SFEBES2015 Poster Presentations Neoplasia, cancer and late effects (31 abstracts)
Somatostatin responsive ACTH and precursor excess in a midgut mesentery NET
G K Dimitriadis 1, , A Nasoodi 1 , S Khan 1 , W Shatwell 1 , L Chambers 1 , C Tomkins 1 , C Darby 1 , K Gopalakrishnan 1 , H S Randeva 1, , N Murthy 1 & M O Weickert 1,
1University Hospitals Coventry and Warwickshire, The Arden NET CoE, WISDEM centre, Coventry, West Midlands, UK; 2Warwick Medical School, University of Warwick, Coventry, West Midlands, UK.
Introduction/Background: ACTH production from a midgut mesentery NET is extremely rare (1). A 62y old woman presented with hypokalaemia (2mmol/L) and hyperpigmentation, 11y after surgery of a pT3N1Mx non-functional G1 NET with SRS positive, non-resectable but stable, residual mass encasing mesenteric vessels. Serum cortisol (3261 nmol/L), ACTH (796 ng/L), CgA (530 pmol/L) and urine total cortisol metabolites (33920 μg/24h) including 14 sub-products indicated change of biological behaviour into a functioning NET. Pituitary or pulmonary sources were excluded.
Aims: To test somatostatin (SS) responsiveness on ACTH excess.
Materials and methods: A test dose of SS 100 μg s.c. was applied.
Results: SS resulted in rapid (300 min) improvement of ACTH (222.9 ng/l), cortisol (1700 nmol/l), urine cortisol metabolites (620 min; 4620 μg/24 h) and K+(3.2 mmol/l; 48 h); followed by resistance after 3 wk (cortisol 6362 nmol/l, ACTH 617 ng/l; pro-ACTH and POMC 140; ULN<40 pmol/l), despite SS dose intensification and adding ketoconazole/metyrapone for cortisol excess; resulting in a L3 fracture, reduced mobility and subsequent fatal pneumonia.
Conclusion: Considering the 1–10% cross-reaction of ACTH precursors in ACTH assays (2), precursors were not sufficiently elevated to account for the observed ACTH excess, suggesting production of ACTH precursors by the NET and processing them to ACTH. Treatment with somatostatin was efficient in this context, at least in the short term.
References
(1) Fasshauer et al. BMC Cancer 2006.
(2) Stovold et al. Br J Cancer 2013.
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Endocrine Abstracts
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