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PubMed1986

Magnetic resonance imaging of the adrenal.

Magnetic resonance imaging (MRI) of the adrenals was performed on 50 subjects: 5 normal volunteers, 6 Cushing patients with bilateral adrenal hyperplasia, 14 patients with adrenal adenomas, 3 with adrenal carcinomas, 15 with pheochromocytomas and 7 with metastatic disease to the adrenal. The normal and hyperplastic adrenal glands were imaged in all cases. Using the signal intensity of the adrenals on a T2 weighted image, various forms of adrenal pathology could be differentiated. A ratio of signal intensity of the adrenal mass to the liver was utilized and allowed the differentiation of adrenal adenomas from adrenal carcinomas, pheochromocytomas and metastases. Using the same ratio, metastases could be distinguished from pheochromocytomas as well. MRI appears to be particularly valuable in distinguishing clinically silent adrenal metastases from nonfunctioning adrenal adenomas.

Adenoma↗
PubMed2005

[Development of the human adrenal glands].

The human adrenal is an endocrine gland located at the superior part of the kidney. Composed of the adrenal cortex of mesoblastic origin and the adrenal medulla of neuroectoblastic origin, the human fetal adrenal grows considerably during the first three months of development. From 12 to 18 weeks of development (WD), the weight of the adrenals increases seven-fold. The gland's weight doubles from 18 to 28 WD and from 28 to 36 WD. At birth, the two adrenals weigh on average 10 g. At the 8th week, two zones are individualized in the adrenal cortex: the definitive zone and the fetal inner zone. At the second trimester, according to ultrastructural and biochemical studies, a third zone, called the transition zone, is individualized between the definitive zone and the fetal inner zone. The definitive zone persists, but the origin of the three zones (glomerular, fascicular and reticular) of adult adrenal cortex is not known. The fetal inner zone regresses from the 5th month of gestation and disappears totally one year after birth. At the 8th week, the immature neuroblasts migrate to the definitive zone, then to the fetal inner zone to compose the adrenal medulla, which develops essentially after birth and during the first year. Before the 10th week, the human fetal adrenal is able to produce steroid hormones, in particular dehydroepiandrosterone sulfate (DHEA-S); the secretion of cortisol remains discussed. The development of the human fetal adrenal is complex and is under the control of hormones (ACTH, LH and betaHCG), growth factors (ACTH essentially) and transcription factors (essentially SF1 and DAX-1). Knowledge of morphological and molecular phenomena of this development permits to understand the pathophisiology of congenital adrenal deficiencies.

Adrenal Cortex↗
PubMed2001

Adrenal adenomas: characteristic postgadolinium capillary blush on dynamic MR imaging.

We sought to evaluate dynamic post-gadolinium contrast enhanced magnetic resonance (MR) imaging characteristics of adrenal adenomas with comparison to those of malignant adrenal tumors. MR images, including in- and out-of-phase spoiled gradient echo (SGE) and dynamic gadolinium enhancement, of 35 adrenal adenomas in 34 patients, and 12 malignant adrenal tumors in 12 patients, were reviewed retrospectively. MR images were assessed for the presence of a capillary blush on immediate postgadolinium SGE images, and for rapid washout of contrast on 45-second postgadolinium SGE images. Thirty-five adrenal adenomas (mean size, 3.1 cm) and 12 malignant adrenal tumors (mean size, 7.4 cm) were assessed. Of 35 adrenal adenomas, 25 (71%) showed a homogeneous capillary blush on immediate postgadolinium images. Thirty-three (94%) adrenal adenomas demonstrated rapid washout on 45-second postgadolinium images (P < 0.001). Of 35 adrenal adenomas, 30 (86%) showed diminished signal intensity (SI) on out-of-phase images. Of 12 malignant adrenal tumors, none showed a homogeneous capillary blush on immediate postgadolinium images. Six (50%) malignant tumors showed negligible enhancement, four (33%) showed irregular patchy enhancement, and two (17%) showed peripheral enhancement (P < 0.001). On 45-second postgadolinium images, 11 (92%) of 12 malignant adrenal tumors showed irregular enhancement. In the majority of adrenal adenomas, an initial homogeneous capillary blush and rapid washout are demonstrated on gadolinium-enhanced dynamic MR imaging. Our preliminary results suggest that this may provide useful complementary information to the appearance of adrenal masses on in- and out-of-phase images.

