Concomitant Secretion of Glucocorticoid,Androgens, and Mineralocorticoid by an Adrenocortical Carcinoma: Case Report and Review of Literature

ObjectiveTo present a case of concomitant secretion of cortisol, androgens, and 11-deoxycorticosterone (DOC) by an adrenocortical carcinoma and review the literature in an attempt to identify similar cases.MethodsThe patient’s medical history, physical examination, laboratory data, computed tomographic scan, and histopathologic results were analyzed and summarized in a case report, and an extensive review of the literature was performed.ResultsEndocrinologic data showed excess cortisol production, substantially elevated testosterone and androstenedione levels, and profoundly increased DOC in the setting of suppressed aldosterone. An abdominal computed tomographic scan showed a left adrenal tumor. A left adrenalectomy was performed, and the histopathologic diagnosis was stage II adrenocortical carcinoma. The review of the pertinent literature revealed the absence of any identical cases in the past.ConclusionOur patient presented with a rare case of cosecretion of cortisol, testosterone, androstenedione, and DOC by an adrenocortical carcinoma, resulting in a clinical picture consistent with Cushing’s syndrome, hyperandrogenism, and primary hypermineralocorticoidism. We recommend the routine performance of a DOC assay in the setting of mineralocorticoid excess in association with low plasma aldosterone levels. (Endocr Pract. 2007;13: 408-412)     

Clinical Outcomes in Adrenal Incidentaloma: Experience From one Center

Objective: To investigate the outcome in patients with adrenal incidentaloma (AI).Methods: A retrospective evaluation of 637 patients with AI referred to a tertiary center over 8 years. Radiologic and hormonal evaluations were performed at baseline. Follow-up imaging was carried out if necessary, and hormonal evaluation was performed at 24 months according to national guidelines.Results: The mean age was 62.7 ± 11.6 years, and the mean AI size was 25.3 ± 17.0 mm at presentation. Hormonal evaluation revealed that 85.4% of all tumors were nonfunctioning adenomas, 4.1% subclinical Cushing syndrome (SCS), 1.4% pheochromocytoma, 1.4% primary hyperaldosteronism, 0.8% Cushing syndrome, 0.6% adrenocortical carcinoma, 0.3% congenital adrenal hyperplasia, 2.2% metastasis to adrenals, and 3.8% other lesions of benign origin. Bilateral tumors were found in 11%, and compared to unilateral tumors, SCS was more prevalent. Only 2 cases were reclassified during follow-up, both as SCS, but neither had had a dexamethasone suppression test performed at initial work-up. In patients diagnosed with an adrenal metastasis, 92.9% were deceased within 2 years. Excluding those with malignant tumors, 12.9% of patients died during the study period of up to 11 years due to other causes than adrenal.Conclusion: Most AIs were benign, but a small fraction of tumors were functional and malignant. The prognosis of patients with adrenal metastasis was extremely poor, but otherwise, the mortality rate was similar to that for the general population. Follow-up of AIs <4 cm with an initial nonfunctional profile and benign radiologic appearance appears unwarranted, but screening for congenital adrenal hyperplasia should be considered.Abbreviations: 17OHP = 17-hydroxyprogesterone ACC = adrenal cortical carcinoma ACTH = adrenocorticotropic hormone AI = adrenal incidentaloma CAH = congenital adrenal hyperplasia CT = computed tomography CS = Cushing syndrome DST = dexamethasone suppression test HPA = hypothalamic-pituitary-adrenal axis MRI = magnetic resonance imaging SCS = subclinical Cushing syndrome T2DM = type 2 diabetes mellitus UFC = urinary free cortisol     

Corticotropin-Independent Macronodular Adrenal Hyperplasia Associated With Insulinoma

