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PubMed2003

A case of aldosterone-producing adrenocortical adenoma associated with a probable post-operative adrenal crisis: histopathological analyses of the adrenal gland.

We describe a case of aldosterone-producing adrenocortical adenoma (APA) associated with a probable post-operative adrenal crisis possibly due to subtle autonomous cortisol secretion. The patient was a 46-year-old female who suffered from severe hypertension and hypokalemia. CT and MRI scans revealed a 2-cm diameter adrenal mass. The patient's plasma aldosterone level was increased, and her plasma renin activity was suppressed, both of which findings were consistent with APA. Cushingoid appearance was not observed. Morning and midnight serum cortisol and plasma adrenocorticotropic hormone (ACTH) levels were all within the normal range. Her serum cortisol level was suppressed to 1.9 microg/dl as measured by an overnight 1-mg dexamethasone suppression test, but was incompletely suppressed (2.7 microg/dl) by an overnight 8-mg dexamethasone suppression test. In addition, adrenocortical scintigraphy showed a strong uptake at the tumor region and a complete suppression of the contra-lateral adrenal uptake. After unilateral adrenalectomy, she had an episode of adrenal crisis, and a transient glucocorticoid replacement improved the symptoms. Histopathological studies demonstrated that the tumor was basically compatible with APA. The clear cells in the tumor were admixed with small numbers of compact cells that expressed 17alpha-hydroxylase, suggesting that the tumor was able to produce and secrete cortisol. In addition, the adjacent non-neoplastic adrenal cortex showed cortical atrophy, and dehydroepiandrosterone sulfotransferase immunoreactivity in the zonae fasciculata and reticularis was markedly diminished, suggesting that the hypothalamo-pituitary-adrenal (HPA) axis of the patient was suppressed due to neoplastic production and secretion of cortisol. Together, these findings suggested that autonomous secretion of cortisol from the tumor suppressed the HPA axis of the patient, thereby triggering the probable post-operative adrenal crisis. Post-operative adrenocortical insufficiency should be considered in clinical management of patients with relatively large APA, even when physical signs of autonomous cortisol overproduction are not apparent.

3-Hydroxysteroid Dehydrogenases↗
PubMed1992

Production of active and inactive renin by adrenal explant cultures and the existence of a prorenin activating enzyme in the adrenal gland.

We previously demonstrated high levels of inactive renin (IR) in nephrectomized rat plasma which provided evidence for extra-renal sources of IR. However, the sources of IR were unknown. This study examined whether the adrenal gland is capable of producing active renin (AR) and IR, using explants of adrenal capsules (glomerulosa portions) from control and nephrectomized (Nepex) rats. Explants from both control and Nepex rats produced large quantities of IR and small quantities of AR. The productions of both IR and AR in Nepex rats were significantly greater than in control rats. High potassium culture medium markedly increased IR and slightly, but significantly, enhanced AR in both control and Nepex rats. On the other hand, sodium had little effect on either IR or AR. A renin-angiotensin system has been reported in the adrenal gland. Recently, a prorenin activating enzyme was demonstrated in the kidney and the aortic wall. The next study was performed to demonstrate the existence of a prorenin activating enzyme in the adrenal gland, using inactive renin from culture medium from Nepex rat explants as the substrate. A 26 KD component in adrenal zona glomerulosa tissues isolated by Sephacryl S-200 column chromatography, converted IR to AR in IR rich medium. The pH optimum for prorenin activation by the enzyme was 6.5. Inhibitor studies indicate that this enzyme is a serine protease. These data suggest that (1) the adrenal gland is an extra-renal source of inactive renin and (2) a prorenin activating enzyme exists in the adrenal gland.

Adrenal Glands↗
PubMed1984

Adrenal and extra-adrenal pheochromocytomas: an ultrastructural and formaldehyde-induced fluorescence study with catecholamine content.

