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PubMed2002

Steroidogenic factor-1 is essential for compensatory adrenal growth following unilateral adrenalectomy.

While the orphan nuclear receptor steroidogenic factor-1 (SF-1) has been shown to function as an induction factor to define adrenocortical cell lineage, it remains unclear whether SF-1 plays an additional role as a growth promoting agent in the adult adrenal cortex. The proliferative potential of the adrenal cortex in adult SF-1(+/-) mice was examined using the model of compensatory adrenal growth following unilateral adrenalectomy (uADX). While the right adrenal gland of wild-type (wt) mice grew significantly after uADX, the adrenal of SF-1(+/-) mice exhibited a blunted, statistically nonsignificant weight increase. Accordingly, a profound increase in the proliferation marker proliferating cell nuclear antigen could be detected only in wt mice after uADX but not in the SF-1(+/-) mice. The proposed key regulator in adrenal compensatory growth, the recently cloned adrenal secretory serine protease was up-regulated in the remaining adrenal of wt mice, whereas this increase was blunted in SF-1(+/-) mice. While no differences in preadipocyte factor-1, the presumed marker of primitive adrenocortical cells, were detectable in the adrenals of wt and SF-1(+/-) mice, an increase in the ACTH receptor as well as agouti-related protein was observed only in wt animals but not in the SF-1(+/-) mice following uADX. Taken together, these results reflect a primary inability of adrenal cortical cells of SF-1(+/-) mice to undergo compensatory adrenal growth in response to uADX.

Adrenal Glands↗
PubMed1986

Contribution of the adrenal gland to the production of androstenedione and testosterone during the first two years of life.

Androstenedione and testosterone were measured in whole adrenal glands of 56 previously healthy boys who died suddenly between birth and 2 yr of age. In each adrenal gland, the concentration of androstenedione considerably exceeded that of testosterone. The highest concentrations were found during the first week of life (median, 295 ng/g; range, 98-320 ng/g). Thereafter, values decreased rapidly until the end of the first year of life (median, 10 ng/g; range, 4.4-22.7 ng/g). Adrenal testosterone concentrations averaged 15% of those of androstenedione in the same gland and similarly decreased until the end of the first year. The decrease of adrenal androgen concentrations paralleled the involution of the fetal adrenal zone. A close correlation existed between the concentration of androstenedione in adrenal tissue and plasma. However, no correlation existed between adrenal and plasma testosterone. When the adrenals and testes of the same infant were compared, there was 10 times more androstenedione in the adrenals than in the testes during the first 2 yr of life. The testes contained more testosterone than the adrenals only during the first 4 months. Thus, in infant boys the adrenals are the main source of androstenedione during the first 2 yr. After the sixth month of life, they also are the main source of testosterone.

Adrenal Glands↗
PubMed2000

Complete sequencing and messenger ribonucleic acid expression analysis of the MEN I gene in adrenal cancer.

Adrenal cancer is a rare sporadic disease that has also been observed in the context of multiple endocrine neoplasia type I (MEN I). Adrenal lesions occur in up to 40% of MEN I patients. Loss of heterozygosity of the 11q13 band harboring the menin gene has been reported in more than 50% of patients with adrenal cancer. Despite this high index of suspicion, former screening studies did not reveal mutations of the MEN I gene in 28 patients. We identified loss of heterozygosity of 11q13 microsatellites in five of five patients (100%). In 40%, heterozygosity was retained in codon 418 of the MEN I gene. Complete direct DNA sequencing data of the entire coding region and adjacent splice sites of the MEN I gene were obtained in 14 patients with sporadic adrenal cancer. In only one of them a heterozygous missense mutation, R176Q (exon 3), was identified. Due to the heterozygous pattern and unknown biological effect of this mutation, it is not clear whether there is a causal relationship with adrenal cancer. The total mutation frequency in sporadic adrenal cancer is 1 of 14 (7%). Menin messenger RNA expression was identified in 14 of 14 patients (100%). Transcriptional inactivation of the menin gene is, hence, unlikely to cause loss of its tumor suppressor function in adrenal cancer. Furthermore, we examined three patients who presented adrenal cancer in the context of sporadic multiglandular endocrine tumor disease previously diagnosed on clinical grounds to be MEN I syndrome. An opal stop codon mutation was identified in codon 126 (exon 2) in the adrenal cancer of one of these patients. Formation of the adrenal cancer in this patient may be rather coincidental because the mutation was present in a heterozygous pattern. There was no mutation of the menin gene in the two other patients. This may mean that formation of adrenal cancer in the context of multiglandular endocrine disease denotes an entity different from MEN I in some patients.