ObjectiveTo report a case of corticotropin-independent macronodular adrenal hyperplasia (AIMAH) associated with an insulinoma.MethodsWe describe the clinical, radiographic, laboratory, and histopathologic findings of the study patient; review the current protocols for management of AIMAH; and discuss the disease etiology.ResultsA 64-year-old woman with multiple intradermal facial nevi experienced intermittent light-headedness, tremor, and confusion and was found to have a venous plasma glucose concentration of 52 mg/dL. Hypoglycemia and hyperinsulinemia after 18 hours of fasting suggested the presence of an insulinoma. Hepatic venous sampling for insulin after selective arterial calcium injection localized the insulinoma to the pancreatic head. The insulinoma was excised, and there was no recurrence over the 5 years the patient was in our care. During the workup for insulinoma, bilateral adrenal masses were incidentally discovered on computed tomography. Twenty-hour urinary free cortisol excretion was elevated and serum corticotropin was suppressed. Overt signs of Cushing syndrome were not present, and subsequent urinary cortisol measurements were within the reference range for several years. After 4 years, Cushing syndrome developed and bilateral adrenalectomy was performed. AIMAH was diagnosed on the basis of histopathologic findings.ConclusionsThis appears to be the first reported case of AIMAH associated with an insulinoma. In the absence of other stigmata of multiple endocrine neoplasm type 1 and in the presence of multiple nevi, it may represent a novel endocrine syndrome. (Endocr Pract. 2011;17:e43-e47)     

An Unusual Variant of Cushing Syndrome

ObjectiveTo discuss the initial clinical manifestations of primary pigmented nodular adrenocortical disease.MethodsWe present a case report of a 4-year-old boy who had the classic clinical features of Cushing syndrome. Results of hormonal investigations are reviewed, and histopathologic findings are illustrated.ResultsInvestigations revealed adrenocorticotropic hormone (corticotropin)-independent Cushing syndrome. Findings on magnetic resonance imaging of the pituitary gland and abdomen were within normal limits. The patient underwent bilateral adrenalectomy. The histopathologic features were consistent with primary pigmented nodular adrenocortical disease.ConclusionPrimary pigmented nodular adrenocortical disease should be suspected in patients with corticotropin- independent Cushing syndrome who have normal findings on adrenal imaging. (Endocr Pract. 2008;14:717-720)     

The Glucocorticoid Receptor and its Expression in the Anterior Pituitary and the Adrenal Cortex: A Source of Variation in Hypothalamic-Pituitary-Adrenal Axis Function; Implications for Pituitary and Adrenal Tumors

ObjectiveTo review the expression of the glucocorticoid receptor (GR) in anterior pituitary and adrenocortical cells and tumors derived from these tissues as well as factors that may influence its expression.MethodsWe present an overview of the relevant literature, with a focus on data generated from our studies.ResultsThe expression of the GR is an essential element of the negative feedback that closes the loop formed by corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol in the context of the hypothalamicpituitary-adrenal (HPA) axis. Although the GR expression in anterior pituitary cells—and in particular the corticotrophs—was first demonstrated several years ago, it was not known until relatively recently where, by what cells, and in what form the GR is expressed in the adrenal cortex.The variability in the expression of the GR in pituitary and adrenocortical cells may underlie the substantial differences in HPA axis function across individuals, especially when testing for tumors associated with hypercortisolemia. This expression is influenced by a multitude of tissue-specific factors, which may explain why it is so difficult to interpret (or reproduce) studies that are based on GR functional polymorphisms on different cohorts of patients or even different sets of laboratory animals.ConclusionThis review highlights the variability in expression and function of the GR in pituitary and adrenocortical cells as one of the reasons for the appreciable differences in HPA axis function across individuals. Particular attention was paid to interactions that may affect the interpretation of diagnostic testing of the HPA axis in patients with pituitary adenomas (Cushing disease) or adrenocortical tumors (Cushing syndrome). (Endocr Pract. 2011;17:941-948)     

Adrenocortical Neoplasms With Myelolipomatous and Lipomatous Metaplasia: Report of 3 Cases