Adenoma↗
PubMed2002

Predictive value of benign percutaneous adrenal biopsies in oncology patients.

PURPOSE: Percutaneous CT guided biopsy is accepted as a safe procedure for the diagnosis of indeterminate adrenal masses in oncologic patients. The purpose of this study was to evaluate the accuracy of a 'negative for tumour' adrenal biopsy in the oncologic patient population by assessing subsequent outcome including clinical course, size and imaging characteristics of the adrenal lesions on follow-up imaging studies and pathological findings at re-biopsy or following adrenal mass resection. MATERIALS AND METHODS: Retrospective analysis of 225 oncological patients (FM, 128;87; age range 33-87 years, mean age 66 years) who had undergone CT guided biopsies of an adrenal mass over a 5-year period was performed. Those patients with a report consistent with 'negative for malignancy' were evaluated by reviewing the medical records for patient demographics, primary malignancy, histology of adrenal tumour, subsequent surgical interventions, repeat adrenal biopsy under image guidance, by open surgery or at autopsy, subsequent abdominal imaging in which the adrenal gland was imaged, and long-term outcome including hospital admissions, or death. RESULTS: Of the 225 CT-guided adrenal biopsies performed, 41 (18%) were negative for neoplasm. The primary neoplasm in these 41 patients included lung cancer (n=32), breast (n=5), renal cell carcinoma (n=2), bladder (n=1), and prostate (n=1). The size of the adrenal lesions ranged from 2.8-5 cm. Of the 41 biopsies, which were negative for tumour; 10 were identified as adenomas and the rest showed benign adrenal cortical cells or hyperplasia on cytopathology and histopathology. Repeat biopsies were obtained in 13/41 (31%) patients; whereas 2/41 (5%) had their adrenal gland analyzed on post mortem examination. None of these 15 repeat evaluations yielded tumour. CONCLUSION: In oncological patients, pathological analysis of tissue samples obtained by CT-guided percutaneous biopsy, suggesting benign aetiology, is reliable and predicts a benign course on long-term follow-up. A negative or benign pathology result for a CT guided percutaneous adrenal biopsy can be regarded as a true negative evaluation in oncological patients with no necessity to repeat the biopsy.

Adenoma↗
PubMed2006

Prolactin and the expression of suppressor of cytokine signaling-3 in the sheep adrenal gland before birth.

The fetal pituitary-adrenal axis plays a key role in the fetal response to intrauterine stress and in the timing of parturition. The fetal sheep adrenal gland is relatively refractory to stimulation in midgestation (90-120 days) before the prepartum activation, which occurs around 135 days gestation (term=147+/-3 days). The mechanisms underlying the switch from adrenal quiescence to activation are unclear. Therefore, we have investigated the expression of suppressor of cytokine signaling-3 (SOCS-3), a putative inhibitor of tissue growth in the fetal sheep adrenal between 50 and 145 days gestation and in the adrenal of the growth-restricted fetal sheep in late gestation. SOCS-3 is activated by a range of cytokines, including prolactin (PRL), and we have, therefore, determined whether PRL administered in vivo or in vitro stimulates SOCS-3 mRNA expression in the fetal adrenal in late gestation. There was a decrease (P<0.005) in SOCS-3 expression in the fetal adrenal between 54 and 133 days and between 141 and 144 days gestation. Infusion of the dopaminergic agonist, bromocriptine, which suppressed fetal PRL concentrations but did not decrease adrenal SOCS-3 mRNA expression. PRL administration, however, significantly increased adrenal SOCS-3 mRNA expression (P<0.05). Similarly, there was an increase (P<0.05) in SOCS-3 mRNA expression in adrenocortical cells in vitro after exposure to PRL (50 ng/ml). Placental and fetal growth restriction had no effect on SOCS-3 expression in the adrenal during late gestation. In summary, the decrease in the expression of the inhibitor SOCS-3 after 133 days gestation may be permissive for a subsequent increase in fetal adrenal growth before birth. We conclude that factors other than PRL act to maintain adrenal SOCS-3 mRNA expression before 133 days gestation but that acute elevations of PRL can act to upregulate adrenal SOCS-3 expression in the sheep fetus during late gestation.

Adrenal Cortex↗
PubMed1990

Regulation of the primate fetal adrenal cortex.