Twenty-one adrenal and 6 extra-adrenal pheochromocytomas were studied by light and electron microscopy, and formaldehyde-induced fluorescence (FIF). These morphological findings were compared to the content of tumor catecholamines. Based on predominancy of the cell types, pheochromocytomas were classified into three groups: basophilic, chromophobic and oxyphilic (oncocytic) types. The basophilic type was characterized by basophilic cytoplasm of the tumor cells with hematoxylin and eosin (H & E) stain, green cytoplasmic fluorescence with FIF and numerous epinephrine type of electron dense granules with electron microscopy. Its epinephrine content was compatible to the normal adrenal medulla. The basophilic type was only of adrenal origin. Chromophobic and oxyphilic tumors contained predominantly norepinephrine, and showed yellow-green or light brown cytoplasmic fluorescence by FIF. By electron microscopy, various granules of different sizes and shapes of the norepinephrine type were noted. Extra-adrenal pheochromocytoma cells demonstrated dark brown cytoplasmic fluorescence by FIF. Morphological findings of the extra-adrenal tumor corresponded to those of chromophobic type adrenal pheochromocytoma. The tumors contained only norepinephrine.

Adrenal Gland Neoplasms↗
PubMed1989

Prenatal development of the adrenal in pig Sus scrofa dom. Part II. Adrenal cortex development in the second part of pregnancy.

The development of the adrenal cortex in pig fetuses between the 50 and 112 day of pregnancy were investigated with histological and histochemical methods and in electron microscope. Three consecutive generations of the cortical cells were observed. They had features of steroidogenic cells and differed with mature of mitochondria and in amount of SER and in enzyme activity. The earliest differentiated fetal cortical cells demonstrated alkaline phosphatase activity and giant mitochondria. They were translocated from the periphery to the center of the adrenal, where they degenerated and disappeared in the late pregnancy. The second generation--transitional cortical cells appeared about 70 day of development. They have pleomorphic mitochondria and abundant SER and low alkaline phosphatase activity. The last generation--the definitive cortical cells differentiated from 100 day of development and their number increased till the parturition. They had active 3-beta-hydroxysteroid dehydrogenase, spherical mitochondria and characteristic concentric whorls of SER. A probable role of the three generations of cortical cells is was discussed. In the subcapsular region of fetal adrenal undifferentiated and differentiating cells were observed, forming glomerularlike groups. Their role in the formation of cortical blastema and future zona glomerulosa was discussed. In the first part of the studies the formation of the mesenchymal primordium of the adrenal cortex was examined in early fetuses of domestic pig, and then differentiation of mesenchymal cells into steroidogenic cortical cells. The changes encountered then at the ultrastructural level consisted of an increased area of SER and greater number of mitochondria. At the same time, the shape of mitochondria altered and the cristae from lamellar became tubular. In the period around 50 day of development fetal adrenal was already a separate organ, with a capsule, composed of cords of fetal cortical cells divided by the blood vessels and strands of chromaffinoblasts penetrating the adrenal. Fetal cortical cells were characterized by alkaline phosphatase activity. The following study presents farther development of the adrenal cortex till the time of birth.

Adrenal Cortex↗
PubMed2006

Diagnostic accuracy of chemical-shift MR imaging to differentiate between adrenal adenomas and non adenoma adrenal lesions.

PURPOSE: The objective of this study was to evaluate the diagnostic accuracy of chemical-shift (CS) magnetic resonance (MR) imaging in the differential diagnosis of adenoma and nonadenoma adrenal masses. MATERIALS AND METHODS: We enrolled 36 patients (9 men, 27 women, mean age 51.3+14.4 years) with unilateral (n=31) or bilateral (n=5) adrenal masses incidentally discovered during imaging examinations [ultrasound (US), computed tomography (CT)] performed for other indications. A total of 41 adrenal lesions were evaluated (mean diameter 3.0+2.2 cm). Histology (n=19), biopsy (n=3) or clinical-imaging follow-up (n=19) demonstrated 29 adenomas, five pheochromocytomas, three cysts and four carcinomas. MR imaging was performed using the following breath-hold sequences: T1-fast field echo (FFE) [repetition time (TR)/echo time (TE)=236/4.6 ms], T2-turbo spin echo-single shot (TSE-SSh) (TR/TE=831/80 ms), T1-DUAL-FFE (TR=236, double TE=4.6/2.3 ms in phase and out of phase) and T1-FFE after gadolinium-DTPA (Gd). Axial and coronal imaging planes were used, with a slice thickness of 3-5 mm. MR images were qualitatively assessed for signal intensity of the adrenal mass relative to the liver on T1, T2, CS and T1-Gd scans; diagnostic criteria for adenomas were isointensity or hypointensity on both T1 and T2 scans, out-of-phase CS signal loss and mild transient enhancement after Gd. RESULTS: Analysis of T1-T2 signal intensity showed diagnostic accuracy, sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of 80%, 72%, 100%, 100% and 60%, respectively. In contrast, analysis of CS and T1-Gd signal intensity showed diagnostic accuracy, sensitivity, specificity, PPV and NPV for both sequences of 93%, 90% (p<0.05 vs. T1-T2 analysis), 100%, 100% and 80% (p<0.05 vs. T1-T2 analysis), respectively. CONCLUSIONS: CS MR imaging significantly improves characterization of adrenal masses compared with conventional T1-T2-weighted images, providing accuracy similar to that of the T1 sequence after Gd. Therefore, the CS sequence is strongly recommended for MR study of adrenal masses, and its use might obviate the need for Gd administration.

