Journal articles: 'Cushing's syndrome – Treatment'

1

LUFT, ROLF. "The Treatment of Cushing's Syndrome." Acta Medica Scandinavica 124, no. 3 (April 24, 2009): 227–51. http://dx.doi.org/10.1111/j.0954-6820.1946.tb09204.x.

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SARTOR, OLIVER, and GORDON B. CUTLER. "Mifepristone: Treatment of Cushing's Syndrome." Clinical Obstetrics and Gynecology 39, no. 2 (June 1996): 506–10. http://dx.doi.org/10.1097/00003081-199606000-00024.

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MIURA, KIYOSHI. "Medical treatment for Cushing's syndrome." Nihon Naika Gakkai Zasshi 83, no. 9 (1994): 1627–32. http://dx.doi.org/10.2169/naika.83.1627.

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Atkinson, A. B. "The treatment of Cushing's syndrome." Clinical Endocrinology 34, no. 6 (June 1991): 507–13. http://dx.doi.org/10.1111/j.1365-2265.1991.tb00332.x.

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Terzolo, Massimo, Silvia Bovio, Anna Pia, Giangiacomo Osella, Giorgio Borretta, Alberto Angeli, and Giuseppe Reimondo. "Subclinical Cushing's syndrome." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 8 (November 2007): 1272–79. http://dx.doi.org/10.1590/s0004-27302007000800013.

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Subclinical Cushing's syndrome (CS) is attracting increasing interest since the serendipitous discovery of an adrenal mass has become a rather frequent event owing to the routine use of sophisticated radiologic techniques. Cortical adenoma is the most frequent type of adrenal incidentaloma accounting for approximately 50% of cases in surgical series and even greater shares in medical series. Incidentally discovered adrenal adenomas may secrete cortisol in an autonomous manner that is not fully restrained by pituitary feedback, in 5 to 20% of cases depending on study protocols and diagnostic criteria. The criteria for qualifying subclinical cortisol excess are controversial and presently there is no consensus on a gold standard for the diagnosis of this condition. An increased frequency of hypertension, central obesity, impaired glucose tolerance, diabetes and hyperlipemia has been described in patients with subclinical CS; however, there is still no clear demonstration of the long-term complications of this condition whose management remains largely empirical. Either adrenalectomy or careful observation associated with treatment of the metabolic syndrome have been suggested as treatment options.

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Shukla, Lekhansh. "Cushing's Syndrome and Treatment-Resistant Depression." Indian Journal of Psychological Medicine 39, no. 2 (March 2017): 213–14. http://dx.doi.org/10.4103/0253-7176.203114.

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MILLER, JEFFREY W., and LAWRENCE CRAPO. "The Medical Treatment of Cushing's Syndrome." Endocrine Reviews 14, no. 4 (August 1993): 443–58. http://dx.doi.org/10.1210/edrv-14-4-443.

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Rao, D. "Reversible Cardiomyopathy in Cushing Syndrome-A Rare Presentation." Indian Journal of Cardiovascular Disease in Women WINCARS 01, no. 03 (September 2016): 035–38. http://dx.doi.org/10.1055/s-0038-1656478.

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AbstractCushing syndrome (CS) is the result of extended exposure to excessive glucocorticoids from endogenous or exogenous sources. Cushing's syndrome (CS) is associated with reduced life quality and increased mortality, mostly due to cardiovascular disease. We report the case of a 26-year-old female patient who presented with heart failure who was found to have Cushing syndrome and recovered after supportive treatment.

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Pilmis, Benoit, Hélène Coignard-Biehler, Vincent Jullien, Olivier Hermine, Philippe Touraine, Marc Lecuit, and Olivier Lortholary. "Iatrogenic Cushing's Syndrome Induced by Posaconazole." Antimicrobial Agents and Chemotherapy 57, no. 11 (August 26, 2013): 5727–28. http://dx.doi.org/10.1128/aac.00416-13.

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ABSTRACTIatrogenic Cushing's syndrome is an undesirable outcome of glucocorticoids treatment. It can be increased by pharmacologic interactions. Glucocorticoid therapy, given in association with ritonavir, and some azole treatments are causes of iatrogenic Cushing's syndrome. We present a patient with common-variable immunodeficiency who received 7 years of itraconazole therapy for bronchial colonization withAspergillusin combination with inhaled fluticasone without any Cushingoid symptoms. After a switch to posaconazole, the patient developed Cushingoid symptoms.

