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PubMed1999

[Cushing syndrome by ectopic ACTH secretion: analysis of the physiopathologic mechanism of hypokalemia. Report of two cases].

We report a 42 years old male and a 66 years old female with a Cushing syndrome caused by ectopic ACTH secretion secondary to a carcinoid tumor. These patients had both severe hypokalemia, resistant to medical treatment and that subsided with bilateral adrenalectomy and supplementation with dexametasone. Cushing syndrome caused by ectopic ACTH secretion is characterized by a severe and rapidly evolving hypercortisolism. Hypokalemia is present in 90% of cases and is probably caused by a defect in 11 beta hydroxysteroid dehydrogenase, that limits the binding of cortisol to aldosterone receptor, metabolizing it to cortisone. Therefore, this alteration will increase the mineralocorticoid action of cortisol.

ACTH Syndrome, Ectopic↗
PubMedDate not supplied

An infantile Cushing syndrome due to misuse of topical steroid.

Chronic low-dose exogenous steroid therapy in children can result in hypothalamic-pituitary-adrenal axis dysfunction. However, the development of Cushing syndrome from topical steroid therapy is unusual. A 9-month-old girl with a diagnosis of Cushing syndrome caused by long-term topical clobetasol propionate application was evaluated. The patient was found to have severe adrenal suppression. Limiting the use of steroid-containing drugs, prescription of less potent agents, especially during infancy, and warning of parents about potential side effects are very important.

Administration, Cutaneous↗
PubMed2006

Hypertension in Cushing's syndrome.

Cushing's syndrome can be exogenous, resulting from the administration of glucocorticoids or adrenocorticotrophic hormone (ACTH), or endogenous, secondary to increased secretion of cortisol or ACTH. Hypertension is one of the most distinguishing features of endogenous Cushing's syndrome, as it is present in about 80% of adult patients and in almost half of children and adolescents patients. Hypertension results from the interplay of several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which may be increased. The therapeutic goal is to find and remove the cause of excess glucocorticoids, which, in most cases of endogenous Cushing's syndrome, is achieved surgically. Treatment of Cushing's syndrome usually results in resolution or amelioration of hypertension. However, some patients may not achieve normotension or may require a prolonged period of time for the correction of hypercortisolism. Therefore, therapeutic strategies for Cushing's-specific hypertension (to normalise blood pressure and decrease the duration of hypertension) are necessary to decrease the morbidity and mortality associated with this disorder. The various pathogenetic mechanisms that have been proposed for the development of glucocorticoid-induced hypertension in Cushing's syndrome and its management are discussed.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2005

Dexamethasone infusion testing in the diagnosis of Cushing's syndrome.

Cushing's syndrome and its various aetiologies is a markedly difficult diagnosis to make given its subtle signs, sometime cyclical nature, and the lack of a single definitive diagnostic test. Although a great variety of diagnostic tests have been developed to assist in the diagnosis, even with the best clinical acumen, biochemistry and medical imaging the diagnosis can remain elusive. The long low and high dose oral dexamethasone suppression test is cumbersome, costly and often requiring an extended inpatient stay. The utility of the dexamethasone suppression test would be greatly enhanced if it could be performed as a short outpatient procedure. In this study we sought to confirm and refine the clinical utility of the high dose 4 mg intravenous dexamethasone suppression test as an alternative diagnostic test for Cushing's syndrome. There were a total of 31 subjects: 8 patients with proven pituitary Cushing's disease, 3 with primary adrenal tumors, 10 with pseudo-Cushing's syndrome and 10 healthy controls. All subjects with pseudo-Cushing's syndrome suppress serum cortisol at +5 and at +24 hours. In subjects with pituitary Cushing's disease, 7 out of 8 (88%) had serum cortisol suppressed at +5 hours but rebounded at +24 hours to at least 70% of the original serum level. Primary adrenal tumors showed a pattern of non-suppression throughout. The 4 mg intravenous dexamethasone suppression test is excellent in ruling out pseudo-Cushing's syndrome. This test is much simpler and more convenient than the oral dexamethasone suppression test in confirming clinical suspicion of pituitary Cushing's disease.

Adrenal Gland Neoplasms↗
PubMed1999

Contemporary evaluation and management of Cushing's syndrome.

