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PubMed2002

Steroidogenic acute regulatory protein expression is decreased in the adrenal gland of the growth-restricted sheep fetus during late gestation.

Functional development of the adrenal cortex is critical for fetal maturation and postnatal survival. In the present study, we have determined the developmental profile of expression of the mRNA and protein of an essential cholesterol-transporting protein, steroidogenic acute regulatory protein (StAR), in the adrenal of the sheep fetus. We have also investigated the effect of placental restriction (PR) on the expression of StAR mRNA and protein in the growth-restricted fetus. Adrenal glands were collected from fetal sheep at 82-91 days (n = 10), 125-133 days (n = 10), and 140-144 days (n = 9) and from PR fetuses at 141-145 days gestation (n = 9) (term = 147 +/- 3 days gestation). The adrenal StAR mRNA:18S rRNA increased (P < 0.05) between 125 days (7.44 +/- 1.61) and 141-144 days gestation (13.76 +/- 1.88). There was also a 13-fold increase (P < 0.05) in the amount of adrenal StAR protein between 133 and 144 days gestation in these fetuses. However, the amount of StAR protein (6.9 +/- 1.7 arbitrary densitometric units [AU]/microg adrenal protein) in the adrenal of the growth-restricted fetal sheep was significantly reduced, when compared with the expression of StAR protein (17.1 +/- 1.9 AU/microg adrenal protein) in adrenals from the age-matched control group. In summary, there is a developmental increase in the expression of StAR mRNA and protein in the fetal sheep adrenal during the prepartum period when adrenal growth and steroidogenesis is dependent on ACTH stimulation. We have found that, while the level of expression of StAR protein is decreased in the adrenal gland of the growth-restricted fetus during late gestation, this does not impair adrenal steroidogenesis. Our data also suggest that the stimulation of adrenal growth and steroidogenesis in the growth-restricted fetus may not be ACTH dependent.

Adrenal Glands↗
PubMed2001

Immunoexpression of inhibin alpha-subunit in adrenal neoplasms.

Inhibin normally is produced by ovarian granulosa cells and testicular Sertoli cells. Extragonadal inhibin expression also has been detected in the placenta, pituitary gland, and liver. It may be difficult to make a distinction between adrenal cortical tumors, pheochromocytoma, and metastatic carcinomas including renal cell and hepatocellular carcinoma. Immunohistochemical expression of inhibin alpha-subunit was evaluated to determine whether any usefulness of immunostaining could be found for inhibin alpha-subunit in the differential diagnosis of adrenal glandular lesions. The authors performed immunostaining against inhibin alpha-subunit on 5 cases of normal adrenal gland, 1 case of adrenal cortical hyperplasia, 25 cases of adrenal cortical adenoma, 6 cases of adrenal cortical carcinoma, 21 cases of pheochromocytoma, 8 cases of metastatic carcinoma, and 10 cases of primary renal cell carcinoma. Normal adrenal gland showed a strong immunoreactivity against inhibin alpha-subunit, especially in the inner layer of the adrenal cortex, representing the zona reticularis, but adrenal medulla was negative for inhibin alpha-subunit. Adrenal cortical hyperplasia associated with Cushing's syndrome showed a strong, diffuse immunoreactivity for inhibin alpha-subunit. Immunoreactivity against the inhibin alpha-subunit was identified in all cases of adrenal cortical adenoma and carcinoma, especially in the adrenal cortical neoplasm with Cushing's syndrome, which showed a strong reactivity. However, immunoreactivity was absent in two metastatic carcinomas from the liver and colon and most of the pheochromocytomas, except three cases with weak focal positivity for inhibin alpha-subunit. Four cases of metastatic renal cell carcinoma and 10 cases of primary renal cell carcinoma revealed no immunoreactivity. Metastatic adenocarcinoma from the prostate showed a weak immunoreactivity for inhibin alpha-subunit. Metastatic hepatoblastoma was negative against inhibin alpha-subunit with endogenous biotin blocking. Immunoexpression for inhibin alpha-subunit is useful for making distinction between adrenal cortical tumors, pheochromocytoma, and metastatic carcinoma. Inhibin alpha-subunit may be valuable as part of a diagnostic immunohistochemical panel in adrenal glandular lesions.

Adolescent↗
PubMedDate not supplied

Retrospective review of the ultrasonographic features of adrenal lesions in 21 ferrets.