ObjectiveTo present pathologic and radiographic features of 3 patients with adrenocortical neoplasms—2 with uncertain malignant potential and 1 adenoma with areas of myelolipomatous and lipomatous metaplasia.MethodsWe describe 3 patients who had adrenocortical neoplasms with foci of myelolipomatous and lipomatous metaplasia. For each patient, the clinical and pathologic data are reviewed.ResultsAll 3 patients were women, with a mean age at presentation of 58 years. The lesion size averaged 6.8 cm (range, 3.9 to 11.0), and the mean gland weight was 128.8 g (range, 32.5 to 249). Two patients showed imaging findings compatible with adrenal myelolipoma. Pathologically, 2 of the lesions were classified as adrenocortical neoplasms of uncertain malignant potential, and 1 lesion was classified as an adrenocortical adenoma. All 3 lesions contained myelolipomatous foci throughout the neoplasm, and 2 of the tumors contained several pure lipomatous foci.ConclusionAdrenocortical neoplasms, including those associated with an uncertain malignant potential, may be associated with areas of myelolipomatous and lipomatous metaplasia. Imaging studies may result in a false diagnosis of a benign adrenal myelolipoma and potential undertreatment in such patients. (Endocr Pract. 2009;15:128-133)     

Adrenal Cortical Carcinoma With Late Pulmonary Metastases Causing Clinicical Cushing’s Syndrome: Case Report With Immunohistochemical Analysis Of Steriodogenic Enzyme Production

ObjectiveTo present a case of pulmonary metastases from adrenocortical carcinomas (ACC) that were secreting fully-functional cortisol resulting in clinical Cushing’s syndrome and to compare the steroidogenic enzyme expression in the primary tumor and lung.MethodsWe analyzed and summarized the patient’s medical history, physical examination results, labora tory data, imaging studies, and histopathologic results. The original tumor and the pulmonary metastases were then immunohistochemically evaluated for steroidogenic enzymes.ResultsInitial endocrinological workup revealed hyperandrogenism and adrenocorticotropic hormone (ACTH) independent Cushing’s due to a 4 cm left adrenal mass. The patient was initially diagnosed with an adrenal adenoma. Four years later, the patient developed recurrent Cushing’s syndrome. Repeat magnetic resonance imaging (MRI) showed no adrenal masses; however, chest computed tomography (CT) showed multiple bilateral lung nodules and biopsy revealed metastases of adrenal origin. Upon immunohistochemical analysis, side chain cleavage, 17α hydroxylase, 3β hydroxysteroid dehydrogenase, and 21 hydroxylase immunoreactivity were detected in both the original and pulmonary metastatic lesions with patterns of disorganized steroidogenesis. Dehydroepiandrosterone sulfotransferase (DHEA-ST) immunoreactivity was detected in the original tumor but not in the lung metastases.ConclusionThis case demonstrates some inter esting features of ACC that pose challenges to its management, including the difficulties in establishing the pathologic diagnosis, the potential for fullyfunctional steroidogenesis even in late metastases, and the plasticity of steroidogenic potential in tumor cells. (Endocr Pract. 2012;18:e138-e143)     

Virilizing Adrenal Ganglioneuroma in a Woman with Subclinical Cushing Syndrome

ObjectiveTo describe a patient with a virilizing adrenal ganglioneuroma and subclinical Cushing syndrome.MethodsDetailed clinical, laboratory, radiologic, and pathologic findings are presented, and the pertinent literature is reviewed.ResultsA 56-year-old postmenopausal woman was referred for evaluation of a 3.6- by 3.0-cm right adrenal mass, which had been diagnosed during a work-up for hirsutism. A bilateral oophorectomy done 2 months before the presentation failed to correct the elevated testosterone levels. On examination, she had severe hirsutism on her face, chest, back, and extremities, as well as male pattern baldness and clitoromegaly. Biochemical evaluation showed elevated total and free serum testosterone levels of 319 ng/dL (reference range, 20 to 70) and 78 pg/mL (reference range, 1 to 9), respectively, values in the adult male range. The serum dehydroepiandrosterone sulfate level was 117 μ/dL (reference range, 10 to 152), and the urine free cortisol was 10.4 μg/24 h (reference range, < 45). A laparoscopic adrenalectomy revealed a 5.0-cm adrenal ganglioneuroma containing nests of adrenocortical cells. On the first day postoperatively, the serum cortisol level was < 1.0 μg/dL. At 1 month after adrenalectomy, the total and free testosterone levels had declined to 16 ng/dL and 3.1 pg/mL, respectively. At 2 months postoperatively, normal results of a cosyntropin stimulation test (basal and peak cortisol levels of 13.6 and 20.0 μg/dL, respectively) indicated recovery of the hypothalamic-pituitary-adrenal axis.ConclusionTo our knowledge, this is the first case report of a virilizing adrenal ganglioneuroma with this unique pathologic finding and concomitant subclinical Cushing syndrome. (Endocr Pract. 2008;14:584-587)     

