Hormonal and morphological data were investigated in 202 consecutive patients with adrenal incidentalomas (171 unilateral and 31 bilateral) in an attempt to assess subclinical hyperfunction or malignancy. In addition to the classical evaluation, scintiscan was carried out in a large number of these patients. In unilateral incidentalomas, 83% showed normal hormonal function, whereas 17% had biochemical signs of adrenal overactivity (hyperaldosteronism in 3, hypercortisolism in 17, medullary hyperfunction in 9). [75Se]Methylnorcholesterol scintigraphy depicted malignant, space-occupying lesions as decreased or absent radiotracer uptake by the mass, and cortical adenomas as increased or normal uptake. In cortical adenomas a relationship between radiocholesterol uptake and degree of functional autonomy was demonstrated. [123I]Metaiodobenzilguanidine scintiscan visualized 7 of 8 pheochromocytomas. In bilateral incidentalomas, abnormal adrenal function was more frequent, accounting for 29% of cases (hyperaldost...

Incidentally discovered adrenal tumors : Endocrine and scintigraphic correlates

It is well established that incidentally discovered adrenal masses constitute a rather common finding in clinical practice and one of the most frequent problems about which endocrinologists' opinion is requested In recent years the widespread use of sensitive and noninvasive diagnostic techniques, such as ultrasonography, computed tomography (CT) and magnetic resonance imaging (MRI), greatly expanded the observation of patients with clinically silent (or apparently silent) adrenal incidentalomas Although up to now great experience, as far as epidemiological, imaging and hormonal aspects, has been accumulating, some issues are still open The main questions are concerned with a) which is the simplest and less expensive way to initially evaluate and then follow-up such patients, b) which is the nature of the lesions, c) are there any markers of a possible evolution towards hypersecretory syndromes, d) which, and when, patients have to be treated, ie operated on This article will review most established knowledges on the topic and will suggest strategies for clinical purposes,trying to answer the above mentioned questions

The clinical evaluation of silent adrenal masses

Objective: An increased response of 17-hydroxyprogesterone to ACTH stimulation has been observed in adrenal incidentaloma and linked to an impairment of either 21-hydroxylase or of 11b-hydroxylase activity. To analyse this question further, we investigated the steroidogenic pathways in a series of 17 adrenal incidentalomas. Design and Patients: 17 patients (7 women, 10 men; mean age, 62 6 12 years) with non-histologically analyzed adrenal incidentalomas were prospectively evaluated. Methods: The following variables were investigated: 24-h urinary methanephrines and free cortisol excretion; plasma levels of ACTH and dehydroepiandrosterone; overnight dexamethasone suppression test; 1‐24 ACTH stimulation test with measurement of: cortisol, 11-deoxycortisol, 17hydroxyprogesterone, aldosterone, 11-deoxycorticosterone, progesterone, 17-hydroxypregnenolone, D4-androstenedione, dehydroepiandrosterone and 21-deoxycortisol. Results: Discordant features of subclinical hypercorticism were noted in one case. No patient had dehydroepiandrosterone sulfate levels in the normal range for his or her age. Peak 17hydroxyprogesterone and peak 21-deoxycortisol disclosed impairment of 21-hydroxylase in 11 and 10 cases respectively. An increased 11-deoxycortisol/cortisol ratio identified reduced activity of 11b-hydroxylase in 11 patients. Eight patients displayed features of mild 17,20-lyase impairment, which was related to 21-hydroxylase dysfunction. Whereas only 2 patients showed no enzyme modification, 9 displayed alterations of at least two pathways. Conclusion: In our hands, a combination of enzyme dysfunction was frequently observed. Shared biochemical mechanisms could explain combined 17,20-lyase and 21-hydroxylase alterations, whereas coexistence of 21-hydroxylase (particularly when based on peak 21-deoxycortisol) and 11b-hydroxylase is more puzzling.