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B. N., Anil Kumar, and Sandeep Grover. "Cushing's Syndrome Masquerading as Treatment Resistant Depression." Indian Journal of Psychological Medicine 38, no. 3 (May 2016): 246–48. http://dx.doi.org/10.4103/0253-7176.183095.

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Haugen, H. N., and Hugo Jensen. "Diagnosis and Surgical Treatment of Cushing's Syndrome." Acta Medica Scandinavica 168, no. 2 (April 24, 2009): 141–46. http://dx.doi.org/10.1111/j.0954-6820.1960.tb06655.x.

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12

Levitsky, Lynne L. "Cognitive dysfunction following treatment of Cushing's syndrome." Nature Clinical Practice Endocrinology & Metabolism 2, no. 12 (December 2006): 666–67. http://dx.doi.org/10.1038/ncpendmet0344.

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Divers, M. J. "Ketoconazole treatment of Cushing's syndrome in pregnancy." American Journal of Obstetrics and Gynecology 163, no. 3 (September 1990): 1101. http://dx.doi.org/10.1016/0002-9378(90)91159-a.

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Ferriere, Amandine, and Antoine Tabarin. "Cushing's syndrome: Treatment and new therapeutic approaches." Best Practice & Research Clinical Endocrinology & Metabolism 34, no. 2 (March 2020): 101381. http://dx.doi.org/10.1016/j.beem.2020.101381.

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Razenberg, A. J., J. W. F. Elte, A. P. Rietveld, H. C. T. van Zaanen, and M. Castro Cabezas. "A ‘smart’ type of Cushing's syndrome." European Journal of Endocrinology 157, no. 6 (December 2007): 779–81. http://dx.doi.org/10.1530/eje-07-0538.

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Cushing's syndrome results from lengthy and inappropriate exposure to excessive concentrations of either endogenous or exogenous glucocorticoids. This case report describes a patient with a novel type of Cushing's syndrome due to the use of party drugs. A 35-year-old woman had gained 8 kg body weight in 5 months and complained of anxiety. She showed a Cushing-like appearance and mild hypertension (blood pressure, BP 150/95 mmHg). She reported daily use of increasing doses of γ-hydroxybutyric acid (GHB), a popular party drug. ACTH plasma levels were in the upper normal range (41 ng/l), with normal plasma cortisol (0.36 μmol/l). She showed an abnormal overnight 1 mg dexamethasone suppression test (cortisol 0.38 μmol/l). The urinary excretion of free cortisol in 24 h was also increased (0.47 μmol/24 h). CT scanning of the abdomen showed normal adrenals. After stopping GHB intake she lost 7 kg body weight and her BP normalized (BP 135/80 mmHg). GHB is a popular party drug in the Netherlands, but it is also used as a narcotic and for the treatment of narcolepsy. We hypothesize that GHB may bind to the pituitary gland γ-aminobutyric acid-B receptors leading to ACTH overproduction.

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Rizk, Ahmed, Juergen Honegger, Monika Milian, and Tsambika Psaras. "Treatment Options in Cushing's Disease." Clinical Medicine Insights: Oncology 6 (January 2012): CMO.S6198. http://dx.doi.org/10.4137/cmo.s6198.

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Endogenous Cushing's syndrome is a grave disease that requires a multidisciplinary and individualized treatment approach for each patient. Approximately 80% of all patients harbour a corticotroph pituitary adenoma (Cushing's disease) with excessive secretion of adrenocorticotropin-hormone (ACTH) and, consecutively, cortisol. The goals of treatment include normalization of hormone excess, long-term disease control and the reversal of comorbidities caused by the underlying pathology. The treatment of choice is neurosurgical tumour removal of the pituitary adenoma. Second-line treatments include medical therapy, bilateral adrenalectomy and radiation therapy. Drug treatment modalities target at the hypothalamic/pituitary level, the adrenal gland and at the glucocorticoid receptor level and are commonly used in patients in whom surgery has failed. Bilateral adrenalectomy is the second-line treatment for persistent hypercortisolism that offers immediate control of hypercortisolism. However, this treatment option requires a careful individualized evaluation, since it has the disadvantage of permanent hypoadrenalism which requires lifelong glucocorticoid and mineralocorticoid replacement therapy and bears the risk of developing Nelson's syndrome. Although there are some very promising medical therapy options it clearly remains a second-line treatment option. However, there are numerous circumstances where medical management of CD is indicated. Medical therapy is frequently used in cases with severe hypercortisolism before surgery in order to control the metabolic effects and help reduce the anestesiological risk. Additionally, it can help to bridge the time gap until radiotherapy takes effect. The aim of this review is to analyze and present current treatment options in Cushing's disease.

