Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADRENALECTOMY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,675 records · Page 93Linked to original sources

The role of corticoids, adrenalectomy, phenobarbital and pentobarbital in the promotion of DEN-hepatocarcinogenesis.

This paper shows there is a good correlation between the disturbance of the proliferation control and the plasma Corticosterone circadian pattern on the one hand and the promotion of diethylnitrosamine (DEN) initiated precancerous lesions on the other. In normal rats, phenobarbital (PB) or adrenalectomy, which both decrease plasma corticosterone levels, induce chronic liver growth, enhance the mitotic response to partial Hepatectomy and eliminate the mitotic circadian rhythms. In rats treated by DEN, the same treatments increase the proliferation advantage of PAS positive precancerous cells and promote tumorogenesis. Daily corticosterone injections inhibits liver growth even after hepatectomy both in normal and DEN-treated rats. Under carcinogenic conditions (DEN for 6 weeks), corticoid injections inhibit the selective growth of precancerous cells and the death by cancer occurs later. Pentobarbital (PE), administrated at the same subsedative doses as PB, does not change plasma corticosterone levels nor the mitotic control and does not enhance the carcinogenesis initiated by DEN. The "promoting effect" is closely linked to the disturbance of the biological corticosterone activity that normally synchronizes the liver cell proliferation by temporary inhibition of DNA synthesis for some hours every day (14-16). The role played by corticosterone in the selective growth of precancerous foci (glycogenesis type I) is discussed in the light of the hypothesis (1-2) according to which modification of the carbohydrate metabolism is closely related to the process of hepatocarcinogenesis.

Adrenalectomy↗

Primary hyperaldosteronism and adrenal incidentaloma: an argument for physiologic testing before adrenalectomy.

OBJECTIVE: To determine the frequency of nonfunctioning adrenal masses in patients with primary hyperaldosteronism. DESIGN: A case series. SETTING: A tertiary care hypertension clinic. PATIENTS: Twenty-seven consecutive patients with primary hyperaldosteronism. MEASUREMENTS: Blood pressure, serum electrolytes, supine and upright plasma renin, cortisol and aldosterone levels, selective adrenal vein aldosterone and cortisol levels, adrenal computed tomography (CT) scans and pathology reports. RESULTS: There was considerable overlap in the clinical features and laboratory investigations for patients with unilateral aldosteronoma and those with bilateral adrenal hyperplasia. Of the 27 patients who had confirmed primary hyperaldosteronism investigated at this centre, 25 had a definitive diagnosis assigned on the basis of postural stimulation tests, adrenal CT scans, and bilateral adrenal vein sampling, surgery or a combination of test results. Of this group, 18 had adrenal masses visualized on CT. However, only 13 of these 18 patients had an adrenal aldosteronoma subsequently proven by selective adrenal vein sampling or surgery, or both; the other 5 patients were found to have bilateral adrenal hyperplasia with nonfunctioning adrenal masses. CT had a sensitivity of 100% for the diagnosis of aldosteronoma, but the specificity was only 58% and the positive predictive value was only 72%. The likelihood ratio for the diagnosis of aldosteronoma in patients with primary hyperaldosteronism and an adrenal mass on CT was only 2.4. CONCLUSION: Given the poor specificity of CT in patients with primary aldosteronism, full biochemical and physiologic testing should be done before adrenalectomy in patients with suspected adrenal aldosteronoma.

Adenoma↗

Surgical approach to adrenal neoplasms: laparoscopic versus open adrenalectomy.

There are a number of different approaches available to surgically remove the adrenal gland. These can be broadly classified into two general categories, open and laparoscopic. There is no one best method for all patients. Surgeons, skilled in all aspects of adrenal surgery, should choose an approach for adrenalectomy based on patient and tumor related factors. Once advantages and disadvantages of a specific procedure, with these factors in mind, are weighed, the best approach for the individual patient should be chosen.

Adrenal Gland Neoplasms↗

[Laparoscopic adrenalectomy. An alternative to open surgery of minor adrenal tumors].

In the period February 1994 to November 1995 11 laparoscopic adrenalectomies were performed at our institution (seven women, four men). A transperitoneal approach was used in both right- and left-sided operations. Results were collected retrospectively. Indications for surgery were: Conn's syndrome (four), Cushing's syndrome (two), phaecromocytoma (four), and incidentaloma (one). The operations took median 170 minutes (range 105-250 minutes). Median size of the tumour was 4 cm range 1(1/2)-5 cm). No significant peri- or postoperative complications were recorded. The patients were discharged from the surgical unit median two days after surgery. Laparoscopic operation emerges as an alternative to open operation when dealing with smaller adrenal tumours. Because of the small number of patients, these operations have to be restricted to a few centres where both internists, anaesthesiologists and surgeons with expertise in this field are found.

