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PubMed1995

Regulatory patterns of plasma pituitary-adrenal and pituitary-thyroid hormone secretions: indication for adrenal factor inhibiting adrenal response to ACTH.

Although organization and hormonal regulation of the hypothalamic-pituitary-adrenocortical (HPA) and the hypothalamic-pituitary-thyroid (HPT) axes share a remarkable degree of similarities, distinctive patterns of their plasma hormone secretions are observed. We measured plasma levels of ACTH-cortisol (PA) and hTSH-T3 (PT) pairs of hormones in 24-hour sequential blood specimens sampled at 30-minute intervals from 3 patients with suspected adrenal disorders and 4 normal volunteers and found the same percentage of discordant secretions of the PA and PT hormones but significantly greater coefficients of variations of the PA values than the PT values (p < 0.002). This confirms that plasma PT hormones are more tightly self-regulated between themselves than plasma PA hormones. Moreover, cluster analysis of the 24-hour plasma hormonal fluctuations revealed one or more ACTH-cortisol hyposecretory clusters only in subjects with a normal status of adrenal function. There was no similar hTSH-T3 hyposecretory cluster detected in any one of the 7 subjects. Based on these results, we postulate that there is some adrenal factor normally exerting a subtle antagonistic action against ACTH and causes the incidence of such ACTH-cortisol hyposecretory cluster.

Adrenocorticotropic Hormone↗
PubMed1994

Bilateral adrenal hemorrhage and adrenal insufficiency in a patient with lymphomatous adrenal infiltration following administration of a fusion toxin (DAB486 interleukin-2).

DAB486IL-2 is a novel fusion toxin in which the ADP-ribosyltransferase and membrane-translocating domains of diphtheria toxin have been combined with the interleukin-2 (IL-2) gene, creating a recombinant protein capable of selectively intoxicating cells bearing the high-affinity IL-2 receptor. Clinical activity has been documented in Hodgkin disease and the non-Hodgkin lymphomas; toxicities have been minimal and include mild hepatic transaminitis, proteinuria, and hypersensitivity reactions. In this report, a patient with tumor-stage cutaneous T-cell lymphoma developed clinical adrenal failure with bilateral adrenal hemorrhage and necrosis 7 weeks after completing a 5-day course of treatment with DAB486IL-2. The relationship of fusion toxin therapy to the development of this unusual toxicity is discussed.

Adrenal Gland Diseases↗
PubMed1986

Pituitary-adrenal function after transplantation in rats: dependence on age of the adrenal graft.

Comparisons of resting plasma adrenocorticotropin (ACTH) and corticosterone in the morning and afternoon were made among adult rats bearing regenerated adult adrenal grafts, neonatal (day 1) adrenal grafts, adult adrenal capsule grafts, or intact adrenals. In the morning plasma ACTH and corticosterone were similar in all rats. In the afternoon, plasma ACTH was elevated in rats bearing neonatal adrenal grafts or adult adrenal capsule grafts, but not in rats bearing whole adult adrenal grafts. There was no difference in afternoon plasma corticosterone among rats bearing transplanted adrenals, although afternoon plasma corticosterone was decreased in rats bearing transplants compared with rats with intact adrenals. Thus the increased plasma ACTH after adrenal transplantation cannot be explained entirely by decreases in resting plasma corticosterone. Adrenal responsiveness to ACTH was tested at 5 wk after transplantation in the afternoon by measuring the plasma corticosterone response to submaximal doses of ACTH. The responsiveness was decreased in rats bearing transplants. In addition, responsiveness was inversely related to the age of the grafted adrenal tissue. Adrenals regenerated from adult adrenals were more responsive than adrenals regenerated either from neonatal adrenals or from adult adrenal capsules. The findings suggest that following adrenal transplantation reestablishment of normal pituitary-adrenocortical function does not occur in rats bearing adrenals regenerated from immature adrenal cells. In addition, comparable alterations occur after regeneration of adrenal tissue from neonatal adrenal cells and adult adrenal capsular cells. Elevated plasma ACTH associated with adequate plasma corticosterone in rats bearing adrenals regenerated from immature adrenal cells may result from chronic alteration in responsiveness to steroid feedback.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed2004

Dopamine receptor expression and function in human normal adrenal gland and adrenal tumors.