Clinical signs and follow-up information were recorded. Histopathologic diagnoses were obtained for 25 adrenal glands in 21 ferrets. Adrenal lesions included ten adenocarcinomas, nine adenomas, one hyperplasia and one cortical cyst. Four adrenal glands (all right-sided) were diagnosed as unspecified adrenal tumors but lacked a definite histopathologic diagnosis (adenoma vs. adenocarcinoma) due to incomplete surgical resection and consequent small sample sizes. Bilateral adrenal lesions were identified in 4 ferrets (19%). Adrenal shape, size, echogenicity, laterality, and the presence of vascular invasion were evaluated with ultrasound. Size and shape were variable and not specific to lesion type. Both benign and malignant adrenal tumors (adenomas, adenocarcinomas) appeared most often as masses with increased thickness and a normal length (11/23), less frequently as larger masses with increased thickness and length (4/23) or as nodules focally deforming the normal adrenal shape (6/23). The only cortical cyst appeared as a nodule. Three adrenal glands had a normal size and shape and were diagnosed as adenomas (2) or hyperplasia (1). Therefore treatment may be warranted based solely on clinical signs if adrenal glands are ultrasonographically normal. Vascular invasion was not identified ultrasonographically. However, focal absence of periglandular fat resulting in contact of 8 adrenal glands with either caudal vena cava (6), aorta (1) or liver (1) identified ultrasonographically, correlated with incomplete surgical resectability (6/8) and histopathologic diagnoses of carcinoma (4/8) or unspecified tumors (4/8). Therefore, a focal absence of periglandular fat between the adrenal gland and the large vessels or liver, deviation or compression of the large vessels by the adrenal lesion may indicate malignancy. Adrenal tumors (benign and malignant) were often associated with a prominent uterus, uterine stump or prostate with or without prostatic cysts.

Adenocarcinoma↗
PubMed1995

Regulation of neuropeptide Y and its mRNA by glucocorticoids in the rat adrenal gland.

The effects of glucocorticoids on adrenal neuropeptide Y (NPY) and NPY mRNA levels have been investigated on adult male rats of the Wistar strain subcutaneously injected twice a day with dexamethasone (5 mg/day), metyrapone (66 mg/day) or solvent (NaCl 0.9%) for 2.5 days and sacrificed 2 h after the last injection. Dexamethasone induced a significant decrease in both the adrenal weight (30%) and the plasma corticosterone concentration (85%) but a significant increase of the adrenal NPY content (about 25%) as well as of its mRNA (0.8 kb) (> 100%), revealed by Northern blot analysis and by in situ hybridization. Dexamethasone was unable to affect significantly dopamine (DA), norepinephrine (NE) and epinephrine (E) content of the adrenals; in contrast, it induced a significant decrease (30%) of the plasma NE level. Metyrapone elicited a drop of the plasma corticosterone level (80%), but a rise (near 150%) of the plasma ACTH concentration associated with an increase (19%) of the adrenal weight, a significant increase (30%) in the amount of adrenal NPY as well as a rise (> 200%) of NPY mRNA content of the adrenal. Such treatment increased DA and NE (40%), and decreased E (> 30%) content of the adrenals. Metyrapone-induced changes of catecholamine concentrations in the plasma were similar to that observed in the adrenal gland. Data suggest that the increase in adrenal NPY mRNA content induced by dexamethasone is more likely due to humoral effect rather than nervous effect of this synthetic glucocorticoid on the adrenal medulla. A neural mechanism as splanchnic nerve activation in response to severe corticosterone deficiency is a reasonable hypothesis to explain the increase in adrenal NPY mRNA induced by metyrapone, although there are probably other, nonneural mechanisms by which metyrapone could stimulate adrenal NPY. Present data are consistent with glucocorticoid regulation of NPY gene expression and/or steady-state level of NPY mRNA in the adrenal gland.

Adrenal Glands↗
PubMed1980

Adrenocorticotropin inhibits compensatory adrenal growth after unilateral adrenalectomy.

