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PubMed2004

Cystic adrenal neoplasms.

BACKGROUND: Cystic lesions of the adrenal gland are uncommon and demonstrate a spectrum of histologic changes and may vary from pseudocysts to malignant cystic neoplasms. METHODS: The authors analyzed a series of primary cystic lesions of the adrenal gland to evaluate the clinicopathologic features and histologic spectrum and to determine features that are helpful in distinguishing benign from malignant cystic adrenal tumors. RESULTS: A total of 41 cases of macroscopically cystic lesions among patients who underwent surgery at the Mayo Clinic were identified over a 25-year period. Of these 41 cases, 32 were pseudocysts, 8 were endothelial cysts, and 1 was an epithelial cyst. Of the 32 pseudocysts, 6 were associated with adrenal neoplasms, including 2 adrenal cortical carcinomas, 2 adrenal cortical adenomas, and 2 pheochromocytomas. One pheochromocytoma case was identified in association with an endothelial cyst. Both patients with cystic adrenal cortical carcinomas died of disease. CONCLUSIONS: Adrenal neoplasms, including adrenal cortical carcinomas, may be associated with benign-appearing cysts. Extensive pathologic sampling of resected tissues is important to rule out malignancy in patients with cystic adrenal lesions.

Adolescent↗
PubMed1987

[Silent adrenal gland tumors in patients with adrenogenital syndrome].

Adrenal tumors accidently detected by CT scan are increasingly seen in patients without clinical signs of adrenal diseases. We studied whether enhanced adrenal stimulation is of importance in the development of adrenal tumors. For this purpose 22 patients with adrenogenital syndrome (AGS) were studied by CT scan. One of these patients suffered from C-11 beta-hydroxylase-, one from C-3 beta-hydroxy steroid dehydrogenase-, and 20 from C-21-hydroxylase deficiency. The average adrenal size of these patients was 506 +/- 79 mm2 as compared to 132 +/- 8 mm2 in the controls (P less than 0.001). Only two patients with the late onset form revealed adrenal glands of normal size. There was a significant correlation between adrenal size and patients' age (P less than 0.01). Females with the simple virilizing form revealed adrenal glands larger than those of the late onset form (640 +/- 169 vs 308 +/- 56 mm2). Eighteen patients with AGS exhibited one (n = 11) or several (n = 7) adrenal tumors, the size of which was 5-9 mm in diameter in 9, 10-20 mm in 7, and more than 50 mm in 2 patients. There was a significant correlation between adrenal hyperplasia and tumor diameter (P less than 0.001). No correlation was found between tumor size and plasma concentrations of testosterone or 17-hydroxyprogesterone, patients' age at the time of diagnosis, or clinical signs of androgenization. Again, tumors were larger in females suffering from the simple virilizing form of AGS than in those with the late onset form (14.8 +/- 5.5 vs 7.7 +/- 0.8 mm).(ABSTRACT TRUNCATED AT 250 WORDS)

17-alpha-Hydroxyprogesterone↗
PubMed1995

Adrenal cortical and medullary imaging.

Adrenal disease can be manifested by endocrine dysfunction or anatomic abnormalities detected by cross-sectional imaging modalities. With the advent of newer and more reliable in vitro assays and a better understanding of the spectrum of adrenal pathology, the physician can now adopt a more accurate and cost-effective approach to the diagnosis of adrenal disease. Both functional and anatomic imaging modalities can play an important role in the evaluation of the incidental adrenal mass, the early detection of adrenal metastases, differentiation of the various causes of Cushings's syndrome, selection of patients for potentially curative surgery in primary aldosteronism and adrenal hyperandrogenism, and localization of pheochromocytomas and neuroblastomas. The usefulness of the adrenal cortical radiopharmaceutical, 131I-6-beta-iodomethylnorcholesterol (NP-59), and the adrenal medullary radiopharmaceuticals, 131I and 123I-metaiodobenzylguanidine (MIBG), is detailed for these various clinical settings and the role of NP-59 and MIBG is contrasted to that of the cross-sectional modalities, computed tomography and magnetic resonance imaging (MRI). Incidental adrenal masses are common, but malignancies are few. Imaging studies select those patients who require a further evaluation by biopsy examination or adrenalectomy. In the hyperfunctioning endocrine states, such as Cushing's syndrome, primary aldosteronism, adrenal androgenism, and pheochromocytoma, correlation of biochemical findings with both functional and anatomic imaging is necessary to avoid inappropriate and ineffective surgical intervention, yet not miss an opportunity for curative resection. Lastly, MIBG and MRI are complementary in the detection and staging of neuroblastoma.

