan and/or niacin can be deficient in these patients leading to symptoms including pellagra. Suppletion of tryptophan might facilitate serotonin production and is therefore undesirable in patients with serotonin producing NETs. In malnourished people, pellagra is effectively treated with niacin suppletion. However, in serotonin producing NET patients data on niacin status are scarce and suppletion of niacin receives hardly attention. We therefore aimed to assess niacin status before and after niacin suppletion in serotonin producing NET patients.


We identified serotonin producing NET patients based on elevated platelet serotonin and/or urinary 5-hydroxyindolacetic acid (5-HIAA) levels, who had received niacin suppletion (mean dose 144 mg daily) for low plasma tryptophan levels and/or pellagra associated symptoms. Pre-suppletion plasma tryptophan levels and niacin status based on the urinary niacin metabolite N1-methylnicotinamide (N1-MN) before (n = 42) and after suppletion (in 34 paired samples) were assessed. Healthy individuals (n = 133) served as controls.


The mean pre-suppletion plasma tryptophan level was 32 ± 11 µmol/L (reference value 40-70 µmol/L). Pre-suppletion N1-MN levels were lower in patients (median 17.9 µmol/24 h, range 2.6-70) compared to controls (median 43.7 µmol/24 h, range 9.5–169.3, p < 0.0001). Before suppletion niacin levels were below normal in 45% of the patients. Urinary 5-HIAA level negatively correlated with niacin status (p = 0.022, r = -0.352). Niacin suppletion increased N1-MN levels to high normal levels (median 55.4 µmol/24 h, range 7.4–489) in 86% of the niacin deficient patients.


In serotonin producing NET patients low niacin status is prevalent and therefore, N1-MN deserves to be included in standard biochemical evaluation. Niacin suppletion in serotonin producing NET patients normalizes niacin status in most niacin deficient patients. A prospective study is warranted.


All authors have declared no conflicts of interest.