Iatrogenic Cushing Syndrome in Patients Receiving Inhaled Budesonide and Itraconazole or Ritonavir: Two Cases and Literature Review

ObjectiveTo present two cases of iatrogenic Cushing syndrome caused by the interaction of budesonide, an inhaled glucocorticoid, with ritonavir and itraconazole.MethodsWe present the clinical and biochemical data of two patients in whom diagnosis of Cushing syndrome was caused by this interaction. We also reviewed the pertinent literature and management options.ResultsA 71-year-old man was treated with inhaled budesonide for a chronic obstructive pulmonary disease and itraconazole for a pulmonary aspergillosis. The patient rapidly developed a typical Cushing syndrome complicated by bilateral avascular necrosis of the femoral heads. Serum 8:00 AM cortisol concentrations were suppressed at 0.76 and 0.83 µg/dL on two occasions. The patient died 4 days later of a massive myocardial infarction. The second case is a 46-year-old woman who was treated for several years with inhaled budesonide for asthma. She was put on ritonavir, a retroviral protease inhibitor, for the treatment of human immunodeficiency virus (HIV). In the following months, she developed typical signs of Cushing syndrome. Her morning serum cortisol concentration was 1.92 µg/dL. A cosyntropin stimulation test showed values of serum cortisol of <1.10, 2.65, and 5.36 µg/dL at 0, 30, and 60 minutes, respectively, confirming an adrenal insufficiency. Because the patient was unable to stop budesonide, she was advised to reduce the frequency of its administration and eventually taper the dose until cessation.ConclusionClinicians should be aware of the potential occurrence of iatrogenic Cushing syndrome and secondary adrenal insufficiency due to the association of inhaled corticosteroids with itraconazole or ritonavir. (Endocr. Pract. 2013;19:e138-e141)     

Diagnostic Challenges in Adrenocortical Carcinoma: Recommendations for Surveillance after Surgical Resection of Selected Adrenal Nodules

ObjectiveTo discuss challenges in the diagnosis of adrenocortical carcinoma and to suggest surveillance measures after removal of selected adrenal nodules.MethodsWe present the case of a 65-year-old man with worsening hypertension and new-onset hypokalemia attributed to primary hyperaldosteronism due to a 3-cm right adrenal nodule.ResultsA laparoscopic right adrenalectomy was performed, and the histologic diagnosis was a benign adenoma. The patient’s hypertension and hypokalemia improved postoperatively but recurred 8 months later, and florid Cushing’s syndrome developed. Magnetic resonance imaging showed an 8-cm mass in the right adrenal bed and multiple hepatic metastatic lesions. Fine-needle biopsy confirmed the presence of adrenocortical carcinoma.ConclusionDespite a comprehensive biochemical, radiologic, and histologic assessment, the diagnosis of adrenocortical carcinoma can be missed. Particularly, we caution against undue reliance on the initial tumor size. We recommend that abdominal imaging be performed every 3 months for the first year and every 6 months for the second year after surgical removal of selected adrenal nodules. (Endocr Pract. 2007;13:636-641)     

Cushing Syndrome in a Young Woman Due to Primary Pigmented Nodular Adrenal Disease

