Tumours of endocrine glands.
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Adenocarcinoma↗
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Results for “ADRENAL CORTEX NEOPLASMS”
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Tumours of the adrenal gland.
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Adrenal Cortex↗
Technical aspects of adrenalectomy via operative laparoscopy.
Adrenalectomy is usually performed through a transabdominal or a posterior approach. These approaches are associated with a painful syndrome postoperatively and long hospital stay. We report a series of five successful laparoscopic adrenalectomies, performed on: a 35-year-old male with a 5-cm right nonfunctioning tumor; a 32-year-old female with a 1.8-cm right aldosterone-producing adenoma; a 17-year-old female with a 4-cm right adrenocortical adenoma; and a 33-year-old female with bilateral 3.5-cm right and 4.5-cm left pheocromocytoma. Single right adrenalectomy lasted between 2 h and 2 h 30 min and bilateral adrenalectomy 5 h and 30 min. No transfusion was required. The hospital stay was between 3 and 4 days. This technique adequately removes adrenal tumors surgically and results in less postoperative pain and rapid recovery.
Adolescent↗
Androgen producing adrenocortical carcinoma.
Two cases of androgen secreting adrenocortical carcinoma have been described by light and electron microscopy. The histological and ultrastructural features of the tumour cells were similar to those of compact cells of zona reticularis and to those described in virilizing adenomas. They possess numerous mitochondria with lamellar and tubular cristae, abundant smooth endoplasmic reticulum, lipofuscin bodies and scanty lipid. Irregularly shaped, crenated mitochondria, with outpouchings of the outer limiting membrane have also been observed. The clusters of neoplastic cells were surrounded by basement membrane which demonstrated a focal discontinuity, probably reflecting malignancy of the tumours. Hyperplasia of smooth endoplasmic reticulum and the presence of outpouchings of the mitochondrial outer limiting membrane might be the morphological manifestation of endocrine activity of the tumours.
17-Ketosteroids↗
Wilms' tumor and adrenocortical carcinoma with hemihypertrophy and hamartomas.
A girl with hemihypertrophy and hamartomas, now 14 years old, had Wilms' tumor and subsequently developed adrenocortical carcinoma. The occurrence of the two tumors with the signs of an inborn defect of growth control supports the hypothesis that both tumors can be caused by the same etiologic factors, which are also teratogenic. An alternative explanation of induction of the second tumor by previous radio- and chemotherapy is discussed. Possible relationships between our case and the syndrome of Wiedemann and Beckwith are pointed out.
Adolescent↗
Scintigraphy of incidentally discovered bilateral adrenal masses.
The purpose of this study was to determine the patterns of iodine-131 6 beta-iodomethylnorcholesterol (NP-59) imaging and the correlation with computed tomography (CT)-guided adrenal biopsy and follow-up in patients with bilateral adrenal masses. To this end we investigated a consecutive sample of 29 euadrenal patients with bilateral adrenal masses discovered on CT for reasons other than suspected adrenal disease. Adrenal scintigraphy was performed using 1 mCi of NP-59 injected intravenously, with gamma camera imaging 5-7 days later. In 13 of the 29 patients bilateral adrenal masses were the result of metastatic involvement from lung carcinoma (5), lymphoma (3), adrenocarcinoma of the colon (3), squamous cell carcinoma of the larynx (1), and anaplastic carcinoma of unknown primary (1). Among these cases the NP-59 scan demonstrated either bilaterally absent tracer accumulation (in eight, all with bilateral metastases proven by CT-guided biopsy or progression on follow-up CT) or marked asymmetry of adrenocortical NP-59 uptake (in five). Biopsy of the adrenal demonstrating the least NP-59 uptake documented malignant involvement of that gland in five of five patients. In two patients an adenoma was found simultaneously in one adrenal with a contralateral malignant adrenal mass. In each of these cases, the adenoma demonstrated the greatest NP-59 uptake. In 16 patients diagnosis of adenoma was made on the basis of (a) CT-guided adrenal biopsy of the gland with the greatest NP-59 uptake of the pair (n = 4), or (b) adrenalectomy (n = 2), or (c) absence of change in the size of the adrenal mass on follow-up CT scanning performed 6 months to 3 years later (n = 10).(ABSTRACT TRUNCATED AT 250 WORDS)
Adosterol↗
Structural, genetic and pharmacological identity of the rat alpha 2-adrenergic receptor subtype cA2-47 and its molecular characterization in rat adrenal, adrenocortical carcinoma and bovine retina.
