Winkelmann W, Deuss U, Allolio B, Hummerich W, Kaulen D, Brosch H, Guyot A, Arnold C
Klin Wochenschr. 1984 Nov 2;62(21):1018-24. doi: 10.1007/BF01711724.
We measured basal and dexamethasone-suppressed plasma ACTH in 246 patients with bronchogenic carcinoma (105 with small-cell carcinoma); in 138 of these patients (67 with small-cell carcinoma) basal and pentagastrin-stimulated serum calcitonin was also determined. In addition, in a subgroup of 120 patients (58 with small-cell carcinoma) plasma ADH with reference to plasma osmolality was also assayed. Non-suppressible plasma ACTH was found in 45% of patients with small-cell carcinoma but only in isolated cases of large-cell carcinoma, adenocarcinoma, and squamous-cell carcinoma. Serum calcitonin was increased in 28% of patients with small-cell carcinoma but only in few patients with other tumor types. Stimulation of calcitonin by pentagastrin was ineffective. Plasma ADH was inappropriately high in 47% of patients with small-cell carcinoma. Strikingly high also was the incidence of increased ADH concentrations in patients with large-cell (40%), adenocarcinoma (46%), and squamous-cell carcinoma (29%). By measuring plasma ACTH after dexamethasone suppression and ADH with reference to osmolality, the sensitivity of these tumor markers in detecting pathological hormone secretion is markedly increased. In small-cell carcinoma the simultaneous measurement of ACTH, ADH, and calcitonin gives a high yield of positive results (74%), indicating that this set of tumor markers is a promising aid in diagnosis and therapy control.