Adolescent↗
PubMed2005

Management of adrenal insufficiency in different clinical settings.

Adrenal insufficiency is a rare disease, but its prevalence is increasing. The most frequent cause of primary adrenal insufficiency in western countries is autoimmune adrenalitis, whereas secondary adrenal insufficiency is most often caused by pituitary tumours and their treatment (e.g., surgery). Chronic glucocorticoid replacement consists of hydrocortisone 15-25 mg/day in divided doses and dose monitoring is largely based on clinical judgement. Fludrocortisone 0.05-0.2 mg/day is given for substitution in mineralocorticoid deficiency aiming at normotension, normokalaemia and a plasma renin activity in the upper normal range. It has recently been shown that, despite adequate glucocorticoid and mineralocorticoid replacement well being in patients with adrenal insufficiency is still impaired. Several studies have demonstrated that dehydroepiandosterone 25-50 mg/day p.o. may improve mood, fatigue, well-being and, in women, also sexuality, suggesting that dehydroepiandosterone should become part of the standard treatment regime. However, large Phase III trials of dehydroepiandosterone for adrenal insufficiency are still lacking and it has not yet been approved for the treatment of this disease. Patients with adrenal insufficiency are at risk of adrenal crisis, usually precipitated by major stress, such as severe infection or surgery. Early dose adjustments are required to cover the increased glucocorticoid demand in stress. Careful and repeated education of patients and their partners is the best strategy to avoid this life-threatening emergency. Some recent studies suggest that during sepsis some patients with intact adrenal function may develop transient relative adrenal insufficiency and benefit from administration of hydrocortisone plus fludrocortisone. However, the pathophysiology and diagnosis criteria of relative adrenal insufficiency and its treatment remain unsettled issues.

Acute Disease↗
PubMed2000

Long-term testosterone treatment prevents gonadal and adrenal tumorigenesis of mice transgenic for the mouse inhibin-alpha subunit promoter/simian virus 40 T-antigen fusion gene.

We have developed a transgenic (TG) mouse model for tumorigenesis of gonadal somatic cells using a 6 kb fragment of the mouse inhibin-alpha subunit promoter (Inh-alpha) fused with the simian virus 40 T-antigen (Tag) coding sequence. Gonadal tumors, of Leydig or granulosa cell origin, develop in the TG mice with 100% penetrance by the age of 5-8 months. Conspicuously, if the mice are gonadectomized, they develop adrenal tumors. Gonadal and adrenal tumorigenesis in these mice seem to be gonadotropin dependent. On the other hand, testosterone stimulates the proliferation of a cell line (C alpha 1) established from one of the adrenal tumors. The purpose of the present study was therefore to investigate further whether testosterone affects the growth of these gonadal and adrenal tumors in vivo. Two experimental models were used: (1) Tag TG/hypogonadotropic (hpg) double mutant mice and (2) castrated Tag TG mice. Both were treated between 1-2 and 7-8 months of age with Silastic rods (length 2 cm) containing testosterone. None of the control or testosterone-treated Tag/hpg mice developed gonadal or adrenal tumors. The castrated Tag TG mice displayed, upon microscopical examination, early stages of adrenal tumors, whereas those receiving testosterone did not show such changes. Testosterone increased the weights of gonads in the Tag/hpg mice, and those of uteri and seminal vesicles in both groups. In contrast, the adrenal weights were significantly reduced in both groups by testosterone treatment. Gonadal histology of the testosterone-treated mice showed hyperplasia of testicular Leydig cells and ovarian stroma. Spermatogenesis was induced by testosterone in the Tag/hpg mice. Adrenal histology of the testosterone-treated animals demonstrated the disappearance of the X-zone. Serum levels of FSH in testosterone-treated Tag/hpg mice were significantly increased, while those of serum LH were decreased. In conclusion, the present result indicate that the suppression of gonadotropins by testosterone implants in castrated Inh-alpha/Tag TG mice prevents the tumorigenesis of their adrenals. In intact Tag/hpg mice, testosterone implants were not able to induce gonadal or adrenal tumorigenesis. Although testosterone treatment was able to induce interstitial cell hyperplasia in gonads of the Inh-alpha/Tag mice, direct gonadotropin action is responsible for gonadal and adrenal tumorigenesis.

