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PubMed1977

Transmission and scanning electron microscopic observations of mouse adrenocortical adenoma cells (Y-1) in non-stimulated and stimulated states.

ACTH sensitive murine adrenocortical adenoma cells (Y-1) were examined by transmission and scanning electron microscopes under non-stimulated and stimulated conditions. They showed the ultrastructural characteristics which were fairly different from those of the original adrenocortical cells of LAF1 mice. The smooth-surfaced endoplasmic reticulum (sER) were poorly developed, and the mitochondrial cristae showed lamellar rather than tubular or tubulo-vesicular type. Administration of ACTH induced rounding-up of the Y-1 cells with slight increase in sER, BUt no mitochondria with vesicular inner structure appeared. The effects of dbcAMP on the morphology of the Y-1 cells were similar to those of ACTH except that the rounding-up occurred more rapidly and uniformly.

Adenoma↗
PubMed2004

Case of combined adrenal cortical adenoma and myelolipoma.

We report a case of myelolipoma 10 mm in size within a functional cortical adenoma that was 33 x 22 x 17 mm in size. A 29-year-old woman was referred to hospital for transient hypertension. A right adrenal tumor was detected by computed tomography (CT) scan and magnetic resonance imaging (MRI). Her cortisol levels indicated a loss of the normal diurnal pattern, and urinary 17-hydroxycorticosteroids was elevated. She underwent a right adrenalectomy under the diagnosis of adrenal adenoma with Cushing's syndrome. The tumor was fairly well encapsulated by a thin layer of connective tissue. The major tumor portion was composed of two distinct cell types, clear cells and eosinophilic cells, arranged in an alveolar structure. These findings were representative of cortical adenoma. The adrenal cortical adenoma centrally included well-demarcated adipose tissue admixed with scattered islands of myelopoietic elements: erythroblasts, myeloid cell series and lymphocytic cells, which was eventually recognized as myelolipoma. Recently, adrenal myelolipoma has commonly been found because of the ease of detecting it as an incidentaloma by CT scan or MRI. However, the present adrenal myelolipoma case is uncommon because it is combined with a functioning cortical adenoma. Only six similar cases have previously been reported in English and Japanese publications. Furthermore, in the present case, the myelolipoma formed a tumor nodule, and to our knowledge, this is the first reported case of a radiographically recognizable tumor nodule. We discuss the etiology of myelolipoma and suggest that myelolipoma can develop in the course of endocrine hyperfunction.

Adenoma↗
PubMed1988

Primary adrenal tumours--a ten-year experience.

The experience of 31 patients with primary adrenal tumours seen in one teaching hospital over a 10-year period is reviewed. There were 10 patients who had benign cortical adenomas; 11 had adrenal cortical carcinomas, and 10 had phaeochromocytomas, one of which was malignant. During the review period, a primary adrenal mass was discovered in 5% of 2951 autopsies performed in the study institution. The diagnosis and management of these uncommon tumours is reviewed.

Adenoma↗
PubMed1994

Adrenalectomy: expanded indications for the extraperitoneal approach.

The adrenal glands can be removed surgically by the anterior transperitoneal approach, or by the extraperitoneal approaches, either posteriorly or posterolaterally. While the extraperitoneal routes have become accepted as the preferred approach to the adrenal glands for small benign cortical adenomas, many authors still recommend the anterior transperitoneal route as the preferred operative approach for phaeochromocytoma, large tumours, adrenal cancers or bilateral hyperplasia. A series of 51 consecutive adrenalectomies performed for a wide range of adrenal disorders is presented, including phaeochromocytoma and large malignant tumours. In 47 cases the tumours were successfully removed through an extraperitoneal approach, with minimal morbidity. The anterior approach had to be employed in only four cases, and in three of these there was pre-operative evidence of tumour invasion into either the major vessels or the liver. The extraperitoneal approach to the adrenal gland is technically simple and can be performed quickly, with a low postoperative morbidity and should be regarded as the routine approach for almost all adrenal procedures.

Adrenal Cortex Neoplasms↗
PubMed1978

A testosterone-secreting adrenal cortical adenoma.

A virilizing, gonadotrophin-responsive adrenal cortical adenoma was removed from a 54-year-old woman. Following removal of the tumour, which contained and secreted androgens and estradiol, serum gonadotrophins rose to menopausal levels and the patient experienced menopausal symptoms. Pre-operative attempts to localize the source of androgens were unsuccessful.

