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PubMed1995

Adrenal surgery for hypercortisolism--surgical aspects.

BACKGROUND: Patients with endogenous hypercortisolism are thought to be at high risk for adrenalectomy and may experience significant postoperative surgical mortality/morbidity. METHODS: From 1981 through 1991, 91 patients underwent adrenal resection for endogenous hypercortisolism. Causes were adrenal-dependent Cushing's syndrome (50%), pituitary-dependent Cushing's syndrome (27%), and an ectopic adrenocorticotropic hormone-secreting tumor (23%). Causes of adrenal-dependent Cushing's syndrome were adrenocortical adenoma (72%), bilateral nodular hyperplasia (20%), and adrenocortical carcinoma (8%). Comparative mean length of hospitalization for patients undergoing unilateral anterior versus posterior approach was 8 versus 6 days, and bilateral anterior versus posterior was 11 versus 6 days. RESULTS: Operative mortality was 2.6%. Only one patient had a wound infection, and no patient had either a venous thrombosis or a pulmonary embolism. Delayed wound healing occurred in three patients. CONCLUSIONS: (1) Adrenal surgery can be performed today with low morbidity/mortality. (2) Although there is an effect of hypercortisolism on wound healing, infection, diabetes, hypertension, coronary artery disease, and pulmonary embolism, it was possible to perform adrenalectomy surgically with acceptable morbidity and mortality. (3) These results may serve as a standard against which laparoscopic adrenalectomy may be compared.

Adenoma↗
PubMed1997

Adrenomedullin gene expression and its different regulation in human adrenocortical and medullary tumors.

Adrenomedullin (ADM) is a polypeptide originally discovered in a human pheochromocytoma and is also present in normal adrenal medulla. It has been proposed that ADM could be involved in the regulation of adrenal steroidogenesis via paracrine mechanisms. Our aim was to find out if ADM gene is expressed in adrenocortical tumors and how ADM gene expression is regulated in adrenal cells. ADM mRNA was detectable by Northern blotting in most normal and hyperplastic adrenals, adenomas and carcinomas. The average concentration of ADM mRNA in the hormonally active adrenocortical adenomas was about 80% and 7% of that in normal adrenal glands and separated adrenal medulla respectively. In adrenocortical carcinomas, the ADM mRNA concentration was very variable, but on average it was about six times greater than that in normal adrenal glands. In pheochromocytomas, ADM mRNA expression was about ten times greater than that in normal adrenals and three times greater than in separated adrenal medulla. In primary cultures of normal adrenal cells, a protein kinase C inhibitor, staurosporine, reduced ADM mRNA accumulation in a dose- and time-dependent fashion (P < 0.01), whereas it simultaneously increased the expression of human cholesterol side-chain cleavage enzyme (P450 scc) gene (a key gene in steroidogenesis). In cultured Cushing's adenoma cells, adrenocorticotropin, dibutyryl cAMP ((Bu)2cAMP) and staurosporine inhibited the accumulation of ADM mRNA by 40, 50 and 70% respectively (P < 0.05), whereas the protein kinase C activator, 12-O-tetradecanoyl phorbol 13-acetate (TPA), increased it by 50% (P < 0.05). In primary cultures of pheochromocytoma cells, treatment with (Bu)2cAMP for 1 and 3 days increased ADM mRNA accumulation two- to threefold (P < 0.05). Our results show that ADM mRNA is present not only in adrenal medulla and pheochromocytomas, but also in adrenocortical neoplasms. Both protein kinase A- and C-dependent mechanisms regulate ADM mRNA expression in adrenocortical and pheochromocytoma cells supporting the suggested role for ADM as an autocrine or paracrine (or both) regulator of adrenal function.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2003

Ectopic adrenocorticotropin (ACTH) and corticotropin-releasing hormone (CRH) production in the adrenal gland: basic and clinical aspects.

