Lipid abnormalities in patients with adrenal incidentalomas: role of subclinical hypercortisolism and impaired glucose metabolism

Masserini, Benedetta; Morelli, Valentina; Palmieri, Serena; Eller-Vainicher, Cristina; Zhukouskaya, Volha V.; Cairoli, Elisa; Orsi, Emanuela; Beck‐Peccoz, Paolo; Spada, Anna; Chiodini, Iacopo

doi:10.1007/s40618-014-0232-0

Cited by 30 publications

(16 citation statements)

References 27 publications

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“…T2D occurs in roughly one third of patients with SH. However, as expected, there is a high variability between studies, with prevalence of T2D that range from 5% to 69%, which could be explained by several factors, such as the different (28,29). The presence of impaired glucose metabolism, visceral fat accumulation and lipid abnormalities concur to the dysmetabolic frame that is common in patients with SH.…”

Section: Overview Of Associated Co-morbiditiesmentioning

confidence: 65%

Subclinical hypercortisolism: a state, a syndrome, or a disease?

Dalmazi¹,

Pasquali²,

Beuschlein³

et al. 2015

European Journal of Endocrinology

113

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Subclinical hypercortisolism (SH), defined as alterations of the hypothalamus-pituitary-adrenal axis in the absence of clinical signs or symptoms related to cortisol secretion, is a common finding in patients with adrenal incidentalomas. The clinical correlates of this pathological condition have become clearer over the last few years. The aim of this review is to summarize the co-morbidities and the clinical outcomes of patients with SH. According to the analysis of the results of the studies published within the last 15 years, hypertension and type 2 diabetes are a common finding in patients with SH, occurring roughly in 2/3 and 1/3 of the patients respectively. Moreover, several additional cardiovascular and metabolic complications, like endothelial damage, increased visceral fat accumulation and impaired lipid metabolism have been shown to increase the cardiovascular risk of those patients. Accordingly, recent independent reports investigating the natural history of the disease in a long-term follow-up setting have shown that patients with SH have a higher incidence of cardiovascular events and related mortality. Moreover, longitudinal studies have also shown increased incidence of osteoporotic vertebral fractures. Future research is needed to improve the diagnostic performance of hormonal tests, by assessment of the complete steroid profile with more accurate assays, and to define the efficacy of surgical vs medical treatment in a randomizedcontrolled setting.

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Section: Overview Of Associated Co-morbiditiesmentioning

confidence: 65%

Subclinical hypercortisolism: a state, a syndrome, or a disease?

Dalmazi¹,

Pasquali²,

Beuschlein³

et al. 2015

European Journal of Endocrinology

113

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“…However, in a subgroup of sCS patients no significant improvement was observed after adrenalectomy (122). Moreover, in another cohort of adrenal adenoma patients, the occurrence of dyslipidaemia was associated with the presence of impaired glucose metabolism rather than to the subtle cortisol hypersecretion per se (123). Patients undergoing long-term treatment with GCs causing typical Cushingoid fat deposition were demonstrated to have higher LDL and lower HDL cholesterol compared to GC-treated patients without the typical pattern of fat distribution (124).…”

Section: Dyslipidemia In Csmentioning

confidence: 97%

Metabolic comorbidities in Cushing's syndrome

Ferraú

Korbonits

2015

European Journal of Endocrinology

137

119

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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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“…In another retrospective study of 150 patients with AIs, 48.9 % was diagnosed with dyslipidemia [18]. No significant difference in the prevalence of dyslipidemia between those with a cortisol-producing tumor and those with a non-functioning tumor (52.9 vs. 48.5 %, p > 0.05) was found [17], as well as, in a large (n = 338) retrospective study by Masserini et al (40.9 vs. 34.7 %, p = 0.29) [12]. However, Rossi et al found higher prevalence of dyslipidemia in sCS patients compared with those harboring non-functioning adenomas (50 vs. 21 %) [19].…”

Section: Discussionmentioning

confidence: 75%

“…Lipid abnormalities in patients with AIs have been also described, though evidence is limited and a clear lipid profile in relation to AIs has not been recognized. Dyslipidemia in patients with AIs is thought to be associated with subclinical hypercortisolism, though it may also be associated with IR and impaired glucose metabolism (IGM) [12]. In the recent European Society of Endocrinology clinical practice guideline on AIs, dyslipidemia is considered as a comorbidity possibly associated with AIs with ACS, previously known as "subclinical Cushing syndrome" (sCS) [13], though evidence is stronger for T2DM and hypertension.…”

Section: Introductionmentioning

confidence: 99%

Could Lipid Profile be Used as a Marker of Autonomous Cortisol Secretion in Patients with Adrenal Incidentalomas?

et al. 2018

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Adrenal incidentalomas (AIs) have been associated with an increased risk of metabolic syndrome and dyslipidemia, though evidence regarding the latter is limited. Lipid abnormalities in patients with AIs have been associated with subclinical hypercortisolism. The current study aims to test whether lipid profile in patients with AIs predicts "autonomous cortisol secretion" (ACS). Patients with AIs found on either computerized tomography (CT) or magnetic resonance imaging (MRI), were included in a prospective cohort study. All patients were followed up for at least three years. Alterations in their hormonal and lipid profiles were recorded. Ninety-four patients (69 women) harboring 111 AIs were included. There were no differences between patients with ACS and those without, with respect to their baseline lipid profile [total cholesterol, low-density-lipoprotein cholesterol (LDL-C), triglycerides, high-density lipoprotein cholesterol (HDL-C) and non-HDL-C] and blood pressure (systolic and diastolic). Non-HDL-C concentrations decreased over time (Repeated Measures ANOVA, p=0.013), despite patients' body mass index (BMI) remaining unchanged. Logistic regression analysis revealed that the only predictor of ACS was the size of AIs, as calculated by CT or MRI. The current study demonstrated that lipid profile at baseline or during follow-up cannot predict ACS in patients with AIs. However, larger AIs may have a greater probability of ACS.

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Lipid abnormalities in patients with adrenal incidentalomas: role of subclinical hypercortisolism and impaired glucose metabolism

Abstract: In the absence of alterations of glucose metabolism the presence of a subtle cortisol excess has no effect on lipid pattern. IGM seems to influence the lipid metabolism regardless of the presence of SH.

Cited by 30 publications

References 27 publications

Subclinical hypercortisolism: a state, a syndrome, or a disease?

Subclinical hypercortisolism: a state, a syndrome, or a disease?

Metabolic comorbidities in Cushing's syndrome

Could Lipid Profile be Used as a Marker of Autonomous Cortisol Secretion in Patients with Adrenal Incidentalomas?

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