Adenoma↗
PubMed1998

A case of mid-trimester intrauterine fetal death with Cushing's syndrome.

A 34-year-old woman was diagnosed with Cushing's syndrome after her first pregnancy ended in intrauterine fetal death at 25 weeks' gestation. She subsequently had a successful pregnancy after treatment of her disease. Although patients with Cushing's syndrome rarely conceive, abortion, preterm labor, and intrauterine growth retardation are common when they do.

Adrenal Cortex Neoplasms↗
PubMed1983

Advances in the techniques of localisation of adrenal tumours and their influence on the surgical approach to the tumour.

The results of attempts to localise adrenal tumours in 65 patients are presented. In the first series (1966-1978) adrenal phlebography and adrenal vein sampling located 18 of 20 (90%) of adrenocortical tumours and 18 of 19 (94%) phaeochromocytomas were defined by angiography and venous sampling. In the second series CT located 7 of 8 adrenocortical and all 6 intra-abdominal phaeochromocytomas. Scintigraphy located all 9 adrenocortical tumours and both of the phaeochromocytomas examined. Confidence in the ability of newer techniques allows the use of a flank incision in most cases, thus reducing the operative morbidity.

Adrenal Cortex Neoplasms↗
PubMed2002

Role of interleukin-6 in stress response in normal and tumorous adrenal cells and during chronic inflammation.

Interleukin-6 (IL-6) is the end-product of a cytokine signaling cascade and is secreted by specialized immune cells during inflammation. It has a great influence on many functions, including differentiation, stimulation, and activation of immune cells, or other cells of neuroendocrine origin. Thus, IL-6 serves as a key messenger in its communication with the neuroendocrine system, and serves as a potent activator of the hypothalamic-pituitary-adrenal axis at all levels. Changes in the levels of expression of this cytokine and its receptor have been observed during chronic inflammatory disease, and have been associated with tumorigenesis. Therefore, we studied the effect of IL-6 on normal and adenomatous human adrenal cells in vitro. The expression of IL-6 receptor mRNA was quantified within the same tissue. IL-6 potently stimulated cortisol secretion from dispersed normal human adrenal cells. We found immunoreactivity for the IL-6 receptor on cultured cells and paraffin-embedded sections of adrenal tissues. Further, there was a more pronounced expression of IL-6 mRNA in adrenal adenomas of patients with Cushing's syndrome, compared to normal human adrenals. Despite this fact, the sensitivity of cells of adenomatous adrenal glands to IL-6 was significantly decreased relative to cells from normal controls. These results were confirmed employing the permanent adrenocortical cancer cell line model NCI-H295. We infer that the loss of responsivity of tumorous adrenal cells to IL-6, and in part corticotropin, is an important step in the process of adrenal tumorigenesis by which regulation by differentiating proteins is bypassed.

Adenoma↗
PubMed1982

Functioning adrenocortical tumour in a dog.

Naturally-occurring hyperadrenocorticism was diagnosed in an 11-year-old female Dachshund with signs of polydipsia, polyuria, pendulous abdomen, weakness, depression and lethargy, and laboratory test abnormalities comprising lymphocytopaenia, eosinopaenia, hypercholesterolaemia and increased plasma alkaline phosphatase concentration. While awaiting hormonal test results, an adrenocorticolytic drug (o,p'-DDD) was administered for 14 days, during which the patient deteriorated. Hormonal assays suggested a functioning adrenocortical tumour, but the poor condition of the patient precluded adrenalectomy. An adrenocortical carcinoma with hepatic metastases was found at necropsy.

Adrenal Cortex Neoplasms↗
PubMed1994

Endocrine and neurogenic regulation of the orphan nuclear receptors Nur77 and Nurr-1 in the adrenal glands.