Adrenal Gland Neoplasms↗
PubMed2001

Developmental regulation of corticotrophin receptor gene expression in the adrenal gland of the ovine fetus and newborn lamb: effects of hypoxia during late pregnancy.

Responsiveness of the fetal sheep adrenal gland to adrenocorticotrophin (ACTH) increases in late pregnancy, resulting in increased glucocorticoid production. Development of this responsiveness is an important determinant of fetal hypothalamic-pituitary-adrenal function and depends, in part, on the potential for ACTH binding to adrenal tissue. In the present study, we have examined the developmental pattern of ACTH receptor (ACTH-R) expression during the latter half of pregnancy and in neonatal and adult life. As hypoxaemia induces increases in cortisol and ACTH secretion, in addition to increasing fetal adrenal responsiveness, a further aim of this study was to investigate whether hypoxaemia was associated with altered expression of the ACTH-R gene. Whole adrenal glands were removed from fetal sheep, lambs and adult sheep at different stages of development for measurement of ACTH-R mRNA. Moderate hypoxaemia was induced for 48 h beginning on days 124-128, or on days 132-134 of gestation, by decreasing the maternal fractional inspired oxygen. ACTH-R mRNA was detected by northern blotting using a cDNA cloned in our laboratory and by in situ hybridisation. ACTH-R mRNA (3.6 kb major transcript) was detected in adrenal tissue at day 63 of gestation. Its relative abundance increased significantly (P<0.05) between days 126-128 and 140-141 of pregnancy, increased further with the onset of spontaneous labour, and remained increased in newborn lambs at 7 h-7 days after birth. ACTH-R mRNA levels then decreased in adrenal tissue from lambs and adult sheep (P<0.05). Hypoxaemia for 48 h significantly increased ACTH-R mRNA expression in adrenals of the older fetuses (days 134-136) compared with that in controls (P<0.05), but was without effect in younger fetuses. We conclude that levels of ACTH-R mRNA in the fetal adrenal gland increase as term approaches, coincident with the endogenous prepartum surge in plasma ACTH and cortisol. Sustained hypoxaemia resulted in an upregulation of mRNA encoding for ACTH-R, but only in older fetuses and in association with a sustained increase in plasma cortisol. These results are consistent with cortisol, ACTH, or both, contributing to increased fetal adrenal responsiveness, by increasing expression of fetal adrenal receptors for ACTH.

Adrenal Glands↗
PubMed1994

Adrenal hemorrhage in abused children: imaging and postmortem findings.

OBJECTIVE: Adrenal hemorrhage associated with child abuse has received little attention in published reports. We review imaging studies or pathologic findings of adrenal hemorrhage in five cases of proved child abuse. SUBJECTS AND METHODS: The imaging findings in three children with adrenal hemorrhage were analyzed retrospectively. All three had abdominal CT scans and skeletal radiographs. One also had abdominal sonograms and MR images. The pathologic findings in two other abused children with adrenal hemorrhage who died of head injuries were also studied. In all five cases, a history of trauma was not initially known; child abuse was later confirmed. RESULTS: Unilateral hemorrhage in the right adrenal gland was found in all patients. Enhanced CT scans of the abdomen showed a low-attenuation, oval mass separating the limbs of the adrenal gland. Sonograms in one case showed a small, heterogeneous mass in the right adrenal gland. MR images obtained 3 weeks later showed an area of high signal intensity within the right adrenal gland on both T1- and T2-weighted images, consistent with subacute hemorrhage. In both deceased children, autopsy showed hemorrhage in the right adrenal gland, mainly within the medulla with some extension beyond the capsule in one case. All five children had associated abdominal visceral injuries or rib fractures or both, on the same side as the hemorrhage. CONCLUSION: Imaging findings of adrenal hemorrhage are similar to those previously described in patients with accidental trauma. Pathologic sections of the gland reveal predominantly medullary involvement with hemorrhage. The presence of adrenal hemorrhage in a child should prompt a search for other associated injuries and raise the possibility of unsuspected trauma.