To determine the interaction between ACTH and compensatory adrenal growth after unilateral adrenalectomy, we have studied the adrenals of young male rats treated with saline, ACTH, dexamethasone, or hypophysectomy and left or sham adrenalectomy (Adx or Sham). ACTH injected at the time of adrenal surgery inhibited the normal increase in [3H]thymidine incorporation into right adrenal DNA at 12 or 18 h (P < 0.05), but increased the RNA content. ACTH treatment (2, 4, or 8 U twice daily) in Shams caused a dose-dependent increase in adrenal weight and the RNA to DNA ratio at 24 h and, subsequently, a dose-dependent increase in adrenal DNA content at 72 h. ACTH treatment of Adx prevented the increase in adrenal DNA content at 24 h (P < 0.05), while increasing the RNA to DNA ratio (P < 0.05) in a dose-dependent manner. Treatment of rats with dexamethasone decreased adrenal weight and RNA content and attenuated the normal response to Adx. ACTH (1 U) at the time of adrenalectomy or sham operation in hypophysectomized rats abolished the normal difference between right adrenal weights in the two groups at 3 days. Adrenal growth occurred in rats hypophysectomized and adrenalectomized 24 h previously compared to Sham controls. These results show that adrenal growth mediated by ACTH is a different cellular process (hypertrophy) from that growth triggered by unilateral adrenalectomy (hyperplasia). Treatment with a long acting preparation of ACTH causes adrenals in rats from both the Sham and Adx groups to grow, and the process of ACTH-mediated adrenal growth inhibits the rapid proliferative response to unilateral adrenalectomy. A proliferative response may occur by 3 days during treatment with large doses of long acting ACTH. Treatment at adrenalectomy with synthetic alpha ACTH-(1-24) abolished the normal increase in adrenal weight at 20 h.

Adrenal Glands↗
PubMed1987

Corticotropin-releasing factor in the dog adrenal medulla is secreted in response to hemorrhage.

To characterize the nature of CRF-like immunoreactivity (CRF-LI) in the dog adrenal, adrenal medullary, adrenal cortical, or hypothalamic tissue was extracted and subjected to RIA after partial purification on C-18 cartridges or Sephadex G-50. Using N- and C-terminal-directed antisera against rat/human (r/h) CRF, significant levels of CRF-LI were found in the adrenal medulla and hypothalamus, but not in the adrenal cortex. Immunocytochemical analysis revealed that CRF-immunoreactive cells were located in the adrenal medulla, many of them concentrated in the vicinity of blood vessels and at the border between adrenal medulla and cortex. However, the cortex was devoid of any CRF-positive cells. On reverse phase HPLC, CRF-LI in the adrenal medulla coeluted with synthetic r/hCRF. In a bioassay system, using dispersed rat anterior pituitary cells, purified adrenal CRF caused a dose-dependent increase in ACTH secretion parallel to the r/hCRF standard, indicating that dog adrenal medulla contains authentic r/hCRF. Evidence of CRF-LI secretion from the adrenal was supported by its presence in adrenal venous, but not in peripheral arterial, plasma. Adrenal venous plasma CRF-LI coeluted with r/hCRF on reverse phase HPLC after affinity chromatographic purification. The CRF-LI secretory rate in conscious trained dogs was 68 +/- 19 pg/min (concentration, 27 +/- 5 pg/ml). In response to 20% hemorrhage, the CRF-LI secretion rate rose 3-fold within 15 min and was associated with increased catecholamine secretion. The existence of a biologically active CRF-like substance in the dog adrenal medulla and its secretion in conjunction with catecholamines after a hemorrhage suggest a physiological role for this peptide other than pituitary or central nervous system regulation.

Adrenal Medulla↗
PubMed2003

Diagnostic and prognostic value of fas and telomeric-repeat binding factor-1 genes in adrenal tumors.

It is often difficult to distinguish histologically between an adrenal cortical cancer and a benign adenoma, or to predict the prognosis of patients with adrenal cortical cancers. In this investigation, we examined whether apoptosis-regulating genes, bcl-xL and fas, and a telomere-related gene, telomeric-repeat binding factor-1 (TRF-1), differ between adrenal cortical cancers and benign adrenal tumors. Tissues from 4 adrenal cortical cancers were compared with 7 normal adrenal tissues, 17 cortical adenomas, 4 cortical hyperplasias, and 20 pheochromocytomas for expressions of bcl-xL and fas by RT-PCR, and for expressions of TRF-1 by real-time quantitative RT-PCR. All benign adrenal tissues expressed both the antiapoptosis gene, bcl-xL, and proapoptosis gene, fas, but the adrenal cortical cancers expressed only bcl-xL and not fas. TRF-1 increased by more than 30-fold in the adrenal cortical cancers, compared with benign adrenal tissues, and inversely correlated with the prognosis of patients with the adrenal cortical cancers. This lack of expression of fas in adrenal cortical cancer may help to distinguish it from benign adrenal tumors. The level of TRF-1 expression may be helpful prognostically for patients with adrenal cortical cancers.

