Manage psychiatric symptoms in Cushing’s syndrome by controlling cortisol levels and usual psychiatric therapy

2017 ◽  
Vol 33 (11) ◽  
pp. 529-534
Author(s):  
2020 ◽  
Vol 26 (4) ◽  
pp. 3443-3448
Author(s):  
Tatyana Telbizova ◽  
◽  
Ivan Aleksandrov ◽  
Mariana Arnaoudova ◽  
◽  
...  

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.


2000 ◽  
pp. 472-476 ◽  
Author(s):  
NA Huizenga ◽  
WW De Herder ◽  
JW Koper ◽  
P de Lange ◽  
D AJ v Lely ◽  
...  

OBJECTIVE: Glucocorticoids (GCs) serve a variety of important functions throughout the body. The synthesis and secretion of GCs are under the strict influence of the hypothalamo-pituitary-adrenal axis. The mechanisms of action of GCs are mediated by the intracellular glucocorticoid receptor (GR). Over the years, many studies have been performed concerning the regulation of GR expression by GC concentrations. METHODS: In the present study, we determined the characteristics of the GR in peripheral mononuclear blood leukocytes (PBML) from thirteen patients with endogenous Cushing's syndrome and fifteen control subjects, using a whole cell dexamethasone binding assay. Furthermore, cortisol concentrations were determined in order to investigate a possible relationship between serum cortisol levels and receptor characteristics. RESULTS: There were no differences in mean receptor number between patients and controls. On the other hand, a significantly lower ligand affinity was identified in cells from patients with Cushing's syndrome compared with controls. A complete normalisation of the ligand affinity was observed after treatment in the only patient tested in this respect, whereas the receptor number was not affected. In patients, there was a statistically significant negative correlation between cortisol concentrations and ligand affinity, which was not found in controls. CONCLUSION: Receptor down-regulation does not occur in PBML from patients with endogenous Cushing's syndrome. On the other hand, there seems to be a diminished ligand affinity which possibly reflects receptor modification in response to exposure to the continuously high cortisol levels in patients with Cushing's syndrome. This assumption is substantiated by the fact that in one patient a normalisation of the ligand affinity after complete remission of the disease was seen.


2013 ◽  
Vol 12 (1) ◽  
pp. 23 ◽  
Author(s):  
Alice Tang ◽  
Anthony J O’Sullivan ◽  
Terry Diamond ◽  
Andrew Gerard ◽  
Peter Campbell

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Ricardo Álvarez Martínez ◽  
Rosa María Tomé Rodríguez ◽  
María Álvarez Ariza ◽  
Carlos Spuch ◽  
Jose M. Olivares

This is a case of a patient affected by Cushing syndrome that was admitted at the hospital due to hormonal problems. He had presented psychiatric symptoms that were mistakenly considered not directly connected to the pathology causing the clinical condition, but a mere psychological reaction to it.


Drugs ◽  
2017 ◽  
Vol 77 (8) ◽  
pp. 829-842 ◽  
Author(s):  
Alicia Santos ◽  
Eugenia Resmini ◽  
Juan Carlos Pascual ◽  
Iris Crespo ◽  
Susan M. Webb

2009 ◽  
Vol 118 (02) ◽  
pp. 133-138 ◽  
Author(s):  
S. Thomson ◽  
G. Koren ◽  
L.-A. Fraser ◽  
M. Rieder ◽  
T. C. Friedman ◽  
...  

2005 ◽  
Vol 153 (2) ◽  
pp. 207-210 ◽  
Author(s):  
A Bhattacharyya ◽  
K Kaushal ◽  
D J Tymms ◽  
J R E Davis

Steroid withdrawal syndrome (SWS) usually refers to relapse of the disease being treated after withdrawal of glucocorticoid therapy, or the symptoms of adrenal insufficiency which occur when glucocorticoids are rapidly reduced or stopped. A less well-recognised form of SWS is that which develops when patients experience a symptom complex similar to that of adrenal insufficiency despite acceptable cortisol levels. We describe three patients who presented with this form of SWS following surgical treatment for endogenous Cushing’s syndrome. All responded well to a short-term increase in the dose of glucocorticoid replacement therapy, with the median duration of the syndrome being 10 months (range 6–10 months). Trough serum cortisol levels above 100 nmol/l, with peaks between 460 and 750 nmol/l were documented in the first two patients at presentation with SWS. It is thought that the syndrome may result from development of tolerance to glucocorticoids, and mediators considered to be important in its development include interleukin-6, corticotrophin-releasing hormone, vasopressin, and central noradrenergic and dopaminergic systems. The exact underlying mechanism for SWS remains unclear. However, with increasing recommendations for use of lower doses of replacement glucocorticoids, its incidence may increase. Physicians need to be aware of this condition, which is self-limiting and easily treated by a temporary increase in the dose of glucocorticoid replacement therapy. It is possible that a slower glucocorticoid tapering regimen than that used in the standard postoperative management of patients undergoing pituitary surgery may reduce the risk of development of SWS.