Significant advances in our understanding of the regulation of fetal adrenal growth, differentiation, and steroidogenesis have been made in the past several years. In vitro studies employing molecular biological techniques have demonstrated that the placenta and several fetal tissues synthesize growth factors and/or oncogene-related products, which have the capacity to modulate growth and maturation of the fetal adrenal. Moreover, there is evidence that the fetal adrenal itself produces IGF-I and IGF-II and that the mRNAs for these growth factors are responsive to ACTH and perhaps other peptides originating in the fetal pituitary and/or the placenta. Most fascinating are the studies demonstrating that growth factors may also regulate the pattern of steroidogenesis elicited by the fetal adrenal. For example, TGF beta modulates binding, internalization, and degradation of LDL-cholesterol in adult adrenals while IGF-I increases fetal adrenal steroidogenesis by mechanisms that do not involve induction of P-450scc or enhanced metabolism of LDL. These studies, coupled with the observation that activation of protein kinase C by EGF or bFGF can block ACTH and/or other cAMP-induced increases in the activity of P-450(17 alpha), provide new insight into the subcellular mechanisms that underlie the regulation of fetal adrenal function. However, in vivo investigations must be aggressively pursued because the latter provide a major and perhaps exclusive means to elucidate the complex and multiple mechanisms that are apparently operative in utero in the regulation of fetal adrenal development. Moreover, in vivo studies remain the only valid means to delineate whether the factors that have been shown to modulate fetal adrenal function in vitro are indeed operable in vivo. Thus, in vivo investigations have shown that a multifactorial regulation of the fetal adrenal exists in utero in which PRL and perhaps other peptides as well as ACTH selectively stimulate fetal adrenal androgen production. Moreover, in vivo studies have demonstrated that a feedback mechanism operates in utero whereby estrogen produced in the placenta from androgen precursors of fetal adrenal origin feeds back to modulate the responsivity of the fetal adrenal to tropic peptides perhaps by regulating peptide binding to cell membrane receptors and/or other mechanisms. Evidence has also been provided from in vivo studies to support the concept that the placenta via metabolism of maternal cortisol and cortisone regulates fetal pituitary production of ACTH by modulating the extent to which maternal cortisol arrives at the fetus.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex↗
PubMed1991

Hormonally regulated inhibin gene expression in human fetal and adult adrenals.

Inhibin subunit expression has recently been shown to occur in rat and sheep adrenals. We now show the presence of inhibin subunit mRNAs in human fetal and adult adrenal tissue specimens and cultured adrenocortical cells. Northern blot analysis revealed that inhibin alpha-subunit gene is as strongly expressed in fetal adrenals as in fetal testes, whereas adult adrenals expressed alpha-subunit mRNA to a lesser extent. beta A-Subunit mRNA was detectable in placenta, and beta B mRNA was found in testes. With reverse transcription-polymerase chain reaction analysis all inhibin subunit mRNAs (alpha, beta A, and beta B) could be found in fetal adrenal samples. In cultured fetal and adult adrenal cells ACTH and dibutyryl cAMP increased inhibin alpha-subunit mRNA 3- to 4-fold. beta A mRNA was spontaneously induced in cultured adrenal cells. 12-O-Tetradecanoyl phorbol-13-acetate, a protein kinase-C regulator, increased beta A mRNA levels 9.6- and 3.3-fold in fetal and adult adrenal cultures, respectively. 12-O-Tetradecanoyl phorbol-13-acetate treatment abolished ACTH-induced alpha-subunit mRNA accumulation in both fetal and adult cultures. Our results show that inhibin genes are expressed in human fetal adrenals and testes during the second trimester of gestation. Adult adrenals also express inhibin genes, although to a lesser extent than fetal adrenals. Both cAMP- and protein kinase-C-dependent pathways regulate inhibin subunit gene expression in adrenocortical cells. These findings suggest that inhibins/activins are produced locally in human adrenals, where they could function as paracrine or autocrine regulators of adrenal growth and steroidogenesis.

Adrenal Cortex↗
PubMed2002

Functional scintigraphy of the adrenal gland.