3-Iodobenzylguanidine↗
PubMed2002

Unique cases of unilateral hyperaldosteronemia due to multiple adrenocortical micronodules, which can only be detected by selective adrenal venous sampling.

Primary aldosteronism is classified as aldosterone-producing adenoma (APA), idiopathic hyperaldosteronism (IHA), unilateral adrenal hyperplasia (UAH), primary adrenal hyperplasia (PAH), adrenal cancer, and glucocorticoid-remediable aldosteronism. We describe here 4 cases of primary aldosteronism due to unilateral hyperaldosteronemia, demonstrating unique histopathologic findings, such as unilateral multiple adrenocortical micronodules in the affected adrenals. Thirty-three patients with primary aldosteronism were consecutively admitted; 27 of them were treated by unilateral adrenalectomy. Four of them also had unilateral adrenal hypersecretion of aldosterone by selective adrenal venous sampling and adrenocortical multiple micronodules without an adenoma. These patients had hyporeninemic hyperaldosteronism with normokalemic hypertension. In these patients, furosemide plus upright test failed to increase plasma renin activity (PRA); the ratio of plasma aldosterone concentration (PAC) to PRA at 90 minutes after captopril administration was similar to that in patients with IHA and APA. Aldosterone concentrations were increased in each unilateral adrenal vein, and poorly encapsulated multiple adrenocortical micronodules from 2 to 3 mm in diameter were microscopically detected in the resected adrenal glands. Immunohistochemical analysis of steroidogenic enzymes, including cholesterol side chain cleavage, 3beta-hydroxysteroid dehydrogenase, 21-hydroxylase, 17alpha-hydroxylase, and 11beta-hydroxylase, indicated that the cortical cells within these micronodules were active in aldosterone production, while the non-nodular zona glomerulosa cells were inactive. We conclude that the clinical and pathologic characteristics of our 4 cases with unilateral multiple adrenocortical micronodules (UMN) are distinct from those of APA, IHA, UAH, and PAH. Furthermore, unilateral hyperaldosteronemia induced by UMN may be frequently misdiagnosed, because standard imaging tests, which cannot always detect tiny abnormalities of adrenals, showed "normal adrenal glands" in these patients. Thus, primary aldosteronism due to UMN should be carefully examined for differential diagnosis of each form of hyperaldosteronemia.

Adenoma↗
PubMed2002

Adrenal gland volume after spinal cord injury.

OBJECTIVE: Spinal cord injury in adult men may result in hypothalamic-pituitary-adrenal axis dysfunction. Atrophy of adrenal glands was speculated in these patients. This study was undertaken to clarify the functional-anatomic correlation between adrenal volume and body surface area in subjects with spinal cord injury with impaired adrenal reserve. DESIGN: Twenty male subjects with chronic spinal cord injury with impaired adrenal reserve were identified by adrenocorticotropic hormone stimulation test from a group of 42 subjects. All subjects with spinal cord injury and healthy volunteers underwent computed tomographic imaging with contiguous 3-mm section over adrenal glands for volumetric measurements. Ten pairs of subjects with spinal cord injury and controls with matched height and weight were included in the statistical analysis. RESULTS: Significantly increased relative adrenal volumes were noted among subjects with chronic spinal cord injury and impaired adrenal reserve as compared with the body weight-matched and height-matched control group. CONCLUSIONS: Increased relative adrenal volumes were found after chronic spinal cord injury. Hyperplasia of the zona glomerulosa may be the cause of increased relative adrenal volume after chronic spinal cord injury.

Adrenal Glands↗
PubMed1989

Relationship between fetal adrenal morphology and anterior pituitary function.

