The steroid metabolism exploration for the diagnosis of Connshing syndrome
- Authors: Paltsman Z.V.1, Shustov S.B.1, Vorokhobina N.V.1, Kalugina V.V.1, Velikanova L.I.1, Kuznetsova A.V.1, Galakhova R.K.1
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Affiliations:
- North-Western State Medical University named after I.I. Mechnikov
- Issue: Vol 16, No 4 (2024)
- Pages: 64-73
- Section: Original research
- URL: https://journal-vniispk.ru/vszgmu/article/view/276652
- DOI: https://doi.org/10.17816/mechnikov636729
- ID: 276652
Cite item
Abstract
BACKGROUND: Reports of the synchronous glucocorticoid-mineralocorticoid activity in patients with Cushing’s syndrome and primary hyperaldosteronism have been found in the literature for fifty years, but there are few evidence-based studies on this issue.
AIM: To study mineralocorticoid and glucocorticoid secretion in patients with unilateral, bilateral tumours and bilateral hyperplasia of the adrenal cortex exploring urine and blood steroid metabolomes by chromatography methods.
MATERIALS AND METHODS: 114 patients with corticotrophin-independent Cushing’s syndrome, autonomous cortisol secretion and primary hyperaldosteronism were examined. The state of the pituitary-adrenal cortex system was assessed by classical methods of immunochemical analysis and functional tests. The corticosteroid metabolomics was studied in biological fluids using high-performance liquid chromatography and gas chromatography-mass spectrometry. In accordance with functional activities and type of hyperplasia, all the patients were divided into 8 subgroups: Cushing’s syndrome and corticosteroma (n = 19), Cushing’s syndrome and bilateral adenomas (n = 9), Cushing’s syndrome and bilateral macronodular hyperplasia (n = 8); autonomus cortisol secretion and unilateral adrenal adenoma (n = 19), autonomus cortisol secretion and bilateral adenomas (n = 14) and autonomus cortisol secretion with bilateral macronodular hyperplasia (n = 11); primary hyperaldosteronism with unilateral aldosteroneproducing adrenal adenoma (n = 15) and bilateral hyperplasia (n = 19). The group of healthy subjects was a control group (n = 22). Family hyperaldosteronism and adrenocortical cancer were excluded. Patients’ urinary corticosteroid excretion and blood steroid levels were compared using the nonparametric Mann–Whitney test.
RESULTS: Chromatographic methods have shown the presence of mineralocorticoid and glucocorticoid co-secretion in the patients with primary hyperaldosteronism: increased urine excretion of free cortisol 51 (27–90) ng/ml (p = 0.001) and its metabolite tetrahydrocortisol — 850 (720–994) μg/24 h (p = 0.0002) in the patients with Conn syndrome. As well as free cortisol 35 (32–72) µg/24 h (p = 0.002), tetrahydrocortisol — 1036 (490–1482) µg/24 h (p = 0.0049), 5α-tetrahydrocortisol — 1194 (411–1873) µg/24 h (p = 0.0048), 5α-tetrahydrocorticosterone — 339 (172–356) µg/24 h (p = 0.0008) in the patients with bilateral adrenal hyperplasia and hyperaldosteronism in comparison with the healthy persons. Glucocorticoid-mineralcorticoid activity was found among the patients with autonomous cortisol secretion and bilateral adrenal tumours: by increased levels of 18-hydroxycorticosterone in blood — 2.7 (1.3–3.5) ng/ml (p = 0.002). The patients with autonomous cortisol secretion and a single tumour had an increase of 18-hydroxycorticosterone in urine — 35 (33–55) µg/24 h (p = 0.0048) in comparison with the healthy subjects. The group of patients with corticotrophin-independent Cushing’s syndrome and unilateral corticosteroma was distinguished from the control group by high level of 18-hydroxycorticosterone in blood — 2.4 (1.0–4.3) ng/ml (p = 0.001) and urine — 42 (30–123) µg/24 h (p = 0.003).
CONCLUSIONS: Mixed glucocorticoid and mineralocorticoid activity of adrenal cortical tumor cells was revealed among the patients with Cushing’s syndrome, with autonomous cortisol secretion and primary hyperaldosteronism using chromatographic methods.
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##article.viewOnOriginalSite##About the authors
Zhanna V. Paltsman
North-Western State Medical University named after I.I. Mechnikov
Author for correspondence.
Email: zhannapaltsman@yandex.ru
ORCID iD: 0009-0005-6683-5494
SPIN-code: 4552-5998
Russian Federation, Saint Petersburg
Sergey B. Shustov
North-Western State Medical University named after I.I. Mechnikov
Email: Sergei.Shustov@szgmu.ru
ORCID iD: 0000-0002-9075-8274
SPIN-code: 5237-2036
MD, Dr. Sci. (Medicine), Professor
Russian Federation, Saint PetersburgNatalia V. Vorokhobina
North-Western State Medical University named after I.I. Mechnikov
Email: natvorokh@mail.ru
ORCID iD: 0000-0002-9574-105X
SPIN-code: 4062-6409
MD, Dr. Sci. (Medicine), Professor
Russian Federation, Saint PetersburgValentina V. Kalugina
North-Western State Medical University named after I.I. Mechnikov
Email: kaluginavav@gmail.com
ORCID iD: 0000-0002-2812-6911
SPIN-code: 3996-7284
MD, Cand. Sci. (Medicine)
Russian Federation, Saint PetersburgLyudmila I. Velikanova
North-Western State Medical University named after I.I. Mechnikov
Email: velikanova46@gmail.com
ORCID iD: 0000-0002-9352-4035
SPIN-code: 5586-4851
MD, Dr. Sci. (Biology), Professor
Russian Federation, Saint PetersburgAlla V. Kuznetsova
North-Western State Medical University named after I.I. Mechnikov
Email: all-kuznetsova@yandex.ru
ORCID iD: 0000-0003-4990-5946
MD, Cand. Sci. (Medicine), Associate Professor
Russian Federation, Saint PetersburgRavilya K. Galakhova
North-Western State Medical University named after I.I. Mechnikov
Email: rgalakhova@gmail.com
ORCID iD: 0000-0003-3599-3199
SPIN-code: 1865-2310
MD, Cand. Sci. (Medicine), Associate Professor
Russian Federation, Saint PetersburgReferences
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