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PubMed2004

[CT and MRI in the differential diagnosis of lesions of the adrenal gland].

Adrenal gland tumors are often incidental findings during imaging of the upper abdomen. In the majority of cases, benign adrenal gland tumors, especially nonfunctioning adenomas, are diagnosed, although the evaluation of dignity is essential in order to avoid unnecessary biopsy and tumor extirpation. Lipid-containing adrenocortical adenomas and nonadenomas can be differentiated with high diagnostic accuracy and specificity by computed tomography (CT) and magnetic resonance imaging (MRI). The fat content of these lesions can be correlated with CT attenuation values or with signal decrease in chemical shift imaging in MRI. Furthermore, low-fat adenomas can be distinguished from nonadenomas with delayed contrast enhancement and washout characterization. For the differentiation of non-fat-containing nonadenomas (metastases, lymphoma, pheochromocytoma, and inflammatory processes), morphological imaging criteria in CT and MRI (signal alterations, contrast media enhancement), clinical signs and laboratory test are essential in order to establish the diagnosis. The localization of functioning adenomas can be easily performed with CT and MRI. Both imaging techniques reveal typical findings of lesions-like cysts and myelolipomas.

Adenoma↗
PubMed1998

[Physiology and functional investigation of adrenal glands].

Adrenal glands are composed of a cortex producing 3 steroid hormones, namely cortisol, aldosterone and androgens, and a medulla synthesizing catecholamines. The regulation of the corticotropic axis explains the present investigation of this endocrine function including static measurements (plasmatic and urinary cortisol) and dynamic testing which are either stimulatory tests (Synacthene tests) or inhibitory tests (dexamethasone and metyrapone tests). Similarly, the physiology of the renin angiotensin system explains the exploration of the mineralo-corticoid function, which includes measurements of both qualitative and quantitative modifications of renin and aldosterone. Finally, the adrenal medulla in case of pheochromocytoma can produce an excess of catecholamines, which can be measured, themselves or their metabolites in the plasma or urines.

Adrenal Cortex↗
PubMed1995

Gastric adaptation to stress: role of sensory nerves, salivary glands, and adrenal glands.

BACKGROUND: Single exposure to water immersion and restraint stress (WRS) in rats produces acute gastric mucosal damage, but repetitive WRS insults lead to gastric adaptation to stress ulcerogenesis. This study was designed to assess the mechanism of this adaptation, particularly the role of sensory nerves, salivary glands, adrenal glands, and gastric acid secretion. METHODS: WRS was applied for a standard period of 3.5 h, either once or repeated every other day for up to 8 days in intact rats and in animals with capsaicin-induced deactivation of sensory nerves, vagotomy, salivectomy, adrenalectomy, and inhibition of gastric acid secretion by H2-blocker. RESULTS: WRS applied once produced multiple gastric erosions accompanied by a significant increase in gastric acid secretion and a decrease in gastric blood flow (GBF) and DNA synthesis. Repeated WRS insults resulted in a significant decrease in the number of gastric lesions, reaching a maximum after four consecutive exposures to WRS. This adaptation to stress ulcerogenesis was accompanied by a decrease in gastric acid secretion and an increase in GBF and mucosal generation of DNA synthesis. Salivectomy, which decreased the luminal content of epidermal growth factor (EGF) (by about 80%), markedly attenuated this adaptation, and this was reversed by the addition of exogenous EGF. Capsaicin-induced ablation of sensory nerves eliminated gastric adaptation to WRS, and this was accompanied by a significant decrease in the GBF, but pretreatment with calcitonin gene-related peptide restored gastric adaptation to stress in capsaicin-denervated rats. Selective vagotomy and adrenalectomy failed to affect gastric adaptation to WRS, whereas gastric acid inhibition by ranitidine enhanced this adaptation. CONCLUSIONS: The stomach is able to adapt to repeated stress insults by enhancing GBF and DNA synthesis, and this adaptation is mediated, at least in part, by sensory nerves and EGF.

Adaptation, Physiological↗
PubMed1991

[Magnetic resonance imaging of the adrenal gland].