Adrenal Gland Diseases↗
PubMed2002

A103 immunostaining in the diagnosis of adrenal cortical tumors: an immunohistochemical study of 316 cases.

CONTEXT: The monoclonal antibody A103 recognizes an antigen on melanoma cells known as Melan-A or MART-1. Recent studies have shown that A103 also reacts with adrenal cortical cells and may be useful in the diagnosis of adrenal cortical tumors. However, only small numbers of some of the tumors in the differential diagnosis of adrenal cortical neoplasms have been studied. OBJECTIVE: To study the specificity of A103 immunohistochemistry in a large number of tumors in the differential diagnosis of adrenal cortical neoplasms. DESIGN: Formalin-fixed, paraffin-embedded tissue from 21 adrenal cortical tumors, 16 cases of metastatic carcinoma to the adrenal, 10 pheochromocytomas, and 269 extra-adrenal carcinomas was evaluated for A103 immunoreactivity using a commercially available antibody (Novocastra, Newcastle, UK). RESULTS: Positive staining was seen in all of the adrenal cortical tumors but in none of the adrenal metastases or pheochromocytomas. In the 269 extra-adrenal carcinomas, A103 immunoreactivity was limited to a single ovarian serous carcinoma. CONCLUSION: A103 immunostaining is useful in distinguishing adrenal cortical neoplasms from other carcinomas and pheochromocytoma.

Adrenal Cortex Neoplasms↗
PubMed1999

Congenital adrenal hyperplasia: not really a zebra.

Congenital adrenal hyperplasia was once considered a rare inherited disorder with severe manifestations. Mild congenital adrenal hyperplasia, however, is common, affecting one in 100 to 1,000 persons in the United States and frequently eluding diagnosis. Both classic and nonclassic forms of the disease are caused by deficiencies in the adrenal enzymes that are used to synthesize glucocorticoids. The net result is increased production from the adrenal gland of cortisol precursors and androgens. Even mild congenital adrenal hyperplasia can result in life-threatening sinus or pulmonary infections, orthostatic syncope, shortened stature and severe acne. Women with mild congenital adrenal hyperplasia often present with hirsutism, oligomenorrhea or infertility. Congenital adrenal hyperplasia is diagnosed by demonstration of excess cortisol precursors in the serum during an adrenal corticotropic hormone challenge. Diagnosis of congenital adrenal hyerplasia in fetuses that are at risk for congenital adrenal hyperplasia can be determined using human leukocyte antigen haplotype or by demonstration of excess cortisol precursors in amniotic fluid. Treatment includes carefully monitored hormone replacement therapy. Recognition of the problem and timely replacement therapy can reduce morbidity and enhance quality of life in patients that are affected by congenital adrenal hyperplasia.

17-alpha-Hydroxyprogesterone↗
PubMed1999

[Effects of mitotane therapy in dogs with pituitary dependent Cushing syndrome on the adrenal gland size--an ultrasonographic study].

The effect of mitotane therapy on adrenal gland size was evaluated in 13 dogs with pituitary dependent hyperadrenocorticism. Ultrasonographic measurements were obtained before and during mitotane therapy. During therapy both adrenal glands were shorter and thinner (median during therapy: left adrenal gland 19.4 mm long, 5.4 mm thick, right adrenal gland 18.1 mm long, 6.1 mm thick) than before mitotane therapy (median before therapy: left adrenal gland 23.6 mm long, 8.3 mm thick, right adrenal gland 21.6 mm long, 8.1 mm thick). Statistical evaluation showed a significant reduction in size. But ultrasonographic measurement of adrenal gland size is not useful in the evaluation of adrenal reserve during mitotane therapy. Inadequate adrenal reserve was not identified and adrenal size measurement by ultrasonography was not helpful to differentiate adequate and inadequate control of adrenal cortisol secretion during mitotane therapy.

Adrenal Glands↗
PubMed1991

Control of adrenal androgen secretion.