Adrenal Cortex Neoplasms↗
PubMed2004

Study of migration of neural crest cells to adrenal medulla by three-dimensional reconstruction.

Adrenal medullary cells are derived from the neural crest. To study the formation process of the adrenal medulla in the embryonic period, we visualized chromaffin cells of rat embryos at 13 to 17 days of gestation using anti-tyrosine hydroxylase (TH) antiserum, and created three-dimensional images from serial tissue sections. Between 13 and 15 days of gestation, TH-positive cells (chromaffin cells) migrated from a group of TH-positive cells present dorsal to the adrenal primordium via the medial cranial end of the adrenal primordium into the adrenal primordium. At or after 16 days of gestation, the adrenal capsule was formed except on the ventral aspect of the cranial end of the adrenal gland, from which TH-positive cells penetrated into the adrenal gland. The reconstructed images showed that TH-positive cells were present contiguously from the sympathetic chain ganglia through a group of TH-positive cells ventral to the adrenal gland into the adrenal cortex, and that the group of TH-positive cells ventral to the adrenal gland communicated with the preaortic ganglion present ventral and caudal to the adrenal gland. These results suggest that neural crest cells use the same pathway to migrate to the sympathetic chain ganglia dorsal to the adrenal gland, to the adrenal gland, and to the preaortic ganglion.

Adrenal Medulla↗
PubMed1995

MR imaging of adrenal masses: value of chemical-shift imaging for distinguishing adenomas from other tumors.

OBJECTIVE: CT and conventional MR imaging are helpful in characterizing adrenal tumors, but a specific diagnosis is not achieved for a substantial number of lesions. Chemical-shift imaging relies on the different resonance frequencies of protons in water and triglyceride molecules and therefore may permit a more specific diagnosis of adrenal adenomas, which are known to contain abundant lipid. The purpose of this study was to evaluate the usefulness of chemical-shift MR imaging in the differentiation of adrenal adenomas from other adrenal masses. SUBJECTS AND METHODS: Forty-one adrenal masses (17 nonhyperfunctioning adenomas, two aldosteronomas, six pheochromocytomas, one ganglioneuroma, five adrenal carcinomas, one lymphoma, seven metastases, one case of extramedullary hematopoiesis, and one leiomyosarcoma) suspected clinically or identified by sonography or CT in 38 patients were prospectively evaluated with MR imaging. Pathologic proof of diagnosis was obtained for 28 lesions, and stability on imaging follow-up (mean, 19 months) was accepted as proof of diagnosis of benign adenoma for 13 lesions. In-phase T1-weighted spin-echo sequences (500/20 [TR/TE]) and opposed-phase gradient-echo sequences (142/6.3, flip angle = 90 degrees) of the adrenal regions were applied. Quantitative analysis of signal intensity loss in the adrenal lesions relative to reference tissues (liver, muscle, and spleen) on in-phase and opposed-phase sequences was done to differentiate adenomas from nonadenomas. Region-of-interest signal intensity measurements were obtained in a standard fashion by selection of the largest possible representative sample. RESULTS: Using liver as the reference standard, we found that mean signal intensity ratios were 0.47 (range, 0.23-0.97) for adrenal adenomas and 0.88 (range, 0.65-1.32) for nonadenomas; signal intensity ratios for two adenomas overlapped those of the nonadenomas. Using muscle as the reference standard, we found that mean signal intensity ratios were 0.44 (range, 0.22-0.66) for adrenal adenomas and 0.85 (range, 0.59-1.39) for nonadenomas; signal intensity ratios for two adenomas overlapped those of the nonadenomas. Using spleen as the reference standard, we found that mean signal intensity ratios were 0.45 (range, 0.27-0.73) for adrenal adenomas and 0.97 (range, 0.8-1.18) for nonadenomas, with no overlap. The mean signal intensity ratios were significantly different between adenomas and nonadenomas for all three reference tissues (p < .001). CONCLUSION: Our results show that chemical-shift MR imaging is an important new technique that enables the differentiation of adrenal adenomas from other adrenal masses, reducing the need for biopsy and prolonged imaging follow-up in patients with adrenal tumors.