Adrenal Gland Neoplasms↗

[Video laparoscopic adrenalectomy. The authors' personal experience].

Personal experience on two cases of laparoscopic adrenalectomy, operated, one on the right and the other on the left side, during 1996 is reported. The surgical technique, using a lateral decubitus and a transperitoneal approach is described, as well as the postoperative outcome. The laparoscopic approach to adrenal surgery seems to be "ideal", since it has a low "trauma ratio" (surgical procedure/access) with an anatomical an virtually bloodless dissection.

Adenoma↗

[Subtotal retroperitoneoscopic adrenal gland resection--an alternative to adrenalectomy?].

Primary adrenal tumors were removed in 24 patients by the posterior retroperitoneoscopic approach, maintaining tumor-free parts of the ipsilateral adrenal gland. These partial adrenal resections did not cause a significantly different operating time or blood loss compared to 58 complete adrenalectomies performed during the same period. All 20 patients with hormonally active tumors are biochemically and clinically cured (mean follow-up 18 months). In selected cases the retroperitoneoscopic subtotal adrenal gland resection is a safe procedure, which can potentially maintain the function of the adrenal gland's cortex.

Adrenal Gland Neoplasms↗

Neurogenic influences of bilateral adrenalectomy on monoamine oxidase.

Bilateral adrenalectomy (10 days) increased the monoamine oxidase activity of the rat heart, vas deferens, spleen, superior cervical ganglion, and hypothalamus but not that of the rest of the brain, kidney, and liver. Experiments were made to determine whether the increased activity was due to neurogenic influences and whether the enhanced activity of monoamine oxidase was intra- or extraneuronally located. Ganglionic blockade with chlorisondamine failed to alter the rise in cardiac monoamine oxidase. Likewise, superior cervical ganglion monoamine oxidase was unaffected by surgical denervation. 6-Hydroxydopamine abolished the increase in monoamine oxidase activity of the vas deferens, spleen, and superior cervical ganglion but failed to alter that of the kidney, hypothalamus, and the rest of the brain. Cardiac monoamine oxidase was reduced markedly by 6-hydroxydopamine, but the remaining activity was still significantly elevated over the respective control values. The data suggest that the increase in organ monoamine oxidase is predominantly of neuronal origin and that this increase is not due to transsynaptic induction.

Adrenal Glands↗

Suppression of neuropeptide Y-elicited eating by adrenalectomy or hypophysectomy: reversal with corticosterone.

Neuropeptide Y (NPY) injected into the paraventricular hypothalamus (PVN) stimulates a robust eating response in the satiated rat. To examine whether the NPY-feeding system interacts with the pituitary-adrenal axis, the eating response to PVN injections of NPY (78 pmol) was tested in adult male rats before and after sham surgery, adrenalectomy (ADX), hypophysectomy (HYPX), and/or corticosterone (CORT) replacement therapy. In unoperated or sham groups, NPY elicited 5.7-8.8 g of food intake in 1 h as compared to 0.4-1.1 g for vehicle-injected animals. In ADX groups, the NPY-elicited response was reduced by 60-71%, to between 2.4 and 2.8 g. Likewise, the average response of the HYPX group was reduced by 69%, to 1.7 g. Corticosterone replacement, via subcutaneous implant of a 100 mg CORT pellet, normalized the NPY-induced feeding response in both the ADX and HYPX groups. These findings suggest that the hypothalamic NPY-feeding system is largely dependent upon circulating CORT and that no other adrenal or pituitary hormone is essential.

Animals↗

Effect of pharmacological adrenalectomy on corticotropin-releasing factor-like and arginine vasotocin immunoreactivities in the brain and pituitary of the eel: immunocytochemical study.

Metopirone, a blocker of the 11 beta-hydroxylase, was used to suppress cortisol synthesis in the eel, producing a pharmacological adrenalectomy. After 1 and 2 days, corticotropin-releasing factor (CRF) immunoreactivity was reduced in the preoptic nucleus (PON) and was increased in the rostral neurohypophysis (NH) where CRF fibers ended in close proximity to ACTH cells. After 4 days, immunoreactive (ir) CRF increased in the PON or was similar to that of controls, and was reduced in the rostral NH. It was not affected in the caudal NH among intermediate lobe (IL) ramifications. Arginine vasotocin (AVT) immunostaining was often slightly increased in the PON, but changes were not apparent in the pituitary and AVT-ir fibers remained very scarce in the rostral NH. Metopirone significantly increased the cross-sectional area of CRF- and AVT-ir perikarya in the parvocellular region and the number of these perikarya as well as the ratio of CRF to AVT cell bodies in the totality of the PON. Colocalization of CRF and AVT, barely detected in control eels, occurred in 9.6% of CRF perikarya after 1-2 days, but in only 2.4% after 4 days. ACTH cells were rapidly and markedly stimulated. These immunocytochemical studies suggest that CRF synthesis, axonal transport, and release are increased in metopirone-treated eels, acting on the pituitary to stimulate ACTH release and interrenal cell activity. The participation of AVT in ACTH cell stimulation is less clear. These data are compared to those reported in mammals.