Dopamine is known to play a role in the modulation of aldosterone and catecholamine secretion from the adrenal gland, where dopamine receptors (DR), in particular the DR type 2 (D(2)), have been found to be expressed. DR expression has also been demonstrated in some types of benign adrenal tumors. The aims of the current study were to evaluate DR expression and D(2) localization in the normal adrenal gland and in different types of benign and malignant adrenal tumors, as well as to evaluate the in vitro effects of the dopamine agonists bromocriptine and cabergoline on hormone secretion in nontumoral adrenal cells. Adrenal tissues from 25 patients, subjected to adrenal surgery for different diseases, were studied. These included three normal adrenals; five adrenal hyperplasias; four aldosterone-secreting, two cortisol-secreting, and two clinically nonfunctioning adrenal adenomas; two aldosterone-secreting, two cortisol-secreting, and two androgen-secreting adrenal carcinomas; and three pheochromocytomas. In all tissues, DR and D(2) isoform (D(2long) and D(2short)) expression was evaluated by RT-PCR. D(2) localization was also evaluated by immunohistochemistry using a specific polyclonal antibody, whereas D(2)-like receptor expression was evaluated by receptor-ligand binding study, using the radiolabeled D(2) analog (125)I-epidepride. The effects of bromocriptine and cabergoline on baseline and ACTH and/or angiotensin II-stimulated aldosterone, cortisol, and androstenedione secretion were evaluated in cell cultures derived from five different adrenal hyperplasia. At RT-PCR, both D(1)-like and D(2)-like receptors were expressed in all normal and hyperplastic adrenals. D(2) and D(4) were expressed in aldosterone- and cortisol-secreting adenomas, cortisol-secreting carcinomas, and clinically nonfunctioning adenomas, whereas no DR was expressed in aldosterone- and androgen-secreting carcinomas. D(2), D(4), and D(5) were expressed in pheochromocytomas. In all D(2)-positive tissues, both D(2) isoforms were expressed, with the exception of one case of aldosterone-secreting adenoma and the cortisol-secreting carcinomas, in which only the D(2long) isoform was expressed. D(2)-like receptor expression was confirmed at receptor-ligand binding study. At immunohistochemistry, D(2) was mainly localized in the zona glomerulosa and reticularis of the adrenal cortex and, to a lesser extent, in the zona fasciculata and medulla of normal and hyperplastic adrenal tissue. In the positive tumors, D(2) was localized in the tumoral cells. At the in vitro study, a significant inhibition of both baseline and ACTH-stimulated aldosterone secretion was found after high-dose cabergoline, but not bromocriptine, administration; and a significant inhibition of angiotensin-II-stimulated aldosterone secretion was found after both bromocriptine and cabergoline administration in the adrenal hyperplasias. In conclusion, the current study demonstrated that both D(1)-like and D(2)-like receptors are expressed in the normal adrenal gland and in a percentage of adrenal adenomas or carcinomas. Bromocriptine and cabergoline induce only a minor inhibition of the secretion of adrenal hormones in the nontumoral adrenal gland in vitro, not excluding, however, the possible effective use of dopamine agonists in vivo in the treatment of adrenal tumors.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Ultrasonographic adrenal gland measurements in dogs without evidence of adrenal disease.