Cushing's syndrome, characterized by unregulated cortisol secretion, may be caused by a variety of adrenal, pituitary, or other tumors. The best biochemical test for establishing the diagnosis is determination of 24-h urinary free cortisol. The specific causes for Cushing's syndrome may be further differentiated by plasma adrenocorticotrophic hormone (ACTH). Primary adrenal cortical diseases are associated with low levels of ACTH and are considered ACTH-independent. Pituitary disease and the ectopic ACTH syndrome are associated with normal or elevated ACTH levels and are considered ACTH-dependent. Adrenal forms of Cushing's syndrome may result from either adenoma or carcinoma. The diagnostic approach to Cushing's syndrome and the clinical, biochemical, and radiographic features that distinguish adrenal adenoma and carcinoma are the subjects of this paper. 65-75% of CS [14, 15]. Most cases of Cushing's disease are the result of pituitary adenomas; however, corticotrope hyperplasia is responsible for a small minority of cases. Ectopic production of ACTH from a variety of tumors (bronchial carciniod, thymoma, oat-cell carcinoma, pheochromocytoma, islet-cell tumor, and prostate cancer) accounts for 10-15% of CS. Primary adrenocortical diseases account for the remaining 20-30% of CS, including benign adenoma (10-15%), adrenocortical carcinoma (5-10%), and adenomatous hyperplasia (5%). The purpose of this review is to present a contemporary approach to the evaluation and management of patients with Cushing's syndrome, emphasizing the primary adrenal etiologies pertinent to urologists.

Cushing Syndrome↗
PubMed2005

Evaluation and treatment of Cushing's syndrome.

Cushing's syndrome results from sustained pathologic hypercortisolism caused by excessive corticotropin (ACTH) secretion by tumors in the pituitary gland (Cushing's disease, 70%) or elsewhere (15%), or by ACTH-independent cortisol secretion from adrenal tumors (15%). The clinical features are variable, and no single pattern is seen in all patients. Those features most specific for Cushing's syndrome include abnormal fat distribution, particularly in the supraclavicular and temporal fossae, proximal muscle weakness, wide purple striae, and decreased linear growth with continued weight gain in a child. Patients with characteristics of glucocorticoid excess should be screened with measurements of saliva or urine cortisol or dexamethasone suppression testing. The diagnosis of Cushing's syndrome should be followed by the measurement of plasma ACTH concentration to determine whether the hypercortisolism is ACTH-independent. In ACTH-dependent patients, bilateral inferior petrosal sinus sampling with measurement of ACTH before and after administration of ACTH-releasing hormone most accurately distinguishes pituitary from ectopic ACTH secretion. Surgical resection of tumor is the optimal treatment for all forms of Cushing's syndrome; bilateral adrenalectomy, medical treatment, or radiotherapy are sought in inoperable or recurrent cases. The medical treatment of choice is ketoconazole. The prognosis is better for Cushing's disease and benign adrenal causes of Cushing's syndrome than adrenocortical cancer and malignant ACTH-producing tumors.

Adrenalectomy↗
PubMed1990

Diagnosis of corticotropin-producing bronchial carcinoid tumors causing Cushing's syndrome.

Cushing's syndrome due to ectopic production of adrenocorticotropic hormone (corticotropin) has been recognized for many years. Traditionally, clinicians have thought that most cases were due to lung carcinomas and that the clinical manifestations differed from those for pituitary-dependent Cushing's syndrome. We report two cases of corticotropin-producing bronchial carcinoid tumors that were clinically and biochemically indistinguishable from pituitary-dependent Cushing's syndrome. Review of the literature revealed that bronchial carcinoid tumors are the most common cause of Cushing's syndrome due to ectopic secretion of corticotropin. On biochemical and anatomic studies, they are frequently indistinguishable from pituitary-dependent Cushing's syndrome and thus may be difficult to diagnose. Inferior petrosal sinus sampling for corticotropin and computerized imaging of the chest may be the best aids in making the diagnosis.

ACTH Syndrome, Ectopic↗
PubMed1975

Pituitary carcinoma with liver metastases and Cushing syndrome. Report of a case.

