Advances in the epidemiology, pathogenesis, and management of Cushing’s syndrome complications

Arnaldi, Giorgio; Mancini, Tatiana; Tirabassi, Giacomo; Trementino, Laura; Boscaro, Marco

doi:10.1007/bf03345431

Cited by 70 publications

(67 citation statements)

References 171 publications

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“…Chronic hypercortisolism has multiple deleterious effects on growth, and some of them are uncoupled from GH/IGF1 secretion impairment. Indeed, GCs (i) impair gonadal function, mainly via inhibiting gonadotropin secretion and GnRH transcription, but also by interfering with testicular function and sex hormone-binding globulin synthesis in the liver; (ii) exert catabolic actions on bone and muscle; (iii) negatively affect calcium/vitamin D metabolism; and (iv) exert direct inhibitory effects on the growth plate (153,154).…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

Metabolic comorbidities in Cushing's syndrome

Ferraú

Korbonits

2015

European Journal of Endocrinology

143

121

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Cushing's syndrome (CS) patients have increased mortality primarily due to cardiovascular events induced by glucocorticoid (GC) excess-related severe metabolic changes. Glucose metabolism abnormalities are common in CS due to increased gluconeogenesis, disruption of insulin signalling with reduced glucose uptake and disposal of glucose and altered insulin secretion, consequent to the combination of GCs effects on liver, muscle, adipose tissue and pancreas. Dyslipidaemia is a frequent feature in CS as a result of GC-induced increased lipolysis, lipid mobilisation, liponeogenesis and adipogenesis. Protein metabolism is severely affected by GC excess via complex direct and indirect stimulation of protein breakdown and inhibition of protein synthesis, which can lead to muscle loss. CS patients show changes in body composition, with fat redistribution resulting in accumulation of central adipose tissue. Metabolic changes, altered adipokine release, GC-induced heart and vasculature abnormalities, hypertension and atherosclerosis contribute to the increased cardiovascular morbidity and mortality. In paediatric CS patients, the interplay between GC and the GH/IGF1 axis affects growth and body composition, while in adults it further contributes to the metabolic derangement. GC excess has a myriad of deleterious effects and here we attempt to summarise the metabolic comorbidities related to CS and their management in the perspective of reducing the cardiovascular risk and mortality overall.

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Section: European Journal Of Endocrinologymentioning

confidence: 99%

Metabolic comorbidities in Cushing's syndrome

Ferraú

Korbonits

2015

European Journal of Endocrinology

143

121

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“…CS is associated with increased mortality rate compared to general population mainly due to cardiovascular disease, direct consequence of the several comorbidities associated with CS, but also to infectious diseases, and consequent sepsis as result of the immunosuppression induced by hypercortisolism [5][6][7][8][9][10][11][12]. However, the mortality rate seems to be strongly dependent by the disease status.…”

Section: Introductionmentioning

confidence: 99%

The degree of urinary hypercortisolism is not correlated with the severity of cushing’s syndrome

et al. 2016

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Cushing syndrome (CS) is characterized by increased morbidity and mortality compared to the general population. However, there are patients who have more clinical aggressive forms than others. Aim of the study is to evaluate whether the degree of hypercortisolism, defined by the number of times urinary free cortisol (UFC) levels exceed the upper limit of the normal range (ULN), is related to the worsening of phenotypic features, as well as metabolic and cardiovascular parameters, in a cohort of CS patients. A cross-sectional study was conducted on 192 patients with active CS, consecutively presenting at the outpatients' clinic of the University Hospitals of Ancona, Naples, and Palermo. Patients were grouped into mild (UFC not exceeding twice the ULN), moderate (2-5 times the ULN), and severe (more than 5 times the ULN) hypercortisolism. Thirty-seven patients (19.3 %) had mild, 115 (59.8 %) moderate, and 40 (20.9 %) severe hypercortisolism. A significant trend of increase among the three groups was demonstrated for 8-, 16-, and 24-h serum cortisol levels (p \ 0.001) and serum cortisol after low dose of dexamethasone suppression test (p = 0.001). No significant trend of increase was found regarding phenotype and comorbidities. The degree of hypercortisolism by itself does not appear to be a sufficient parameter to express the severity of CS. Therefore, estimating the severity of CS according to biochemical parameters remains a challenge, while the clinical phenotype and the associated comorbidities might be more useful to assessing the severity of the CS.

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“…Diabetes, hypertension, cardiovascular diseases, coagulopathy and hypothyroidism are more frequently seen in CS. [30] These systemic disorders may be associated with pelvic atherosclerosis and cause sexual dysfunction. It is worth to remember that, in our study, nearly 50% of the patients with CS had at least one complication associated with hypercortisolism which could lead to sexual dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Sexual function in women with Cushing’s Syndrome: A controlled study

Keskin

Özkaya

Ortaç

et al. 2018

Turkish Journal of Urology

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Objective: The aim of this study is to determine the severity of female sexual dysfunction (FSD), quality of life, and depression status in female patients with Cushing's syndrome (CS). Material and methods:This study included 29 sexually active women with CS and 30 healthy age and body mass index matched women. The Female Sexual Function Index (FSFI) questionnaire, Beck Depression Inventory (BDI) and Short Form Health Survey (SF-36) were filled by each participant. Plasma levels of FSH, LH, PRL, cortisol, DHEA-S, 17-hydroxyprogesterone, androstenedione, free testosterone, total testosterone and estradiol were measured.Results: Female sexual dysfunction was present in 88.9% of the women with CS and 24.1% of the control group. The CS group showed a lower total FSFI score [16.6 (IQR: 5-23)] compared to the healthy women [26.8 (IQR: 25.5-30.4) (p<0.001)]. The FSFI scores in the arousal, lubrication, orgasm, pain and satisfaction domains were all lower in the women with CS (p<0.001). Both summary scores of the SF-36 were reduced in women with Cushing's syndrome compared to the control group (p=0.001). The BDI scores of patients were significantly higher than those of the control subjects (p=0.007). In patients with CS, levels of LH, estradiol, and DHEA-S04 were significantly lower while cortisol (p<0.05), and 17 hydroxyprogestrone levels were higher than control subjects (p<0.05). Conclusion:This study showed that majority of the women with CS had FSD. This may be related to the inhibitory effect of cortisol on sex hormones.

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Advances in the epidemiology, pathogenesis, and management of Cushing’s syndrome complications

Cited by 70 publications

References 171 publications

Metabolic comorbidities in Cushing's syndrome

Metabolic comorbidities in Cushing's syndrome

The degree of urinary hypercortisolism is not correlated with the severity of cushing’s syndrome

Sexual function in women with Cushing’s Syndrome: A controlled study

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