Adrenal imaging was performed using magnetic resonance (MR) was in 100 patients who had no clinical or biochemical evidence of adrenal abnormality and in 19 patients with 24 adrenal lesions (adenoma in 5, hyperplasia in 2, metastasis in 5, (lung cancer in 1, hepatoma in 4) adrenal cancer in 1, pheochromocytoma in 3, neuroblastoma in 3). Normal adrenal glands showed intermediate intensity between muscle and liver, and were detected in over 90% of cases on T1-weighted images (T1-weighted SE, inversion recovery). Adenomas and hyperplasias had the same intensity as normal glands. Medullary masses showed extreme hyperintensity on T2-weighted images and could be differentiated from cortical masses. Neuroblastomas were detected as hyperintense tumors with intratumoral hemorrhage and necrosis on T2-weighted MR images. Metastatic adrenal tumors from lung cancer were hyperintense on T2-weighted images, while metastasis from hepatoma showed low intensity on the same pulse sequence. In diagnosing adrenal metastasis, we must compare and contrast the tumor intensity and structure with those of the primary lesions. MR is considered a useful modality in characterizing adrenal tissue.

Adenoma↗
PubMedDate not supplied

[Myelolipoma of the adrenal gland].

Adrenal myelolipomas are rare, nonfunctioning, benign neoplasms of the adrenal gland. The authors describe their experience of a case and they report the review of the literature. They illustrate what's etiopathogenetic theories, modern diagnostic technology "of imaging" and different surgical approaches need to be adapted to the excision of the adrenal myelolipomas.

Adrenal Gland Neoplasms↗
PubMed2004

Dopamine receptor expression and function in human normal adrenal gland and adrenal tumors.

Dopamine is known to play a role in the modulation of aldosterone and catecholamine secretion from the adrenal gland, where dopamine receptors (DR), in particular the DR type 2 (D(2)), have been found to be expressed. DR expression has also been demonstrated in some types of benign adrenal tumors. The aims of the current study were to evaluate DR expression and D(2) localization in the normal adrenal gland and in different types of benign and malignant adrenal tumors, as well as to evaluate the in vitro effects of the dopamine agonists bromocriptine and cabergoline on hormone secretion in nontumoral adrenal cells. Adrenal tissues from 25 patients, subjected to adrenal surgery for different diseases, were studied. These included three normal adrenals; five adrenal hyperplasias; four aldosterone-secreting, two cortisol-secreting, and two clinically nonfunctioning adrenal adenomas; two aldosterone-secreting, two cortisol-secreting, and two androgen-secreting adrenal carcinomas; and three pheochromocytomas. In all tissues, DR and D(2) isoform (D(2long) and D(2short)) expression was evaluated by RT-PCR. D(2) localization was also evaluated by immunohistochemistry using a specific polyclonal antibody, whereas D(2)-like receptor expression was evaluated by receptor-ligand binding study, using the radiolabeled D(2) analog (125)I-epidepride. The effects of bromocriptine and cabergoline on baseline and ACTH and/or angiotensin II-stimulated aldosterone, cortisol, and androstenedione secretion were evaluated in cell cultures derived from five different adrenal hyperplasia. At RT-PCR, both D(1)-like and D(2)-like receptors were expressed in all normal and hyperplastic adrenals. D(2) and D(4) were expressed in aldosterone- and cortisol-secreting adenomas, cortisol-secreting carcinomas, and clinically nonfunctioning adenomas, whereas no DR was expressed in aldosterone- and androgen-secreting carcinomas. D(2), D(4), and D(5) were expressed in pheochromocytomas. In all D(2)-positive tissues, both D(2) isoforms were expressed, with the exception of one case of aldosterone-secreting adenoma and the cortisol-secreting carcinomas, in which only the D(2long) isoform was expressed. D(2)-like receptor expression was confirmed at receptor-ligand binding study. At immunohistochemistry, D(2) was mainly localized in the zona glomerulosa and reticularis of the adrenal cortex and, to a lesser extent, in the zona fasciculata and medulla of normal and hyperplastic adrenal tissue. In the positive tumors, D(2) was localized in the tumoral cells. At the in vitro study, a significant inhibition of both baseline and ACTH-stimulated aldosterone secretion was found after high-dose cabergoline, but not bromocriptine, administration; and a significant inhibition of angiotensin-II-stimulated aldosterone secretion was found after both bromocriptine and cabergoline administration in the adrenal hyperplasias. In conclusion, the current study demonstrated that both D(1)-like and D(2)-like receptors are expressed in the normal adrenal gland and in a percentage of adrenal adenomas or carcinomas. Bromocriptine and cabergoline induce only a minor inhibition of the secretion of adrenal hormones in the nontumoral adrenal gland in vitro, not excluding, however, the possible effective use of dopamine agonists in vivo in the treatment of adrenal tumors.