The purpose of this retrospective study was to determine measurements of adrenal glands from longitudinal sonograms, in a large population of dogs and to correlate these measurements to age, sex and descriptors of body size. Dogs were selected from the clinic population presented for routine abdominal ultrasonography between September, 1991 and March, 1994. Dogs with elevated serum cholesterol or alkaline phosphatase levels, polyuria/polydipsia, and/or clinical diagnoses of adrenal pathology were excluded. Dogs with ultrasound-documented abnormalities (mass lesions, abnormal architecture) of either adrenal were not considered. Age, sex, weight and breed were recorded, and the body surface area of each dog was calculated. Adrenal length and caudal polar width were determined from longitudinal, two-dimensional ultrasound images. Adrenal measurements were compared with body size measurements and age using least squares linear regression analysis and the correlation coefficient (r) and coefficient of determination (r2) calculated. One hundred and ninety three dogs were included in the study, with a weight and body surface area range of 1.8-72 kg and 0.2-1.8 m2, respectively. The left adrenal gland (n = 182) length range was from 10.7 to 50.2 mm, and the range of the caudal polar widths was 1.9 to 12.4 mm. Right adrenal gland (n = 85) length range was from 10 to 39.3 mm, and the range of the caudal polar widths was from 3.1 to 12 mm. In dogs where both adrenal gland lengths were measured (n = 74), the right adrenal gland length was less than that of the left in 46 dogs, equal to the left in one dog, and greater than the length of the left in 27 dogs. The strongest linear association was noted between the left adrenal gland length and body weight (kg, r = 0.71, p < 0.0001) or body surface area (m2, r = 0.71, p < 0.0001). Similar significant association was noted between the right adrenal gland length and body weight (kg, r = 0.69, p < 0.0001). A significant positive association was also noted between age and left adrenal gland length, (r = 0.25, p = 0.009). The summation of all four adrenal measurement values (left length and width, right length and width) did slightly improve the correlation (r = 0.74, p < 0.0001) when compared with body weight (kg). There was not a significant difference in the adrenal measurements with regard to sex. With regard to the correlation coefficient values, there was no advantage noted to calculating the body surface area from body weight. The causes for the low degrees of the correlation between adrenal size and the variables investigated in this study are unknown; measurement error, effects of non-adrenal illness on adrenal size, and a non-linear or complex linear relationship between adrenal gland size (as measured by longitudinal parameters) and descriptors of body size are among possible explanations.

Adrenal Glands↗
PubMed2004

Changing role of imaging-guided percutaneous biopsy of adrenal masses: evaluation of 50 adrenal biopsies.

OBJECTIVE: Prior series of percutaneous imaging-guided biopsies of adrenal masses before the advent of dedicated CT and MRI of the adrenal glands have shown that 40-57% of adrenal masses biopsied were adenomas-benign lesions requiring no further evaluation or treatment. This study was performed to assess the effect of dedicated adrenal imaging with CT and MRI on the rate of percutaneous imaging-guided biopsies of adrenal masses. MATERIALS AND METHODS: We reviewed 50 consecutive adrenal mass biopsies performed during a 48-month period. The patient demographics, technique of biopsy, pathology results, and results of any prior dedicated adrenal imaging with MRI or CT protocols were noted. RESULTS: Only six (12%) of 50 biopsies were adenomas. Five of these six cases were preceded by dedicated adrenal CT or MRI. Thirty-five cases were metastatic disease, four were adrenal cortical carcinoma, three were pheochromocytoma, and two biopsies were nondiagnostic. Overall, 20 of 50 cases were preceded by a dedicated adrenal CT or MRI examination to exclude an adenoma; in 21 of the remaining 30 cases, the imaging characteristics before biopsy were inconsistent with the potential diagnosis of an adenoma and dedicated adrenal CT or MRI was not recommended. CONCLUSION: The number of adrenal adenomas biopsied has declined markedly with the introduction of dedicated adrenal CT and MRI for adrenal adenomas. Percutaneous imaging-guided biopsy is useful in confirming the presence and nature of suspected metastatic deposits to the adrenal gland and in diagnosing or excluding adrenal adenomas in patients with equivocal imaging characteristics.

Adenoma↗
PubMed2000

Rat adrenal transplants are reinnervated: an invalid model of denervated adrenal cortical tissue.

Adrenal autotransplantation is a widely used approach to investigate the potential for neural modulation of adrenal cortical function. It is believed that regenerating adrenal transplants are not reinnervated, thereby providing a model to investigate adrenal function in the absence of neural modulation. However, the hypothesis that adrenal transplants become reinnervated has not been directly tested. The purpose of the present study was to characterize the time course, extent, and nature of the reinnervation of the regenerating adrenal transplant and to assess whether the recovery of steroidogenic function and enzyme expression correlates temporally with the presence of innervation. Using immunohistofluorescent detection of tyrosine hydroxylase (TH), neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP), the innervation of regenerating adrenals was assessed 14-30 days after transplantation of adrenal capsules beneath the kidney capsule in rats. Extensive reinnervation by TH-, NPY-, and VIP-positive fibres was present by 14 days after transplantation including regions of the adrenal capsule and cortex, with only minimal reinnervation by CGRP-positive fibres up to 30 days. TH- and NPY-positive chromaffin cells were also observed in the regenerating transplants. In addition, there was marked recovery of steroidogenic function and steroidogenic enzyme expression up to 30 days. The finding that nerve fibres are present in the transplants during the re-establishment of steroidogenic function and enzyme expression suggests that innervation may modulate the regeneration and functional recovery of adrenal transplants. In an attempt to prevent reinnervation of transplants, adrenal capsules were autotransplanted to denervated kidneys. Immunohistochemical analysis showed that, despite extensive denervation of the kidney tissue, the reinnervation and regeneration of the adrenal transplants still occurred. These data demonstrate the marked capacity of the regenerating adrenal to become reinnervated and reinforces the conclusion that adrenal transplants are an invalid model of denervated adrenal cortical tissue.

