Bilateral Adrenalectomy (bilateral + adrenalectomy)

Distribution by Scientific Domains


Selected Abstracts


Retroperitoneal endoscopic adrenalectomy is safe and effective

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 11 2010
J. M. J. Schreinemakers
Background: The aim of this study was to review an experience with retroperitoneal endoscopic adrenalectomy (REA). This is the procedure of choice for adrenal tumours at this institution. Methods: Between 1997 and 2008, 112 REAs were performed in a single university centre. Data were retrieved retrospectively from a prospectively collected database, including information on patient demographics, surgical procedure, complications and hospital stay. Results: One hundred and twelve REAs were carried out successfully in 105 patients, including seven bilateral adrenalectomies. Thirty-nine patients with unilateral adrenal disease had a phaeochromocytoma, of whom 16 had multiple endocrine neoplasia syndrome type 2, 21 patients had Cushing's disease and 20 had Conn's disease. Median body mass index was 27 (interquartile range 23,29) kg/m2. The median duration of unilateral operations was 100 (90,130) min with a median blood loss of 5 ml. Median tumour size was 3·1 (2·0,4·4) cm. Conversion from REA to open surgery was needed in two patients. Seven patients experienced postoperative complications (2 major, 5 minor). One patient needed a reoperation. The median postoperative hospital stay was 3 days. A learning curve with a significant decrease in operating time was observed over the years. Conclusion: REA appears to be a safe and effective surgical technique for adrenal gland tumours up to 6 cm in diameter, with a minimal complication rate. Copyright © 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source]


The Trophic Effects of Oestrogen on Male Rat Anterior Pituitary Lactotrophs

JOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2009
L. A. Nolan
Rapid but often transient changes in mitotic and apoptotic activity are important components of the pituitary response to changes in the hormonal environment. For example, bilateral adrenalectomy and orchidectomy each result in a wave of increased mitosis lasting approximately 1 week, mediated by the same population of trophically active and, to a large extent, endocrinologically inactive cells. By contrast to these tonic inhibitors of pituitary trophic activity, reports of a progressive increase in lactotroph numbers during pregnancy suggest that oestrogen is a potent and persistent pituitary mitogen. By comparing the amplitude and duration of male rat anterior pituitary mitotic responses to oestrogen treatment, to adrenalectomy, and to a combination of the two, the present study aimed to further clarify the characteristics of the oestrogen-induced trophic response, in particular whether lactotrophs are the predominant cell type involved. Adrenalectomy produced a wave of increased mitotic activity, which resolved within 7 days as expected, whereas oestrogen induced a significant increase in mitotic activity, which was sustained for the 14-day duration of the study. The trophic effects of combining adrenalectomy and oestrogen treatment were not additive in that the statistically insignificant upward trend in mitotic index during the first few days compared to oestrogen treatment alone was entirely abolished by oestrogen pre-treatment. The increase in mitotic activity in lactotrophs induced by oestrogen either with or without adrenalectomy did not result in an increase in the relative size of the prolactin-positive compared to prolactin-negative pituitary parenchymal cell numbers by the end of the study. Despite the marked increase in the lactotroph population that is reported during pregnancy, these data indicate that at least the early (i.e. within 2 weeks) mitotic response to pharmacological doses of oestrogen increases mitotic activity in the lactotroph subpopulation by only 5,8% relative to other cellular subpopulations. Unexpectedly, the mitotic response to oestrogen principally occurs in non-prolactin-containing cells and results in the recruitment, amongst other trophically responsive populations, of the entire subpopulation of prolactin-, adrenocorticotrophic hormone- and luteinising hormone-negative cells that respond mitotically to adrenalectomy. Oestrogen therefore has a previously unrecognised non-cell type-specific trophic effect in the pituitary that obscures the relative expansion of the lactotroph population by inducing concurrent increases in numbers of prolactin-negative cells, the nature of which at least in part remains to be determined. [source]


Aberrant G-protein coupled receptor expression in relation to adrenocortical overfunction

CLINICAL ENDOCRINOLOGY, Issue 1 2010
André Lacroix
Summary The aberrant adrenal expression and function of one or several G-protein coupled receptors can lead to cell proliferation and abnormal regulation of steroidogenesis in unilateral adenomas, carcinomas or in ACTH-independent macronodular adrenal hyperplasia (AIMAH). Excess cortisol secretion leading to either sub-clinical or overt Cushing's syndrome is the most prevalent phenotype reported to date. In a few patients, aberrant regulation of androgen excess has been reported. More recently, initial studies suggest that similar mechanisms are involved in the renin-independent regulation of aldosterone secretion in primary aldosteronism. In recent years, cases of familial AIMAH have been identified, and specific aberrant hormone receptors are functional in the adrenal of affected members. The identification of aberrant receptors can offer specific pharmacological approach to prevent disease progression and control abnormal steroidogenesis; alternatively, unilateral or bilateral adrenalectomy remains the treatment of choice. [source]


Ectopic ACTH syndrome caused by pulmonary carcinoid tumourlets

CLINICAL ENDOCRINOLOGY, Issue 6 2001
S. Tofé Povedano
The differential diagnosis of Cushing's syndrome is a major challenge to clinical endocrinologists, especially those infrequent cases referred to as occult ectopic ACTH syndromes. Although bronchial carcinoids are well known to be a cause of Cushing's syndrome due to ectopic ACTH secretion, very few cases of carcinoid tumourlets causing an ACTH ectopic syndrome have been reported, and their origin remains controversial. For some authors, tumourlets and typical carcinoids represent distinct pathological entities, whilst others hold that tumourlets are merely microscopic carcinoid tumours. We report a patient with an aggressive Cushing's syndrome that required bilateral adrenalectomy, diagnosed 22 years before a 3-cm lung nodule became apparent on routine chest X-ray. The biopsy after lung surgery revealed a typical peripheral bronchial carcinoid surrounded by tumourlets. Both tumourlets and carcinoid tumour showed strongly positive ACTH immunostaining. Recently, Arioglu et al. (1998) reported a case of Cushing's syndrome caused by pulmonary carcinoid tumourlets, concluding that this entity should be considered in the differential diagnosis of occult ectopic ACTH syndrome. Furthermore, we consider that the carcinoid tumourlets found in our patient, were the initial source of ACTH, leading to Cushing's syndrome with a rapid onset, and that a loss of cell proliferation control in one of such tumourlets many years later, could have resulted in the development of a typical carcinoid tumour, reinforcing the theory of a common origin of these lesions. [source]