Over the last 30 years nuclear medicine imaging of the adrenal gland and its lesions has been achieved by the exploitation of a number of physiological characteristics of this organ. By seeking and utilising features which are quantitatively or qualitatively different from those of the adjacent tissues, functional depiction of the adrenal gland and its diseases, which in most cases retain the basic physiology of their tissue of origin, including both the cortex and the medulla, are now a useful clinical reality. Agents widely used in clinical practice include: (a) uptake and storage of radiolabelled cholesterol analogues via the low density lipoprotein (LDL) receptor and cholesterol ester storage pool in the adrenal cortex ((131)I-6-beta-iodomethyl-norcholesterol, (75)Se-selenomethyl-norcholesterol); (b) catecholamine type I, presynaptic, uptake mechanism and intracellular granule uptake and storage mechanism in the adrenal medulla and extra-adrenal paraganglia ((131)I-, (123)I- and (124)I-meta-iodo-benzyl-guanidine (MIBG), (18)F-metafluoro-benzyl-guanidine); (c) cell surface receptor binding of peptides/neurotransmitters/modulators such as for the family of five subtypes of somatostatin receptors ((123)I-tyr-octreotide, (111)In-DTPA-octreotide, (111)In-DOTA-octreotide and many others); (d) although not specific for the adrenal gland, increased glycolysis by tumours, particularly the most malignant varieties, (18)F-2-fluoro-d-deoxyglucose can thus be expected to depict certain malignant lesions such as malignant pheochromocytomas (particularly the minority which are not detected by MIBG) and adrenal incidentalomas (particularly when they occur in patients with known extra-adrenal malignancies). There are a variety of adrenal tissue characteristics with potential for exploitation but which are not currently in clinical use, and which may, nevertheless, have potential as imaging agents. These include: (a) inhibitors of adrenal cortical steroid hormone synthesis enzymes (e.g. radiolabelled analogues of metyrapone); (b) radiolabelled lipoproteins which bind to adrenocortical LDL receptors; (c) inhibitors of catecholamine biosynthesis enzymes (e.g. radiolabelled analogues of tyrosine and related amino acids); (d) cell surface receptors for various peptides and hormones which may be over-expressed on adrenal cortical or adrenal medullary tumours (e.g. radiolabelled analogues of ACTH on adrenocortical cells of zona fasciculata or zona glomerulosa origin, neurotransmitter/hormone message peptides binding to cell surface receptors such as bombesin, vasoactive intestinal polypeptide, cholecystokinin and opiate peptides); (e) the adrenal cortex can also synthesise cholesterol ab initio from acetate, and preliminary studies with (11)C-acetate positron emission tomography have shown interesting results.

Adrenal Gland Diseases↗
PubMed1984

Guanfacine and clonidine: the effects on adrenal medullary function in spontaneously hypertensive rats.

The effect of guanfacine on adrenal medullary function was investigated in anesthetized spontaneously hypertensive rats (SHR). This effect was compared with the clonidine-induced adrenal suppressant action. Sympathetic adrenal nerve activity and adrenal catecholamine secretion rate were determined and used for the analysis of adrenal medullary function. Intravenous administration of guanfacine (30-100 micrograms/kg) produced a decrease in both adrenal nerve activity and adrenal catecholamine secretion rate that paralleled a decrease in arterial blood pressure and heart rate. The ED50 of the guanfacine-induced decrease in adrenal nerve activity was 300 micrograms/kg, and the ED50 of clonidine was 30 micrograms/kg. This guanfacine dose produced decreases up to about 20% of the pretreatment values in both epinephrine and norepinephrine secretion rates from the adrenal medulla. Moreover, guanfacine produced a significant decrease of adrenal plasma flow rate. The adrenal plasma flow rate did not change significantly after clonidine administration. These findings suggest that the adrenal suppressant effect induced by guanfacine is predominantly due to its central action and that the vasoconstriction due to the peripheral action of guanfacine is partly related to its adrenal suppressant effect in SHR.

Adrenal Glands↗
PubMed1998

Primary hyperaldosteronism and adrenal incidentaloma: an argument for physiologic testing before adrenalectomy.