Adrenal Cortex Neoplasms↗
PubMed2004

Assessment of parallel acquisition techniques in adrenal magnetic resonance imaging: does increased temporal resolution significantly improve visualization of adrenal lesions?

RATIONALE AND OBJECTIVES: To compare conventional radiofrequency coil reception techniques with parallel coil array acquisition methods in adrenal tissue visualization and to evaluate the dependence of temporal resolution on image quality in adrenal magnetic resonance magnetic resonance (MR) imaging. MATERIAL AND METHODS: Using a 1.5 T MR imager, conventional and parallel sampled sequences were acquired in 10 healthy volunteers and 10 patients with adrenal lesions. The imaging protocol consisted of: conventional (TR/TE 4,730/125 ms; FA 150 degrees; NA 1; AT 25 s), and two parallel imaging SMASH techniques (TR/TE 4,090/125 ms; FA 150 degrees; NA 1 resulting in an AT of 12 s, as well as NA 2 resulting in an AT of 24 s) with generalized autocalibration T(2)-weighted turbo spin echo sequences with 5 mm slice thickness, 1.6 mm in-plane resolution, and an acceleration factor 2. Severity of breathing motion and aliasing artifact and overall image quality were rated on five-point scales and evaluated with student's t test; a differential receiver operating characteristic (DROC) analysis was performed. RESULTS: Adrenal gland findings included adenomas, metastases, and hemorrhages. Acceleration of conventional turbo spin echo sequence with one signal average led to an increase in diagnostic power (DROC 0.362) as well as significant improvement in overall image quality (P(Volunteers) =.017; P(Patients) =.042) and reduction of breathing motion artifact in patients (P(Patients) =.012) while improving the temporal resolution. Parallel imaging with two signal averages resulted in further improvement of image quality over conventional imaging (DROC 0.303), (P(Volunteers) =.045; P(Patients) =.022), in the same acquisition time as the conventional method. CONCLUSION: Parallel acceleration of sequences used for adrenal tissue visualization leads to a significant increase in diagnostic quality by significantly reducing breathing motion artifacts without sacrificing contrast indispensable for adrenal lesion characterization.

Adenoma↗
PubMed1998

Adrenal insufficiency in an adult on inhaled corticosteroids; recovery of adrenal function with inhaled nedocromil sodium.

BACKGROUND: Whereas oral corticosteroids and high-dose inhaled corticosteroids may be associated with suppression of the hypothalamic-pituitary-adrenal axis, medium-dose inhaled corticosteroids have not been reported to be associated with clinically significant adrenal insufficiency in the adult. OBJECTIVE: A case study of adrenal responsiveness after prolonged medium-dose inhaled corticosteroids and after replacement of steroid therapy by inhaled nedocromil sodium is described. METHODS: Standard 250-microg dose ACTH (cosyntropin) stimulation tests were followed after replacement of inhaled triamcinolone acetonide therapy by nedocromil sodium. RESULTS: A 55-year-old woman who had been on inhaled triamcinolone acetonide, 1600 microg/day for 12 years, presented with symptoms of adrenal hypofunction upon inhaled corticosteroid taper. An ACTH stimulation test confirmed adrenal insufficiency. She was switched to inhaled nedocromil sodium with improvement in her clinical syndrome and normalization of her ACTH stimulation test. CONCLUSION: Withdrawal from prolonged use of inhaled medium-dose corticosteroids may be associated with clinically significant adrenal insufficiency in adults. Steroid sparing agents may be considered for those on long-term inhaled corticosteroid therapy.