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Dang, Cuong Nguyen, and Peter Trainer. "Pharmacological management of Cushing's syndrome: an update." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 8 (November 2007): 1339–48. http://dx.doi.org/10.1590/s0004-27302007000800020.

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The treatment of choice for Cushing's syndrome remains surgical. The role for medical therapy is twofold. Firstly it is used to control hypercortisolaemia prior to surgery to optimize patient's preoperative state and secondly, it is used where surgery has failed and radiotherapy has not taken effect. The main drugs used inhibit steroidogenesis and include metyrapone, ketoconazole, and mitotane. Drugs targeting the hypothalamic-pituitary axis have been investigated but their roles in clinical practice remain limited although PPAR-gamma agonist and somatostatin analogue som-230 (pasireotide) need further investigation. The only drug acting at the periphery targeting the glucocorticoid receptor remains Mifepristone (RU486). The management of Cushing syndrome may well involve combination therapy acting at different pathways of hypercortisolaemia but monitoring of therapy will remain a challenge.

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Johanssen, Sarah, and Bruno Allolio. "Mifepristone (RU 486) in Cushing's syndrome." European Journal of Endocrinology 157, no. 5 (November 2007): 561–69. http://dx.doi.org/10.1530/eje-07-0458.

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AbstractContextMifepristone (RU 486) blocks the action of cortisol by binding to the glucocorticoid receptor and, therefore, is of potential therapeutic value in Cushing's syndrome. However, research in endogenous hypercortisolism has been hampered by the controversy related to the use of mifepristone for inducing abortion. Currently, new studies are planned to better define the role of RU 486 in Cushing's syndrome. This paper reviews the available evidence concerning the therapeutic effects and adverse events of RU 486 in Cushing's syndrome.Evidence acquisitionOriginal articles and reviews were identified using a PubMed search strategy covering the time period until February 2007.Evidence synthesisTreatment of Cushing's syndrome with mifepristone has been reported in a total of 18 patients, with daily doses ranging from 5 to 30 mg/kg. Case reports indicate that the mifepristone-induced receptor blockade may lead to significant clinical improvement in patients with Cushing's syndrome in whom surgery and inhibitors of adrenal steroidogenesis fail to control hypercortisolism. Due to its rapid onset of action, mifepristone may be particularly useful in acute crises, e.g. in cortisol-induced psychosis. Side effects include adrenal insufficiency and, as a result of its antiprogestin action, endometrial hyperplasia in long-term treatment. Adrenal insufficiency can be assessed only by careful clinical evaluation, as the hormonal parameters are not reliable during receptor blockade, and is rapidly reversed by exogenous dexamethasone. Well-designed larger clinical trials are needed to better assess the value of this interesting drug in the treatment of Cushing's syndrome.

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19

Reincke, Martin, Katrin Ritzel, Andrea Oßwald, Christina Berr, Günter Stalla, Klaus Hallfeldt, Nicole Reisch, Jochen Schopohl, and Felix Beuschlein. "A critical reappraisal of bilateral adrenalectomy for ACTH-dependent Cushing's syndrome." European Journal of Endocrinology 173, no. 4 (October 2015): M23—M32. http://dx.doi.org/10.1530/eje-15-0265.

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ObjectiveOur aim was to review short- and long-term outcomes of patients treated with bilateral adrenalectomy (BADx) in ACTH-dependent Cushing's syndrome.MethodsWe reviewed the literature and analysed our experience with 53 patients treated with BADx since 1990 in our institution.ResultsBADx is considered if ACTH-dependent Cushing's syndrome is refractory to other treatment modalities. In Cushing's disease (CD), BADx is mainly used as an ultima ratio after transsphenoidal surgery and medical therapies have failed. In these cases, the time span between the first diagnosis of CD and treatment with BADx is relatively long (median 44 months). In ectopic Cushing's syndrome, the time from diagnosis to BADx is shorter (median 2 months), and BADx is often performed as an emergency procedure because of life-threatening complications of severe hypercortisolism. In both situations, BADx is relatively safe (median surgical morbidity 15%; median surgical mortality 3%) and provides excellent control of hypercortisolism; Cushing's-associated signs and symptoms are rapidly corrected, and co-morbidities are stabilised. In CD, the quality of life following BADx is rapidly improving, and long-term mortality is low. Specific long-term complications include the development of adrenal crisis and Nelson's syndrome. In ectopic Cushing's syndrome, long-term mortality is high but is mostly dependent on the prognosis of the underlying malignant neuroendocrine tumour.ConclusionBADx is a relatively safe and highly effective treatment, and it provides adequate control of long-term co-morbidities associated with hypercortisolism.