A comparative study of adrenal morphology between normal fetuses and those with anencephaly or congenital adrenal hyperplasia (CAH) was performed in order to examine the hypothesis that fetal adrenal mass and structure are adrenocorticotrophin (ACTH)-dependent throughout gestation. Combined adrenal weight in 102 normal fetuses was used to establish a reference range for the gestational ages of 15-27 weeks. During this period, mean adrenal weight showed a 6-fold linear increase. In 38 anencephalic fetuses of similar gestation age, adrenal weight was below the normal range and did not show a rise. Three fetuses with CAH (18, 22 and 30 weeks gestation) had adrenal weights considerably above the normal range. Adrenal cortical thickness was significantly increased in CAH fetuses, largely as a consequence of cell hypertrophy, whereas decreased cortical thickness in the anencephalic group represented cellular hypoplasia. Conspicuous secretory granules in the cytoplasm was the electron-micrographic feature of the adrenal gland in the 22-week fetus with CAH. These observations are consistent with close dependency of fetal adrenal growth and development upon fetal pituitary function from an early age, mediated primarily through ACTH.

Adrenal Cortex↗
PubMed1981

Prostaglandin E-binding sites in the fetal adrenal.

Prostaglandin E2 (PGE2) is specifically and reversibly bound by particulate fractions from adrenals from fetal calves and lambs. These binding sites appear to be located primarily in the adrenal medulla and have properties very similar to those which we have detected in adult human, bovine, and ovine adrenal medulla. The rate constant for the association reaction between [3H]PGE2 and its binding sites in fetal calf adrenals is 1.8 X 10(5) M-1 sec-1. The [3H]PGE2-binding site complex dissociates in a biphasic manner, with rate constants of 6.7 X 10(-4) sec-1 and 4.2 X 10(-5) sec-1 for the fast and slow phases, respectively. The Kd values for the interactions of PGE2 with particulate fractions from adrenals of fetal calves and lambs are 2.3 and 3.5 nM, respectively. The [3H]PGE2-binding sites are very specific for PGE1 and PGE2. The affinities of other prostaglandins (PGF2 alpha greater than PGA2 greater than 13,14-dihydro-15-oxo-PGE2 greater than PGD2 greater than 6-oxo-PGF1 alpha) are 130- to 1300-fold lower. We have detected binding sites in adrenals from fetal calves as early as 112 days of gestation. The concentration of binding sites in fetal calf adrenals increases from 0.11 to 0.18 pmol/mg protein between about 130 days of gestation and term. The concentration of binding sites in fetal lamb adrenals (approximately 0.07 pmol/mg protein) does not change appreciably between about 100 days of gestation and term. These results suggest that PGE-binding sites are present in fetal adrenal medulla in mid- and late gestation and are consistent with a role for PGEs in controlling catecholamine release from the fetal adrenal.

Adrenal Cortex↗
PubMed1998

Expression of Ob receptor in normal human adrenals: differential regulation of adrenocortical and adrenomedullary function by leptin.

The major effects of leptin, an adipostatic hormone produced in fat tissue, are exerted through the hypothalamic-pituitary-adrenal axis and the systemic sympathetic/adrenomedullary system at the level of the central nervous system. Here, we examined the direct effects of leptin on the adrenal gland, a peripheral end organ of both the hypothalamic-pituitary-adrenal axis and the sympathetic/adrenomedullary system. As cortical and chromaffin tissues are intermingled in the human adrenal, we employed the novel technique of laser capture microdissection to analyze these systems separately. Functional full-length leptin receptor messenger ribonucleic acid and all human isoforms Ob219.1-3 were demonstrated by RT-PCR in both cortical and medullary tissue. Immunohistochemical staining of leptin receptor protein, however, demonstrated a strong signal only in the adrenal cortex, whereas there was weak positive staining in the medulla. Corticotropin (ACTH)-induced adrenal aldosterone, cortisol, and dehydroepiandrosterone secretion was inhibited by leptin in a concentration-dependent manner, whereas this hormone had no significant effect on catecholamine release by primary cultures of human adrenal chromaffin cells. Leptin itself was not expressed in human adrenal tissue, excluding a local paracrine or autocrine function of this peptide. In conclusion, this is the first report identifying functional leptin receptor in human adrenal tissue and showing a differential action of leptin on human adrenocortical and chromaffin hormone production. This peripheral action of leptin on the adrenal gland provides an additional important link between the human stress response and body weight regulation.