Administration, Inhalation↗
PubMed1991

Aldosterone synthesis in salt-wasting congenital adrenal hyperplasia with complete absence of adrenal 21-hydroxylase.

BACKGROUND: Congenital adrenal hyperplasia due to 21-hydroxylase deficiency is a disorder of cortisol and aldosterone biosynthesis that results from mutations in the CYP21 gene encoding the adrenal 21-hydroxylase P-450c21. It can cause severe salt wasting in newborns that requires long-term treatment with glucocorticoids and mineralocorticoids. We describe a spontaneous partial recovery from this disorder in a 19-year-old woman who had discontinued treatment. METHODS: We measured plasma and urinary levels of adrenal hormones, plasma renin activity, and sodium balance longitudinally in the patient and four other patients in whom adrenal hyperplasia had been diagnosed in infancy and in whom DNA analysis had predicted a complete absence of functional P-450c21. The ratio of plasma renin activity to urinary aldosterone was used as a measure of the response of the adrenal zona glomerulosa. Two patients underwent intravenous infusion of [3H]progesterone for the measurement of extraadrenal production of 21-hydroxylated precursors of aldosterone. RESULTS: The patient who had discontinued her medication excreted a normal amount of aldosterone (20.0 nmol per square meter of body-surface area per day) while following a diet low in sodium. Her ratio of plasma renin activity to urinary aldosterone-18-glucuronide excretion was 1.7 after three days of sodium restriction, as compared with a ratio of 4.7 at the age of nine years (normal range, 0.03 to 0.1). The percentage of extraadrenal conversion of progesterone to deoxycorticosterone was low. The four other patients had variable responses to sodium restriction after the neonatal period (range for plasma renin activity:urinary aldosterone-18-glucuronide, 1.9 to 19.4). CONCLUSIONS: Although patients with salt-wasting 21-hydroxylase deficiency have functionally equivalent mutations in their CYP21 genes, they may vary from one another and over time in their ability to produce mineralocorticoids. This variation may be attributable to another adrenal enzyme with 21-hydroxylase activity.

Adolescent↗
PubMed1981

The 21-hydroxylase activity in the glomerulosa and fasciculata of the adrenal cortex in congenital adrenal hyperplasia.

In the two clinical syndromes of congenital adrenal hyperplasia due to a 21-hydroxylation defect of adrenal steroidogenesis, the simple virilizing and the salt-wasting forms, the 21-hydroxylase activity was studied considering the zona fasciculata and the zona glomerulosa of the adrenal cortex as two separate glands under different regulation. To test this hypothesis, we stimulated adrenal steroidogenesis by ACTH infusion or dietary sodium restriction in eight patients with congenital adrenal hyperplasia (four patients with the simple virilizing form and four with the salt-wasting form of congenital adrenal hyperplasia) and in six normal children. Both the 17-hydroxy and 17-deoxy pathways of adrenocortical steroid biosynthesis were examined by measuring serum concentrations of 17-hydroxyprogesterone, cortisol, progesterone, deoxycorticosterone, corticosterone, and aldosterone and the excretion of free deoxycorticosterone, 18-hydroxydeoxycorticosterone, corticosterone, 18-hydroxycorticosterone, cortisol, and aldosterone. We considered the steroids 18-hydroxycorticosterone and aldosterone to be primarily of zona glomerulosa origin. These studies indicated that the zona fasciculata of both the salt-wasting and the simple virilizing forms is defective in 21-hydroxylation of 17-hydroxy and 17-deoxy steroids. The zona glomerulosa demonstrated deficient 21-hydroxylation only in the salt-wasting form, whereas in the simple virilizing form, the glomerulosa was spared this defect.

Adrenal Cortex↗
PubMed1986

Adrenal androgen hyperresponsiveness to adrenocorticotropin in women with acne and/or hirsutism: adrenal enzyme defects and exaggerated adrenarche.