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20

Chan, Li F., Helen L. Storr, Ashley B. Grossman, and Martin O. Savage. "Pediatric Cushing's syndrome: clinical features, diagnosis, and treatment." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 8 (November 2007): 1261–71. http://dx.doi.org/10.1590/s0004-27302007000800012.

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Cushing's syndrome (CS) results from prolonged exposure to supraphysiological levels of circulating glucocorticoids, endogenously or exogenously derived. Although rare in childhood, CS remains a difficult condition to diagnose and treat. A multidisciplinary approach and close collaboration with adult colleagues is adopted at most large centres that manage pediatric CS patients. Although pediatric protocols are derived from adult data, significant differences exist between adult and childhood CS. Furthermore, long term outcome parameters including final height, bone mineral density, reproductive function, body composition and psychological health pose challenges for pediatric care. This article will aim to provide an overall view of pediatric CS highlighting some of the differences between adult and pediatric CS.

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Labeur, M., E. Arzt, G. K. Stalla, and M. Paez-Pereda. "New Perspectives in the Treatment of Cushing's Syndrome." Current Drug Targets - Immune, Endocrine & Metabolic Disorders 4, no. 4 (December 1, 2004): 335–42. http://dx.doi.org/10.2174/1568008043339703.

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22

Doppman, JL, EH Oldfield, GP Chrousos, L. Nieman, R. Udelsman, GB Cutler, and DL Loriaux. "Rebound thymic hyperplasia after treatment of Cushing's syndrome." American Journal of Roentgenology 147, no. 6 (December 1986): 1145–47. http://dx.doi.org/10.2214/ajr.147.6.1145.

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23

Feelders, Richard A., John Newell-Price, Rosario Pivonello, Lynnette K. Nieman, Leo J. Hofland, and Andre Lacroix. "Advances in the medical treatment of Cushing's syndrome." Lancet Diabetes & Endocrinology 7, no. 4 (April 2019): 300–312. http://dx.doi.org/10.1016/s2213-8587(18)30155-4.

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Choi, Y. J., M. S. Lee, and Y. S. Chung. "P5 Growth hormone treatment for iatrogenic Cushing's syndrome." Growth Hormone & IGF Research 20 (January 2010): S41. http://dx.doi.org/10.1016/s1096-6374(10)70105-2.

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25

Hughes, Lissett, and Shalet. "Growth hormone status following treatment for Cushing's syndrome." Clinical Endocrinology 51, no. 1 (July 1999): 61–66. http://dx.doi.org/10.1046/j.1365-2265.1999.00738.x.

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26

Munoz, M. C., F. Doreste, O. Ferrer, J. Gonzalez, and J. A. Montoya. "Pergolide treatment for Cushing's syndrome in a horse." Veterinary Record 139, no. 2 (July 13, 1996): 41–43. http://dx.doi.org/10.1136/vr.139.2.41.

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van der Pas, R., F. W. G. Leebeek, L. J. Hofland, W. W. de Herder, and R. A. Feelders. "Hypercoagulability in Cushing's syndrome: prevalence, pathogenesis and treatment." Clinical Endocrinology 78, no. 4 (March 12, 2013): 481–88. http://dx.doi.org/10.1111/cen.12094.

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Schteingart, David E. "Drugs in the medical treatment of Cushing's syndrome." Expert Opinion on Emerging Drugs 14, no. 4 (November 26, 2009): 661–71. http://dx.doi.org/10.1517/14728210903413522.

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Fleseriu, Maria, Richard J. Auchus, Rosario Pivonello, Roberto Salvatori, Sabina Zacharieva, and Beverly M. K. Biller. "Levoketoconazole: a novel treatment for endogenous Cushing's syndrome." Expert Review of Endocrinology & Metabolism 16, no. 4 (July 4, 2021): 159–74. http://dx.doi.org/10.1080/17446651.2021.1945440.

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Vilar, Lucio, Maria da Conceição Freitas, Lúcia Helena C. Lima, Ruy Lyra, and Claudio E. Kater. "Cushing's syndrome in pregnancy: an overview." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 8 (November 2007): 1293–302. http://dx.doi.org/10.1590/s0004-27302007000800015.