Adrenal Cortex↗
PubMed2005

Evaluation of adrenal function in patients with growth hormone deficiency and hypothalamic-pituitary disorders: comparison between insulin-induced hypoglycemia, low-dose ACTH, standard ACTH and CRH stimulation tests.

OBJECTIVES: Patients with organic growth hormone deficiency (GHD) or with structural hypothalamic-pituitary abnormalities may have additional anterior pituitary hormone deficits, and are at risk of developing complete or partial corticotropin (ACTH) deficiency. Evaluation of the integrity of the hypothalamic-pituitary-adrenal axis (HPA) is essential in these patients because, although clinically asymptomatic, their HPA cannot appropriately react to stressful stimuli with potentially life-threatening consequences. DESIGN AND METHODS: In this study we evaluated the integrity of the HPA in 24 patients (age 4.2-31 years at the time of the study) with an established diagnosis of GHD and compared the reliability of the insulin tolerance test (ITT), short synacthen test (SST), low-dose SST (LDSST), and corticotropin releasing hormone (CRH) test in the diagnosis of adrenal insufficiency. RESULTS: At a cortisol cut-off for a normal response of 550 nmol/l (20 microg/dl), the response to ITT was subnormal in 11 subjects, 6 with congenital and 5 with acquired GHD. Four patients had overt adrenal insufficiency, with morning cortisol concentrations ranging between 66.2-135.2 nmol/l (2.4-4.9 microg/dl) and typical clinical symptoms and laboratory findings. In all these patients, a subnormal cortisol response to ITT was confirmed by LDSST and by CRH tests. SST failed to identify one of the patients as adrenal insufficient. In the seven asymptomatic patients with a subnormal cortisol response to ITT, the diagnosis of adrenal insufficiency was confirmed in one by LDSST, in none by SST, and in five by CRH tests. The five patients with a normal cortisol response to ITT exhibited a normal response also after LDSST and SST. Only two of them had a normal response after a CRH test. In the seven patients with asymptomatic adrenal insufficiency mean morning cortisol concentration was significantly higher than in the patients with overt adrenal insufficiency. ITT was contraindicated in eight patients, and none of them had clinical symptoms of overt adrenal insufficiency. One of these patients had a subnormal cortisol response to LDSST, SST, and CRH, and three exhibited a subnormal response to CRH but normal responses to LDSST and to SST. CONCLUSION: We conclude that none of these tests can be considered completely reliable for establishing or excluding the presence of secondary or tertiary adrenal insufficiency. Consequently, clinical judgment remains one of the most important issues for deciding which patients need assessment or re-assessment of adrenal function.

Adolescent↗
PubMed1980

Sonography of the adrenal glands: normal glands and small masses.

To evaluate sonographic imaging of the normal adrenal glands, anterior transverse and longitudinal scans were made on 200 patients who had no evidence of adrenal disease. In 78 additional patients who were suspected of having adrenal masses, anterior and posterior transverse and longitudinal scanning and longitudinal oblique scanning were done. Anterior transverse scanning proved to be the best single method of scanning the adrenal gland and small adrenal masses. The normal adrenal gland which is 3-6 mm thick and adrenal masses as small as 1.3 cm can be delineated. Although the frequency of visualizing normal adrenal glands (78.5% on the right and 44% on the left) with sonography is not as high as with CT, masses are more readily detected than the normal glands. The accuracy for detecting adrenal masses is very high, with a false-negative rate of only 3%. Sonography can be a useful screening test for many patients who are suspected of having adrenal masses. However, for obese patients the image is degraded and a higher false-positive rate (3.5%) is obtained. CT provides better resolution for such patients.

Adenoma↗
PubMed1990

[Direct evidence of alpha-adrenoceptor binding in rat and human adrenal glands].