The human adrenal gland secretes large amounts of androgens and androgenic precursors as compared with the adrenal glands of other species. In part, this pattern of secretion is regulated by ACTH, analogous to the control of cortisol. However, in many instances, including adrenarche, puberty, aging, and severe illness, secretion of adrenal androgens and cortisol diverge for reasons which are not clear. Factors endogenous to the adrenal gland may have a role in the modulation of adrenal androgen secretion. These include the centripetal blood supply of the adrenal gland, availability of cofactors of steroidogenic enzymes, and intrinsic properties of adrenal cells or enzymes. However, these mechanisms may, in turn, be modified by factors exogenous to the adrenal gland. Possible evidence for a regulatory role for such known substances as growth hormone, IGF-1, gonadotropins, estrogens, angiotensins, prostaglandins, insulin, EGF, and POMC-related peptides is discussed. Furthermore, pituitary or extrapituitary substances, in addition to known hormones, may have a role in the control of adrenal androgen secretion. Several lines of evidence include the inability of ACTH to maintain a normal adrenal androgen/cortisol ratio in adrenally suppressed patients, or experimentally, in hypophysectomized chimpanzees. Evidence for such factors derived from fetal and adult human pituitary gland is discussed.

Adrenal Glands↗
PubMed1987

Preoperative lateralisation of aldosteronomas by aldosterone/cortisol ratios in adrenal venous plasma.

Data from adrenal scintigraphy with 6 beta-[131I]-iodomethyl-19-norcholesterol (AS), computed tomography (CT), adrenal venography and adrenal venous sampling were compared for their accuracy in locating small aldosteronomas in 17 patients. Final confirmation of location was by surgery. Seventeen out of 18 adrenals whose aldosterone/cortisol (A/C) ratio was 5.0 x 10(-3) or higher were found to have aldosteronomas (94.4%). All 14 adrenals whose A/C ratios were less than 5.0 x 10(-3) contained no aldosteronomas (100%). AS successfully lateralised nine out of 17 aldosteronomas (52.9%), CT 3 out of 5 (60.0%), adrenal venography 12 out of 17 (70.6%), adrenal venous aldosterone concentration 12 out of 15 (80.0%). The most frequent problem with adrenal venous sampling was the varying degrees of mixture with non-adrenal venous blood, mainly from renal vein and inferior vena cava blood. The A/C ratio of adrenal venous plasma proved to be the most useful diagnostic tool, using cortisol concentration as an indicator of any non-adrenal venous mixture.

Adenoma↗
PubMed1983

The influence of age on the activity of the renin-angiotensin system in rats with adrenal-regeneration hypertension.

In female rats aged 21 and 80 days, uninephroadrenalectomy with enucleation of the remaining adrenal was performed and 0.17 mol X l-1 saline offered as the only drinking fluid. The changes of plasma concentration of renin (PRC), and its substrate (RSC) and renal renin activity (RRA), considered as an indicator of the secretory activity of the regenerating adrenal were studied 5, 10, 20, 40 and 60 days after the adrenal enucleation to look for possible age differences related to the higher susceptibility of immature rats to the hypertensive influence of the regenerating adrenal. It has been found that: 1. In adrenal-enucleated rats the saline-induced decrease of RRA was delayed for a shorter time period in immature rats than in adult ones (5 vs. 10 days), during which blood pressure, saline consumption and RSC were lowered. The decrease of PRC was retarded in the older group only. 2. In rats with regenerating adrenals the PRC and RRA decrease was greater in animals subjected to enucleation of the remaining adrenal gland when immature, than in those operated when adult. At the end of the experiment this age difference disappeared. 3. The age difference in PRC and RRA suppression appeared during the period, when neither blood pressure nor saline consumption were higher in immature rats than in adult ones. 4. In rats with regenerating adrenals the renal mass was greater than in saline drinking controls. In the younger group, which in contrast to the adult one developed hypertension, this increase was greater and directly related to the blood pressure level from the 20th post-enucleation day onwards. It is being suggested that the changes of PRC, RRA and RSC observed up to the 10th post-enucleation day indicates relative adrenal insufficiency, the shorter duration of which in immature rats reflects their higher sensitivity to mineralocorticoids produced by the regenerating adrenal. This also manifests itself by greater PRC and RRA suppression in this age group. The haemodynamic results of the greater RRA suppression in the not yet fully developed kidneys of immature rats may facilitate the development of a "vicious circle" mechanism between blood pressure and hypertensive renal damage and thus contribute to the higher sensitivity to adrenal-regeneration hypertension.

Adrenal Cortex↗
PubMed1995

Ultrasonographic evaluation of the adrenal glands in dogs.