Adrenal Gland Neoplasms↗
PubMed1991

The modification and expression of 21-hydroxylase gene in normal human adrenal gland and adrenal cancer.

Genomic DNA and total RNA from three adrenal cancer tissues were analyzed by hybridization with human 21-hydroxylase gene. Southern blot analysis with restriction enzyme Eco RI revealed major fragments at 18, 13 and 9 kilobase (kb) in normal adrenal glands. In two of three adrenal cancers, however, the band at 18 kb was either absent or decreased and the 9 kb fragment showed an increase in its intensity. Normal liver, kidney and leucocytes has only 18 and 13 kb while lacking the 9 kb fragment. Using Taq I, Bam HI or Bgl II, we found no difference in restriction fragment patterns between adrenal cancer and normal tissues. Cleavage with Hpa II after digestion with Bgl II showed that significantly more DNA was digested into low-molecular weight fragments in adrenal cancer and the normal adrenal gland than those in other normal tissues. By Northern blot analysis, there was difference of signal intensity of hybridizing mRNA between the adrenal cancers and normal adrenal glands. These results suggest that the Eco RI site in the flanking region of the 21-hydroxylase gene may be modified in adrenal cancer tissue, and that inadequate 21-hydroxylase is present in some forms of adrenal cancers.

Adrenal Cortex Hormones↗
PubMed1986

Chromaffin cell heterogeneity of process formation and neuropeptide content under control and nerve growth factor-altered conditions in cultures of chick embryonic adrenal gland.

Adrenal glands from embryonic day 11 (E-11) chicks were cryostat-sectioned, and it was determined that tyrosine hydroxylase-like immunoreactive (TLI) cells, somatostatin-like immunoreactive (SLI) cells, and methionine-enkephalin-like immunoreactive (ELI) cells occupied chromaffin regions of the gland. Similar age adrenals were dissociated, and the cells were cultured under serum-free conditions. Cultured TLI cells, ELI cells, and SLI cells were characterized according to cell size, cell number, and neurite formation. ELI and SLI cells composed two largely separate populations, with SLI cells tending to have larger cell areas, to be more numerous, and to be less likely to form neurites than ELI cells. The population of TLI cells, although unique in itself, was diverse and numerous enough to include all or portions of the neuropeptide-immunoreactive populations. Neurites of some cells from each of the above populations were strongly immunoreactive for alpha neurofilament protein, and for NAPA73 neurofilament-associated protein. However, neurites could also be observed in all populations that showed poor immunoreactivity for these cytoskeletal proteins. Exogenously added NGF significantly increased neurite-like process formation among TLI and ELI cells, but not among SLI cells. Reductions in the number of neurite-like processes following treatment with anti-nerve growth factor (NGF) were not significant for any of the populations. However, if shorter and broader process were included, anti-NGF caused a significant reduction in total cell processes among TLI and ELI cells. Anti-NGF inhibition of process formation among ELI cells could be reversed with exogenous NGF. Neither NGF or anti-NGF treatments showed a significant effect on cell numbers among TLI and ELI populations. The implications are that a compound of antigenic and physiological similarity to mouse salivary NGF is made by embryonic chick adrenal cells in culture, but the effects of NGF do not appear to be the same for all neural-crest-derived cells from the adrenal, and greater heterogeneity of phenotypes may exist among chromaffin cells than has previously been accepted. Some questions are also raised concerning the neurite-like nature of processes formed by some chromaffin cells in vitro.

Adrenal Medulla↗
PubMed2002

Giant myelolipoma of the right adrenal gland.