2010 ◽  
Vol 56 (4) ◽  
pp. 44-51
Author(s):  
E I Marova ◽  
I A Voronkova

The cyclic Cushing's syndrome is a rare disease characterized by multiple episodes of elevated cortisol levels alternating with periods of its normal secretion. The so-called hypercorticism cycles may be either regular or episodic with intercycle intervals as long as a few days to several years. Most researchers agree that the reliable diagnosis of cyclic Cushing's syndrome should be based on laboratory detection of 3 peaks and 2 falls of plasma cortisol level. Cyclic Cushing's syndrome may be either ACTH dependent or independent. A review of 65 verified cases indicates that this condition may be caused by pituitary corticotropinoma (54%), ectopic ACTH-producing tumour (26%), and adrenal tumour (roughly 11%). The cause of the disease remains uncertain in 9% of the patients. Pathophysiological mechanisms of cyclic Cushing's syndrome are poorly known. In certain cases of bilateral macronodular adrenal hyperplasia or adrenal corticosteroma, it may be associated with the presence of ectopic receptors or anomalous expression of normally located receptors. The majority of the patients presenting with cyclic Cushing's syndrome exhibit symptoms of classical hypercorticism that manifest themselves either on a permanent or cyclic basis. In a small number of patients, clinical signs of cyclic Cushing's syndrome are virtually absent. Variations of the clinical picture and conflicting results of hormonal assays taken together make cyclic Cushing's syndrome difficult to diagnose. Therefore, physicians must be aware of this condition and actively search for it in all patients believed to have an enhanced cortisol production despite normal results of laboratory analysis. Frequent changes of urinary or salivary free cortisol levels are reliable and convenient criteria for cyclic Cushing's syndrome in patients suspected to have this condition. Results of cortisol stimulation or suppression tests are likely to lead to a false conclusion due to spontaneous falls and rises in serum cortisol levels at the time of analysis. Given laboratory confirmation of cyclic Cushing's syndrome, subsequent studies should be focused on the elucidation of its cause. The average life expectancy of patients with cyclic Cushing's syndrome remains to be determined.


Author(s):  
Salvatore Cannavò ◽  
Serafinella Patrizia Cannavò

Summary Factitious Cushing’s syndrome (CS) is a very rare form of Münchausen syndrome. Its presentation and course are extremely heterogeneous, and diagnosis is generally challenging. We report the case of a 52-year-old woman who was initially investigated because of the occurrence of cushingoid features. Nevertheless, endocrine work-up showed very low morning plasma ACTH and serum cortisol levels. In addition, it also demonstrated central hypopituitarism and hypogonadotropic hypogonadism. Head MRI showed a small pituitary mass. Based on these results, and probably overlooking the initial clinical suspicion, general practitioner (GP) referred the patient to our Endocrine Unit for hypopituitarism. At inspection, moon face, central obesity, and bruising were evident. Multiple ulcerative skin lesions were also concentrated in the right arm and leg. Dermatology evaluation suggested that the lesions were self-provoked. For several days, the patient denied the assumption of corticosteroids, but we finally discovered that the GP’ nurse had prescribed betamethasone without the GP’s knowledge for about 2 years. In conclusion, the surreptitious assumption of corticosteroids is very rare, but the physicians should be aware that pituitary function could be impaired by high doses of corticosteroids, mimicking hypopituitarism. In these patients, a multidisciplinary approach and environmental investigation can be useful to diagnose factitious CS. Learning points Surreptitious assumption of corticosteroids can cause heterogeneous presentation, ranging from Cushing’s syndrome to multiple hypopituitarism. Suppression of ACTH and cortisol levels in a patient with cushingoid features firstly suggests surreptitious assumption of corticosteroids. A multidisciplinary approach can be extremely useful in patients with suspected factitious Cushing’s syndrome. Sometimes, to prove surreptitious assumption of corticosteroids needs environmental investigation.


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