Adenoma↗
PubMed1995

Characterization of adrenal masses (< 5 cm) by use of chemical shift MR imaging: observer performance versus quantitative measures.

OBJECTIVE: The purposes of this study were to evaluate the ability of chemical shift MR imaging to differentiate 1- to 5-cm adrenal adenomas from metastases and to compare subjective interpretation with several different quantitative measures. SUBJECTS AND METHODS: Forty-three patients with 46 proved adrenal lesions (28 adenomas and 18 metastases) had MR imaging with a gradient-echo breath-hold technique and echo time varied to obtain in-phase and out-of-phase images. Qualitative analysis of the MR images was done by three experienced observers, who reported their confidence in diagnosing the benignity versus the malignancy of the adrenal masses on the basis of signal loss on out-of-phase images. Quantitative analysis was performed by calculating the difference in signal intensity between in-phase and out-of-phase images by use of regions of interest (signal intensity index) and by use of adrenal-liver, adrenal-spleen, and adrenal-muscle signal intensity ratios. Results between quantitative and qualitative measures were compared by use of receiver operating characteristic (ROC) analysis. RESULTS: The mean signal intensity was significantly different between adenomas and metastases on out-of-phase images (64 versus 98) (p < .0005) but not in-phase images (130 versus 122) (p = .47). The adrenal-spleen ratio discriminated between adenomas and metastases better than did the adrenal-liver ratio, the adrenal-muscle ratio, or the signal intensity index. No significant difference in interpretation among the three observers was evident (areas under the ROC curves, 0.93, 0.95, and 0.96). The performance of the observers was comparable to the results obtained with the adrenal-spleen ratio measurement (area under the ROC curve, 0.97). CONCLUSION: Experienced observers were able to differentiate adrenal adenomas from metastases just as well as quantitative measures. The adrenal-spleen ratio is the best quantitative means of distinguishing benign from malignant adrenal masses. Chemical shift MR imaging is a good but imperfect discriminator of adrenal adenomas.

Adenoma↗
PubMed2004

Characterization of the normal adrenal gland with 18F-FDG PET/CT.

UNLABELLED: Prior studies have documented increased (18)F-FDG adrenal activity in both benign and malignant pathologic conditions. When whole-body PET imaging is performed without CT anatomic coregistration, however, the normal adrenal gland is difficult to recognize. The purpose of this study was to investigate the normal adrenal appearance and standardized uptake value (SUV) using (18)F-FDG PET/CT imaging. METHODS: Twenty patients with lymphoma with normal-appearing adrenal glands on prior CT examination (less than a 5% pretest likelihood of adrenal involvement) were studied. PET/CT imaging was performed 2 h after intravenous administration of (18)F-FDG. Unenhanced CT scans were acquired for attenuation correction and anatomic coregistration. PET images were reconstructed using an ordered-subsets expectation maximization algorithm and were corrected for body weight, dose, and radioactive decay. Ability to confirm visualization of the adrenal glands was determined for (18)F-FDG PET alone and for (18)F-FDG PET/CT by a consensus of 2 readers, and uptake of (18)F-FDG in the adrenal gland was compared with liver activity and scored visually (0 = no visualization, 1 = activity less than in liver, 2 = activity equal to liver activity, and 3 = activity greater than in liver). RESULTS: The 2 readers agreed on visualization of the adrenal glands with PET alone for 2 of 40 (5%) glands. With PET/CT, the readers agreed on visualization of 27 of 40 (68%) adrenal glands. Visual scores for normal adrenal activity ranged from 0 to 3, and maximum SUVs ranged from 0.95 to 2.46. Visual scoring of adrenal activity correlated well with both mean and maximal SUV (mean SUV vs. visual score: slope = 0.96, r = 0.88; maximum SUV vs. visual score: slope = 0.99, r = 0.87). CONCLUSION: PET/CT permits more reliable visualization of normal adrenal glands than does PET alone. Visual assessment of adrenal uptake correlates well with SUV measurement, and readers of PET/CT need to be aware of the wide range of normal adrenal uptake.

Adrenal Glands↗
PubMed1990

[Adrenal tumors associated with renal cell carcinoma].