The hypothalamic-pituitary-adrenal (HPA) axis is integrated in the human stress system and controls the metabolism of many cell systems in the body. Therefore, hypofunction or hyperfunction of the HPA axis potentially threatens the life of the whole organism. Noncontrolled overproduction of its key regulators, CRH and ACTH, causes dysfunction of the stress system. Ectopic secretion of these compounds may be part of extraadrenal paraneoplastic syndromes caused by various benign or malignant tumors. However, ectopic ACTH and CRH may originate from the adrenal itself. A local CRH/ACTH system exists in the normal human adrenal medulla. Overproduction of CRH and ACTH has been documented in pheochromocytomas causing Cushing's syndrome. Finally, ectopic production of ACTH causing Cushing's syndrome has also been demonstrated in adrenocortical cells. This suggests a marked plasticity within the HPA axis and the neuroendocrine cell system.

Adrenal Cortex Neoplasms↗
PubMed1989

[Morphometric characteristics of the cells in non-tumoral processes and tumors of the adrenal glands].

A comparative morphometric study of the cells was carried out by the Integral-2MT television cytologic analyzer, and the DNA quantitative estimation by flow cytofluorometry in 31 patients with adrenal tumors and hyperplastic involvements. The shifts in all the morphometric parameters in cortical adenoma and hyperplasia were found statistically insignificant, with similar (diploid) DNA cytograms. The differences in all the morphometric parameters (except the cellular and nuclear shape) were statistically significant in pheochromocytoma and hyperplasia of the cortex, with the pheochromocytoma DNA histograms showing higher counts of cells with DNA content higher than 2S. Assessment of the total group of malignant tumors of the adrenals (malignant pheochromocytoma, cortical carcinoma) has shown statistically significant differences in the mean characteristics (except cellular and nuclear shape) of these tumors and adrenocortical hyperplasia. In adrenocortical carcinoma 2 of the 3 histograms were aneuploid with a considerable count of cells with DNA content higher than 2S. The objective parameters may be used in the differential cytologic diagnosis of nontumor involvements and tumors of the adrenals.

Adenoma↗
PubMed1995

[The value of fine needle puncture in adrenal gland tumors].

UNLABELLED: The value of fine needle biopsy (FNB) in adrenal masses was investigated in 33 patients presenting with such masses. Representative material was obtained 18 times from 19 patients with a history of tumour. 4 of them were diagnosed to be genuinely benign and 14 to be genuinely malignant. Further representative material was obtained 13 times from 14 patients with incidental findings of adrenal masses. The material gained by puncturing was classified correctly as benign in 9 cases, and twice it was considered benign although the tumours later proved malignant. In one case a clinically not suspected malignant lesion was detected by FNB, while in another case a malignant lesion was suspected by FNB, whereas a benign tumour was proven by means of surgery. The share of malignant diagnoses corresponded with the size of tumour, ascertained by the application of ultrasound or CT. The rate of malignant adrenal masses, which were found incidentally, increased from 7 cm onwards; however, the rate of malignant adrenal masses obtained from patients with a history of tumour increased distinctively already from 4 cm onwards. From 11 patients out of 33, adrenal tissue was obtained and classified as benign lesion (adenoma), although, by means of FNB and the conditions for reasons of method, a well differentiated carcinoma cannot be excluded. CONCLUSION: FNB is indicated for non-functioning tumours examined in patients with a history of tumour, furthermore, for incidental findings of the size between 4-6 cm. A diagnostic approach to adrenal masses is suggested.

Adrenal Cortex Neoplasms↗
PubMed1995

Overlapping expression of immunohistochemical markers and synaptophysin mRNA in pheochromocytomas and adrenocortical carcinomas. Implications for the differential diagnosis of adrenal gland tumors.

