scholarly journals The role of high performance liquid chromatography in the functional state of the adrenal glands before and after surgical treatment for corticosteroma

2020 ◽  
Vol 11 (2) ◽  
pp. 30-37
Author(s):  
M. O. Buinova ◽  
N. V. Vorokhobina ◽  
L. I. Velikanova ◽  
E. G. Strelnikova ◽  
V. L. Baranov

Objective: It is to evaluate the functional state of the adrenal cortex after surgical treatment in patients with corticosteromas for optimize of tactic of postoperative management.Materials and methods: We examined 143 patients (43 men and 100 women) aged 51.3 ± 10.1 years with incidentaloma of adrenal glands and 27 healthy peopels (control group) aged 45.5 ± 5.7 years. Cushing's syndrome was detected in 22 patients, autonomous cortisol secretion was detected in 43. All patients had an analysis of the complaints, objective, laboratory and instrumental data in the preoperative and early postoperative periods. Assessment of levels glucocorticoid and mineralocorticoid hormones in biological fluids was carried out by immunoassay and high performance liquid chromatography.Results: The signs of adrenal cortex insufficiency in the early postoperative period were obtained in 77.3% of patients with Cushing's syndrome and in 25% of patients with autonomous cortisol secretion according to immunoassay and high performance liquid chromatography. An increase of level of corticosterone in the serum of blood in the preoperative period indicate the possibility development of adrenal insufficiency in the early postoperative period in all patients. Аn increase of levels of 11-deoxycortisol and 18-OH-corticosteronein in the serum of blood аnd urinary excretion of free cortisone, 18-OH-corticosterone and 6β-hydroxycortisol indicate the possibility development of adrenal insufficiency in the early postoperative period in patients with Cushing's syndrome.Conclusions: The determination of cortisol and aldosterone precursors by high performance liquid chromatography increases the accuracy of the diagnosis of glucocorticoid and mineralocorticoid function of the adrenal cortex in patients with Cushing's syndrome and with autonomous cortisol secretion in the early postoperative period.

2015 ◽  
Vol 172 (6) ◽  
pp. 677-685 ◽  
Author(s):  
Anne Thiel ◽  
Anna-Carinna Reis ◽  
Matthias Haase ◽  
Gerald Goh ◽  
Matthias Schott ◽  
...  

ObjectiveCortisol excess due to adrenal adenomas or hyperplasia causes Cushing's syndrome. Recent genetic studies have identified a somatic PRKACAL206R mutation as a cause of cortisol-producing adenomas. We aimed to compare the clinical features of PRKACA-mutant lesions with those of CTNNB1 mutations, and to search for similar mutations in unilateral hyperplasia or tumors co-secreting aldosterone.Design, patients, and methodsIn this study, 60 patients with cortisol excess who had adrenalectomies at our institution between 1992 and 2013 were assessed, and somatic mutations were determined by Sanger sequencing. A total of 36 patients had overt Cushing's syndrome, the remainder were subclinical: 59 cases were adenomas (three bilateral) and one was classified as hyperplasia. Four tumors had proven co-secretion of aldosterone.ResultsAmong cortisol-secreting unilateral lesions without evidence of co-secretion (n=52), we identified somatic mutations in PRKACA (L206R) in 23.1%, CTNNB1 (S45P, S45F) in 23.1%, GNAS (R201C) in 5.8%, and CTNNB1+GNAS (S45P, R201H) in 1.9%. PRKACA and GNAS mutations were mutually exclusive. Of the co-secreting tumors, two (50%) had mutations in KCNJ5 (G151R and L168R). The hyperplastic gland showed a PRKACAL206R mutation, while patients with bilateral adenomas did not have known somatic mutations. PRKACA-mutant lesions were associated with younger age, overt Cushing's syndrome, and higher cortisol levels vs non-PRKACA-mutant or CTNNB1-mutant lesions. CTNNB1 mutations were more significantly associated with right than left lesions.ConclusionsPRKACAL206R is present not only in adenomas, but also in unilateral hyperplasia and is associated with more severe autonomous cortisol secretion. Bilateral adenomas may be caused by yet-unknown germline mutations.


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