Abstract
We have studied a young untreated patient with low-renin hypertension. All the clinical tests were in normal range, except plasma renin activity, which was low. Also all traditional tests evaluating the adrenal function were normal. A test of supraphysiological ACTH stimulation revealed a partial enzymatic defect of adrenal 11-hydroxylase. The patient has been treated with dexamethasone (0.75 mg once daily), during 4 weeks. At the end of the treatment blood pressure reached normal values. The traditional adrenal function tests are not sufficient to exclude enzymatic abnormalities and their possible involvement in the pathogenesis of hypertension.
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References
Biglieri E.G., Herron M.A., Brust N. 17-hydroxylation deficiency in man. J. Clin. Invest. 45: 1946, 1966.
Biglieri E.G. Adrenal enzymatic defects resulting in hypertension. In: Genest J., Koiw E., Kuchel O. (Eds.), Hypertension. McGraw-Hill, Inc., New York, 1977, p. 789.
Mantero F., Scaroni C., Armanini D., Boscaro M., Fallo F., Masarotto P., Opocher G., Sonino N. Hypertension due to adrenal enzymatic defects. In: Mantero F., Biglieri E.G., Edwards C.R.W. (Eds.), Endocrinology in hypertension. Academic Press, London, New York, 1982, p. 111.
Honda M., Nowaczynski W., Guthrie G.P. jr., Messerli F.H., Tolis G., Kuchel O., Genest J. Response of several adrenal steroids to ACTH-stimulation in essential hypertension. J. Clin. Endocrinol. Metab. 44: 264, 1977.
De Simone G., Tommaselli A.P., Rosi R., Valentino R., Lauria R., Scopacasa F., Lombardi G. Partial deficiency of adrenal 11 -hydroxylase. A possible cause of primary hypertension. Hypertension 7: 204, 1985.
Melby J.C., Dale S.L., Grekin R.J., Gaunt R., Wilson T.E. 18-hydroxy-deoxycorticosterone (18-OHDOC) secretion in experimental and human hypertension. Recent Prog. Horm. Res. 28: 287, 1972.
Haruyama K., Yamazaki M., Toki T., Fukuchi S. Two cases of low-renin hypertension thought to be due to excessive secretion of unknown mineralocorticoid. Jpn. Cire. J. 46: 156, 1982.
Chamontin B., Ribot C., Guttard J., Bayard F., Salvador M. Hypertension arterielle de la jeune femme controlée par glucocorticoide. Arch. Mal. Coeur 37: 91, 1980.
Newsome H.H. jr., Clements A.S., Borum E.H. The simultaneous assay of cortisol, corticosterone, 11 — deoxycortisol, and cortisone in human plasma. J. Clin. Endocrinol. Metab. 34: 473, 1972.
Dahl L.K. Sait and hypertension. Am. J. Clin. Nutr. 25: 231, 1972.
Henry J.P. Stress and salt-intake in hypertension. Psychosom. Med. 35: 276, 1973.
Pang S., Levine L.S., Lorenzen F., Chow D., Pollack M., Dupont B., Genel M., New M.I. Hormonal studies in obligate heterozygotes and siblings of patients with 11-beta-hydroxylase deficiency congenital adrenal hyperplasia. J. Clin. Endocrinol. Metab. 50: 586, 1980.
Hermus A.R., Pieters G.F., Smals A.G., Benraad T.J., Kloppenborg P.W. Plasma adenocorticotropin, cortisol and aldosterone responses to corticotropin-releasing factor: modulatory effect of basal cortisol levels. J. Clin. Endocrinol. Metab. 58: 187, 1984.
Hoefnagels W.H., Drayer J.I., Smals A.G., Benraad T.J., Kloppenborg P.W. Nocturnal, daytime and postural changes of plasma aldosterone before and during dexamethasone in adenomatous and idiopathic aldosteronism. J. Clin. Endocrinol. Metab. 51: 1334, 1980.
Ganguly A., Pratt J.H., Weinberger M.H., Grim C.E., Fineberg N.S. Differing effects of metoclopramide and adrenocorticotropin on plasma aldosterone levels in glucocorticoidsuppressible hyperaldosteronism and other forms of hyperaldosteronism. J. Clin. Endocrinol. Metab. 57: 388, 1983.
Biglieri E.G. Syndrome of primary aldosteronism and hypertension. In: Mantero F., Biglieri E.G., Edwards C.R.W. (Eds.), Endocrinology in hypertension. Academic Press, London, New York, 1982, p. 69.
Nowaczynski W., Kuchel O., Genest J., Messerli F.H., Honda M., Tolis G., Seth K., Parvin-Pande R., Kubo S., Grose J., Ledoux F., Lebel M. Dynamic aldosterone and 18-hydroxydeoxycorticosterone studies in labile and stable benign essential hypertension. J. Steroid Biochem. 6: 767, 1975.
Mitra S., Genuth S.M., Berman L.B., Vertes V. Aldosterone secretion in anephric patients. N. Engl. J. Med. 286: 61, 1972.
Messerli F.H., Genest J., Nowaczynski W., Kuchel O., Honda M., Latour Y., Dumont G. Splanchnic blood flow in essential hypertension and in hypertensive patients with renal artery stenosis. Circulation 51: 1114, 1975.
Edwards C.R.W., Al-Dujaili S., Boscaro M., Gow I., Williams B.C. Peptidergic and monoaminergic regulation of aldosterone secretion. In: Mantero F., Biglieri E.G., Edwards C.R.W. (Eds.), Endocrinology of hypertension. Academic Press, London, New York, 1982, p. 11.
Carey R.M., Ayers C.R. Labile hypertension. Precursor of sustained hypertension? Am. J. Med. 61: 811, 1976.
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Tommaselli, A.P., De Simone, G., Di Lorenzo, L. et al. Low-renin primary hypertension in a young patient treated with dexamethasone. J Endocrinol Invest 9, 77–81 (1986). https://doi.org/10.1007/BF03348069
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DOI: https://doi.org/10.1007/BF03348069