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Tachykinins in Carcinoid Tumors: Their Use as a Tumor Marker and Possible Role in the Carcinoid Flush^*

Department of Internal Medicine, University Hospital (I.N., K.O.), Uppsala; and the Department of Clinical Chemistry, Karolinska Hospital (E.T.-N.), and the Department of Pharmacology, Karolinska Institute Stockholm, Sweden

Address all correspondence and requests for reprints to Dr. Ingrid Norheim, Department of Internal Medicine, University Hospital, S- 751 85 Uppsala, Sweden.

The plasma concentrations of various tachykinins were measured before and during flushing episodes in 16 patients with metastatic carcinoid tumors. The flushing attacks were induced by iv injection of pentagastrin or ingestion of food or alcohol. Tachykinins, such as neurokinin A (NKA) and neuropeptide K (NPK), increased 2-fold during flushing episodes in 12 patients, and the plasma concentrations of substance P increased to a varying extent in 3 patients. Chromatographic analysis of plasma samples taken before and during flushing episodes in 2 patients indicated the presence of individual spectra of tachykinins. In addition, the plasma concentration of tachykinin [TKLI(K12)], using an assay that detects NKA, NPK, kassinin, eledoisin, and NKB, but not substance P and physalemin, and the urinary excretion of 5-hydroxyindole acetic acid (5-HIAA) were measured in 20 patients with midgut carcinoid tumors before and during treatment with human leucocyte interferon. The overall changes in the 2 tumor markers were concordant in 18 of the 20 patients. Thus, the Spearman correlation coefficient between the percent changes in urinary 5- hydroxyindole acid excretion and plasma TKLI(K12) was 0.54 (P < 0.001). The patients who had a decrease in the tumor markers also had a decrease in flushing episodes and diarrhea. Plasma TKLI(K12) is a convenient tumor marker for the diagnosis and follow-up of patients with carcinoid tumors of midgut origin. The combined use of both tumor markers strengthens the diagnosis and may improve the evaluation of response during treatment. (J Clin Endocrinol Metab 63: 605, 1986

^* This work was supported by the Swedish Medical Research Council (O3X-07464); Swedish Cancer Research Fund (1925-B85-O2XA); Nordisk Insulinfond; Konung Gustav 5:s jubileumsfond (84556); Smith Cline, and French; Swedish Society for Medical Sciences; funds of the Karolinska Institute; and funds of Uppsala Univeristy.

Received December 10, 1985.

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