OBJECTIVE: To determine normal adrenal gland size by means of ultrasonography in dogs and to determine the value of ultrasonography in the diagnosis of pituitary-dependent hyperadrenocorticism (PDH) in dogs. DESIGN: Prospective observational study. ANIMALS: 62 dogs: 20 healthy dogs, 20 dogs with non-endocrine disease, and 22 dogs with untreated PDH. PROCEDURE: Length and maximum and minimum diameter of the adrenal glands were measured ultrasonographically. Multiple regression and correlation analyses were used to determine whether body weight, kidney length, aortic diameter, or age was related to adrenal gland size. Two-tailed t-tests and multiple linear regression analysis were used to compare values between groups. Sensitivity and specificity of using ultrasonographic measurement of adrenal gland size as a diagnostic test for PDH were determined. RESULTS: There was a significant linear relationship between adrenal gland length, but not maximum and minimum diameters, and body weight, aortic diameter, and kidney length in healthy dogs and in dogs with nonendocrine diseases. Length, maximum diameter, and minimum diameter of the right adrenal gland and maximum and minimum diameters of the left adrenal gland were significantly greater in dogs with PDH than in healthy dogs and dogs with nonendocrine diseases. As a diagnostic test for PDH, ultrasonographic measurement of maximum or minimum diameter of the left adrenal gland gave the best combination of sensitivity and specificity. For maximum diameter of the left adrenal gland, sensitivity was 77% and specificity was 80%. For minimum diameter of the left adrenal gland, sensitivity was 73% and specificity was 85%. CLINICAL IMPLICATION: Ultrasonography of the adrenal glands is a valuable diagnostic procedure in dogs suspected of having pituitary-dependent hyperadrenocorticism.

Adrenal Glands↗
PubMed1995

Role of the adrenal medulla in control of blood pressure and renal function during frusemide-induced volume depletion.

OBJECTIVE: To examine the role of the adrenal medulla in reflex control of mean arterial pressure (MAP), heart rate and renal function parameters during frusemide-induced volume depletion. DESIGN: Frusemide (6 mg/kg per h) was administered intravenously to two groups of chronically instrumented rats with either sham adrenal medullectomy (n = 15) or adrenal medullectomy (n = 11). RESULTS: Adrenal medullectomy reduced adrenal adrenaline concentration by 99% and plasma adrenaline concentration by 97%. Plasma corticosterone levels were similar in the two groups, which suggests that adrenal cortical function was not affected by adrenal medullectomy. Although frusemide did not affect arterial pressure in the sham-operated rats, MAP fell by 21 +/- 3 mmHg (mean +/- SEM) during frusemide diuresis in the rats with adrenal medullectomy. Heart rate was lower in the rats with adrenal medullectomy than in the sham-operated rats throughout the study. There were no major differences in renal haemodynamics or overall renal water and sodium handling between the two groups but, at the time of maximal activation of compensatory sodium reabsorption, fractional sodium excretion in the distal nephron segment was significantly higher in the rats with adrenal medullectomy than in the sham-operated rats. CONCLUSIONS: Adrenal medullary adrenaline release is essential in the control of MAP during frusemide-induced volume depletion. Circulating adrenaline might contribute, by modifying distal tubular sodium reabsorption, to compensatory sodium reabsorption during frusemide-induced volume depletion.

Adrenal Medulla↗
PubMed1993

Metrazole induces the sequential activation of c-fos, proenkephalin, and tyrosine hydroxylase gene expression in the rat adrenal gland: modulation by glucocorticoid and adrenocorticotropic hormone.