Subsequent to the first alpha 2-adrenergic receptor (alpha 2-AR) gene cloning of alpha 2-C10 from human platelet, cloning of the first rodent alpha 2-AR cDNA, cA2-47, was reported. Based on the structural and limited pharmacological comparison, it was concluded that the rodent receptor is a molecular and pharmacological analog of the human receptor, which is pharmacologically classified as the alpha 2A-AR. A later study slightly revised the structure of the human receptor. Thus, the precise structural comparison of the rat receptor to the human platelet receptor is no longer valid. Another rat alpha 2-AR gene, RG20, was then cloned and was also found to be a structural analog of the human alpha 2-C10. It, however, varied slightly from the alpha 2A subtype pharmacology, but matched the newly defined alpha 2D subtype pharmacology. It was, therefore, concluded that RG20 encodes the alpha 2D subtype. The structural and pharmacological relationship of RG20 with cA2-47 is not known, although it has been tacitly assumed that both are the identical alpha 2D receptor subtypes. The present study addresses this and other issues relating to the precise structural, genetic and pharmacological relationship of cA2-47 with the human platelet alpha 2-C10 receptor, and also the localization of cA2-47 transcript in certain rat tissues. The results show that the cA2-47 receptor shows a high degree of sequence identity to the alpha 2-C10 receptor, yet important differences exist between them. The sequence identity of cA2-47 receptor to the RG20 receptor is almost, but not quite complete. The cA2-47 gene is not present in the human and the human gene is not present in the rat; that cA2-47 receptor subtype is pharmacologically similar to the RG20 receptor subtype, both being of the alpha 2D subtype. The cA2-47 receptor transcript in addition to being found in the rat brain is present in the rat adrenal gland, testes, adrenocortical carcinoma and the bovine retina.
Adrenal Cortex Neoplasms↗
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↗
Adenosine 3',5'-cyclic monophosphate and adrenal tumor cell morphology.
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Adrenal Cortex Neoplasms↗
Magnetic resonance imaging of the adrenal glands.
Applications of nuclear magnetic resonance (NMR) to the adrenal gland have received considerable attention in recent years. Using high field strength magnets and surface coil technology, images of normal and abnormal adrenal glands have been obtained that compare favorably, and in some instances excel, computed tomography (CT) with respect to both image quality and, to a greater degree, differentiation of pathology. This article reviews the current state of magnetic resonance (MR) imaging of normal and abnormal adrenal glands, compares MR with CT imaging, and indicates where NMR spectroscopy has been of greatest value to date in the study of adrenal gland disease.
Adenoma↗
Computed tomography of myelolipoma in the accessory adrenal gland.
A case of myelolipoma arising from an accessory adrenal gland is reported. The accessory adrenal gland is a developmental anomaly, recognized often in the periadrenal fatty tissue at post-mortem examination. Myelolipoma of accessory adrenal gland should be considered when a suprarenal fat-containing tumor is seen separately from a normal-shaped adrenal gland.
Adrenal Cortex Neoplasms↗
Substance P in human adrenal medulla and in sympathetic tumours.
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Adenoma↗
Unique association of non-functioning pheochromocytoma, ganglioneuroma, adrenal cortical adenoma, hepatic and vertebral hemangiomas in a patient with a new intronic variant in the VHL gene.
We analyzed the clinical, hormonal, immunohistochemical and genetic features in a 69-yr-old Caucasian woman with a very rare "composite and mixed pheochromocytoma". This was characterized by right adrenal pheochromocytoma associated with homolateral ganglioneuroma and controlateral adrenal cortical adenoma. The three tumors, incidentally discovered, proved to be non-functioning (normal secretion of catecholamines and of other neuroendocrine peptides, glucocorticoids, mineralcorticoids and androgens). Accordingly, the patient showed no sign or symptom of endocrine disease. Computed tomography (CT) and magnetic resonance (MR) demonstrated a typical adenomatous lesion on the left adrenal gland with precocious uptake of the radiotracer on radioidine (131I)-norcholesterol adrenal scintigraphy, while the controlateral gland showed hyperdensity on CT, hyperintensity on MR and no uptake at adrenal scintigraphy. In addition, CT and MR revealed a vertebral and two hepatic hemangiomas. The right adrenal gland was surgically removed and, microscopically, pheochromocytoma and ganglioneuroma areas appeared intermixed without a predominant component. The former showed strong immunoreactivity for chromogranin, synaptophysin, vascular endothelial growth factor (VEGF) and CD34, while the latter appeared positive for neuron-specific enolase (NSE) and S-100. Peripheral blood genomic DNA analysis revealed a new intronic variant (5557A > G) in the von Hippel-Lindau gene (VHL) not observed in our control population.