We experienced two cases with renal cell carcinoma who showed enlargement of the contralateral adrenal gland. In case 1, the enlarged adrenal gland was a non-functioning adrenal adenoma, and in case 2, it was a metastatic adrenal tumor. Non-functioning adrenal adenomas are benign tumors of the adrenal cortex often found incidentally at autopsy or on computed tomography (CT) studies of the upper abdomen. Adrenal adenomas have been reported to occur in 9.5-14% of patients with renal cell carcinoma, while the incidence being 1.5-8.7% in the general population. Since metastases of renal cell carcinoma to the adrenal glands are not uncommon, it is important to distinguish between non-functioning adrenal adenomas and metastatic tumors. Therefore, we studied the incidence of adrenal tumors (including metastatic tumors and benign tumors) in patients with renal cell carcinoma who underwent the abdominal CT study in our hospital. From 1982 to 1989, CT had been performed in 67 patients with renal cell carcinoma. Six adrenal masses were identified with CT in these patients. Three out of the 6 patients probably had metastatic tumors and one of the 3 adrenal masses was pathologically diagnosed as metastatic tumor. The other three masses were benign on pathology and only one of them was pathologically diagnosed as non-functioning adrenal adenoma. The incidence of adrenal adenomas on the CT study was lower than that of previous studies based on autopsy. The reasons of this difference in results between their studies and ours are not clear.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1981

[Effect of clonidine on the function of adrenal medulla in rats (author's transl)].

The present experiments were undertaken to elucidate the effect of clonidine on the function of adrenal medulla both in normotensive rats and spontaneously hypertensive rats (SHR). In urethane anesthetized rats, efferent discharge rate of splanchnic nerve and sympathetic adrenal nerve branch (adrenal nerve) was recorded. Plasma catecholamine concentration of adrenal venous blood was determined radioenzymatically. Catecholamine secretion rate from left adrenal gland was calculated. In normotensive rats, clonidine produced a significant decrease in efferent nerve activity of the splanchnic nerve and adrenal nerve. It was also demonstrated that clonidine produced a significant decrease in adrenaline secretion rate from adrenal gland. Statistically insignificant decrease in noradrenaline secretion rate from adrenal gland was observed. Clonidine induced hyperglycemia was not related to the rapid fall in adrenal efferent nerve activity induced by clonidine. In debuffered rats, clonidine produced a decrease in the adrenal efferent nerve activity. In SHR, clonidine produced a significant decrease in adrenal efferent nerve activity and adrenaline secretion rate from adrenal gland. With regard to the response of adrenal efferent nerve activity to clonidine, decreased activity appeared more remarkably in normotensive rats as compared with that in SHR. These findings suggest that clonidine decreases adrenaline secretion rate from the adrenal glands by central actions in rats.

Adrenal Medulla↗
PubMed1993

[Antiphospholipid syndrome. A new cause of bilateral hemorrhage of the adrenal glands. 4 cases].

Four cases of adrenal insufficiency due to bilateral adrenal haemorrhage in patients with antiphospholipid syndrome are reported. The 1st patient had repeated episodes of thrombosis on a background of altered general condition; he was examined by computed tomography (CT) which showed enlarged and presumably tumoral adrenal glands; adrenal insufficiency was present and improved under hormone replacement therapy; the thrombotic episodes were attributed to the antiphospholipid antibodies; after a 5-year follow-up the antiphospholipid syndrome remained alone, and further examinations showed progressive adrenal atrophy. The 2nd patient had systemic lupus erythematosus with thrombocytopenia; because of abdominal pain CT was performed, showing bilateral adrenal enlargement; treatment with intravenous pulses of cyclophosphamide and high-dose immunoglobulins combined with corticosteroids failed, and splenectomy was performed disclosing an old adrenal haematoma which was evacuated. The 3rd patient had bilateral and asymmetrical adrenal hypertrophy at CT; subsequently, systemic lupus erythematosus was diagnosed with anti-prothrombinase and anticardiolipin accounting for the initial findings; follow-up examinations showed the formation of pseudocysts in the adrenals; following myocardial infarction the patient died of cerebral haemorrhage, and autopsy confirmed the presence of old, bilateral adrenal haematomas. The 4th patient had recurrent vein thrombosis associated with distal ischaemia, which prompted CT in search of a neoplasia; this examination revealed 2 large adrenal haematomas while anticardiolipin antibodies were found. In patients with antiphospholipid syndrome any functional or morphological abnormality of the adrenals should prompt a search for bilateral adrenal haemorrhage. Conversely, in all cases of adrenal insufficiency a search for antiphospholipid antibodies should be part of all aetiological investigations, and this search should be carried out prior to withdrawing corticosteroids in cases of systemic lupus erythematosus with antiphospholipid antibodies.