In order to determine whether or not alpha-adrenoceptors are present in adrenal glands, radioligand receptor binding assay was performed in both Sprague-Dawley (SD) rat and human adrenal gland membranes. Radioligand binding assay using 3H-prazosin as an alpha 1-adrenoceptor ligand and 3H-yohimbine as an alpha 2-adrenoceptor ligand, clearly demonstrated alpha 1 and alpha 2 receptors present in both rat and human adrenal gland membranes. Maximal binding capacity (Bmax) and dissociation constant (Kd) of 3H-prazosin binding to the rat adrenal gland were 12.5 fmol/mg protein, and 0.11 nM, respectively. Those for the membrane preparations from adrenal cortex and medulla of the normal human were 16.3 fmol/mg protein, 0.34 nM and 16.3 fmol/mg protein, 0.27 nM, respectively. And those of the human pheochromocytoma were 25.6 fmol/mg protein, 0.15 nM, respectively. On the other hand, Bmax and Kd of 3H-yohimbine binding in the rat adrenal gland to were 22.9 fmol/mg protein, and 4.28 nM, respectively. Those for the membrane preparations from adrenal cortex and medulla of the normal human were 40.4 fmol/mg protein, 5.15 nM and 12.2 fmol/mg protein, 5.39 nM, respectively. And those of the human pheochromocytoma were 35.8 fmol/mg protein, and 1.08 nM, respectively. Bmax (35.8 fmol/mg protein) of 3H-yohimbine binding in the pheochromocytoma was significantly (p less than 0.01) greater than that (12.2 fmol/mg protein) in the human normal adrenal medulla, while Kd (1.08 nM) of this binding in the human pheochromocytoma was significantly (p less than 0.01) lower than that (5.39 nM) in the human normal adrenal medulla. Our data suggest that the alpha 2 receptor had greater affinity and binding site density to its agonist in the human pheochromocytoma than in the human normal adrenal medulla.

Adrenal Gland Neoplasms↗
PubMed2005

[Diagnosis and surgical treatment of adrenal tumors].

Adrenal surgery is necessary for the management of functioning adrenal tumors, such as aldosterone-producing adenoma, cortisol-producing adenoma, and pheochromocytoma. The role of adrenal imaging in primary hyperaldosteronism is to separate the surgically resectable unilateral aldosteronoma from bilateral hyperplasia. Once the clinical diagnosis of primary hyperaldosteronism is confirmed, adrenal computed tomography (CT) with 3-mm sections should be the first imaging study. If the results of CT and NP-59 scintigraphy are equivocal, adrenal venous sampling is necessary. Cortisol-producing adrenocortical adenomas are seen as adrenal masses 2.5 cm or larger in diameter in CT scanning. When an adrenal mass measures more than 5 cm in diameter, a functioning adrenal carcinoma should be considered. Symptomatic pheochromocytomas are almost always 2 cm or larger. On MR scanning, pheochromocytomas are extremely bright on T2-weighted images. In patients with ectopic pheochromocytomas, 131I-MIBG scintigraphy should be mandatory. In the past decade, laparoscopic adrenalectomy has replaced open adrenalectomy as a standard operative procedure for benign adrenal tumors. Adrenal-sparing laparoscopic surgery has recently become a feasible option in patients with hereditary bilateral pheochromocytomas.

Adrenal Cortex Neoplasms↗
PubMed1990

Sub-clinical Cushing's syndrome in patients with adrenal gland incidentalomas. Pitfalls in diagnosis and management.

Widespread use of contemporary imaging techniques (ultrasound, computerized axial tomography, and magnetic resonance imaging scans) have led to the incidental discovery of asymptomatic adrenal neoplasms with increasing frequency. Patients with such adrenal "incidentalomas" typically have no clinical manifestations of adrenal cortical hyperfunction at the time of discovery. We have studied 122 patients with asymptomatic adrenal masses ranging in size from 2 to 7 cm in diameter from 1978 to 1988. Selected patients, after adrenal metastases, pheochromocytoma, myelolipomas, and cysts were ruled out, were further evaluated for adrenal cortical hyperfunction by measuring urinary 17-hydroxysteroids, 17-ketosteroids, and free cortisol, serum A.M., P.M. cortisol, and plasma ACTH levels. These values were also measured before and after dexamethasone suppression. NP-59 adrenal scintiscans were performed on all patients. Six patients were identified with sub-clinical Cushing's syndrome. Baseline cortisol levels were normal in each of these patients. Loss of diurnal rhythm appeared to be the most sensitive indicator of abnormal adrenal cortical function. When adrenalectomy is performed in such patients, especially when contralateral adrenal gland suppression is evidenced by NP-59 scanning or other biochemical assessment, perioperative steroids should be administered in a manner similar to that used for patients with symptomatic Cushing's syndrome. Unilateral adrenalectomy in a patient with an asymptomatic adrenal adenoma, insufficiently studied, may result in Addisonian crisis.