/pdf/apparent-activities-of-21-hydroxylase-17alpha-hydroxylase-3iz8vtci5e.pdf

Apparent activities of 21-hydroxylase, 17alpha-hydroxylase and 17,20-lyase are impaired in adrenal incidentalomas

Mineralocorticoid hypertension is most often caused by autonomous overproduction of aldosterone, but excess of other mineralocorticoid precursors can lead to a similar presentation. 11-Deoxycorticosterone (DOC) excess, which can occur in 11-β hydroxylase or 17-α hydroxylase deficiencies, in DOC-producing adrenocortical tumours or in patients taking 11-β hydroxylase inhibitors, may cause mineralocorticoid hypertension. We report a 35-year-old woman who in the third trimester of pregnancy was found to have a large adrenal mass on routine obstetric ultrasound. On referral to our unit, persistent hypertension and long-standing hypokalaemia was noted, despite good compliance with multiple antihypertensives. Ten years earlier, she had hypertension noted in pregnancy which had persisted after delivery. A MRI scan confirmed the presence of a 12 cm adrenal mass and biochemistry revealed high levels of DOC and low/normal renin, aldosterone and dehydroepiandrosterone, with normal catecholamine levels. The patient was treated with antihypertensives until obstetric delivery, following which she underwent an adrenalectomy. Histology confirmed a large adrenal cortical neoplasm of uncertain malignant potential. Postoperatively, blood pressure and serum potassium normalised, and the antihypertensive medication was stopped. Over 10 years of follow-up, she remains asymptomatic with normal DOC measurements. This case should alert clinicians to the possibility of a diagnosis of a DOC-producing adrenal tumours in patients with adrenal nodules and apparent mineralocorticoid hypertension in the presence of low or normal levels of aldosterone. The associated diagnostic and management challenges are discussed.

Learning points:

Hypermineralocorticoidism is characterised by hypertension, volume expansion and hypokalaemic alkalosis and is most commonly due to overproduction of aldosterone. However, excess of other mineralocorticoid products, such as DOC, lead to the same syndrome but with normal or low aldosterone levels.


The differential diagnosis of resistant hypertension with low renin and low/normal aldosterone includes congenital adrenal hyperplasia, syndrome of apparent mineralocorticoid excess, Cushing’s syndrome, Liddle’s syndrome and 11-deoxycorticosterone-producing tumours.


DOC is one intermediate product in the mineralocorticoid synthesis with weaker activity than aldosterone. However, marked DOC excess seen in 11-β hydroxylase or 17-α hydroxylase deficiencies in DOC-producing adrenocortical tumours or in patients taking 11-β hydroxylase inhibitors, may cause mineralocorticoid hypertension.


Excessive production of DOC in adrenocortical tumours has been attributed to reduced activity of the enzymes 11-β hydroxylase and 17-α hydroxylase and increased activity of 21-α hydroxylase.


The diagnosis of DOC-producing adrenal tumours is challenging because of its rarity and poor availability of DOC laboratory assays.






Background
Mineralocorticoid-induced hypertension is common and normally associated with autonomous aldosterone overproduction (primary hyperaldosteronism). However, other mineralocorticoid hormones such 11-deoxycorticosterone (DOC) may be responsible for a similar condition (1, 2). The rarity of DOC-producing adrenocortical tumours (3) and poor availability of laboratory assays to measure mineralocorticoid products other than aldosterone cause diagnostic challenges. This case highlights the diagnostic challenges, with the patient’s diagnosis remaining hidden for at least 10 years.

/pdf/hypertension-due-to-a-deoxycorticosterone-secreting-adrenal-d6i579opxl.pdf

Hypertension due to a deoxycorticosterone-secreting adrenal tumour diagnosed during pregnancy

A convenient synthesis of 18-hydroxycorticosterone and 18-hydroxy-11-desoxycorticosterone via stereospecific hypoiodination of 20-hydroxysteroids

The aim of this study was to find out whether the dysfunction of aldosterone pathway, previously proposed as a marker of secretory adrenal carcinoma, is also found in nonsecretory adrenal carcinomas, which pose even more difficult diagnostic problems even for patients with hypertension accompanied or not by hypokalemia. The exploration consisted of using the same method (RIA preceded by a chromatographic step) to determine the plasma levels of the following steroids in the mineral corticosteroid pathway: deoxycorticosterone (DOC), 18-hydroxydeoxycorticosterone (18-OHDOC), corticosterone (B), 18 hydroxycorticosterone (18 OH B), and aldosterone. The subjects included 16 adults, each presenting with an endocrinologically asymptomatic adrenal mass associated for some patients with hypokalemia and hypertension (8 with adrenal carcinoma, 2 with adrenal metastasis from other forms of cancer, and 6 adenomas). These results show that even in nonsecretory adrenal carcinoma, there is a dysfunction of the aldosterone...

Plasma levels of aldosterone versus aldosterone precursors: a way to estimate the malignancy of asymptomatic and nonsecretory adrenal tumors: a French Retrospective Multicentric Study.

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Plasma levels of aldosterone versus aldosterone precursors: a way to estimate the malignancy of asymptomatic and nonsecretory adrenal tumors: a French Retrospective Multicentric Study.