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PubMedDate not supplied

Progestogens and Cushing's syndrome.

We report 3 patients where Medroxyprogesterone Acetate (MPA = Provera) and Megestrol Acetate (Megace) in doses used for therapy of breast cancer, caused clinical hypercortisolism and Cushing's syndrome. Studies of the toxicity of Medroxyprogesterone Acetate list the commonest adverse events at 500 mg/day as weight gain, water retention, increased blood pressure, tremor, moon face, sweating, muscle cramps, vaginal bleeding and increased appetite. Glucocorticoid-like effects are seen in up to 30% of patients treated for longer than 6 weeks with mostly large doses of the order of 1500 mg/day but Cushing's syndrome has been reported in patients taking 400 mg/day. Neither the glucocorticoid-like effects or Cushing's syndrome have been previously observed with Megestrol Acetate. In the elderly female population receiving progestogens for neoplastic disease the progestogen itself could be an appreciable cause of morbidity both by causing glucocorticoid-like effects and Cushing's syndrome but also by lack of awareness of the danger of sudden withdrawal of these compounds when the hypothalmic-pituitary-adrenal (HPA) axis is suppressed. The signs and symptoms could be easily overlooked unless appropriate testing for Cushing's syndrome is carried out. While the progestogen may have to be continued indefinitely a dose decrease may be feasible with reduction of morbidity.

Adrenocortical Hyperfunction↗
PubMed1998

Hormonal characteristics of primary aldosteronism due to unilateral adrenal hyperplasia.

A case of unilateral adrenocortical hyperplasia is presented. A 46-year-old woman with a 7-year history of hypertension and a 1-year-history of hypokalemia was diagnosed with primary aldosteronism. Computed tomography, magnetic resonance imaging, venous sampling and adosterol scintigraphy exhibited a functioning left adrenal mass. The plasma aldosterone concentration increased markedly when furosemide with upright posture and either captopril or adrenocorticotropin were administered. Plasma renin activity was suppressed below the detectable range. Aldosterone secretion displayed a circadian rhythm and was not suppressed by dexamethasone administration. The resected left adrenal mass was pathologically diagnosed as adrenocortical nodular hyperplasia. Unilateral adrenal hyperplasia involving the zona glomerulosa rarely has been reported, with varying and incompletely characterized hormonal characteristics. This case report and literature review suggest unilateral adrenal hyperplasia as a rare cause of hyperaldosteronism with characteristics intermediate between idiopathic hyperaldosteronism and aldosterone-producing adrenocortical adenoma, resembling the functional features of the adenoma more closely.

Adrenal Cortex↗
PubMed1989

Effects of the opiate agonist loperamide on pituitary-adrenal function in patients with suspected hypercortisolism.

In the present work the possible use of loperamide, an opiate agonist, in the dynamic evaluation of patients with suspected hypercortisolism was investigated. The effects of loperamide on plasma ACTH and cortisol levels were evaluated in normal subjects and in 58 patients with suspected Cushing's syndrome. The results were compared to those obtained after the overnight dexamethasone suppression test. In normal subjects plasma ACTH and cortisol levels were significantly (p less than 0.005) suppressed by both loperamide (16 mg po) and dexamethasone (1 mg po). In 17 patients, in whom the diagnosis of Cushing's syndrome was confirmed by subsequent investigations, neither loperamide or dexamethasone inhibited cortisol (from a baseline of 606 +/- 55 nmol/L) to a nadir of 502 +/- 43 nmol/L and 539 +/- 50 nmol/L, respectively) and ACTH concentration (from a basal level of 70.1 +/- 11.8 pg/ml to a nadir of 46.0 +/- 8.6 pg/ml and 54.3 +/- 7.5 pg/ml, respectively). In 34 patients, in whom the suspect of hypercortisolism was ruled out, either loperamide or dexamethasone suppressed the pituitary-adrenal axis: cortisol and ACTH levels significantly fell from 417 +/- 24 nmol/L and 28.3 +/- 3.5 pg/ml to 60 +/- 6 nmol/L and 14.4 +/- 1.4 pg/ml after loperamide and to 26 +/- 4 nmol and 16.4 +/- 1.7 pg/ml after dexamethasone. In 7 patients discordant responses were observed. In 3 patients treated with antiepileptic drugs ACTH and cortisol levels were inhibited by loperamide, but not by dexamethasone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocortical Hyperfunction↗
PubMed1997

[Reactive thymus dysplasia following therapy for ACTH-producing tumors].

UNLABELLED: Surgical or conservative treatment of ACTH-producing tumors results in acute drop of the previously excessively high cortisol levels. The following associated pathophysiological changes also occur in the organism's recovery from stress, such as trauma, operation or chemotherapy of tumors. Both cases result in a regeneration of the immune system, which might even be exalted. The corresponding radiographic feature is the "rebound" enlargement of the thymus occurring about six months after remission of hypercortisolism. Histological examination reveals benign thymus hyperplasia. Especially in cases of still unknown primary tumor the appearance of this anterior mediastinal mass can lead to misdiagnosis. We present the cases of two patients with diffuse thymic hyperplasia following surgical and medical correction of hypercortisolism. One patient suffered from classic Cushing's disease responding to transsphenoidal resection of an ACTH-secreting pituitary microadenoma. Six months later CT of the chest incidentally demonstrated an anterior mediastinal mass known as thymic hyperplasia. The second patient presented with an ectopic, still unkown source of ACTH-production. Six months after medical correction of hypercortisolism CT of the thorax showed an enlargement of the anterior mediastinum. Thymectomy was performed in order to exclude thymus carcinoid. Histological examination revealed benign thymus hyperplasia with negative immunostaining. CONCLUSION: Radiologists and clinicians should be familiar with the pathophysiological changes resulting from precipitously dropping cortisol levels in order to prevent diagnostic errors and unnecessary operations.