Adrenal Gland Diseases↗
PubMed1983

Computed tomography in adrenal disease.

Ninety-eight patients with suspected adrenal disease were examined by computed tomography (CT). In 73 patients adrenal disease was confirmed on biochemical and other grounds (Cushing's syndrome (38), primary aldosteronism (8), phaeochromocytoma (12), androgen excess (7), Addison's disease (1) and non-functioning adrenal masses (7)). The CT appearances of hyperplasia and benign and malignant adrenal tumours are described in detail. Ninety-six per cent of the adrenal glands were identified, and all but one of the 39 adrenal mass lesions were correctly identified and localised by CT. The failure to identify some adrenal glands and one adrenal tumour was related to a paucity of intra-abdominal fat. Two abdominal ectopic phaeochromocytoma were not identified (in one patient because the appropriate area was not scanned). The 25 patients examined with unproven adrenal disease had normal glands on CT. That some hyperplastic glands appear normal on CT precludes its use as a screening procedure for biochemically unproven adrenal disease. Computed tomography allows the differentiation of adrenal hyperplasia from functioning adrenal tumours, and the differentiation of benign from malignant lesions with a high degree of certainty; it is the method of choice for the identification and localisation of adrenal tumours.

Addison Disease↗
PubMed2002

Increased angiotensin II AT(1) receptor expression in paraventricular nucleus and hypothalamic-pituitary-adrenal axis stimulation in AT(2) receptor gene disrupted mice.

Angiotensin II AT(2) receptor gene-disrupted mice have increased blood pressure and response to angiotensin II, behavioral alterations, greater response to stress, and increased adrenal AT(1) receptors. We studied hypothalamic AT(1) receptor binding and mRNA by receptor autoradiography and in situ hybridization, adrenal catecholamines by HPLC, adrenal tyrosine hydroxylase mRNA by in situ hybridization and pituitary and adrenal hormones by RIA in AT(2) receptor-gene disrupted mice and wild-type controls. To confirm the role of adrenal AT(1) receptors, we treated wild-type C57 BL/6J mice with the AT(1) antagonist candesartan for 2 weeks, and measured adrenal hormones, catecholamines and tyrosine hydroxylase mRNA. In the absence of AT(2) receptor transcription, we found increased AT(1) receptor binding in brain areas involved in the regulation of the hypothalamic-pituitary-adrenal axis, the hypothalamic paraventricular nucleus and the median eminence, and increased adrenal catecholamine synthesis as shown by higher adrenomedullary tyrosine hydroxylase mRNA and higher adrenal dopamine, norepinephrine and epinephrine levels when compared to wild-type mice. In addition, in AT(2) receptor gene-disrupted mice there were higher plasma adrenocorticotropin (ACTH) and corticosterone levels and lower adrenal aldosterone content when compared to wild-type controls. Conversely, AT(1) receptor inhibition in CB57 BL/6J mice reduced adrenal tyrosine hydroxylase mRNA and catecholamine content and increased adrenal aldosterone content. These results can help to explain the enhanced response of AT(2) receptor gene-disrupted mice to exogenous angiotensin II, support the hypothesis of cross-talk between AT(1) and AT(2) receptors, indicate that the activity of the hypothalamic-pituitary-adrenal axis parallels the AT(1) receptor expression, and suggest that expression of AT(1) receptors can be dependent on AT(2) receptor expression. Our results provide an explanation for the increased sensitivity to stress in this model.

Adrenal Cortex Hormones↗
PubMed1973

Quantitative relations of fetal and maternal pitiutary-adrenal systems.