ObjectiveTo report a case of Cushing syndrome due to apparently sporadic primary pigmented nodular adrenal disease in a young woman.MethodsWe describe the clinical, biochemical, radiologic, and histologic findings of Cushing syndrome due to the rare condition of primary pigmented nodular adrenal disease.ResultsA 30-year-old woman presented with a 2-year history of worsening itch without rash over her shoulders and arms and weight gain, particularly around the abdomen and face. Careful questioning did not elicit any history of exogenous glucocorticoid use (systemic or topical), including hydrocortisone. On examination, the patient had a slightly rounded and plethoric face, a small buffalo hump, central adiposity, and thin skin with a few small striae on her inner thighs. No features of the Carney complex were observed. Investigations showed hypercor- tisolism with suppressed corticotropin and normal adrenal imaging despite documentation of enlarged adrenal glands at removal. High-dose dexamethasone administration was followed by a decrease in urinary free cortisol excretion rather than a paradoxical rise as previously reported in primary pigmented nodular adrenal disease. No mutations were detected in the PRKAR1A gene.ConclusionsPrimary pigmented nodular adrenal disease should be suspected in patients with corticotropinindependent Cushing syndrome who have normal adrenal imaging. The role of genetic testing in apparently sporadic cases is not established, but cumulative experience may be helpful in defining the frequency of PRKAR1A mutations. (Endocr Pract. 2010;16:84-88)     

A Novel PRKAR1A Mutation Associated With Primary Pigmented Nodular Adrenocortical Disease and the Carney Complex

ObjectiveTo delineate the genetic and phenotypic features of Carney complex in a family with multiple cases of primary pigmented nodular adrenocortical disease (PPNAD).MethodsDetailed clinical, laboratory, genetic, radiologic, and pathologic findings are presented, and the pertinent literature is reviewed.ResultsA 17-year-old girl presented with symptoms and physical findings suggestive of hypercortisolemia, in addition to facial lentigines. She was found to have adrenocorticotropic hormone (ACTH)-independent Cushing syndrome. The adrenal glands appeared normal on computed tomographic scanning. Bilateral surgical adrenalectomy revealed PPNAD. Evaluation of her 14-year-old sister revealed ACTH-independent Cushing syndrome as well as facial lentigines, and adrenalectomy revealed PPNAD as well. Genetic testing of the 2 sisters and their mother (who also had multiple facial lentigines but did not have Cushing syndrome) revealed a novel mutation in the PRKAR1A gene.ConclusionWe describe a novel mutation in the PRKAR1A gene in a family with Carney complex and multiple members with PPNAD. PPNAD should be suspected in cases of ACTH-independent Cushing syndrome, and screening for Carney complex and its complications is recommended in all cases of PPNAD, including first-degree relatives. (Endocr Pract. 2010;16:198-204)     

Virilization of a female infant by a maternal adrenocortical carcinoma

ObjectiveTo describe a possible mechanism underlying the partial virilization of a 46, XX infant by a functional maternal adrenocortical carcinoma (ACC).MethodsWe performed immunocytochemical staining of tumor sections for luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors. In addition, related reports in the literature are discussed.ResultsA previously healthy mother developed a large cortisoland androgen-producing stage III adrenal tumor that did not interfere with conception or early morphogenesis. The tumor eluded detection until after delivery of a partially virilized 46, XX female infant with ambiguous genitalia. Immunohistochemical staining of tumor sections revealed overexpression of the LH/hCG receptor. Virilization of the genetically female fetus may have resulted from hCG-stimulated steroid secretion by the ACC.ConclusionBecause hypercortisolism and hyperandrogenism are associated with menstrual disturbances and spontaneous abortion, pregnancy in patients with functional adrenal tumors is uncommon. Rarely, maternal steroid excess from a functional adrenal tumor has caused 46, XX disordered sex differentiation. This unusual case demonstrates the influence of hCG on the functionality of an ACC and demonstrates the rare phenomenon of virilization of a female infant by a functional maternal adrenal tumor. (Endocr Pract. 2011;17:e26-e31)     