The immediate-early gene c-fos (a nuclear transcription factor) has been viewed as a nuclear "third messenger" or cellular "master switch." Both in vitro and in vivo studies have suggested that the proenkephalin (Penk) and tyrosine hydroxylase (TH) genes are potential targets of this immediate-early gene. We investigated the relationships between the activation of the c-fos gene and the activation of the Penk and TH genes in both rat hippocampus and adrenal using a commonly used model, metrazole (MTZ)-induced convulsions. The administration of MTZ produced a sequential elevation in c-fos, preproenkephalin (PPenk), and TH mRNAs. One hour after MTZ administration, c-fos mRNA was increased about 10-fold in rat hippocampus and about 5-fold in rat adrenal, without a significant change in spinal cord levels. Immunocytochemistry revealed that Fos-like immunoreactivity was greatly increased in both hippocampus and adrenal medulla at 3 hr after MTZ administration. The levels of PPenk and TH mRNAs were significantly increased (5-fold and 3-fold, respectively) in the adrenal 6 hr after MTZ treatment. The effects of MTZ on c-fos, PPenk, and TH mRNAs were dose dependent in both adrenal and hippocampus. In the adrenal, both the basal levels and the MTZ induction of PPenk mRNA were significantly attenuated by hypophysectomy (hypox) and were partially reinstated by adrenocorticotropic hormone (ACTH) replacement. In contrast, the basal levels of c-fos and TH mRNAs were not altered in hypox rat adrenal. ACTH treatment completely blocked the MTZ induction of adrenal c-fos mRNA and the subsequent induction of Fos-like immunoreactivity, whereas MTZ increased PPenk and TH mRNAs nearly 3-fold. Thus, in hypox rats MTZ can increase adrenal c-fos and TH mRNA levels without a corresponding increase in PPenk mRNA, whereas in ACTH-treated rats PPenk and TH mRNA levels in adrenal can be increased by MTZ without a preceding increase in c-fos mRNA. The MTZ induction of c-fos appears neither sufficient nor always necessary for the subsequent MTZ induction of Penk and TH gene expression. We conclude that c-fos, Penk, and TH genes can be differentially regulated in the adrenal of hypox rats or animals treated with ACTH, although they are co-localized in the same medullary cells.

Adrenal Glands↗
PubMed1994

[Distinction between adrenal adenomas and metastases using 0.5 Telsa MR imaging: diagnosis with out-of-phase T2*-weighted gradient-field-echo image].

The purpose of this study was to investigate the ability of MR imaging with a 0.5-T apparatus to distinguish adrenal adenomas from adrenal metastases. The series included 23 adrenal adenomas (18 non-hyperfunctioning adenomas, 5 hyperfunctioning) and 23 adrenal metastases (14 from lung, 5 liver, 3 colon, and 1 stomach cancer). The signal intensity (SI) ratio (adrenal tumor/liver) on T1-, T2-, and T2*-weighted MR images was calculated for adrenal tissue characterization. Adrenal adenomas were more precisely distinguished from adrenal metastases on T2*-weighted images (21/23, 91%) than on T2-weighted images (15/23, 65%). In conclusion, T2*-weighted images were better than routine T2-weighted images in distinguishing adrenal adenomas from adrenal metastases. The reason could be that the total signal intensity of adrenal adenomas which contained some fat components decreased on T2*-weighted images due to an out-of-phase effect.

Adenoma↗
PubMed1998

A comparison of A103 and inhibin reactivity in adrenal cortical tumors: distinction from hepatocellular carcinoma and renal tumors.

Distinguishing adrenal cortical neoplasms from either hepatocellular carcinomas or renal tumors can be difficult. Two recently described antibodies, A103 and inhibin A, are most often reported to be reactive with adrenal cortical neoplasms but with neither hepatocellular carcinoma nor renal cell carcinoma. To compare the sensitivity and specificity of these two antibodies in the diagnosis of adrenal cortical tumors, we stained 22 adrenal cortical adenomas, 4 adrenal cortical carcinomas, 25 hepatocellular carcinomas, and 43 renal tumors, including 33 renal cell carcinomas and 8 oncocytomas, with the A103 and inhibin A using an avidin-biotin complex technique. Fifteen (68%) of 22 adrenal adenomas and 2 (50%) of 4 adrenal cortical carcinomas were reactive with A103. Nineteen (86%) of 22 adrenal adenomas and 3 (75%) of 4 adrenal cortical carcinomas were reactive for inhibin A. None of the renal tumors or hepatocellular carcinomas reacted with A103, but 1 (4%) of 25 hepatocellular carcinomas (a high-grade pleomorphic tumor) and 1 (2%) of 43 renal tumors (a clear-cell renal cell carcinoma) were reactive with inhibin A. The cytoplasmic reactivity for A103 in adrenal tumors was coarsely granular and most common in clear-cell areas. Reactivity for inhibin was either cytoplasmic or membranous and stained both clear-cell and granular areas. We conclude that both antibodies are useful in the immunohistochemical diagnosis of adrenal cortical neoplasms and that A103 is slightly more specific and inhibin slightly more sensitive.

Adenoma↗