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Cushing's syndrome (CS) during pregnancy is a rare condition with fewer than 150 cases reported in the literature. Adrenal adenomas were found to be the commonest cause, followed by Cushing's disease. The gestation dramatically affects the maternal hypothalamic-pituitary-adrenal axis, resulting in increased hepatic production of corticosteroid-binding globulin (CBG), increased levels of serum, salivary and urinary free cortisol, lack of suppression of cortisol levels after dexamethasone administration and placental production of CRH and ACTH. Moreover, a blunted response of ACTH and cortisol to exogenous CRH may also occur. Therefore, the diagnosis of CS during pregnancy is much more difficult. Misdiagnosis of CS is also common, as the syndrome may be easily confused with preeclampsia or gestational diabetes. Because CS during pregnancy is usually associated with severe maternal and fetal complications, its early diagnosis and treatment are critical. Surgery is the treatment of choice for CS in pregnancy, except perhaps in the late third trimester, with medical therapy being a second choice. There does not seem to be a rationale for supportive treatment alone.

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Pivonello, Rosario, Monica De Leo, Alessia Cozzolino, and Annamaria Colao. "The Treatment of Cushing's Disease." Endocrine Reviews 36, no. 4 (August 1, 2015): 385–486. http://dx.doi.org/10.1210/er.2013-1048.

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Abstract Cushing's disease (CD), or pituitary-dependent Cushing's syndrome, is a severe endocrine disease caused by a corticotroph pituitary tumor and associated with increased morbidity and mortality. The first-line treatment for CD is pituitary surgery, which is followed by disease remission in around 78% and relapse in around 13% of patients during the 10-year period after surgery, so that nearly one third of patients experience in the long-term a failure of surgery and require an additional second-line treatment. Patients with persistent or recurrent CD require additional treatments, including pituitary radiotherapy, adrenal surgery, and/or medical therapy. Pituitary radiotherapy is effective in controlling cortisol excess in a large percentage of patients, but it is associated with a considerable risk of hypopituitarism. Adrenal surgery is followed by a rapid and definitive control of cortisol excess in nearly all patients, but it induces adrenal insufficiency. Medical therapy has recently acquired a more important role compared to the past, due to the recent employment of novel compounds able to control cortisol secretion or action. Currently, medical therapy is used as a presurgical treatment, particularly for severe disease; or as postsurgical treatment, in cases of failure or incomplete surgical tumor resection; or as bridging therapy before, during, and after radiotherapy while waiting for disease control; or, in selected cases, as primary therapy, mainly when surgery is not an option. The adrenal-directed drug ketoconazole is the most commonly used drug, mainly because of its rapid action, whereas the glucocorticoid receptor antagonist, mifepristone, is highly effective in controlling clinical comorbidities, mainly glucose intolerance, thus being a useful treatment for CD when it is associated with diabetes mellitus. Pituitary-directed drugs have the advantage of acting at the site responsible for CD, the pituitary tumor. Among this group of drugs, the dopamine agonist cabergoline and the somatostatin analog pasireotide result in disease remission in a consistent subgroup of patients with CD. Recently, pasireotide has been approved for the treatment of CD when surgery has failed or when surgery is not an option, and mifepristone has been approved for the treatment of Cushing's syndrome when associated with impairment of glucose metabolism in case of the lack of a surgical indication. Recent experience suggests that the combination of different drugs may be able to control cortisol excess in a great majority of patients with CD.

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Schott, H. C. "Treatment of pituitary pars intermedia dysfunction (classical Cushing's disease) and metabolic syndrome (peripheral Cushing's syndrome) in horses." Veterinary Dermatology 15, s1 (August 2004): 10. http://dx.doi.org/10.1111/j.1365-3164.2004.00410_2-7.x.

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Albiger, Nora Maria Elvira, Carla M. Scaroni, and Franco Mantero. "Cyclic Cushing's syndrome: an overview." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 8 (November 2007): 1253–60. http://dx.doi.org/10.1590/s0004-27302007000800011.