Adrenal myelolipoma is an unusual, benign and hormonally inactive tumour composed of mature adipose and haematopoietic tissue. In the past, these tumours were accidentally discovered at autopsy. Today, they are found much more frequently and incidentally, mainly because of the widespread use of ultrasonography, computed tomography and magnetic reasonance imaging. Adrenal myelolipoma is usually unilateral and asymptomatic. The case of a 52-year-old female patient, surgically treated for a symptomatic giant myelolipoma of the right adrenal gland, is reported, together with a review of the literature.

Adrenal Gland Neoplasms↗
PubMed1995

[Hemangioma of the adrenal gland].

Adrenal gland haemangioma is an uncommon tumour which finding usually occurs by chance. This paper presents one case of cavernous haemangioma in this location on which surgery was performed successfully. The basic aspects of the case are revised from a pathohistological and diagnostic point of view intended to attempt to suspect its presence preoperatively.

Adrenal Gland Neoplasms↗
PubMed2005

Expression of urocortin 3/stresscopin in human adrenal glands and adrenal tumors.

Urocortin 3 (Ucn 3)/stresscopin (SCP) is a novel peptide of the corticotropin-releasing factor (CRF) family and is a specific ligand for the CRF type 2 receptor. In the present study, we studied expression of Ucn3/SCP in the normal adrenal and adrenal tumors by radioimmunoassay and reverse transcriptase-polymerase chain reaction (RT-PCR). High concentrations of immunoreactive (IR)-Ucn3 were present in the normal portions of adrenal glands (4.2+/-0.51 pmol/g wet weight, mean+/-S.E.M., n = 14), and the levels were higher than those in the brain. IR-Ucn3 was also detected in the tumor tissues of aldosterone-secreting adenomas (6.2+/-0.6 pmol/g wet weight, n = 10), cortisol-secreting adenomas (5.0+/-1.2 pmol/g wet weight, n = 4), and pheochromocytomas (1.9+/-0.4 pmol/g wet weight, n = 7). Reverse phase high performance liquid chromatography showed that IR-Ucn3 in normal portions of adrenal glands and aldosterone-secreting adenomas was eluted mainly in the positions of Ucn3 and SCP with several minor peaks eluting earlier. The RT-PCR showed expression of Ucn3 mRNA in normal portions of adrenal gland (positive ratio; 4/4), aldosterone-secreting adenomas (3/4), cortisol-secreting adenomas (1/3) and pheochromocytomas (6/7). These findings indicate that Ucn3 is produced in normal adrenal and adrenal tumors (both adrenocortical tumors and pheochromocytomas), and suggest that Ucn3 acts as an autocrine or paracrine regulator in normal adrenal and adrenal tumors.

Adenoma↗
PubMed1992

Bilateral primary non-Hodgkin's lymphoma of the adrenal glands with adrenal insufficiency: a case report.

A 72-year-old woman with bilateral non-Hodgkin's lymphoma of the adrenal glands causing adrenal insufficiency is reported. The left-side lymphoma (diffuse large B-cell lymphoma) was removed surgically but the right-side lymphoma could not be removed. Complete response was obtained with subsequent combined chemotherapy and was maintained for 6 months with repeated chemotherapies. However, the patient died of liver recurrence 1 year after admission. In cases of malignant lymphoma forming a bulky mass, surgery with subsequent chemotherapy appears to reduce the cancer volume and improve the therapeutic outcome.

Adrenal Gland Neoplasms↗
PubMed2004

[Mantle cell lymphoma markedly infiltrated into adrenal glands with adrenal insufficiency].

A 66-year-old male was admitted to our hospital complaining of bilateral hypochondrial pain, back pain and loss of weight in May, 2002. Superficial lymph nodes were not palpable on admission. The leukocyte count was 3430/microl, hemoglobin concentration, 13.0g/dl, and platelet count, 174000/microl. LDH, soluble IL-2 receptor, ACTH and cortisol values were out of the normal range (LDH 1368IU/l, sIL-2R 2630U/ml, ACTH 132pg/ml, cortisol 7.4microg/dl). Abdominal CT scan showed bilateral adrenal masses, and abnormal uptake of Ga-scintigraphy was seen correspondent with the bilateral adrenal masses. The histological diagnosis of bilateral adrenal masses cannot be performed because of the bleeding tendency, but atypical cells were observed in the patient's bone marrow aspirate. Surface marker analysis of atypical cells showed CD5+, cyclin D1+, CD19+, CD20+ and HLA-DR+. From these results we diagnosed this case as a mantle cell lymphoma (stage IV B) markedly infiltrated into the adrenal glands with adrenal insufficiency. The bilateral adrenal masses dramatically reduced in size after CHOP chemotherapy with hydrocortisone supplementation. We report on the present case and summarize the reports of adrenal grand-infiltrating lymphomas.