Adenoma↗
PubMed1996

Expression and zonal distribution of CYP2D16 in the guinea pig adrenal cortex: relationship to xenobiotic metabolism.

We recently cloned a CYP2D subfamily member (CYP2D16) from a guinea pig adrenal cDNA library and investigated the expression of CYP2D16 in the guinea pig adrenal cortex and its relationship to adrenal xenobiotic metabolism. A modified sodium dodecyl sulfate-polyacrylamide gel electrophoresis technique revealed three major bands in the molecular mass range of cytochromes P450 in guinea pig adrenal microsomes. Two of the bands were immunoreactive with anti-CYP17 (54 kDa) or anti-CYP21 (52 kDa) antibody. The third band (50 kDa) was immunoreactive with antibody raised against CYP2D1 and with anti-CYP1A1/1A2 antibody. Microsequencing of the 50-kDa band yielded an amino-terminal sequence of 38 amino acids identical to that deducted from the CYP2D16 cDNA. In addition, Northern blot analyses indicated the CYP1A1 was not expressed in the adrenal gland, suggesting that only CYP2D16 composed the microsomal 50-kDa band. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analyses demonstrated greater expression of CYP2D16 in microsomes from the inner zone (zona reticularis) of the adrenal cortex than from the outer zones, coinciding with the major site of adrenal xenobiotic metabolism. Bufuralol-1'-hydroxylase activity, a marker for CYP2D isozymes, was also greater in inner- than in outer-zone microsomal preparations and was highly correlated with CYP2D16concentrations. Northern blot analysis with a full-length CYP2D16 cDNA as the probe gave strong bands with adrenal inner zone RNA preparations and relatively weak bands with outer zone RNA. CYP2D16 mRNA was also detectable in liver and kidney RNA preparations, but at lower levels than in the adrenal inner zone, and it was not detectable in testes, lung, intestines, or heart. Overall, the results demonstrate that CYP2D16 is expressed at highest levels in the inner zone of the guinea pig adrenal cortex and suggest a major role for this isozyme in adrenal xenobiotic metabolism.

Amino Acid Sequence↗
PubMed2006

Adrenal insufficiency in patients with cirrhosis, severe sepsis and septic shock.

Patients with cirrhosis are susceptible to bacterial infection, which can result in circulatory dysfunction, renal failure, hepatic encephalopathy, and a decreased survival rate. Severe sepsis is frequently associated with adrenal insufficiency, which may lead to hemodynamic instability and a poor prognosis. We evaluated adrenal function using short corticotropin stimulation test (SST) in 101 critically ill patients with cirrhosis and severe sepsis. Adrenal insufficiency occurred in 51.48% of patients. The patients with adrenal insufficiency had a higher hospital mortality rate when compared with those with normal adrenal function (80.76% vs. 36.7%, P < .001). The cumulative rates of survival at 90 days were 15.3% and 63.2% for the adrenal insufficiency and normal adrenal function groups, respectively (P < .0001). The hospital survivors had a higher cortisol response to corticotropin (16.2 +/- 8.0 vs. 8.5 +/- 5.9 microg/dL, P < .001). The cortisol response to corticotropin was inversely correlated with various disease severity, Model for End-Stage Liver Disease, and Child-Pugh scores. Acute physiology, age, chronic health evaluation III score, and cortisol increment were independent factors to predict hospital mortality. Mean arterial pressure on the day of SST was lower in patients with adrenal insufficiency (60 +/- 14 vs. 74.5 +/- 13 mm Hg, P < .001), and a higher proportion of these patients required vasopressors (73% vs. 24.48%, P < .001). Mean arterial pressure, serum bilirubin, vasopressor dependency, and bacteremia were independent factors that predicted adrenal insufficiency. In conclusion, adrenal insufficiency is common in critically ill patients with cirrhosis and severe sepsis. It is related to functional liver reserve and disease severity and is associated with hemodynamic instability, renal dysfunction, and increased mortality.