To determine the adrenal contribution to elevated plasma androgens in 31 young hyperandrogenemic women with acne and/or hirsutism, we compared their responses to ACTH with those of 14 normal women. Each subject was given a low dose (10 micrograms/m2) of synthetic ACTH-(1-24) (Cortrosyn) after administration of 1.5 mg dexamethasone the night before the test. Thirty and 60 min responses of plasma 17 alpha-hydroxypregnenolone (17-Preg), 17 alpha-hydroxyprogesterone, (17-prog), dehydroepiandrosterone (DHEA), androstenedione, 11-deoxycortisol, and cortisol were measured. Eighteen (58%) patients had increased responses of at least one 17-ketosteroid or adrenal androgen precursor. All patients had cortisol responses within the range of those of the 14 normal subjects. Nine patients (29%) had evidence of steroid biosynthetic enzyme deficiencies, either mild congenital adrenal hyperplasia or the heterozygote state; after ACTH, 4 of these patients had elevated 17-prog in the range of values in heterozygote carriers of 21-hydroxylase deficiency, 2 had elevated levels of 11-deoxycortisol compatible with 11 beta-hydroxylase deficiency, and 3 had elevated levels of 17-Preg and DHEA, suggestive of 3 beta-hydroxysteroid dehydrogenase deficiency. Another 9 subjects (29%) had 17-ketosteroid (DHEA and/or androstenedione) hyperresponsiveness to ACTH with associated elevated 17-Preg responses. As a group, their patterns suggested relatively deficient 3 beta-hydroxysteroid dehydrogenase and relatively hyperactive C lyase without impairment of cortisol secretion. This pattern resembles exaggerated adrenarche, and we postulate that these 9 patients have hyperplasia of the zona reticularis. Neither basal levels of plasma androgens (free testosterone and DHEA sulfate) nor menstrual history predicted which patients would have abnormal ACTH responses. Although 5 of 11 (45%) patients with acne alone had abnormal responses to ACTH, 10 of 14 patients with acne and hirsutism (71%) had abnormal responses to ACTH. We conclude that an adrenal contribution is found in about half of hyperandrogenemic women with acne and/or hirsutism. This adrenal androgen hyperresponsiveness is heterogeneous. Some patients may have mild forms of congenital adrenal hyperplasia. However, functional androgenic hyperresponsiveness to ACTH, which resembles an exaggeration of adrenarche, is the most common abnormality found. Such findings may provide an explanation for the clinical observation of exacerbations of acne with stress.

3-Hydroxysteroid Dehydrogenases↗
PubMed1996

Human adrenal cells express tumor necrosis factor-alpha messenger ribonucleic acid: evidence for paracrine control of adrenal function.

Tumor necrosis factor (TNF) is gaining increasing importance in clinical medicine. It plays a role in the interaction of the immune system with the hypothalamic-pituitary-adrenal axis. In the present study various morphological methods, including immunohistochemistry, electron microscopy, and in situ hybridization were applied to characterize the localization and distribution of TNF in the human adrenal gland. Double immunostaining revealed an astonishing degree of intermingling of steroid-producing cells and chromaffin cells. Macrophages could be found in all regions of the adrenal gland, but particularly in the transition zone of cortex and medulla. The steroid-producing cells of the inner zone of the cortex express major histocompatibility complex class II molecules. On the ultrastructural level, immune cells, steroid cells, and catecholamine-producing cells were found in direct contact. The combination of immunohistochemistry and in situ hybridization was optimally suited to define the exact cellular source of TNF in the human adrenal. TNF is produced in macrophages, but above all in 17 alpha-hydroxylase-positive cells (steroid-producing cells) in the zona reticularis and medulla. No signal was found in chromaffin cells. TNF may induce major histocompatibility complex class II in human adrenal gland in a paracrine or autocrine manner. It is concluded that TNF may have an important role in normal human adrenal physiology.

Adrenal Cortex↗
PubMed2003

Primary bilateral adrenal intravascular large B-cell lymphoma associated with adrenal failure.