BACKGROUND: The differential diagnosis of cortical versus medullary tumors of the adrenal gland may be a problem in diagnostic pathology. Conflicting results have been reported about the distribution of various immunohistochemical markers in the normal as well as neoplastic adrenal cortex and medulla. EXPERIMENTAL DESIGN: Archival, formaldehyde-fixed, and paraffin-embedded material comprising 27 adrenocortical carcinomas (ACC, meeting Weiss' histologic criteria), 28 pheochromocytomas (PCC), and adjacent nontumorous tissue (13 glands) were analyzed by immunogold-silver staining for the expression of polysialic acid (poly Sia), cytokeratins (CK), synaptophysin (SYN), chromogranin A (CrgA), somatostatin (SOM), calcitonin (CT), and the "adrenocortical marker" D11. Further, SYN mRNA expression was studied by nonradioactive in situ hybridization using digoxigenin-labeled oligonucleotide probes. RESULTS: In the normal adrenal gland, poly Sia was exclusively detected in the medulla and in cortical nerves. In ACCs, SYN immunoreactivity was present in 23 of 27 tumors (85%), D11 was present in 22 of 27 (81%), poly Sia was present focally in 8 of 27 (29%), and CK was present in 7 of 27 (25%). Synthesis of SYN in ACCS was demonstrated by mRNA in situ hybridization. Immunoreactivity for CrgA, SOM, or CT was not detectable. No difference of the marker profiles was seen in the nine clinically hormone-producing (three androgen, five corticosteroid, one mineralocorticoid) ACCs compared with the clinically silent tumors. In PCCs, all 28 tumors were immunoreactive for poly Sia and SYN; CrgA was detectable in 26 of 28 (93%), CT was detectable in 6 of 28 (21%), and SOM was detectable in 2 of 28 (7%) tumors. Staining for D11 or CK was undetectable. By immunohistochemistry, no distinction was possible between the 4 clinically malignant, the 6 multiple endocrine neoplasia type 2A-associated, and the 18 sporadic benign PCCs. CONCLUSIONS: Poly Sia of the neural cell adhesion molecule is consistently detected in normal adrenal medullary cells as well as in PCCs, and is occasionally focally expressed in ACCs. CrgA, CK, and D11 are reliable markers to immunohistochemically distinguish ACC from PCC. Immunoreactivity for SYN and detection of its mRNA in the majority of ACCs indicates the existence of tumor cells sharing both cortical and medullary features. Such focal neuroendocrine differentiation in ACCs can lead to confusion with PCCs.

Adrenal Cortex Neoplasms↗
PubMed1975

ACTH and prostaglandin receptors in human adrenocortical tumors. Apparent modification of a specific component of the ACTH-binding site.

The failure of certain adrenal tumors to respond to ACTH was investigated in vivo be administration of corticotropin-(1-24)-tetracosapeptide (ACTH1-24) and dexamethasone and in vitro by studying the binding properties of ACTH1-24 and prostaglandin E1 (PGE1) and their effect on adenylate cyclase activity of the tumors' crude membranes; in addition, in five cases the stimulation of cortisol production in isolated adrenal cells by both hormones and dibuttyryl cyclic adenosine 3',5'-monophosphate (cAMP) was also studied. The results obtained in 13 hormone-producing tumors of the human adrenal cortex, i.e. 10 carcinomas and 3 adenomas, were compared with those found in normal human adrenal glands. According to the adenylate cyclase responses to ACTH1-24 and PGE1, the tumors fall into different categories. In the first group are six rumors in which the adenylate cyclase was stimulated by both ACTH1-24 and PGE; in addition specific binding could be demonstrated for the two hormones in all six. The binding affinity for 125I-ACTH1-24 was found to be about 10 times higher than that for 125I-ACTH11-24. In the one tumor in which the experiment was performed, bound 125I-ACTH1-24 was displaced by ACTH1-10. These results are similar to the ones found in normal human adrenal preparations. For two rumors of the group in which ACTH did not increase steroidogenesis in vivo, the biochemical abnormality might be located beyond cAMP formation. A second group encompasses six tumors in which the steroidogenesis in vivo and the adenylate cyclase activity were insensitive to ACTH1-24 but in which the enzyme was stimulated by PGE1 and NaF. However, these preparations bound 125I-ACTH1-24 and 125I-ACTH11-24, the binding affinity being similar for both peptides but 10 times lower than the one found in normal adrenal cortex for 125I-ACTH1-24. In the only case of this group where it was tested, ACTH1-10 did not displace bound 125I-ACTH1-24. This result strongly suggests the possibility of a modification or a loss of the receptor site that binds the N-terminal sequency (1-10) of ACTH, the biologically active part of the molecule. In the last tumor, both PGE1 and ACTH were unable to stimulate adenylate cyclase activity and steroid production in a preparation of isolated adrenal cells, although steroidogenesis was stimulated by dibutyryl though steroidogenesis was stimulated by dibutyryl cAMP. No specific binding for PGE1 could be demonstrated. However, 125I-ACTH1-24 and 125I-ACTH11-24 were found to be bound to the tumor with the same affinity.