Adrenal Cortex Neoplasms↗
p53 protein and its messenger ribonucleic acid in human adrenal tumors.
The role of p53 tumor suppressor gene in the pathomechanism of adrenal tumors was investigated by measuring p53 protein and its messenger ribonucleic acid (mRNA) in 12 normal human adrenals as well as in 56 adrenal tumors (7 aldosterone-producing adenomas, 5 adrenocortical adenomas causing Cushing's syndrome, 19 non-hyperfunctioning adrenocortical adenomas, 5 adrenocortical carcinomas, 12 pheochromocytomas, 3 myelolipomas, 4 ganglioneuromas and 1 hemangioma). The p53 protein concentration was significantly increased in aldosterone-producing adenomas (394+/-36 pg/mg cytosolic protein, mean+/-SE, vs 266+/-18 in normal human adrenals), whereas the concentration of this protein in Cushing's adenomas, non-hyperfunctioning adrenocortical adenomas, pheochromocytomas, and in all but one adrenocortical carcinomas was similar to that measured in normal human adrenal tissues. One adrenocortical carcinoma tissue showed very high p53 protein content (3000 pg/mg cytosolic protein). By contrast, myelolipomas (23+/-20) ganglioneuromas (43+/-15) and a hemangioma (11 pg/mg cytosolic protein) had very low p53 protein content. Northern blot analysis revealed the presence of p53 mRNA in each adrenal tissue examined with highest levels in aldosterone-producing and Cushing's adenomas. It is possible that the differences in p53 protein and/or mRNA contents reflect corresponding differences in the pathogenetic importance of p53 alterations in these types of adrenal tumors.
Adenoma↗
False-positive diagnosis of adrenal pheochromocytoma on iodine-123-MIBG scan.
1-123 metaiodobenzylguanidine (1-123 MIBG) scintigraphy is known for its high specificity in detecting pheochromocytoma and other tumors of neural crest origin. In this rare case report, we describe a definite adrenocortical adenoma that demonstrated false-positive uptake at I-123 MIBG scintigraphy and a remarkable accumulation of 75-SE-6-beta-selenomethyl-norcholesterol.
3-Iodobenzylguanidine↗
[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↗
[Hyperaldosteronism persisting after subtotal adrenalectomy].
BACKGROUND: Primary aldosteronism is known to be caused by aldosterone-producing adenoma (APA). Total adrenalectomy is the standard procedure. In contrast to bilateral adrenal diseases (e.g., MEN II pheochromocytomas), there is no consensus about the effect of subtotal adrenalectomy. CASE REPORT: A 44-year-old patient with primary aldosteronism caused by APA underwent subtotal adrenalectomy including removal of one adenoma. Because hypertension and hypokalemia did not disappear and hyperaldosteronism persisted, the patient had to undergo reoperation in which the adrenalectomy was completed. DISCUSSION: Subtotal adrenalectomy in patients with Conn's syndrome is an interesting therapeutic option,whereas its effect is much higher in hereditary diseases of the adrenal gland. The benefit of preserved adrenal tissue has to be weighed against a possible persistence of hyperaldosteronism, especially in cases with normal opposite adrenal glands.
Adrenal Cortex Neoplasms↗
[Value of various imaging modalities for diagnostic work-up of tumors of the adrenal gland].
OBJECTIVE: This paper describes the value of various imaging modalities for diagnostic work-up of tumors of the adrenal gland. METHODS: Results of the literature are reviewed. An optimized examination protocol for computed tomography (CT) and magnetic resonance imaging (MRI) is shown for assessment and differentiation of unclear lesions of the adrenal gland. RESULTS: Measurements of attenuation in the native examination as well as delayed enhancement are the cornerstones in the CT diagnostics of tumors of the adrenal gland. In MRI, chemical-shift imaging and evaluation of signal characteristics in T1- and T2-weighted images are most important for characterization even in unclear cases. CONCLUSION: CT and MRI play the major role in imaging of adrenal gland tumors. Whereas CT is less expensive and widely available,MRI provides advantages in unclear cases because of the excellent tissue contrast and the superior characterization.
Adrenal Cortex Neoplasms↗