Adrenal Cortex↗
PubMed2002

Adrenal antibodies detect asymptomatic auto-immune adrenal insufficiency in young women with spontaneous premature ovarian failure.

BACKGROUND: Auto-immune adrenal insufficiency is a potentially fatal disorder. Young women with spontaneous premature ovarian failure (POF) are at increased risk of developing this condition. METHODS: We further characterized auto-immune adrenal insufficiency in this population by conducting an in-depth cross-sectional evaluation of adrenal function in a series of 123 women. RESULTS: We uncovered a new diagnosis of adrenal insufficiency in four women [3.2%, 95% confidence interval (CI) 0.2-6.4%]. All four tested positive for adrenal antibodies as detected by a clinically available indirect immunofluorescence assay. A positive adrenal antibody test was highly associated with adrenal insufficiency while a negative test was associated with normal adrenal function in all cases (P < 0.001). Adrenal antibodies increased the pretest probability of adrenal insufficiency from 3.2 to 67%. As a screening method the cortisol response during a standard adrenocorticotrophic hormone (ACTH) stimulation test gave two false positive results (1.7%, upper 95% confidence limit 5.0%). CONCLUSIONS: Our findings suggest that measuring adrenal antibodies would be an effective screening method by which to detect auto-immune adrenal insufficiency in young women with spontaneous POF. The standard ACTH stimulation test should be reserved to confirm adrenal insufficiency in women with adrenal antibodies, or those with signs and symptoms of adrenal insufficiency.

Adrenal Glands↗
PubMed1985

Sympathetic adrenal denervation decreases adrenal blood flow without altering the cortisol response to hemorrhage.

To test whether or not adrenal sympathetic innervation is required for the adrenocortical response to small hemorrhage, awake dogs were studied after unilateral adrenal sympathetic denervation. Bilateral adrenal vein cannulas were placed chronically to permit measurement of cortisol, epinephrine, and norepinephrine secretion rates and adrenal blood flow simultaneously from the intact and the denervated adrenal. Plasma ACTH concentration was measured and the presentation rate of ACTH was calculated as the product of plasma ACTH concentration and adrenal plasma flow. Unilateral isolation of the sympathetic chain from the spinal cord at thoracic levels 9-12 (T9-12) had no effect on adrenal blood flow, on the presentation rate of ACTH, or on cortisol secretion after 10 mg/kg hemorrhage. However, thoracic levels 9-12 denervation prevented the secretory response of catecholamines to hemorrhage without lowering basal catecholamine secretion. Unilateral splanchnicotomy, the sectioning of the thoracic and upper lumbar splanchnic nerves, reduced adrenal blood flow and the presentation rate of ACTH, suppressed basal catecholamine secretion, and prevented the catecholamine response to hemorrhage. However, there was no reduction in the secretory response of cortisol to 10% or 20% hemorrhage. These findings suggest that in the absence of sympathetic innervation to the adrenal, increases in adrenal sensitivity to ACTH occur to offset decreased ACTH presentation rate resulting in a normal cortisol response to hemorrhage. However, adrenal sensitivity to exogenous ACTH was not increased in non-hemorrhaged dogs after unilateral splanchnicotomy. Thus, hemorrhage must activate a non-ACTH mechanism that is independent of sympathetic adrenal innervation to augment adrenal sensitivity to ACTH. Sympathetic innervation to the adrenal has profound effects on catecholamine secretion and on adrenal blood flow but is not required for the secretory response of cortisol to small hemorrhage.