nurr77 and nurr-1 are growth factor-inducible members of the steroid/thyroid hormone receptor gene superfamily. In order to gain insight into the potential roles of nur77 in the living organism, we used pharmacologic treatments to examine the expression of nur77 in the mouse adrenal gland. We found that nur77 and nurr-1 are induced in the adrenal gland upon treatment with pentylene tetrazole (Ptz; Metrazole). This induction is separable into distinct endocrine and neurogenic mechanisms. In situ hybridization analysis demonstrates that nur77 expression upon Ptz treatment in the adrenal cortex is localized primarily to the inner cortical region, the zona fasciculata-reticularis, with minimal induction in the zona glomerulosa. This induction is inhibitable by pretreatment with dexamethasone, indicating involvement of the hypothalamic-pituitary-adrenal axis in the activation of adrenal cortical expression. When mice were injected with adrenocorticotrophic hormone (ACTH), nur77 expression in the adrenal gland spanned all cortical layers including the zona glomerulosa, but medullary expression was not induced. Ptz also induces expression of both nur77 and nurr-1 in the adrenal medulla. Medullary induction is likely to have a neurogenic origin, as nur77 expression was not inhibitable by dexamethasone pretreatment and induction was seen after treatment with the cholinergic neurotransmitter nicotine. nur77 is also inducible by ACTH, forskolin, and the second messenger analog dibutyryl cyclic AMP in the ACTH-responsive adrenal cortical cell line Y-1. Significantly, Nur77 isolated from ACTH-stimulated Y-1 cells bound to its response element whereas Nur77 present in unstimulated cells did not. Moreover, Nur77 in ACTH-treated Y-1 cells was hypophosphorylated at serine 354 compared with that in untreated cells. These results, taken together with the previous observation that dephosphorylation of serine 354 affects DNA binding affinity in vitro, show for the first time that phosphorylation of Nur77 at serine 354 is under hormonal regulation, modulating its DNA binding affinity. Thus, ACTH regulates Nur77 in two ways: activation of its gene and posttranslational modification. A promoter analysis of nur77 induction in Y-1 cells indicates that the regulatory elements mediating ACTH induction differ from those required for induction in the adrenal medullary tumor cell line PC12 and in 3T3 fibroblasts.

Adrenal Cortex↗
PubMed2003

Activin induces x-zone apoptosis that inhibits luteinizing hormone-dependent adrenocortical tumor formation in inhibin-deficient mice.

Inhibin and activin are members of the transforming growth factor beta (TGF-beta) family of ligands produced and secreted primarily by the gonads and adrenals. Inhibin-null (INH(-/-)) mice develop gonadal tumors and-when gonadectomized-adrenocortical carcinoma. The mechanisms leading to adrenal tumorigenesis have been proposed to involve the lack of a gonadal factor and/or a compensatory increase in gonadotropins. In order to achieve elevation of gonadotropins without the concomitant loss of a gonadal hormone, we crossed INH(-/-) mice with a transgenic mouse strain that has chronically elevated luteinizing hormone (LH) levels (LH-CTP). Compound INH(-/-)-LH-CTP mice die within 6 weeks of age from severe cancer cachexia induced by large, activin-secreting ovarian tumors. Unexpectedly, INH(-/-)-LH-CTP mice not only fail to develop adrenal tumors but have smaller adrenals, with a regressed x zone, indicating that elevated LH levels are not sufficient to induce adrenal tumor formation. However, following gonadectomy, INH(-/-)-LH-CTP mice develop large, sex steroid-producing adrenal tumors that arise from the x zone, indicating a growth-promoting effect of high levels of LH on the adrenal cortex in the absence of ovarian tumors. In addition, in vivo and in vitro data indicate that activin induces apoptosis specifically in the adrenal x zone. The restricted expression of activin receptor subunits and Smad2 in cells of the adrenal x zone, together with the elevated activin levels in INH(-/-)-LH-CTP mice, supports the conclusion that activin inhibits adrenal tumor growth by inducing x-zone regression.

Activins↗
PubMed1977

Pure oestrogen-secreting feminizing adrenocortical adenoma.

A 6-year-old boy presented with gynaecomastia. There was no clinical or biochemical evidence of excessive androgenic or glucorticoid activity, but urinary oestrogen levels were raised. An adrenocortical adenoma, demonstrated by x-ray, was surgically removed. Oestrogen levels fell immediately. 3 years later the boy shows complete regression of the gynaecomastia and no signs of recurrence.

Adenoma↗
PubMed1978

Unusual case of adrenal cortical carcinoma in a female infant.

Adrenal cortical carcinoma in a 4 1/4-month-old girl was treated by surgery in combination with actinomycin D, cyclophosphamide, and 5-fluorouracil given daily for 5 days every third week for 13 1/2 months. Postoperative hypertension and raised 24-hour 17-hydroxy- and 21-oxosteroids suggested residual microscopical tumour activity. These findings resolved during chemotherapy. The patient is alive and well 22 months after completing chemotherapy. Adrenal cortical carcinoma may rarely mimic neuroblastoma or nephroblastoma when the tumour is not clinically secretory.

Adrenal Cortex Neoplasms↗