Adrenal Glands↗

The influence of adrenalectomy on alpha-adrenoceptor responses in rat cerebral cortex slices.

Experiments were undertaken to examine the effect of depletion of adrenal steroids on neurotransmitter-stimulated cAMP accumulation in rat cerebral cortex slices. Long-term depletion due to bilateral adrenalectomy (ADX) and short term depletion due to the steroid synthesis inhibitor metopirone (MET) caused a significant increase in alpha 1-adrenoceptor-mediated potentiation of beta-adrenoceptor-stimulated cAMP accumulation. The effect of MET was prevented by corticosterone treatment. This effect of ADX was selective in that there was no change in alpha 1-adrenoceptor-mediated inositol phosphate accumulation. In addition, ADX had no effect on potentiation of isoprenaline-stimulated cAMP by either the GABAB agonist baclofen or the phorbol ester, 4 beta-phorbol dibutyrate. However, 2-chloroadenosine-stimulated cAMP accumulation was significantly reduced in ADX rats.

Adrenal Glands↗

Effects of adrenalectomy on AGRP, POMC, NPY and CART gene expression in the basal hypothalamus of fed and fasted rats.

Glucocorticoids regulate body energy balance through both peripheral and central mechanisms. In order to understand the central mechanisms that mediate these effects of glucocorticoids we studied the effects of adrenalectomy (ADX) and food deprivation on the expression of four neuropeptide genes (measured by S1 nuclease protection assay) in the medial basal hypothalamus (MBH), which are known to regulate energy balance: pro-opiomelanocortin (POMC), agouti-related peptide (AGRP), neuropeptide Y (NPY), and cocaine and amphetamine regulated transcript (CART). Adult male rats were ADX or sham operated (SHAM), and studied 1-2 weeks later. In the first study effects of ADX and corticosterone replacement on POMC and AGRP expression were determined. ADX decreased POMC and AGRP gene expression in the MBH by 27 and 38%, respectively, compared to SHAM rats. Corticosterone treatment increased the expression of POMC by 87% and AGRP by 45% in ADX rats. The second study was designed to determine if glucocorticoids are necessary for the fasting induced changes in POMC, AGRP, NPY and CART in the MBH. ADX caused a 20-30% decrease in the expression of all four neuropeptide genes in the MBH. As expected, fasting suppressed POMC and CART expression and increased AGRP and NPY expression. The fasting-induced increases in AGRP and NPY persisted after ADX but no further significant decreases in POMC or CART were noted after fasting in ADX rats. Plasma leptin and insulin declined significantly after ADX and increased with corticosterone replacement; both leptin and insulin declined further in fasted, ADX animals. In conclusion, ADX decreases both anorexigenic, POMC and CART, and orexigenic, AGRP and NPY, neuropeptide gene expression in the MBH. AGRP and NPY decrease after ADX despite the fall in plasma leptin and insulin concentrations which in other situations would increase these neuropeptides. Furthermore, glucocorticoids are not required for fasting-induced upregulation of AGRP and NPY expression.

Adrenal Cortex↗

Aminoglutethimide medical adrenalectomy for advanced prostatic carcinoma.

Complete adrenal suppression with aminoglutethimide has been accomplished in 7 patients with progressive stage D carcinoma of the prostate who had become refractory to orchiectomy and the administration of exogenous estrogens. A favorable response was noted in 3 patients. These preliminary results indicate that this agent may be as useful as surgical adrenalectomy in the treatment of progressive prostatic carcinoma. A brief discussion of the pharmacology of this agent, its mode of administration and the side effects are presented.

Adenocarcinoma↗

Inhibitory avoidance deficit following short-term adrenalectomy in the rat: the role of adrenal catecholamines.

