Volume 6, Issue 8 , Pages e27-e28, August 2008
Carcinoid Syndrome Unmasked by Fluoxetine, a Selective Serotonin Reuptake Inhibitor
Article Outline
A 55-year-old man presented in 1995 with colicky abdominal pain, associated with bloating and borborygmi during a 6-month period. Clinical examination, routine blood tests, abdominal ultrasound scan, and barium enema were normal, and it was thought likely that his symptoms were due to irritable bowel syndrome, and he was discharged.
Two months later his general practitioner referred him back to the clinic. He had started the patient on fluoxetine for depression. The patient had immediately noticed that his previous symptoms had worsened as well as the development of diarrhea and subsequent weight loss. A small-bowel study was carried out (Figure A). A repeat ultrasound at this time revealed a 5-cm lesion in the right lobe of the liver. At subsequent laparotomy there was severe small-bowel distention with visible collapse of the distal ileum. A stenotic lesion was resected.
After surgery and having stopped his selective serotonin reuptake inhibitor (SSRI), he became essentially asymptomatic, despite a gradual increase in the size of his liver lesion to 10 cm. In 2002 he presented for urgent review at the clinic. He reported a sudden deterioration in his condition, with more severe flushing, diarrhea, and an increase in facial color (Figure B). On further questioning it became apparent that his general practitioner had restarted fluoxetine 10 days previously. This was immediately stopped, and his symptoms rapidly improved and have remained settled during ongoing follow-up.
Discussion
This patient's histology confirmed that he had a small-intestinal carcinoid tumor (stricturing lesion on small-bowel study) with lymph node and liver metastases. The small-bowel study also revealed gross proximal dilatation. Figure B shows the classic facial discoloration with telangiectasia.
Carcinoid tumors are responsible for a variety of effects on the gastrointestinal tract, either locally from the tumor itself or systemic and related to the production of biogenic amines, primarily serotonin, from metastases usually within the liver. The systemic symptoms, predominantly diarrhea and flushing, comprise the carcinoid syndrome.
On 2 occasions in this case there was a temporal relationship between starting fluoxetine, an SSRI, and deterioration in symptoms. It seems logical that this deterioration should occur. SSRIs are not neurospecific and increase serotonin levels throughout the body. Approximately 90% of serotonin stores are located within the gastrointestinal tract in conjunction with a high concentration of serotonin-sensitive cells.1 Were this patient's exacerbations simply a result of increased circulating serotonin levels, or could there have been positive feedback promotion of tumor growth?
The case also raises 3 points for the future management of carcinoid patients. First, increasing numbers of patients with irritable bowel symptoms are being prescribed SSRIs. We suggest that any subsequent deterioration in their symptoms should provoke a further search for carcinoid disease. Second, as many as 50% of carcinoid patients have depression,2 and physicians should be aware of the need to avoid SSRIs in the treatment for this. Last, is it possible that SSRIs could have a role as a provocation tool in the often elusive diagnosis of carcinoid?
References
PII: S1542-3565(08)00340-6
doi:10.1016/j.cgh.2008.04.010
© 2008 AGA Institute. Published by Elsevier Inc. All rights reserved.
Volume 6, Issue 8 , Pages e27-e28, August 2008