OBJECTIVE: To determine the frequency of nonfunctioning adrenal masses in patients with primary hyperaldosteronism. DESIGN: A case series. SETTING: A tertiary care hypertension clinic. PATIENTS: Twenty-seven consecutive patients with primary hyperaldosteronism. MEASUREMENTS: Blood pressure, serum electrolytes, supine and upright plasma renin, cortisol and aldosterone levels, selective adrenal vein aldosterone and cortisol levels, adrenal computed tomography (CT) scans and pathology reports. RESULTS: There was considerable overlap in the clinical features and laboratory investigations for patients with unilateral aldosteronoma and those with bilateral adrenal hyperplasia. Of the 27 patients who had confirmed primary hyperaldosteronism investigated at this centre, 25 had a definitive diagnosis assigned on the basis of postural stimulation tests, adrenal CT scans, and bilateral adrenal vein sampling, surgery or a combination of test results. Of this group, 18 had adrenal masses visualized on CT. However, only 13 of these 18 patients had an adrenal aldosteronoma subsequently proven by selective adrenal vein sampling or surgery, or both; the other 5 patients were found to have bilateral adrenal hyperplasia with nonfunctioning adrenal masses. CT had a sensitivity of 100% for the diagnosis of aldosteronoma, but the specificity was only 58% and the positive predictive value was only 72%. The likelihood ratio for the diagnosis of aldosteronoma in patients with primary hyperaldosteronism and an adrenal mass on CT was only 2.4. CONCLUSION: Given the poor specificity of CT in patients with primary aldosteronism, full biochemical and physiologic testing should be done before adrenalectomy in patients with suspected adrenal aldosteronoma.

Adenoma↗
PubMed2004

Endoscopic ultrasound-guided fine-needle aspiration biopsy of the adrenal glands: analysis of 24 patients.

BACKGROUND: Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) biopsy allows the detailed imaging and FNA not only of both intramural and extramural structures and lesions of the gastrointestinal (GI) tract but also of various intraabdominal organs. Thus, EUS-FNA biopsy offers a novel opportunity to evaluate and obtain cytology samples from adrenal gland lesions. The objective of the current study was to determine the utility of EUS-FNA in the diagnosis of adrenal lesions. METHODS: The authors conducted a prospective evaluation of 24 consecutive EUS-FNA biopsy specimens obtained from patients with adrenal lesions. An attending cytopathologist was present on site to assess specimen adequacy and to provide rapid interpretation of air-dried material that had been stained with Diff-Quik (Baxter Scientific Products, McGraw Park, IL). Additional samples were obtained for ThinPrep (Cytyc Corporation, Boxborough, MA) preparation, and cell blocks subsequently were prepared. Appropriate immunohistochemical staining was performed as indicated. The cytologic diagnosis was then analyzed for correlations with the final diagnosis, which was based on relevant correlative cytologic or histologic examination of biopsied/resected pathology materials and/or final clinical follow-up. RESULTS: In total, 24 EUS-FNA biopsy specimens (from 18 males and 6 females) were obtained from adrenal glands. The mean patient age was 62.2 years (range, 48-81 years). Adequate cellularity was noted in all 24 samples. Seven of 24 samples (29%) were reported to be positive for carcinoma. All samples that were diagnosed as metastatic carcinoma were confirmed on subsequent follow-up. EUS-FNA performed simultaneously with adrenal gland aspiration either from the primary site (n = 1) or from metastases to lymph nodes (n = 3) supported diagnoses of metastatic carcinoma. Six of seven samples were metastatic from the lung, and one specimen was a direct extension of a transitional renal cell carcinoma. EUS-FNA biopsy of the right adrenal gland in one patient revealed myelolipoma. In 16 patients, benign adrenal gland cells were noted on EUS-FNA biopsy specimens from enlarged adrenal glands. In 5 samples (31%), signs of adenoma were evident. Morphology alone could not distinguish between adrenal adenoma and adrenal hyperplasia. No significant complications were reported after EUS-FNA biopsy of adrenal glands. CONCLUSIONS: EUS-FNA biopsy is a highly specific and safe technique for confirming the diagnosis of carcinoma metastatic to the adrenal glands. Along with cytologic evaluation, EUS imaging is needed to support the diagnosis of adrenal adenoma.

Adenoma↗
PubMed2005

Adrenal incidentaloma in pregnancy: clinical, molecular and immunohistochemical findings.

