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The Effects of Octreotide on Basal and Stimulated Hormone Levels in Patients with Carcinoid Syndrome^*

Ludwig Institute for Cancer Research (K.Ö.) and the Departments of Internal Medicine (I.N.) and Clinical Chemistry (G.L., L. W.), University Hospital S-751 85 Uppsala
The Department of Clinical Chemistry, Karolinska Hospital (E.T.) S-104 01 Stockholm
The Department of Surgery, Sahlgrenska Hospital (H.A.) S-413 45 Göteborg, Sweden

Address all correspondence and requests for reprints to: Kjell Öberg, Ludwig Institute for Cancer Research, University Hospital, S-751 85 Uppsala, Sweden.

The carcinoid syndrome, a common feature of small intestinal carcinoid tumors with liver metastases, includes flushing, diarrhea, bronchoconstriction, and right heart failure. The etiology of the carcinoid syndrome is not well understood, but serotonin seems to be involved in the diarrhea, whereas tachykinins may play a role in the flush reaction. In a double blind placebo-controlled study, we studied the effect of octreotide in 20 patients with midgut carcinoid tumors and liver metastases. A sc injection of 50 ng octreotide caused a significant (P < 0.001) decrease in median plasma tachykinins and serum pancreatic polypeptide, GH, and insulin for up to 4 h. Administration of octreotide (50 µg, twice daily, sc) caused a 26% decrease in urinary 5-hydroxyindoleacetia acid excretion, butthe number of flushing attacks or bowel movements did not change significantly. A typical flush was provoked by pentagastrin, and plasma tachykinin and serotonin levels were measured. The flush reaction was graded on a 10-point visual analog scale. Octreotide (50 µg, sc) given 45 min before flush stimulation prevented tachykinin release completely and significantly reduced the median flushing score from 8.5 to 2. Placebo administered in the same way did not prevent tachykinin release after pentagastrin administration. Thus, octreotide prevents pentagastrin- induced flushing and the related hormonal changes in patients with the carcinoid syndrome.

^* This work was supported by the Swedish Medical Research Council (Grant 7464), the Swedish Cancer Society (Grant 2313), the Swedish Society for Medical Sciences, funds from the Karolinska Institute, and the Lions Cancer Research Fund.

Received July 15, 1988.

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