Serum Matrix Metalloproteinase-9 Levels in the Diagnosis of Functioning Adrena Tumors

ObjectiveTo investigate whether serum matrix metalloproteinase-9 (MMP-9) levels can be used as a diagnostic tool in determining the functioning status of benign adrenal tumors.MethodsIn this case-control study, medical records of patients with adrenal tumors who consecutively presented to an endocrinology clinic between August 2005 and October 2008 were evaluated. Operation was recommended when the incidentaloma was larger than 4 cm or when a hypersecreting tumor was suspected. A control group of healthy persons matched for age, body mass index, and sex was also enrolled. Patients underwent routine endocrinologic examinations. MMP-9 levels were compared preoperatively and postoperatively. Findings were compared among patients with functioning adrenal tumors, patients with nonfunctioning adrenal tumors, and control participants.ResultsOf 370 patients with adrenal tumors, 50 with adrenal incidentaloma met the inclusion criteria. Twenty- five healthy individuals were enrolled as controls. Group 1 included 20 patients with functioning adrenal tumors (14 with Cushing syndrome and 6 with pheochromocytoma), and Group 2 included 30 patients with nonfunctioning adrenal tumors. MMP-9 levels were higher in patients with nonfunctioning adrenal tumors and functioning adrenal tumors than in control participants (P < .001). MMP-9 levels in patients with functioning adrenal tumors were significantly higher than those in patients with nonfunctioning adrenal tumors (P = .002). After operation, levels decreased significantly in patients with Cushing syndrome and in those with pheochromocytoma; however, patients with Cushing syndrome and pheochromocytoma had similar MMP-9 levels preoperatively and postoperatively. No significant linear correlation existed between tumor volume and MMP-9 levels. A significant positive correlation was determined between preoperative MMP-9 concentrations and 24-hour urinary fractionated metanephrine and epinephrine (r = 0.938, P = .006; r = 0.965, P = .002, respectively), between MMP-9 levels and baseline cortisol levels (r = 0.402, P = .003), and between MMP-9 levels and cortisol levels obtained after dexamethasone suppression testing (r = 0.357, P = .006).ConclusionOur data suggest that serum MMP-9 levels may be useful in differentiating benign subclinical functioning adrenal tumors from benign nonfunctioning adrenal tumors. (Endocr Pract. 2010;16:419-427)     

Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity

The aim of this review is to explore the dysregulation of adrenocortical secretions as a major contributor in the development of obesity and insulin resistance. Disturbance of adipose tissue physiology is one of the primary events in the development of pathologies associated with the metabolic syndrome, such as obesity and type 2 diabetes. Several studies indicate that alterations in metabolism of glucocorticoids (GC) and androgens, as well as aldosterone in excess, are involved in the emergence of metabolic syndrome. Cross talk among adipose tissue, the hypothalamo-pituitary complex, and adrenal gland activity plays a major role in the control of food intake, glucose metabolism, lipid storage, and energy balance. Perturbation of this cross talk induces alterations in the regulatory mechanisms of adrenocortical steroid synthesis, secretion, degradation, and/or recycling, at the level of the zonae glomerulosa (aldosterone), fasciculata (GC and GC metabolites), and reticularis (androgens and androgen precursors DHEA and DHEAS). As a whole, these adrenocortical perturbations contribute to the development of metabolic syndrome at both the paracrine and systemic level by favoring the physiological dysregulation of organs responsive to aldosterone, GC, and/or androgens, including adipose tissue.     