A 38-year-old woman complained of headache, visual impairment, and diabetes insipidus for 18 months prior to rapid onset of Cushing syndrome and amenorrhea. An autopsy disclosed a pituitary carchinoma invading the right cavernous sinus and two liver metastases. The tumor cells were chromophobic and agranular, with scarce polymorphism and rare mitoses. A review of the literature showed that the association of Cushing syndrome to pituitary carcinomas increases in direct proportion to the occurence of metastases. Such association was noted in almost half of the reported cases of pituitary carcinomas with extracranial dissemination.

Adult↗
PubMed1989

Body fat distribution measured with CT: correlations in healthy subjects, patients with anorexia nervosa, and patients with Cushing syndrome.

Computed tomography (CT) was used to study fat distribution in three groups of women of comparable age: 39 healthy volunteers, 15 patients with anorexia nervosa, and seven with Cushing syndrome. Patients with anorexia nervosa had a fivefold decrease in subcutaneous fat and only a twofold decrease in intraabdominal fat compared with the values for the volunteers. Patients with Cushing syndrome had less than a twofold increase in subcutaneous fat and greater than a fivefold increase in intraabdominal fat compared with values for the healthy subjects. These findings suggest that fat in different body compartments responds differently to disease processes and that CT can be used to measure these changes.

Adipose Tissue↗
PubMed1997

[Diagnosis and therapy of Cushing syndrome].

Current diagnostic and therapeutic options in Cushing's syndrome have been retrospectively evaluated on the basis of 40 case histories of the years 1980 to 1994. After biochemical diagnosis, several radiological methods such as 131J-cholesterol-scintigraphy and, in 1 case, selective petrosal sinus blood sampling were employed. Out of 25 patients with central Cushing's syndrome 18 were cured by transsphenoidal pituitary surgery, in 1 case in combination with "Gamma-Knife" therapy. One patient was primarily treated by bilateral adrenalectomy, 5 as second intervention following unsuccessful pituitary surgery. One patient is not fully cured at present. Adrenal cortisol-producing adenomas were successfully treated by unilateral, subtotal or bilateral adrenalectomy in 9, 1 and 2 patients, respectively. Another patient with bilateral adrenal adenomas was treated medically following unilateral adrenalectomy. One patient with a cortisol-producing adrenal carcinoma died shortly after operation. One patient with an ACTH-producing pancreatic islet cell tumor died 1 year after initial remission. Adrenalectomy is the logical therapy in adrenal cortisol-producing adenomas. Improved diagnostic and surgical techniques have reduced bilateral adrenalectomy in patients with central Cushing's syndrome to rare cases in which transsphenoidal surgery (71% success rate) is the therapy of choice.

Adolescent↗
PubMed1989

Cushing's syndrome.

Cushing's syndrome remains one of the great diagnostic challenges to internists and endocrinologists. Urologists have the primary role in the treatment of many of the forms of Cushing's syndrome, especially adrenal tumors and micronodular hyperplasia. As we continue to gain experience with Cushing's disease treated with pituitary surgery and with etopic ACTH syndrome and the other forms of Cushing's syndrome, urologists are likely to become even more involved in the therapy of all types of Cushing's syndrome.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Cushing's syndrome.

Cushing's syndrome results from prolonged exposure to excess glucocorticoids. Patients with Cushing's syndrome may develop multiple metabolic problems including obesity, hyperglycemia, hypertension, depression, low bone mass, muscle atrophy, and hypogonadism. Cutaneous manifestations of hypercortisolism include skin atrophy, excessive bruising, purple striations, poor wound healing, facial plethora, vellous hypertrichosis and hirsutism. Diagnostic tests used to screen for Cushing's syndrome include 24-hour urine cortisol, the 1 mg dexamethasone suppresion test, and late night salivary cortisol. A normal screening test excludes the diagnosis of Cushing's. Patients with an abnormal screening test should be referred to an endocrinologist for complete evaluation of the pituitary-adrenal axis.

Cushing Syndrome↗
PubMedDate not supplied

[Psychiatric symptoms in Cushing syndrome: a clinical case].