Adrenal incidentalomas detected during pregnancy are very rare, and the natural history of these tumors during gestation is unknown. We report a case of a pregnant woman with an adrenal mass discovered serendipitously, who was followed-up during gestation and underwent adrenalectomy shortly after delivery. This allowed the evaluation of both the clinical outcome and the molecular/immunohistochemical correlates. Estrogens may indeed influence the function and proliferation of human adrenal cells, and a state of circulating estrogen excess can represent an in vivo model to test their effect on the adrenals. No evidence of adrenal change in morphology and function was found in our patient throughout pregnancy, as shown by adrenal ultrasound imaging and adrenal hormone measurements. Four months after delivery, the patient underwent laparoscopic right adrenalectomy, and pathologic analysis revealed a 2.7 cm benign adrenocortical adenoma. The diameter of the adrenal mass at ultrasonography correlated highly with post-partum mass diameter measured by abdominal computed tomography (CT). Quantitative expression of both ERalpha and ERbeta by real-time RT-PCR analysis and Western blotting findings did not differ among adenoma, normal adjacent adrenal and normal adrenal control tissues. This case of an adrenal incidentaloma discovered during pregnancy shows that a close observation with endocrine investigations and ultrasonography could be an appropriate approach, delaying the decision of surgical intervention after delivery. Estrogen receptor mRNA levels in the adrenal mass similar to those observed in normal adrenals suggest that estrogen oversecretion during pregnancy was not a risk factor for tumor progression.

Adrenal Gland Neoplasms↗
PubMed1996

The role of radiolabeled somatostatin analogs in adrenal imaging.

We investigated the role of radiolabeled somatostatin analogs (SAs) in adrenal imaging. We evaluated 15 patients (6 men and 9 women, mean age 47 +/- 17 years) with imaging-detected adrenal tumors. Patient population was divided into two groups on the basis of the nature of adrenal lesions. Group 1 consisted of patients with benign adrenal lesions (n = 10). Group 2 consisted of patients with malignant adrenal lesions (n = 5). Pathology examinations were obtained in 13 cases: 7 pheochromocytomas, 2 adenomas, 2 cysts, 1 carcinoma, and 1 fibro-histiocytoma. One patient had a proven diagnosis of non-small-cell lung cancer associated with the presence of a right adrenal mass. The last patient had a clinical diagnosis of Werner syndrome associated with the presence of a large left adrenal mass. All patients underwent scientigraphic studies using radiolabeled SAs, of which indium-111 (In-111) pentetreotide was used in 11 cases and technetium-99m (Tc-99m)-labeled peptides (P-587 or P-829) were used in the remaining four cases. No significant labeled SAs uptake was observed in the majority (8 of 10, 80%) of the benign adrenal lesions (Group 1); however, increased uptake was found in two benign pheochromocytomas. Conversely, significant labeled SAs uptake was observed in the majority (4 of 5, 80%) of the malignant adrenal lesions (Group 2); however, the last lesion (carcinoma) did not show abnormal uptake. Results of this study show that the majority of benign adrenal tumors do not concentrate radiolabeled SAs; conversely, the majority of malignant adrenal lesions show significant SAs uptake, suggesting the presence of somatostatin receptors. This finding may allow the use of somatostatin as a treatment agent in malignant adrenal tumors. Thus, the main role of labeled SAs in adrenal imaging consists of lesion characterization rather than tumor detection and localization.

Adrenal Gland Neoplasms↗
PubMed1999

Synthesis, biological evaluation, and baboon PET imaging of the potential adrenal imaging agent cholesteryl-p-[18F]fluorobenzoate.

Cholesteryl-p-[18F]fluorobenzoate ([18F]CFB) was investigated as a potential adrenal positron emission tomography (PET) imaging agent for the diagnostic imaging of adrenal disorders. We describe the synthesis, biodistribution, adrenal autoradiography, and baboon PET imaging of [18F]CFB. The synthesis of [18F]CFB was facilitated by the use of a specially designed microwave cavity that was instrumental in effecting 70-83% incorporation of fluorine-18 in 60 s via [18F]fluoro-for-nitro exchange. Tissue distribution studies in mature female Sprague-Dawley rats showed good accumulation of [18F]CFB in the steroid-secreting tissues, adrenals and ovaries, at 1 h postinjection. The effectiveness of [18F]CFB to accumulate in diseased adrenals was shown through biodistribution studies in hypolipidemic rats, which showed a greater than threefold increase in adrenal uptake at 1 h and increased adrenal/liver and adrenal/kidney ratios. Analysis of the metabolites at 1 h in the blood, adrenals, spleen, and ovaries of hypolipidemic and control rats showed the intact tracer representing greater than 86%, 93%, 92%, and 82% of the accumulated activity, respectively. [18F]CFB was confirmed to selectively accumulate in the adrenal cortex versus the adrenal medulla by autoradiography. Normal baboon PET imaging with [18F]CFB effectively showed adrenal localization as early as 15 min after injection of the tracer, with enhanced adrenal contrast seen at 60-70 min. These results suggest that [18F]CFB may be useful as an adrenal PET imaging agent for assessing adrenal disorders.