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Cyclic Cushing's syndrome (CS) is a disorder in which glucocorticoid levels are alternately normal and high, the latter occurring in episodes that can last from a few days to several months. It is more common in children than in adults. Cyclic CS may be either of the two different forms of CS (ACTH-dependent or -independent CS). Clinically, it may present with one or many symptoms, depending on the duration of disease activity and the timing of the fluctuations. A serotoninergic influence, cyclic changes in central dopaminergic tone, spontaneous episodic hemorrhage in the tumor, and the action of inflammatory cytokines with antitumor properties are some of the mechanisms suggested to explain the physiopathology of this phenomenon but the exact mechanism remains to be clarified. The cyclic pattern of hypercortisolism can delay the final diagnosis of CS and make it difficult to interpret the results of dynamic tests. Patients may have paradoxical responses to dexamethasone that can reflect increasing or decreasing levels of endogenous activity. Hormone assessments have to be repeated periodically when a diagnosis of CS is suspected. The cyclic pattern can also interfere with medical treatment because patients may show unexpected clinical and biochemical signs of hypocortisolism when cortisol secretion cyclically returns to normal, so an accurate follow-up is mandatory in these patients.

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Telbizova, Tatyana, Ivan Aleksandrov, and Mariana Arnaoudova. "DYNAMICS OF PSYCHIATRIC SYMPTOMS IN CUSHING’S SYNDROME." Journal of IMAB - Annual Proceeding (Scientific Papers) 26, no. 4 (November 19, 2020): 3443–48. http://dx.doi.org/10.5272/jimab.2020264.3443.

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Cushing’s syndrome may present with various psychiatric disorders which can lead to a misdiagnosis at the beginning, deterioration of the course of the disease and life-threatening complications. The most common psychiatric disorder is atypical depression. During the initial stages of the disease, the somatic symptoms of Cushing’s syndrome can be subtle, difficult to identify, especially when the psychiatric symptoms are dominant. Objective: The aim of the present article is to report a case of a 24-year-old woman with a Cushing’s syndrome, caused by the adrenal adenoma. The onset of the disease is a suicidal attempt. Family history is significant for psychiatry disorder. The belated diagnosis led to somatic and psychiatry complications of the disease – sepsis and persisting high suicidal risk. The dynamic change in the patient’s mental state – from a severe depressive episode with atypical symptoms to psychosis with single catatonic symptoms – correlated well with the gradual increase of the plasma cortisol levels. The antidepressant and subsequent antipsychotic medication turned out to be ineffective. The surgical treatment, followed by a normalization of the cortisol levels was a key to the successful outcome and the reduction of self-aggression risk. Conclusion: The early diagnosis and timely treatment of Cushing’s syndrome decrease the risk of multiple complications. The shift from atypical depression to psychosis with catatonic symptoms correlates with the worsening of the hormonal imbalance. The signs of atypical depression in Cushing's syndrome, resistant to the antidepressant medication, could be considered as relatively specific symptoms, guiding specialists to its somatogenic origin for the proper diagnosis.

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Soszynski, P., J. Slowinska-Srzednicka, A. Kasperlik-Zaluska, and S. Zgliczynski. "Endogenous natriuretic factors: atrial natriuretic hormone and digitalis-like substance in Cushing's syndrome." Journal of Endocrinology 129, no. 3 (June 1991): 453–58. http://dx.doi.org/10.1677/joe.0.1290453.

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ABSTRACT In order to investigate the effect of chronic hypercortisolaemia on endogenous natriuretic factors (atrial natriuretic hormone (ANH) and the Na+/K+ pump inhibitor) digitalis-like substance (DLS), and their relation to hypertension, 28 patients with pituitary-or adrenal-dependent Cushing's syndrome and six patients on high-dose prednisone treatment were studied. Plasma ANH levels were increased in patients with Cushing's syndrome (36·0±1·4 (s.e.m.) ng/l) compared with those in healthy controls (28·6±1·3 ng/l, P <0·01). In prednisone-treated patients, ANH levels (43·8±4·5 ng/l) were higher than those in patients with Cushing's syndrome and in controls (P <0·05 and P <0·01 respectively). DLS measured by radioimmunoassay and binding of [3H]ouabain to erythrocytes was not altered in patients with hypercortisolaemia. Slightly decreased DLS activity in the erythrocyte 86Rb uptake inhibition assay was found in patients with Cushing's syndrome (52·9±2·7%) compared with that in controls (60·9±1·8%, P <0·02). With the exception of cortisol (r = 0·52, P<0·01), none of the other factors determined correlated with the mean arterial pressure in patients with Cushing's syndrome. Thus, a chronic excess of endogenous and exogenous glucocorticoids increases plasma levels of ANH, but does not substantially influence DLS activity or plasma levels. Neither natriuretic factor is directly related to hypertension in Cushing's syndrome. Journal of Endocrinology (1991) 129, 453–458

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36

Pivonello, Rosario, Maria Cristina De Martino, Monica De Leo, Libuse Tauchmanovà, Antongiulio Faggiano, Gaetano Lombardi, and Annamaria Colao. "Cushing's syndrome: aftermath of the cure." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 8 (November 2007): 1381–91. http://dx.doi.org/10.1590/s0004-27302007000800025.