Adrenocortical Hyperfunction↗
PubMed1996

Laparoscopic adrenalectomy.

Using the transperitoneal, laparoscopic approach, we performed 67 successful adrenalectomies between June 1993 and July 1995 at Greenslopes Hospital, Brisbane. There were 30 women and 37 men. Syndromes of primary adrenal hormone overproduction--primary aldosteronism (n = 52), pheochromocytoma (n = 6), and hypercortisolism (n = 1)--were present in 59 patients and apparently nonfunctioning adrenal tumors (of which one was malignant) in 8 patients. There was a significant difference in the time of operation between patients weighing < 80 kg and those weighing > 80 kg. Operations on males were slower than those on females, possibly explained by males being significantly heavier. Left-sided tumors outnumbered right-sided tumors; removal of right-sided adrenals took, on average, longer, but this difference was not significant.

Adrenal Gland Neoplasms↗
PubMed1996

Role and operative risk of bilateral adrenalectomy in hypercortisolism.

Transsphenoidal pituitary surgery has radically modified the management of pituitary-dependent hypercortisolism (Cushing's disease). Bilateral adrenalectomy may, however, represent the ultimate treatment in some cases of hypercortisolism. In the present study we report our experience of bilateral adrenalectomy in 82 patients operated on during the last 15 years. The causes of hypercortisolism were Cushing's disease (n = 78), ectopic ACTH syndrome (n = 3), and primary adrenocortical nodular dysplasia (Carney-Meador syndrome) (n = 1). Before operation 37% of the patients had severe symptoms of hypercortisolism. A bilateral posterior approach was undertaken in 58 patients, whereas 18 patients had an anterior transabdominal approach and 6 patients a laparoscopic approach. There were two operative deaths (2.4%). Postoperative complications occurred mostly in cases of advanced disease and were observed in 14 patients (17%), among whom 4 had severe complications. At long-term follow-up, one recurrence of hypercortisolism and 12 Nelson syndromes (15%) were observed. In conclusion, bilateral adrenalectomy carries an acceptable operative risk, and we recommend bilateral adrenalectomy rather than long-term suppressive therapy in patients requiring prompt and definitive control of their hypercortisolism or after pituitary surgery failure.

ACTH Syndrome, Ectopic↗
PubMed2001

Adrenocortical carcinoma in two female children.

Adrenocortical carcinoma is a rare tumor in children. This tumor is more likely to be hormonally active in children than in adults and tends to cause a variety of symptoms, which may mimic other benign endocrinopathies. These tumors are usually diagnosed at advanced stages and portend a dismal prognosis. We describe two cases of adrenocortical carcinoma. One child presented with Cushingoid symptoms secondary to hypercortisolism, including amenorrhea, hirsutism and weight gain. The other child presented with precocious puberty. Both children underwent resection of the tumors. We describe their presenting symptoms, postoperative course, adjuvant therapy and clinical course. Pertinent literature regarding the anatomy of the adrenal gland, pathology of adrenocortical carcinoma, factors influencing outcome, diagnostic modalities and treatment, are discussed.

Adolescent↗
PubMed2000

Intracavernous sinus ectopic adrenocorticotropin-secreting tumours causing therapeutic failure in transsphenoidal surgery for Cushing's disease.

BACKGROUND: The major cause of surgical failure in the treatment of Cushing's disease lies in unsuccessful identification of adenomas. In the present study, we investigated the pathogenesis of negative exploration in transsphenoidal surgery for Cushing's disease by analyzing neuro-imaging studies, endocrinological examination and selective venous sampling. METHODS: Thirty patients with ACTH-dependent Cushing's syndrome that met the endocrinological criteria for Cushing's disease were treated by transsphenoidal microsurgery. Depending on positive or negative identification of adenomas during the surgery, selective adenomectomy, partial hypophysectomy or subtotal hypophysectomy was performed. FINDINGS: All nine patients who underwent selective adenomectomy showed endocrinological remission and did not need any hormone replacement therapy. Of the 12 patients who underwent partial hypophysectomy, 11 showed normalization of hypercortisolism but seven needed permanent replacement of hydrocortisone. Four patients underwent subtotal hypophysectomy because no adenoma could be identified in spite of detailed exploration, and three of them showed remission but with permanent requirements of hydrocortisone and other pituitary hormones. Five patients, whose hypercortisolism persisted after initial surgery, underwent total hypophysectomy as secondary transsphenoidal surgery, and only one of them showed endocrinological remission. Of the six patients with surgical failure, four were thought to be rare cases in whom the ACTH-secreting tumours may have occurred ectopically in the cavernous sinus without direct contact with the pituitary gland. Endocrinologically, these four patients showed a low or no response to corticotropin releasing hormone (CRH) stimulation, and for three of them, radiation therapy to the sellar region including the cavernous sinus was effective for persistent hypercortisolemia. INTERPRETATION: Recognition of an ectopic intracavernous sinus ACTH-secreting tumour as a pathological entity for Cushing's disease may not only enhance the diagnostic accuracy but also be important for determining the optimal surgical mode for persistent Cushing's disease.

Adenoma↗