Adenoma↗
PubMed1975

Selective adrenal venography in an infant with virilizing adrenal cortical carcinoma.

Selective adrenal venography in a 10 month old infant with adrenal cortical carcinoma and virilizing symptoms demonstrated grossly dilated, irregular tumor veins. This was an unexpected finding as at aortography no adrenal arteries which would allow selective catheterization, and only very small neoplastic vessels were seen.

Adrenal Cortex Neoplasms↗
PubMed1996

Adrenaloma: a call for more aggressive management.

We review our experience from the surgical management of 57 patients (24 males, 33 females) with a mean age of 48.5 years who underwent adrenalectomy because of the computed tomography (CT) finding of a "nonfunctioning" adrenal tumor (adrenaloma). We found that CT consistently underestimated the real histologic size of the adrenal tumor (p = 0.001). Of the 57 resected tumors, 23 were cortical adenomas, 7 myelolipomas, 8 adrenal cysts, 11 nodular hyperplasias, 2 primary adenocarcinomas, 2 metastatic carcinomas, and 4 pheochromocytomas. The mean diameter was 5.89 cm and the mean weight 114.07 g. The mean diameter of the resected primary adenocarcinomas was 3.0 cm and 4.5 cm, respectively. The operative mortality was zero and the perioperative morbidity minimal. The mean operating time was 137 minutes (range 60-240 minutes). The posterior approach had the shortest operating time and the laparoscopic approach the shortest hospital stay and the least postoperative need for narcotics. During the 6.2 years mean follow-up period, five patients with preoperative hypertension remained normotensive, and both patients with the resected primary adenocarcinomas are alive without recurrence. We suggest a more liberal surgical approach to patients with adrenalomas because: (1) even small tumors can be malignant or potentially lethal (e.g., pheochromocytomas); (2) some tumors that appear to be nonfunctioning may in reality be functioning; and (3) other nonfunctioning tumors may, with time (and without prior notice), function. The low risk of adrenalectomy especially via the laparoscopic approach can provide an early definitive diagnosis and treatment, avoiding the cost of repeated CT scans and other studies as suggested by the currently prevailing conservative management of these tumors.

Adenocarcinoma↗
PubMed2000

Radiology of the adrenal.

Adrenal incidentalomas are commonly noted on abdominal cross-sectional imaging studies. Most of these lesions are benign, non-functional adrenal adenomas. Certain adrenal lesions have such characteristic radiologic findings that their diagnosis can be made with virtual certainty. This article reviews the radiologic evaluation of adrenal tumors, with particular emphasis on incidentalomas.

Adenoma↗
PubMed1998

Gene expression and roles of angiotensin II type 1 and type 2 receptors in human adrenals.