Adrenal Gland Diseases↗
PubMed1982

[The localization of aldosterone-producing adenoma on computed tomography--a comparative study with adrenal scintigraphy and plasma aldosterone concentration in the adrenal or renal vein].

The evaluation of computed tomography (CT) for detecting aldosterone-producing adenoma in primary aldosteronism was performed by comparison with adrenal scintiscan; determination of aldosterone in adrenal or renal veins, retroperitoneal pneumography and adrenal venography was reliable for diagnosis of adrenal tumors in pheochromocytoma or Cushing's syndrome, but not so effective for small adenoma of primary aldosteronism. An abdominal CT scan was performed on six patients with primary aldosteronism, one with idiopathic hyperaldosteronism and one with glucocorticoid responsive hyperaldosteronism; in an attempt to evaluate the utility of this noninvasive procedure. Diagnosis of hyperaldosteronism was made by demonstrating the elevated plasma aldosterone concentration and aldosterone secretion rate, normal excretion rate of urinary 17-OHCS and 17-KS, and low plasma renin activity. The CT scan correctly predicted unilateral adrenal adenoma in all the patients with primary aldosteronism of which the findings were identical to those demonstrated by surgery. The diameter of these tumors ranged from 10 X 7 X 6 to 19 X 17 X 14 mm. Also the CT scan in idiopathic hyperaldosteronism and glucocorticoid responsive hyperaldosteronism showed bilateral adrenal hyperplasia and bilateral normal adrenal glands, respectively. The pathological findings in these two cases disclosed the adrenal hyperplasia of zona glomerulosa and adrenal hyperplasia of zona subglomerulosa accompanied by a normal thickness of the adrenal gland, respectively. The precision of the CT scan, adrenal scintigraphy and determination of plasma aldosterone in the adrenal or renal veins were almost equal to the diagnosis of the localization of adrenal adenoma. It is concluded that the CT scan is a noninvasive and most useful method for the localization of aldosterone-producing adenoma and helpful in distinguishing adrenal adenoma from adrenal hyperplasia.

Adenoma↗
PubMed1975

Control and localization of rat adrenal cyclic guanosine 3', 5'-monophosphate. Comparison with adrenal cyclic adenosine 3', 5'-monophosphate.

Cyclic AMP and cyclic GMP were measured in rat adrenal glands after either hypophysectomy alone or after hypophysectomy and treatment with ACTH. Adrenal cyclic GMP levels rise in acutely hypophysectomized rats to a maximum at 1 h of approximately 200% of control levels; there is a return to base line at 4-12 h after hypophysectomy. In contrast, adrenal cyclic AMP falls immediately to about 50% of control levels after hypophysectomy and remains at approximately 1 pmol per mg tissue. Doses of ACTH beyond the physiological range markedly suppress adrenal cyclic GMP while producing a 50-fold or greater rise in cyclic AMP in hypophysectomized rats. This pattern of adrenal cyclic GMP rise was unchanged in acutely hypophysectomized animals treated with desamethasone. N-6-2'-0 dibutyryl cyclic AMP acted similarly to the effect of ACTH in bringing about a suppression of adrenal cyclic GMP levels. Physiological i.v. pulse doses of ACTH produced a rapid dose related increase in adrenal cyclic GMP. In vitro incubation of quartered adrenal pairs with 500 mU ACTH produced elevated cyclic AMP levels and suppression of cyclic GMP. Whereas adrenal cyclic AMP fell rapidly to 50% of control levels after hypophysectomy and remained at about 1 pmol per mg tissue for 7 days, adrenal cyclic GMP showed a biphasic rhythm in long-term hypophysectomized animals. After an initial peak at 1 h after hypophysectomy, adrenal cyclic GMP declined to baseline at 4-12 h but thereafter progressively rose with time, eventually reaching levels over 1 pmol per mg tissue. Fluorescent immunocytochemical staining of rat adrenal zona fasciculata showed cyclic AMP largely confined to cytoplasmic elements with little fluorescence contained in nuclei. In constant, cyclic GMP was found discretely positioned in nuclei with prominent fluorescence in nucleoli in addition to cytoplasmic localization. It is concluded that in hypophysectomized rats ACTH, either directly or in conjunction with altertion of adrenal cyclic AMP, appears to be one factor which regulates adrenal cyclic GMP. The direction of cyclic GMP change and the different subcellular localization of the nucleotides suggest divergent roles for cyclic AMP and cyclic GMP in adrenocortical function. Furthermore, our observations suggest a role for adrenal cyclic GMP in nuclear directed events.