A patient with Cushing's syndrome presented psyquiatric manifestations that were diagnosed and treated before diagnosis of Cushing's syndrome. These manifestations were unspecific, unstable and they responded to etiologic treatment but they didn't to syntomatic treatment. This case demonstrates the importance to make a through search for organic factors when there are changes in physical appearance and psyquiatric features are changing through the evolution.

Adult↗
PubMed1992

[Occult bronchial carcinoid tumor producing ACTH simulating Cushing's syndrome].

Cushing's Syndrome raises sometimes important diagnostic and therapeutic problems. A case of Cushing's Syndrome is discussed, induced by ectopic secretion of ACTH by a Benign Bronchial Carcinoid Tumor, which due to its clinical features (asymptomatic and invisible to conventional radiology and associated with typical signs of Chronic Hypercortisolism) and biochemical findings (ACTH only slightly raised and suppression with high doses dexamethasone), simulated an hypophyseal origin, the pulmonary tumor being showed only after 3 years of the diagnosis of Cushing's Syndrome.

Adrenocorticotropic Hormone↗
PubMed1983

Peripheral blood steroid levels in Cushing syndrome due to adrenocortical carcinoma or adenoma.

Measurement of the peripheral vein levels of the steroids in the adrenal biosynthetic pathway affords a further possible definitive method of differentiating adrenocortical carcinoma from adrenal adenoma in the presence of Cushing syndrome. In patients with adrenal carcinoma the blood levels of 17-hydroxyprogesterone, testosterone, androstenedione, and dehydroepiandrosterone are far higher than those seen in association with adenoma. In addition, the adrenal cortical carcinoma appears to have a higher ratio of precursors to product in the early part of the biosynthetic path and a lower one in the distal portion than adrenal adenomas. In Cushing syndrome due to adrenal tumor the measurement of serum cortisol is preferably made after chromatographic separation from 11-deoxycortisol in view of the marked cross reactivity in the protein binding procedure.

Adenoma↗
PubMed2006

Evaluation of the cardiovascular risk in patients with subclinical Cushing syndrome before and after surgery.

BACKGROUND: The widespread use of ultrasound, computerized tomography, and magnetic resonance imaging has led to an increase in the number of incidental adrenal masses identified. Asymptomatic incidentally discovered adrenal masses may indicate that subclinical Cushing syndrome (SCS) is not uncommon. We aimed to evaluate the cardiovascular risk of patients with SCS before and after surgery. METHODS: An autonomous cortisol-producing tumor was detected in 11 of 94 patients with adrenal incidentaloma between 1995 and 2005. Twenty-eight patients suffering from classical Cushing syndrome (CS) associated with unilateral adrenocortical adenoma, who were treated at our department in the same period, served as a control group. Cardiovascular risk factors such as blood pressure, body mass index, and lipid profile were evaluated before and 1 year after surgery. RESULTS: The frequency of hypertension (61% versus 63%), obesity (46% versus 55%), diabetes mellitus (50% versus 36%), hypercholesterolemia (39% versus 36%), and low HDL cholesterol (28% versus 36%) were not significantly different between CS and SCS patients, respectively. Adverse cardiovascular risk profile improved 1 year after adrenalectomy in both groups, although the changes were not significant with respect to body mass index, frequency of diabetes, and hyperlipidemia in SCS patients. But frequency of systolic/diastolic hypertension decreased significantly in this group. CONCLUSIONS: These findings indicate that the increased incidence of cardiovascular risk factors commonly observed in classical CS, is also present in SCS. Unilateral adrenalectomy does not always lead to significant improvements in cardiovascular risk profile in SCS.

Adrenal Cortex Neoplasms↗
PubMed1996

[Thymic carcinoid tumor causing paraneoplastic Cushing syndrome. Diagnostic value of double-labelled tomoscintigraphy].

Cushing's syndromes caused by ectopic corticotropin secretion represent 10 to 15% in the causes of Cushing's syndrome. Somatostatin receptor scientigraphy can be successful in the localization of ACTH-secreting neuroendocrine tumors. We report a case of Cushing's syndrome caused by ectopic corticotropin secretion from a thymic carcinoid tumor. Conventional localization techniques failed but the tumor was detected by a double binding thoracic scintigraphy using 111Indium-octreotide and 99mTechnetium-albumine macroagregates.

Adult↗