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Cushing's syndrome (CS) is a chronic and systemic disease caused by endogenous or exogenous hypercortisolism, associated with an increase of mortality rate due to the clinical consequences of glucocorticoid excess, especially cardiovascular diseases. After cure, usually obtained by the surgical removal of the tumor responsible for the disease, the normalization of cortisol secretion is not constantly followed by the recovery of the clinical complications developed during the active disease, and it is often followed by the development of novel clinical manifestations induced by the fall of cortisol levels. These evidences were mostly documented in patients with pituitary-dependent CS, after surgical resection of the pituitary tumor. Indeed, despite an improvement of the mortality rate, metabolic syndrome and the consequent cardiovascular risk have been found to partially persist after disease remission, strictly correlated to the insulin resistance. Skeletal diseases, mainly osteoporosis, improve after normalization of cortisol levels but require a long period of time or the use of specific treatment, mainly bisphosphonates, to reach the normalization of bone mass. A relevant improvement or resolution of mental disturbances has been described in patients cured from CS, although in several cases, cognitive decline persisted and psychological or psychiatric improvement was erratic, delayed, or incomplete. On the other hand, development or exacerbation of autoimmune disorders, mainly thyroid autoimmune diseases, was documented in predisposed patients with CS after disease remission. The totality of these complications persisting or occurring after successful treatment contribute to the impairment of quality of life registered in patients with CS after disease cure.

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van der Pas, R., W. W. de Herder, L. J. Hofland, and R. A. Feelders. "New developments in the medical treatment of Cushing's syndrome." Endocrine-Related Cancer 19, no. 6 (August 30, 2012): R205—R223. http://dx.doi.org/10.1530/erc-12-0191.

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Cushing's syndrome (CS) is a severe endocrine disorder characterized by chronic cortisol excess due to an ACTH-secreting pituitary adenoma, ectopic ACTH production, or a cortisol-producing adrenal neoplasia. Regardless of the underlying cause, untreated CS is associated with considerable morbidity and mortality. Surgery is the primary therapy for all causes of CS, but surgical failure and ineligibility of the patient to undergo surgery necessitate alternative treatment modalities. The role of medical therapy in CS has been limited because of lack of efficacy or intolerability. In recent years, however, new targets for medical therapy have been identified, both at the level of the pituitary gland (e.g. somatostatin, dopamine, and epidermal growth factor receptors) and the adrenal gland (ectopically expressed receptors in ACTH-independent macronodular adrenal hyperplasia). In this review, results of preclinical and clinical studies with drugs that exert their action through these molecular targets, as well as already established medical treatment options, will be discussed.

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Ludlam, W. H. "Treatment of Adrenocorticotropin-Dependent Cushing's Syndrome: A Consensus Statement." Yearbook of Endocrinology 2008 (January 2008): 336–37. http://dx.doi.org/10.1016/s0084-3741(08)79081-4.

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Forget, Hélène, André Lacroix, and Henri Cohen. "Persistent cognitive impairment following surgical treatment of Cushing's syndrome." Psychoneuroendocrinology 27, no. 3 (April 2002): 367–83. http://dx.doi.org/10.1016/s0306-4530(01)00059-2.

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Tsigos, Constantine, Dimitris A. Papanicolaou, and George P. Chrousos. "Advances in the diagnosis and treatment of Cushing's syndrome." Baillière's Clinical Endocrinology and Metabolism 9, no. 2 (April 1995): 315–36. http://dx.doi.org/10.1016/s0950-351x(95)80354-8.

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Iacobone, M., M. Citton, M. Scarpa, G. Viel, M. Boscaro, and D. Nitti. "Systematic review of surgical treatment of subclinical Cushing's syndrome." British Journal of Surgery 102, no. 4 (February 2, 2015): 318–30. http://dx.doi.org/10.1002/bjs.9742.

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BEVAN, J. S., M. H. GOUGH, M. D. G. GILLMER, and C. W. BURKE. "CUSHING'S SYNDROME IN PREGNANCY: THE TIMING OF DEFINITIVE TREATMENT." Clinical Endocrinology 27, no. 2 (August 1987): 225–33. http://dx.doi.org/10.1111/j.1365-2265.1987.tb01148.x.