Adrenal Glands↗
PubMed1997

Detection of the adrenal glands by endoscopic or transabdominal ultrasound.

BACKGROUND AND STUDY AIMS: The value of transabdominal and endoscopic ultrasound (EUS) in detecting normal adrenal glands is not yet established. The aim of our study was to evaluate whether these techniques can be routinely used to visualize the adrenal glands in patients without suspected adrenal pathology. PATIENTS AND METHODS: Transabdominal ultrasound was validated by examination of 10 corpses and was performed in 80 healthy volunteers (3.5 and 5 MHz). EUS of the left adrenal gland was performed in 154 consecutive patients referred for various other reasons. In 20 patients we attempted to visualize the right adrenal gland as well. RESULTS: Both adrenal glands were correctly identified in all of the 10 corpses once they were opened. In healthy volunteers, the right adrenal gland was visualized by transabdominal ultrasound in 79/80 patients (99 %) and the left adrenal gland in 55/80 patients (69 %). EUS allowed detection of the left adrenal gland in 151/154 patients (98%). In three patients EUS failed because of grossly distorted anatomy. In 6/20 patients we were also able to detect the right adrenal gland by EUS, which was obvious in two cases because of incidentalomas. CONCLUSION: Visualization of the right adrenal gland is almost always possible by transabdominal ultrasound, while its detection by EUS is successful only in some cases. The left gland is more difficult to detect by transabdominal ultrasound, while it can nearly always be seen using EUS. Therefore, a combined transabdominal and endoscopic ultrasonographic approach is useful for visualization of the adrenal glands and may enable diagnosis of even small adrenal masses.

Adrenal Glands↗
PubMed1998

Induction of adrenal scavenger receptor BI and increased high density lipoprotein-cholesteryl ether uptake by in vivo inhibition of hepatic lipase.

Hepatic lipase (HL) and scavenger receptor type B class I (SR-BI) have both been implicated in high density lipoprotein (HDL)-cholesteryl ester uptake in cholesterol-utilizing tissues. Inactivation of HL by gene-directed targeting in mice results in up-regulation of SR-BI expression in adrenal gland (Wang, N., Weng, W., Breslow, J. L., and Tall, A. R. (1996) J. Biol. Chem. 271, 21001-21004). The net effect on HDL-cholesteryl ester uptake is not known. We determined the impact of acute in vivo inhibition of rat adrenal HL activity by antibodies on SR-BI expression and on human and rat HDL-[3H]cholesteryl ether (CEth) uptake in the adrenal gland. Rat HDL was isolated from rats in which HL activity had been inhibited for 1 h. The rats were studied under basal conditions (not ACTH-treated) and after previous treatment with ACTH for 6 days (ACTH-treated). Intravenous injection of anti-HL resulted in 70% lowering of adrenal HL activity in both conditions which were maintained for at least 8 h. In not ACTH-treated rats, inhibition of adrenal HL increased adrenal SR-BI mRNA (5.2-fold) and mass (1. 6-fold) within 4 h. HL inhibition resulted in 41% and 14% more adrenal accumulation of human HDL-[3H]CEth during 4 and 24 h, respectively. The adrenal uptake of rat HDL-[3H]CEth increased by 68%, 4 h after the antibody injection. ACTH treatment increased total adrenal HL activity from 3.7 +/- 0.5 milliunits to 34.0 +/- 17. 2 milliunits, as well as adrenal SR-BI mRNA from 2.9 +/- 0.7 arbitrary units (A.U.) to 86.8 +/- 41.1 A.U. and SR-BI mass from 7.7 +/- 1.8 A.U. to 63.16 +/- 46.7 A.U. The human HDL-[3H]CEth uptake by adrenals was also significantly increased from 0.58 +/- 0.11% of injected dose to 7.24 +/- 1.58% of injected dose. Inhibition of adrenal HL activity did not result in further induction of SR-BI expression and did not affect human HDL-[3H]CEth uptake. These findings indicate that SR-BI expression may be influenced by changes in HL activity. HL activity is not needed for the SR-BI-mediated HDL-cholesteryl ester uptake by rat adrenal glands.