Is Pseudo-Cushing’s Syndrome in a Critically ILL Patient “Pseudo”? Hypothesis and Supportive Case Report

ObjectiveTo propose a new hypothesis regarding the possible role of glucocorticoid excess in patients with an extended acute illness, based on a patient’s presentation and therapy in a critical care situation.MethodsWe present a detailed case report, review the related literature, and suggest the need for prospective studies to determine the appropriate intervention in critically ill patients with pseudo-Cushing’s syndrome.ResultsA 50-year-old woman with diabetes and obesity who underwent vertical banded gastroplasty had postoperative complications, including refractory gastrostomy leakage, peritoneal and abdominal wall infections, and multiorganism sepsis despite intensive antibiotic therapy and surgical drainage procedures. Her physical appearance, elevated and relatively nonsuppressible plasma cortisol levels, and radiologic study supported a tentative diagnosis of Cushing’s syndrome in a critically ill patient. Intravenously administered itraconazole and rectally administered aminoglutethimide were used to suppress endogenous glucocorticoid synthesis. Glucocorticoids were administered at dosages that provided 1/3 to 1/2 of her expected maximal daily cortisol secretion during her complicated hospital course. Insulin resistance declined with adrenal suppression and infection control, and wound healing improved dramatically. Adrenal suppression was discontinued, and she was reevaluated for hypercortisolism. Results of all studies for Cushing’s syndrome were normal and remained so 1 year later.ConclusionIn our patient, substantially increased glucocorticoid levels were associated with severe insulin resistance, retarded wound healing, and persistent infections. Suppression of endogenous cortisol production and replacement with more physiologic concentrations of glucocorticoid were associated with clinical improvement and appeared to contribute to her recovery. Review of the literature leads us to propose the following hypotheses: (1) that considerably increased stress-induced cortisol concentrations in critically ill patients may contribute to adverse outcomes and (2) that therapeutic suppression of the persistent and substantially elevated glucocorticoid levels in selected cases may be a beneficial therapeutic option. (Endocr Pract. 2007;13:153-158)     

Effects of training for two ball games on the saliva response of adrenocortical hormones to exercise in elite sportswomen

In a group of 20 elite female handball or volleyball players, an evaluation was made of the response to a 4-month training period of cortisol, androstenedione and dehydroepiandrosterone in the saliva. At the beginning of the training programme (W₁) and at the 7th (W₇) and 16th weeks (W₁₆), hormone concentrations were measured on awakening (8 a.m.; resting samples), and also before (t ₀) and at the end (t ₁₂₀) of a 2-h exercise session (simulated match) which took place at 6 p.m. The training programme increased the concentrations of adrenal androgens in the saliva at rest (P<0.05) for both groups of subjects, with no change being noted in cortisol concentrations. In contrast, amongst the volleyball players, stressful stimuli produced by an increase in the amount of training did not affect adrenocortical metabolism during exercise. Indeed, a simulated volleyball match resulted in a decrease in salivary cortisol (P<0.05) and androgen concentrations (P<0.05) without regard for the week chosen for the test investigations. In contrast, a simulated handball match caused an increase in cortisol concentrations at W₁ only (P<0.05), with no change in the adrenal androgens concentration in any week of the training programme. The regulators of these hormones during a period of exercise and during the course of a training programme would seem to be different. Accepted: 30 October 1997     

Effect of angiotensin II on secretion of adrenal androgens

To assess the effect of angiotensin II (A II) on the secretion of human adrenal androgens (AA), plasma dehydroepiandrosterone (DHEA), DHEA sulfate (DS) and delta 4-androstenedione (delta 4-A) were measured in eight normal men 60 and 120 min after stimulation of endogenous A II by a bolus injection of 40 mg frusemide, and the direct effect of A II on the secretion of adrenal androgens was examined in cultured human adrenocortical cells in the presence of a low concentration of ACTH. The administration of frusemide led to a significant increase in the plasma DHEA and DS concentration as well as plasma renin activity (PRA) and aldosterone concentration (PAC), but did not change plasma cortisol and delta 4-A. In the culture of human adrenocortical cells, 10(-9)-10(-5) M A II or 10(-13) M ACTH alone did not stimulate the secretion of DHEA, DS and delta 4-A, while 10(-7) and 10(-5) M A II in the presence of 10(-13) M ACTH caused a significant increase in DHEA and DS secretion with no change in delta 4-A. These results suggest that the activated renin-angiotensin system stimulates the secretion of adrenal androgens by a direct effect of A II on adrenal cortical cells.