Adrenal Glands↗
PubMed1991

Magnetic resonance imaging of the adrenal gland in women with late-onset adrenal hyperplasia.

To determine the presence of structural abnormalities of the adrenal in late-onset adrenal hyperplasia, four consecutive patients were studied by MRI before beginning glucocorticoid replacement therapy. Three women were diagnosed as 21-hydroxylase deficient late-onset adrenal hyperplasia by a 17-OHP level greater than 1,000 ng/dL 30 minutes after acute adrenal stimulation, and one patient was diagnosed as 11-hydroxylase deficient late-onset adrenal hyperplasia when her 11-deoxycortisol level was threefold the upper 95th percentile of normal. Two patients with 21-hydroxylase deficient late-onset adrenal hyperplasia had normal adrenal glands on MRI. Another 21-hydroxylase deficient late-onset adrenal hyperplasia patient was noted to have a 2.5 x 3.3-cm left adrenal nodule, which had been documented some 4 years earlier on CT scan and had not changed in size during that interval. This patient was 40 years of age when the diagnosis of late-onset adrenal hyperplasia was established. The patient with 11-hydroxylase deficient late-onset adrenal hyperplasia demonstrated a diffuse enlargement of the left adrenal gland consistent with hyperplasia, with no focal lesions. In conclusion, although patients with late-onset adrenal hyperplasia may often demonstrate nodular or diffuse adrenocortical hyperplasia on MRI, not all patients with endocrinologically evident disease demonstrate such abnormalities, consistent with a lesser degree of ACTH stimulation compared with women with classical congenital adrenal hyperplasia.

Adrenal Glands↗
PubMed1990

Characterization of adrenal autonomy in Cushing's syndrome: a comparison between in vivo and in vitro responsiveness of the adrenal gland.

We measured cortisol and precursor steroid production in response to ACTH, cholera toxin, and forskolin by the dispersed adrenocortical cells prepared from the adrenal glands of 10 patients with different forms of Cushing's syndrome. The cells prepared from the hyperplastic adrenal glands from 4 patients with Cushing's disease responded in a dose-dependent manner to ACTH, cholera toxin, and forskolin. The adrenal cells prepared from 4 encapsulated adrenal adenomas showed no (n = 2), a lowered (n = 1), or a clear (n = 1) response of cortisol release to ACTH. The cells prepared from the adrenal glands of 1 patient with dysplastic micronodular adrenal glands showed a limited response to ACTH, while the cells from an adrenocortical carcinoma, which secreted very little cortisol per cell, were unresponsive to ACTH, cholera toxin, and forskolin. The reaction of the dispersed adrenal cells from these 10 patients to ACTH, cholera toxin, and forskolin showed a close correlation (P less than 0.001 in all instances). This suggests that the defect in autonomous glands is not located at the level of the ACTH receptor, but, rather, involves the adenylate cyclase complex as a whole or its coupling to cAMP-dependent protein kinase. The release into the medium of the cortisol precursors deoxycortisol, 17-hydroxyprogesterone, and progesterone showed that the four autonomous nodules were characterized by a significantly higher deoxycortisol/cortisol ratio in the medium (P less than 0.01), suggesting a relative blockade of 11 beta-hydroxylase in these adrenal adenomas. This was further substantiated in cells from several adrenals by a significant increase in the release of these precursors in response to ACTH in the absence of a cortisol response. We conclude the following. 1) Adrenal adenoma formation in patients with Cushing's syndrome is accompanied by a parallel decrease in the stimulation of the release of steroid hormones in response to ACTH, cholera toxin, and forskolin. This points to a defect in the adenoma cells beyond the ACTH receptor. 2) Adrenal adenoma formation in patients with Cushing's syndrome is accompanied by a relative blockade of 11 beta-hydroxylase activity. 3) By comparing the preoperative dynamic tests of the pituitary-adrenal axis, the plasma ACTH concentration, the morphology of the adrenal glands, and their in vitro responsiveness, a gradual transition from pituitary to (partial) adrenal autonomy could be recognized in several patients.

17-alpha-Hydroxyprogesterone↗