Although stimulation of aldosterone secretion is one of the functions of angiotensin II, the gene expression and biological significance of the angiotensin II receptor subtypes, AT1 and AT2, in the human adrenal have not been characterized. We therefore investigated the transcription levels of the receptor subtype genes and their roles in regulation of steroid secretion by human adrenals. The expression of AT1 and AT2 receptor mRNA was assessed by reverse transcription-polymerase chain reaction followed by Southern blot analysis in normal adrenocortical tissues (n = 6) and a series of adrenal tumour tissues: aldosterone-producing adrenocortical adenoma (n=6), Cushing's syndrome (n = 6) and pheochromocytoma (n = 6). The role of the two receptor subtypes in steroid secretion in vitro was examined by incubating the tissue with angiotensin II(1 microM) with or without the selective AT1 antagonist CV-11974 (1 microM). Both AT1 and AT2 receptor mRNA transcripts were demonstrated in all of the human adrenal tissues tested. Angiotensin II-induced aldosterone secretion was suppressed 50% upon the addition of CV-11974. The selective AT2 agonist CGP-42112 increased aldosterone secretion by 55% over the control, which was not suppressed by CV-11974. Angiotensin II and CGP-42112 did not affect cortisol secretion. These results suggest that both AT2 and AT1 receptors may be involved in the regulation of aldosterone secretion and tumorigenesis of the human adrenals.

Adenoma↗
PubMed1984

[Value of sonography, computed tomography and angiography in adrenal diagnosis].

Between 1979 and 1982, 47 patients with pathological process of the adrenals were surgically treated after preceding thorough non-evasive angiographic diagnosis (6 phaeochromocytomas, 20 adrenal adenomas, 8 adrenal hyperplasias, 5 adrenal carcinomas, 5 adrenal cysts and 3 adrenal metastases). The most consistently accurate results were obtained via adrenal phlebography with an accuracy of 94%. This was followed by non-evasive computed tomography (87%). Compared with the data given in literature, hormone determination in the adrenal venous blood was less favourable (79%). Selective adrenal arteriography, which was used less often, yielded correct results in 83% of the cases, whereas the number of accurate diagnoses achieved via sonography was lowest with 54%.

Adenoma↗
PubMed1975

Selection of patients and operative approach in primary aldosteronism.

A system for discriminating between adrenal adenoma and hyperplasia based on the levels of aldosterone production, plasma renin concentration, severity of electrolyte disturbances, plasma aldosterone patterns during recumbency and after assuming erect posture, and 131I-19-iodocholesterol scan has been developed. Indicated for operation are patients with adenomas whose elevated blood pressure cannot be continuously controlled with usual doses of medication and patients with documented deterioration of target organ function. Adrenalectomy has been performed 83 times in 81 patients with a diagnosis of primary hyperaldosteronism. Results of excision of adrenal adenomas have been excellent with significant lowering of blood pressure in all cases and cure of hypertension in over 60%. Results of total or subtotal adrenalectomy for hyperplasia have been poor with almost all patients still requiring medication for hypertension. Adenomas have always been unilateral, and usually can be localized so that unilateral exploration is curative. Therefore, we have tried to distinguish preoperatively between adenoma and hyperplasia. Anterior transperitoneal adrenalectomy has been effective with few complications, and no postoperative hypercortisolism after unilateral adrenalectomy for adenoma. The unilateral extraperitoneal approach gives shorter morbidity and potentially fewer serious complications.

Adenoma↗
PubMed1978

Adrenal cortical tumors with low attenuation coefficients: a pitfall in computed tomography diagnosis.

Four cases of adrenal tumors with unusually low attenuation coefficients are reported. The tumors presented with values ranging from 8 to 17 EMI units (EU: 500 scale) instead of the expected 30 to 40 EU range of the remainder of our adrenal tumors. Two of these patients had primary aldosteronism and two had Cushing's syndrome. An unusually high lipid content may be responsible for the lucent appearance.

Adrenal Cortex Neoplasms↗