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Sonino, Nicoletta, Marco Boscaro, Agostino Paoletta, Franco Mantero, and Donato Zillotto. "Ketoconazole treatment in Cushing's syndrome: experience in 34 patients." Clinical Endocrinology 35, no. 4 (October 1991): 347–52. http://dx.doi.org/10.1111/j.1365-2265.1991.tb03547.x.

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Ramalingam, Sundhar, Adva Eisenberg, Wen Chi Foo, Jennifer Freedman, Andrew J. Armstrong, Larry G. Moss, and Michael R. Harrison. "Treatment-related neuroendocrine prostate cancer resulting in Cushing's syndrome." International Journal of Urology 23, no. 12 (October 21, 2016): 1038–41. http://dx.doi.org/10.1111/iju.13225.

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Morcos, M., B. Fohr, J. Tafel, F. Pfisterer, A. Hamann, P. Humpert, H. Bode, et al. "Long-Term Treatment of Central Cushing's Syndrome with Rosiglitazone." Experimental and Clinical Endocrinology & Diabetes 115, no. 05 (May 21, 2007): 292–97. http://dx.doi.org/10.1055/s-2007-970162.

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Amado, J. A., C. Pesquera, E. M. Gonzalez, M. Otero, J. Freijanes, and A. Alvarez. "Successful treatment with ketoconazole of Cushing's syndrome in pregnancy." Postgraduate Medical Journal 66, no. 773 (March 1, 1990): 221–23. http://dx.doi.org/10.1136/pgmj.66.773.221.

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Banerjee, R. R., N. Marina, L. Katznelson, and B. J. Feldman. "Mifepristone Treatment of Cushing's Syndrome in a Pediatric Patient." PEDIATRICS 136, no. 5 (October 12, 2015): e1377-e1381. http://dx.doi.org/10.1542/peds.2015-0684.

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Fallo, F. "Effect of surgical treatment on hypertension in Cushing's syndrome." American Journal of Hypertension 9, no. 1 (January 1996): 77–80. http://dx.doi.org/10.1016/0895-7061(95)00299-5.

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Preda, Veronica A., Jonathan Sen, Niki Karavitaki, and Ashley B. Grossman. "THERAPY IN ENDOCRINE DISEASE: Etomidate in the management of hypercortisolaemia in Cushing's syndrome: a review." European Journal of Endocrinology 167, no. 2 (August 2012): 137–43. http://dx.doi.org/10.1530/eje-12-0274.

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Abstract:

This review addresses the practical usage of intravenous etomidate as a medical therapy in Cushing's syndrome. We reviewed the relevant literature, using search terms ‘etomidate’, ‘Cushing's syndrome’, ‘adrenocortical hyperfunction’, ‘drug therapy’ and ‘hypercortisolaemia’ in a series of public databases. There is a paucity of large randomised controlled trials, and data on its use rely only on small series, case study reports and international consensus guideline recommendations. Based on these, etomidate is an effective parenteral medication for the management of endogenous hypercortisolaemia, particularly in cases with significant biochemical disturbance, sepsis and other serious complications such as severe psychosis, as well as in preoperative instability. We suggest treatment protocols for the safe and effective use of etomidate in Cushing's syndrome.

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Munir, Alia, and John Newell-Price. "Nelson's Syndrome." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 8 (November 2007): 1392–96. http://dx.doi.org/10.1590/s0004-27302007000800026.

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Nelson's syndrome is a potentially severe complication of bilateral adrenalectomy performed in the treatment of Cushing's disease, and its management remains difficult. Of all of the features of Nelson's syndrome, the one that causes most concern is the development of a locally aggressive pituitary tumour, which, unusually for pituitary disease, may occasionally cause death from the tumour itself. This feature is especially pertinent given the increasing use in Cushing's disease of laparoscopic bilateral adrenal surgery as a highly effective treatment modality to control cortisol-excess. Despite numerous studies and reports, there is no formal consensus of what defines Nelson's syndrome. Thus, some will define Nelson's syndrome according to the classical description with an evolving pituitary mass after bilateral adrenalectomy, whereas others will rely on increasing plasma ACTH levels, even in the absence of a clear pituitary mass lesion on MRI. These factors need to be borne in mind when considering the reports of Nelson's syndrome, as there is great heterogeneity, and it is likely that overall the modern 'Nelson's syndrome' represents a different disease entity from that of the last century. In the present paper, clinical and epidemiological features of Nelson's syndrome, as well as its treatment modalities, are reviewed.

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Journal articles on the topic 'Cushing's syndrome – Treatment'

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