Adrenal Gland Neoplasms↗
PubMed1984

Interrelationships between the hypothalamus, pituitary gland, ovary, adrenal gland, and the open period for LH release in the hen (Gallus domesticus).

The asynchronous ovulatory cycle of the hen is believed to be the consequence of two interacting systems, one of which is circadian and regulates the timing of the preovulatory LH surge. In support of this proposition, the open period for LH release was shown to oscillate with the same periodicity as the photoschedule when the hens were exposed to 14 L:7 D, 14 L:10 D, and 14 L:14 D. In addition, it was demonstrated that follicular maturation is not affected by or synchronized with the photoperiod. The physiological system that transduces the light/dark cycle into an open period for LH release has not been identified although circumstantial evidence supports the idea that the adrenal gland plays a role in this function. This evidence includes the anatomical juxtaposition of the left ovary and adrenal gland, innervation of steroid-producing cells within the follicle by nerve tracts passing through the adrenal glands, the ability of injections of metyrapone to alter the timing of preovulatory LH release, the ability of injections of corticosterone to induce ovulation when a mature follicle is present in the ovary, and the ability of dexamethasone or infusions of corticosterone to block ovulation. Recently we have also shown that infusions of corticosterone will block the gonadotropic effect of PMSG, will inhibit the photoperiodic response, and do not affect the release of LH in response to injections of GnRH. The addition of corticosterone to incubations of dispersed granulosa cells does not affect their response to LH. These data suggest that corticosterone may modulate the responsiveness of the hypothalamus to tropic stimuli and demonstrate that exposure to corticosterone can alter the responsiveness of some ovarian tissues to gonadotropins.

Adrenal Glands↗
PubMed1998

Ultrastructural and hormonal changes in the contralateral adrenal gland in unilateral adrenal gland ischemia: an experimental study in rats.

While it is well known that unilateral tissue ischemia may result in contralateral damage in some paired organs, there is no universally accepted mechanism to explain why these contralateral changes occur. The aim of the present study was to investigate the ultrastructural and hormonal changes that occur in the contralateral nonischemic adrenal gland after unilateral ischemia of an adrenal gland in a rat model. The animals were divided into four groups of four rats each; namely, a control group which received a sham operation without any ischemic insult, a 2-h ischemic group, a 4-h ischemic group, and an 8-h ischemic group. The left adrenal blood vessels were ligated in all ischemia groups and blood samples were taken for hormonal study 2, 4, and 8 h later, after which bilateral adrenalectomy was performed to determine the ultrastructural changes. The plasma concentrations of aldosterone and cortisol were determined by radioimmunoassays. There was an increase in both aldosterone and cortisol levels related to the duration of the ischemia, but the differences among the groups were not statistically significant. Contralateral ultrastructural damage such as heterochromatin in nuclei, mitochondrial degeneration, endoplasmic reticulum cisternal widening, increased lipid droplets, and lysosomes, were demonstrated electron-microscopically after unilateral adrenal ischemia.

Adrenal Glands↗
PubMed1986

Cavernous hemangioma of the adrenal gland.

Adrenal hemangiomas are rare and seldom found ante mortem. We report a case of adrenal hemangioma that was discovered incidentally and removed surgically. The pertinent literature is reviewed.

Adrenal Gland Neoplasms↗
PubMed1985

Non-Hodgkin's lymphoma limited to the adrenal gland with adrenal insufficiency.

A 81-year-old man presented with bilateral adrenal masses found pathologically to be a large cell, non-follicular center, non-Hodgkin's lymphoma. His clinical course was remarkable for the lack of macroscopic extra-adrenal tumor and for adrenal insufficiency in response to stress and cosyntropin stimulation. This is believed to be the first reported case of a non-Hodgkin's lymphoma limited to the adrenal glands with associated adrenal insufficiency.

Adrenal Gland Neoplasms↗