Impaired retention of an inhibitory avoidance response was observed in rats subjected to adrenalectomy (ADX) up to 120 hr before the single learning trial. Corticosterone substitution failed to normalize this behavioral deficit. Rats ADX 240 hr prior to the learning trial showed a normalized behavior. Adrenomedullectomy (ADXM) 48 or 240 hr before learning caused a similar impairment as in short-term ADX rats. The 240-hr ADX rats subjected to corticosterone substitution showed the same behavioral deficit as short-term ADX rats or ADXM ones. Immediate postlearning subcutaneous injection of adrenaline in a dose range of 0.005-5.0 micrograms/kg or of noradrenaline (0.005-0.5 microgram/kg) to 48-hr ADX rats resulted in a dose-related improvement of later retention behavior. Higher doses of catecholamines were less or ineffective. Postlearning treatment of 48-hr ADXM rats with adrenaline (0.5-500 micrograms/kg) caused a similar pattern of behavioral changes. It is concluded that adrenal catecholamines play an important role in the modulation of consolidation of memory. In addition, the high circulating ACTH levels that follow long-term ADX may correct for the behaviorial deficit induced by the absence of adrenomedullary catecholamines.

Adrenal Glands↗

Dependence of adrenalectomy-induced sodium appetite on the action of angiotensin II in the brain of the rat.

Adrenalectomized rats express a robust sodium appetite that is accompanied by high levels of blood-borne angiotensin II and is caused by angiotensin II of cerebral origin. Blood-borne angiotensin II is elevated in rats consuming NaCl after adrenalectomy, and plasma angiotensin II concentrations are increased further when the animals cannot drink a NaCl solution. These phenomena are the result of the pathological removal of aldosterone, because replacement therapy returned both sodium intake and plasma angiotensin II concentrations to preadrenalectomy levels. The adrenalectomized rat's appetite for sodium is completely suppressed by interference with the central, but not the peripheral, action of angiotensin II. These data demonstrate that the mechanism of the sodium appetite of the adrenalectomized rat is a pathological instance of the angiotensin/aldosterone synergy that governs the sodium appetite of the adrenal-intact, sodium-depleted rat. Because aldosterone has been removed, angiotensin acts alone to produce the appetite. Furthermore, the data show that it is angiotensin II of central origin that is important for sodium appetite expression.

Adrenal Glands↗

Laparoscopic partial adrenalectomy.

The concept of organ- and function-preserving surgery without compromising the primary goal of complete tumour removal has been recently applied in adrenal surgery. This has been accomplished by open surgery in the past. With recent advancements in minimally invasive surgery, partial adrenalectomy by laparoscopic approach has become feasible. The indications, contraindications and worldwide experience have been reviewed for this article.

Journal Article↗

Direct retroperitoneoscopic adrenalectomy in the porcine model.

An experimental protocol was developed to determine the safety and feasibility of retroperitoneoscopic adrenalectomy in the porcine model. We describe the technique and our experience with this exciting new endoscopic surgical modality.

Cholecystectomy, Laparoscopic↗

Medical adrenalectomy for advanced prostatic cancer: clinical and hormonal effects.

We examined the effect of medical adrenalectomy on the clinical and hormonal responses in 50 men with disseminated prostatic carcinoma. Patients refractory to initial hormonal therapy were treated with aminoglutethimide and hydrocortisone (AG-HC) and evaluated by the criteria of the National Prostatic Cancer Project. Eight patients showed a partial response (PR), and 17 remained stable while receiving these medications. Survival times for these two groups averaged 87.8 and 38 weeks, respectively. In contrast, 17 men were unresponsive to this therapy, exhibiting progressive disease with a mean survival time of 18 weeks. Eight patients could not tolerate the drug regimen or were lost to follow-up. Serum and urinary hormone profiles determined serially during AG-HC therapy revealed that all measured serum androgens and estrogens were significantly lowered by AG-HC treatment; however, specific hormones, including free testosterone, dihydrotestosterone, estrone, and estradiol were suppressed to a greater degree in responders (R) as compared with nonresponders (NR). Urinary excretion of 17-ketosteroids did not change during AG-HC therapy, but specific androgen metabolites, including testosterone glucuronide and androstanediol glucuronide, were suppressed by 50% during AG-HC therapy. We showed modest clinical benefit of AG-HC therapy in advanced prostatic cancer. That greater hormonal suppression was associated with greater responsiveness to this therapy raises the hope that further manipulations directed against suppression of extratesticular androgens may be a useful approach as second-line treatment of advanced prostatic cancer.

Aged↗

Etomidate, pharmacological adrenalectomy and the critically ill: a matter of vital importance.

Etomidate is a potent suppressant of adrenal steroidogenesis,effectively inducing reversible pharmacological adrenalectomy. Recent evidence suggests that for every five patients with septic shock given etomidate without corticosteroid supplementation, one patient will die as a consequence. Other critically ill patients are also at possible risk, and this risk requires further exploration. Etomidate will also confound investigations into the effects of disease states on adrenal function, and should therefore be avoided. A moratorium on the use of etomidate in critically ill patients outside clinical trials may be prudent until its safety is established.

Adrenal Cortex Function Tests↗