Adrenal Glands↗
PubMed2002

Adrenal pathology in childhood: a spectrum of disease.

Adrenal lesions in children may present with an asymptomatic adrenal mass lesion, an endocrinopathy, a hypertensive or metabolic crisis or a paraneoplastic syndrome. Some of the underlying disease processes remain localised within the adrenal gland or may develop into disseminated disease. The role of the radiologist is to confirm the adrenal location of a lesion and to document any other foci of disease. Ultrasound, CT, MR imaging and metaiodobenzylguanidine scintigraphy are the most commonly utilised imaging modalities for examining the adrenal glands and their pathologies in children. This paper reviews the spectrum of adrenal disease in childhood and presents the information as a series of radiological appearances: anomalies of adrenal shape, location, number and size, cystic adrenal masses, solid adrenal mass lesions, and adrenal calcifications are all examined. The radiological findings must always be interpreted in conjunction with the patient's age, the clinical history, the findings on physical examination and the available biochemical data.

Adrenal Gland Diseases↗
PubMed1990

Adrenal morphometry in unilateral and sham adrenalectomized Syracuse high and low avoidance rats.

Syracuse high (SHA) and low (SLA) Long-Evans rats, bred for differences in avoidance performance, exhibit dramatic differences in adrenal gland weight. Here we examined adrenal weight and composition (i.e., the size of the medulla, zonae fasciculata/reticularis and glomerulosa) following unilateral adrenalectomy and sham surgery in these strains. Adrenals of SLA animals, regardless of treatment, were heavier and contained larger medullas and cortices than did adrenals of SHA animals. When individual regions were expressed as a percent of total adrenal area, SHA glands (age 31-45 days), although smaller in weight, contained a larger percentage of glomerulosa than did adrenals of SLA animals. Unilateral adrenalectomy produced significant compensatory growth in SHA and SLA animals as indexed by increases in adrenal weight as soon as 7 days after surgery. The adrenal enlargement was the net result of an increase in absolute size of the fasciculata/reticularis (significant 14 days following surgery) and a decrease in the absolute size of glomerulosa (significant 7 days following surgery). These results suggest that SHA and SLA adrenal differences may be the result of genetically determined differential pituitary-adrenal activity.

Adrenal Glands↗
PubMed2002

Effects of orexin on cultured porcine adrenal medullary and cortex cells.

New orexigenic peptides called orexins have recently been described in the neurons of the lateral hypothalamus and perifornical area. No orexins have been found in the adipose tissues or visceral organs, including the adrenal gland. However, expression of the orexin receptor (OXR) in the rat adrenal gland has been reported. With regard to the effects of orexins on peripheral organs, we previously reported that orexins suppress catecholamine synthesis and secretion in the rat pheochromocytoma cell line PC12. To further clarify the pharmacological effects of orexins on peripheral organs, we examined the effects of orexin-A on catecholamine, cortisol, and aldosterone secretion, using cultured porcine adrenal glands. We initially confirmed the expression of the orexin receptor (OXR-1) in cultured porcine adrenal medulla and cortex. Orexin-A (1000 nM) significantly increased the release of both epinephrine (E) and norepinephrine (NE) from porcine adrenal medullary cells. Similarly, orexin-A (> or = 100 nM) significantly increased the release of both cortisol and aldosterone from porcine adrenal cortex cells. Orexin-A (100 nM) significantly inhibited basal and the PACAP-induced increase in cAMP levels in adrenal medullary cells. Conversely, orexin-A (>o = 100 nM) significantly increased the cAMP level in adrenal cortex cells. These results indicate that orexin-A induces the release of catecholamine from porcine adrenal medullary cells, and aldosterone and cortisol from the cortex cells and has opposite effects on cAMP levels in adrenal medulla and cortex.

Adrenal Cortex↗