We report a rare case of bilateral primary adrenal non-Hodgkin's lymphoma with adrenal failure. A 66-year-old woman developed symptoms of adrenal failure. The cause of adrenal failure was suspected to be malignant lymphoma based on the high levels of serum soluble interleukin-2 receptor and LDH. Bilateral adrenalectomy was performed and pathological examination showed intravascular large B-cell lymphoma (IVL). Although complete remission was achieved, recurrence occurred three months later with brain metastases. IVL should be suspected in patients with bilateral adrenal tumors who present with rapidly progressive adrenal failure.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Adrenal insufficiency in a patient with severe hypotension caused by bilateral adrenal hemorrhage.

OBJECTIVE: To describe a patient with adrenal insufficiency and bilateral adrenal enlargement and to review causes of adrenal insufficiency, with special emphasis on adrenal hemorrhage. METHODS: We present the clinical course of a woman with apparent septic shock, who responded poorly to treatment with inotropic agents. The possible cause and management of such cases are discussed. RESULTS: A 44-year-old woman with no prior major illness required medical attention because of severe hypotension, volume depletion, acute renal failure, and shock. Numerous laboratory and radiologic studies were performed to determine the cause of her shock state. She did not respond to several inotropic agents. When she was found to have adrenal insufficiency, initiation of treatment with glucocorticoids promptly alleviated her hypotension. CONCLUSION: Critically ill patients who have sudden unexplained hypotension that does not respond to supportive management should be screened for adrenal insufficiency. The current patient emphasizes the importance of considering this disorder in the differential diagnosis of hypotension that is unresponsive to pressor agents.

Adrenal Gland Diseases↗
PubMed1992

Incidentally found adrenal tumours: results of investigation of the pituitary-adrenal axis.

In the last 7 years 64 patients (48 women, 16 men, aged 25-75 yrs) with incidentally found asymptomatic adrenal tumours have been observed in the Department of Endocrinology. In 11 patients a routine clinical investigations revealed metastatic tumours at the adrenal glands. In the remaining 53 patients the diameter of the adrenal tumours was < or = 3 cm. Only two of them were treated surgically; the rest has been observed regularly and ultrasonographic examinations have been repeated every 3 to 6 months. Twenty three patients with adrenal tumours < 3 cm of diameter were treated by surgery. The macroscopical examination revealed adrenal cortical adenoma in 11 cases, adrenocortical carcinoma in seven, and pheochromocytoma in 5 patients. The investigation of the pituitary-adrenal system (urinary excretion of 17-OHCS before and during dexamethasone administration, 17-KS, "free" corticosteroids, plasma ACTH, cortisol and S-DHA levels) did not reveal any abnormality except that in 10 patients the plasma ACTH concentration was low, especially in the morning. These values were significantly lower as compared with the remaining patients and with control group. One of the possible interpretations is a pituitary suppression by only periodically increased concentrations of the corticosteroids.

Adrenal Gland Neoplasms↗
PubMed1997

Immunoreactive adrenomedullin in human adrenal glands and adrenal tumors.

Adrenomedullin is a potent vasodilator peptide that was isolated from human pheochromocytoma. We developed a sensitive and specific radioimmunoassay for adrenomedullin and studied the presence of adrenomedullin in human adrenal glands and adrenal tumors, including pheochromocytoma. High concentrations of immunoreactive adrenomedullin were found in normal parts of adrenal glands (cortex and medulla) (12.6 +/- 1.0 pmol/g wet wt, N = 7, mean +/- SEM). High concentrations of immunoreactive adrenomedullin were also present in the tumor tissues of pheochromocytoma (4.5 +/- 1.5 pmol/g wet wt, N = 11). Immunoreactive adrenomedullin was detected in some adrenocortical tumors, but these concentrations were much lower than those in the normal adrenal glands and pheochromocytomas. Reverse phase high-performance liquid chromatography of the normal adrenal gland and pheochromocytoma showed a peak eluting in the position of synthetic adrenomedullin 1-52. The present study has shown the presence of high concentrations of immunoreactive adrenomedullin in the normal adrenal glands and pheochromocytomas.

Adenocarcinoma↗
PubMed1994

Immunoreactive C-type natriuretic peptide in human adrenal glands and adrenal tumors.

