Serum thyroid-hormone binding prealbumin (TBPA) and cancer

130s c-094 NEW DATA Oh'THE ADRENAL-POSTP~TUITARYI~BA~CE IN CANCEROUS PATIENTS AND ITS CORRECTION. Bernard-Weil E., Vayre P., Pertuiset B., Legrand S. (CHU Piti&-SalpZtri&e,F-75013 Paris) I-Vasopressin (VP) was one of the first polypeptidic growth factor identified. As corticoids had in general anti-mitogenic effects in vitro, one could wonder if an imbalance between both categories of hormones would play a role in the development of cancerous disease. We performed new investigations in 10 patients with malignant tumor of the digestive tract and in 10 controls, by means of measures of plasmatic rates of cortisol (P), aldosterone, RIA-ADH and free water clearance (CfHZO), during a water load test (20 ml/kg), at 0, 2 and 4 hours. We observed: 1") higher significant values of F in cancerous subjects, i.e. 212 + 8.3, 145.9 2 5.5, 148.3 + 7.6 ng/ml 2 127.5 f 5.5, 61.5 + 2.9, 56.5 2 2.3 ng/ml; 2') h'ighersignificant values of ADH (at 2 hours), i.e. 6.9 + 2.3, 5.8 + 2.7, 4.8 + 1.8 pg/ml vs 4.6 + 3.2, 2.7 + 1.8, 4.0 + 2.0 pgfml; 3") no significant ';iifference values of aidoste&$e; ?Q lower significznt values Gf CfH20, i.e. 1.1 + .2 ml/mn vs 2.7 + 1.1 mlfmn for the first two hours. It was concluded that there was inthe cazcerous patients-an excess of ADH and F, but also an excess of AIM in relation to F, owing to the diuresis changes. Such results, that confirm other similar researches in various types of cancer, should be considered together with the data about the opposite actions of ADH and F upon cell mitosis. IX-To check this imbalance, our computer researches with a mathematical model of the adrenalpostpituitary system gave rise to a therapy combining corticoids and VP. Ten patients with recurrent malignant brain tumors, not improved by high doses of corticoids, received an association of F, VP (at physiological doses) and dexamethasone (at moderate doses of 5 mg/24 h): all the patients showed a more or less change in the CT-scans at short term (15 days) or middle term (9 months), concerning edema, contrast enhancement, tumor volume. Such preliminary results could lead to other attempts in order to modify the endocrine imbalance in caucerous patients. c-095 SERUMTHYROID-HORMJNE BINDING PREXBWIN (TBPA) AND CANCER. L. Li Calzi, S. Eenvenga and F. Trimarchi. Clinica Medica & Semeiotica Medica I, University of Messina, School of Medicine, 98100 Messina, Italy. A wide spectrum of stressful and debilitating conditions, such as trams, bums, surgery, malnutrition, infl.amMtoryand neoplasticprocesses are associated with a drop of TBPA in blocxl. Recently we have developed an accurate, precise and remarkably sensitive RIA for hm Tf%PA(Ann,Cli.Lab.Sci.16:231.1986). with which we have-measured senm~ TBPA Levels in 96 patients (age: 58.4,tiO.9.&rs,mfsD) affected by cancer (pituitary, breast, esophagus, stcmach, colon-rectum, liver, pancreas, thyroid, lung, pleura, non-Hodgkin's lynphanas, chronic myeloid leukemia and polycythemia). TBPA levels in the whole group were significantly (P
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C-096 CORRECTION ETOMIDATE

NORMAL

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OF SEVERE TUMOR-INDUCED HYPERCORTlSOLlSM BY LOW-DOSE NON-HYPNOTIC TREATMENT: ADRENAL RESPONSES IN PATIENTS WITH CUSHINGS SYNDROME AND

VOLUNTEERS.

Schulte,H.M., Allolio, 8. Sippell, W.G., and Ohnhaus, E.E., 1. MedizinischeKlinikund Kinderklinik der Universitat zu Kiel, II. Medizinische Klinik der Universitat zu KBln, F.R. Germany Etomidate (Eta)is a short-acting,imidazole-derived hypnoticagent,widely used for the induction of anesthesia, causing adrenocortical suppression by blockade of the two cytocrome P- 450 dependent Patients with severe endogenous adrenal enzymes llR hydroxylase and desmolase. However, hypercortisolism due to Cushing’s syndrome may benefit from rapid reduction of cortisol secretion to improve their clinical status. We administered Eto to 6 patients with severe hypercortiso~ism for 24 hours. The botus dose of Eto 0.03 mglkg i.v. was foi~owed by a constant infusion of 0.3 m~~kgJbour via an infusion pump. Serum to 12 ugldl until IR-cortisol levels fell from 49 to 7 ug/dl after 11 h and ranged from undetectable etomidate infusion was stopped. Urinary free cortisol excretion decreased from 427 to 67 ug/24 h after Eto and recovered the second day after. Three doses of Eto (0.03; 0.1; 0.3 mg/kg/hour) were administered for 5 hours to a total of 15 normal volunteers in a random order, preceeded by a loading dose of 0.03 mg/kg at 0800 am. ACTH (0.25 mg) was injected at the end of the infusion. Serum IR- cortisol declined rapidly in a dose dependant fashion and rose again after ACTH stimulation only after the lowest Eto- dose. We also measured desoxycosticosterone (DOC), corticosterone (8) and 11-desoxycortisol (S). While B declined in a similar pattern as cortisol, DOC and S showed an inverse course. No side effects were noted. In conclusion, fast correction of severe hypercortisolism seems to be possible with etomidate in a nonsedative dose of 0.1 mg/kg/h.