Glucocorticoid use and serum lipid levels in US adults: The third national health and nutrition examination survey

Choi, Hyon K.; Seeger, John D.

doi:10.1002/art.21329

Cited by 66 publications

(33 citation statements)

References 27 publications

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“…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). In contrast, another study addressing the effects of exogenous GC treatment showed no association between GC use and dyslipidaemia, and unusually, an increased HDL cholesterol level was found in patients treated with GCs who were above 60 years old (125).…”

Section: Dyslipidemia In Csmentioning

confidence: 94%

Metabolic comorbidities in Cushing's syndrome

Ferraú

Korbonits

2015

European Journal of Endocrinology

147

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: Dyslipidemia In Csmentioning

confidence: 94%

Metabolic comorbidities in Cushing's syndrome

Ferraú

Korbonits

2015

European Journal of Endocrinology

147

121

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“…[20] In the third National Health and Nutrition Examination Survey, gluco corticoid use was associated with higher HDL and lower TC/HDL cholesterol ratios. [21] Both glucocorticoid use and endogenous hypercortisolism (Cushing's disease) resulted in elevated TC and LDL cholesterol. Glucocorticoid replacement in hypopituitary patients lowered VLDL, LDL cholesterol, LCAT and CETP.…”

Section: Human Studies With Glucocorticoidsmentioning

confidence: 99%

The influence of glucocorticoids on lipid and lipoprotein metabolism and atherosclerosis

Ross

Marais

2014

S Afr Med J

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Lipoproteins transport lipids in the circulation in four major pathways: (i) a postprandial (exogenous) pathway for chylomicrons; (ii) an endogenous pathway involving very-low-density lipoprotein (VLDL) for triglyceride (TG) transport from the liver; (iii) a lowdensity lipoprotein (LDL) pathway from a proportion of VLDL as a source of cholesterol for cells; and (iv) a reverse cholesterol transport pathway by high-density lipoprotein (HDL).[1] These pathways and the reported effects of glucocorticoids are shown in Fig. 1. Exogenous TG pathwayChylomicrons, comprising 85 -90% TG and containing apolipoprotein B (apo B)-48 (apoB48), apolipoprotein Ai (apoAi) and apolipoprotein Aiv (apoAiv), are produced in enterocytes, traverse the thoracic duct and ultimately reach the systemic circulation. Lipoprotein lipase anchored on cells by heparan sulphate proteoglycans hydrolyses TG at the vascular endothelium, yielding non-esterified fatty acids (NEFAs) and remnants, proportionately richer in cholesterol esters. Chylomicron remnants are rapidly cleared by liver remnant receptors, [2] as a result of apolipoprotein E (apoE) acquired in the circulation. Dietary fat restriction will have a significant impact on severe hypertriglyceridaemia.

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“…Although the literature supports the development of these potentially harmful effects with high-dose glucocorticoid therapy, it has been recognized that there is no firm evidence linking low-dose therapy and CVD in the RA population (7,8). On the contrary, recent studies have suggested that low-dose glucocorticoid treatment is associated with potentially beneficial effects on the cardiovascular (CV) system, such as improvements in the lipid profile (9)(10)(11) as well as insulin sensitivity (12,13). Another recent study demonstrated both favorable and unfavorable effects of glucocorticoids on CV biomarkers (14).…”

mentioning

confidence: 99%

Glucocorticoids and cardiovascular events in rheumatoid arthritis: A population‐based cohort study

Davis¹,

Kremers²,

Crowson³

et al. 2007

Arthritis & Rheumatism

220

122

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Objective. To determine the relationship between glucocorticoid exposure and cardiovascular (CV) events in patients with rheumatoid arthritis (RA).Methods. A total of 603 adult residents of Rochester, Minnesota with incident RA between 1955 and 1995 were followed up through their medical records for a median of 13 years (total of 9,066 person-years). Glucocorticoid exposure was defined 3 ways: tertiles of cumulative exposure; recent use (<3 months) versus past use (>3 months); and average daily dosage (<7.5 mg/day or >7.5 mg/day). CV events, including myocardial infarction, heart failure, and death from CV causes, were defined according to validated criteria. Cox regression models were adjusted for demographic features, CV risk factors, and RA characteristics.Results. Rheumatoid factor (RF)-negative patients with exposure to glucocorticoids were not at increased risk of CV events, irrespective of the glucocorticoid dosage or timing of use, as compared with the reference group of RF-negative patients who had never been exposed to glucocorticoids. In contrast, RFpositive patients were at increased risk of CV events, particularly with higher cumulative exposure, higher average daily dosage, and recent use of glucocorticoids. RF-positive patients with high cumulative exposure to glucocorticoids had a 3-fold increased risk of CV events (hazard ratio 3.06 [95% confidence interval 1.81-5.18]), whereas RF-negative patients with high cumulative exposure were not at increased risk (hazard ratio 0.85 [95% confidence interval 0.39-1.87]).Conclusion. RF-positive but not RF-negative patients were at increased risk of CV events following exposure to glucocorticoids. These findings suggest that glucocorticoids interact with RF status to modulate the occurrence of CV events in patients with RA. The mechanisms underlying this interaction are unknown and should be the subject of further research.

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Glucocorticoid use and serum lipid levels in US adults: The third national health and nutrition examination survey

Cited by 66 publications

References 27 publications

Metabolic comorbidities in Cushing's syndrome

Metabolic comorbidities in Cushing's syndrome

The influence of glucocorticoids on lipid and lipoprotein metabolism and atherosclerosis

Glucocorticoids and cardiovascular events in rheumatoid arthritis: A population‐based cohort study

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