Adrenal Glands↗
PubMed2002

The short synacthen test in the evaluation of adrenal masses in patients with malignancies.

Adrenal computed tomography with determination of Hounsfield units has proved to be sensitive and specific in the differential diagnosis of benign vs. malign adrenal lesions. On the other hand, computed tomography may fail in patients with small adrenal masses of less than 1.0 cm. However, especially in patients with diagnosed malignancies and small adrenal masses which were discovered during the diagnostic staging procedure it is important to determine the origin of the adrenal lesion. An augmented increase in 17alpha-hydroxyprogesterone (17-OHP) levels following corticotropin (1-24) stimulation has been noted in incidentally discovered adrenal masses by several groups. Therefore, we tested the hypothesis that elevated ACTH-stimulated 17-OHP (delta > 2.6 ng/mL) can predict primary adrenal lesions. We evaluated the use of the ACTH test in 85 patients with adrenocortical tumors and in 16 patients who underwent abdominal imaging for staging of a carcinoma other than of adrenal origin. We found an augmented 17-OHP response in 70 (>82%) of patients with known adrenocortical tumors and in 10 (>62%) of patients with adrenal masses and diagnosed malignancies. Results in the latter group have been confirmed in histological studies after operation or puncture. In the group of patients who suffered from a solid malignant tumor and had an adrenal mass, it was thus possible to separate primary from secondary adrenal lesions in 100%. In the group of patients with known adrenocortical tumors, it failed to differentiate between benign and malignant adrenocortical lesion in one case. We therefore think that the ACTH test is a valuable biochemical tool to distinguish primary adrenal tumors from adrenal metastasis derived from other malignancies.

17-alpha-Hydroxyprogesterone↗
PubMed1996

Functional aromatase expression in porcine adrenal gland and testis.

The expression of aromatase cytochrome P450 (P450arom) in the adrenal glands, testes, and placentas of fetal and newborn pigs was investigated. Western immunoblot analysis detected a single 48-50-kDa protein band in these tissues as well as in other porcine tissues known to express P450arom including Day 12 tubular conceptuses, theca interna, and granulosa. Slight differences in migration suggested that the P450arom protein expressed in the testis was larger than that in the adrenal gland, which was, in turn, larger than that in placenta, theca, and granulosa. Consistent with P450arom expression in these tissues, a cDNA encoding porcine P450arom hybridized to a 2.3-kb transcripts in Northern analyses of porcine blastocysts, placentas, and fetal and newborn adrenal glands and testes, as well as in theca and granulosa tissues from preovulatory follicles. No differences in transcript size were detectable among tissues. The identity of P450arom transcripts was confirmed by sequence analysis of partial cDNA clones amplified from porcine fetal adrenal glands, testes, and placentas according to the RACE procedure. The sequences of the adrenal and testis clones were identical but differed from the placental sequence, which represented the first 85 amino acids of porcine P450arom. Specifically, the adrenal and testis clones expressed transcripts that resembled the ovarian isoform of porcine P450arom, rather than the porcine placental isoform, predicting a two-amino acid deletion and 12 predicted amino acid substitutions. P450arom activity was examined to further define expression in these tissues. Activity in adrenal, testis, and placental homogenates was inhibited by 4-hydroxyandrostenedione (4OH-A4) whereas inhibition by etomidate was demonstrated in the adrenal and testis homogenates but not in the placental homogenates. The sensitivity of activity in the newborn porcine adrenal glands and testes to inhibition by etomidate was similar to that of ovarian P450arom activity. The level of P450arom activity was highest in the placenta and lowest in the adrenal gland, and no effect of fetal sex was noted in either tissue. Immunocytochemical studies localized the expression of P450arom in the adrenal gland of newborns to cells at the corticomedullary junction and, with greater intensity, to cells around the developing medullary lobules. The same cells expressed cytochrome P450 17 alpha-hydroxylase, the expression of which also extended throughout the zona fasciculata. The interstitial cells were the site of P450arom expression in the testis, but no expression could be detected in any cells with the spermatic tubules. These data demonstrate that fetal and newborn porcine adrenal glands and testes express an active P450arom that resembles the isoform expressed in the ovary. The localization of adrenal expression suggests a possible role in medullary maturation and function in the fetal and newborn pig.

Adrenal Glands↗