C-type natriuretic peptide (CNP) in human adrenal glands and adrenal tumors was measured with a specific radioimmunoassay for CNP. Tissue immunoreactive (IR-) CNP concentrations were 0.54 +/- 0.40 pmol/g wet tissue (gwt) (mean +/- SD) in 14 pheochromocytomas, 0.69 +/- 0.19 pmol/gwt in six adrenocortical tumors, and 0.49 +/- 0.22 pmol/gwt in seven normal adrenal glands (cortex and medulla mixed). These concentrations were comparable to those found in tissues from human brains. Sephadex G-50 superfine column chromatography and reverse-phase high performance liquid chromatography revealed that IR-CNP in normal adrenal glands and pheochromocytoma consisted of at least two components: a component in low molecular weight form chromatographically identical to CNP-22 and the other, a high molecular weight form very similar to human CNP-53. This study has shown that IR-CNP is present in human adrenal glands and adrenal tumors with similar molecular forms and comparable concentrations to those in the human brain.

Adenoma↗
PubMed1992

Effect of chronic ACTH treatment on guinea-pig adrenal steroidogenesis: steroid plasma levels, steroid adrenal levels, activity of steroidogenic enzymes and their steady-state mRNA levels.

We report here the effects of a 7-day treatment of guinea-pigs with ACTH on adrenal mRNA levels for steroid-transforming enzymes. Adrenal 3 beta-hydroxysteroid dehydrogenase 4-ene-5-ene-isomerase (3 beta-HSD), 17-hydroxylase, 17,20-lyase, 21-hydroxylase and 11-hydroxylase activities were also examined as well as plasma and adrenal steroid levels. Our data reveal that chronic ACTH-treatment stimulated all post-pregnenolone enzyme activities in glomerulosa-fasciculata cells. Plasma steroid levels increased 8 h after the last injection of ACTH and returned to the control levels 24 h later whereas, in the adrenal, the content in steroids in the group sacrificed 8 h after the last injection of ACTH were similar to the values of the control group and decreased markedly 24 h later. It is suggested that the steroid turn-over in the adrenal may be affected by the chronic ACTH-treatment. On the other hand, despite the significant stimulation in steroid-transforming enzyme activities, our data reveal that chronic ACTH administration caused a decrease in mRNA levels for P450c21 and P450c17 while P450scc, 3 beta-HSD and P450c11 remained unchanged. Taken together, these results suggest that in vivo chronic ACTH-treatment of guinea-pigs increases adrenal steroidogenic capacity by increasing steroid secretion and steroid enzyme activity. Moreover, the chronic treatment with ACTH may have a post-transcriptional effect on steroidogenic enzymes gene expression by affecting the half-life of their mRNAs.

3-Hydroxysteroid Dehydrogenases↗
PubMed1989

Prenatal fetal adrenal suppression following in utero diagnosis of congenital adrenal hyperplasia.

Congenital adrenal hyperplasia due to 21-hydroxylase deficiency can result in marked virilization of the external genitalia of affected female subjects. Theoretically, suppression of the fetal pituitary-adrenal axis with glucocorticoid during gestational weeks 9 to 17 should prevent the development of ambiguous genitalia in the female fetus. Prenatal diagnosis of congenital adrenal hyperplasia can be made on elevated amniotic fluid 17-hydroxyprogesterone and adrenal androgen concentrations, and HLA typing of cultured amniotic fluid cells. However, these tests cannot be completed before 16 to 17 weeks of gestation, and maternal therapy would have to be instituted before the exact genetic status of the fetus is known. Chorionic villus sampling during the first trimester provides an alternative to second trimester diagnosis in patients who are at risk for bearing offspring with congenital adrenal hyperplasia. We report the use of dexamethasone suppression at 8 weeks of gestation in a 34-year-old woman whose son had congenital adrenal hyperplasia due to severe salt-losing 21-hydroxylase deficiency and whose biopsy revealed a 46XX chromosomal pattern. Cultured cells from the biopsy confirmed the fetus to be of identical HLA haplotype to the previous affected sibling. At 41 weeks the patient delivered a female neonate with minimal prominence of the clitoris, mildly rugated labia, a single perineal opening and minimal posterior labial fusion. Postnatal tapering of maternal steroids was performed with no long-term sequelae.

Adrenal Hyperplasia, Congenital↗