Even though certain aspects of the fetal pituitary-adrenal system have been extensively studied, much remains to be learned of its basic development and function. In the present work, the effect of maternal hypophysectomy upon quantitative pituitary-adrenal relations in mother and fetus was investigated in pregnant beagle dogs. At 57 days gestation in each of seven normal animals and seven animals 3 wk posthypophysectomy, a cannula for collection of adrenal effluent was placed in a single fetus in utero under halothane anesthesia. A timed fetal adrenal sample was obtained; ACTH (10 mU) was injected into the fetus; 3 min thereafter a second fetal adrenal sample was collected and fetal and maternal peripheral arterial samples were drawn. All fetuses and their adrenal glands were weighed. Concentrations of cortisol and corticosterone were determined by a modification of the double-isotope dilution derivative method of Kliman and Peterson. Mean peripheral cortisol concentrations in mother and fetus were 92 and 94 ng/ml, respectively (ratio 1.0), in normal pregnancies and 11 and 54 ng/ml, respectively (ratio 0.2), in maternal hypophysectomy pregnancies. Weights of fetal adrenal gland pairs of 32 and 44 mg, respectively, in normal and hypophysectomy pregnancies indicate increased fetal ACTH secretion in response to lowered circulating cortisol in the fetus secondary to maternal hypophysectomy. These data demonstrate the presence of an active pituitary-adrenal feedback mechanism in the dog fetus which is partly influenced by maternal pituitary-adrenal function. The shift in the maternal-fetal ratio of peripheral cortisol concentrations from 1.0 to 0.2 occasioned by maternal hypophysectomy neither supports nor rules out the presence of specific placental mechanisms affecting relative concentrations of cortisol in mother and fetus. It does suggest, however, that the relative steroid input into maternal and fetal compartments is one of the factors which influences such concentration ratios. Concentrations of cortisol were significantly higher in fetal adrenal effluent (pre-ACTH) than in fetal peripheral plasma in normal pregnancies, which demonstrates secretion of cortisol by the fetus and shows that corticosteroid of maternal origin does not lead to complete suppression of fetal pituitary-adrenal function. Cortisol secretion rates in response to exogenous ACTH were essentially the same in fetuses in normal and hypophysectomy pregnancies (132 and 128 ng/min, respectively). Thus, fetal adrenal responsiveness to ACTH, i.e., maximum secretory capacity, is not enhanced by increased ACTH stimulation sufficient to induce adrenal hypertrophy in the same fetuses.

Adrenal Cortex Hormones↗
PubMed1985

Mechanism of dissociation of cortisol and adrenal androgen secretion after removal of adrenocortical adenoma in patients with Cushing's syndrome.

We investigated the mechanism of dissociation of cortisol and dehydroepiandrosterone sulfate (DHEA-S) secretion by the adrenal glands after the removal of an adrenal gland containing an adrenocortical adenoma in a patient with Cushing's syndrome. After removal of the adrenocortical adenoma, the serum cortisol rapidly decreased from 24.6 +/- 6.4 micrograms/dl (mean +/- SD, n = 6) to 0.7 +/- 0.5 micrograms/dl. Serum DHEA-S levels were 15 +/- 14 micrograms/dl and 6 +/- 9 micrograms/dl before and after surgery, respectively, and significantly lower than the control values. Serum cortisol levels reverted to normal levels 1.5 to 3 years after the surgery. On the other hand, DHEA-S levels reverted to normal 5 to 7 years after the serum cortisol levels had normalized. Monolayer cultures of normal human adrenal cells obtained at adrenalectomy in patients with advanced breast cancer and atrophic adrenal cells adjacent to the adrenocortical adenoma in patients with Cushing's syndrome were used to study the mechanism of the dissociation of cortisol and DHEA-S secretion. ACTH caused significant increases in the productions of pregnenolone (P5), progesterone (P4), 17-hydroxypregnenolone (17-OH-P5), 17-hydroxyprogesterone (17-OH-P4), DHEA, DHEA-S, androstenedione (delta 4-A), and cortisol. The amounts of 17-OH-P5 and 17-OH-P4 produced by ACTH in atrophic adrenal cells were significantly greater than those in normal adrenal cells. The amounts of DHEA, DHEA-S and delta 4-A produced by ACTH in atrophic adrenal cells were significantly smaller than those of normal adrenal cells. The conversion rate of 17-OH-[3H]P5 to 17-OH-[3H]P4 and 11-deoxy-[3H] cortisol was higher in atrophic adrenal cells than in normal adrenal cells, but the conversion rate to [3H]DHEA, [3H]DHEA-S and [3H]delta 4-A was significantly lower in atrophic adrenal cells than in normal adrenal cells. These results suggest that the dissociation of cortisol from DHEA-S after the removal of adrenocortical adenoma is a probably due to diminished C17,20-lyase activity in the remaining atrophic adrenal gland.

Adenoma↗