1988
DOI: 10.1016/s0002-9343(88)80234-1
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Relationship between corticosteroid exposure and plasma lipid levels in heart transplant recipients

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Cited by 111 publications
(37 citation statements)
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“…[5] Lipid and lipoprotein changes with corticosteroids Dyslipidaemia, hyperglycaemia and hyper tension are the most significant cardiovascular adverse effects resulting from glucocorticoid therapy, [6] but mechanistic insights are incomplete. Documented changes in human lipid profiles on varying doses of prednisone [7][8][9][10] include elevated VLDL, TG and LDL cholesterol, and either increased or decreased HDL cholesterol.…”
Section: Reverse Cholesterol Transportmentioning
confidence: 99%
“…[5] Lipid and lipoprotein changes with corticosteroids Dyslipidaemia, hyperglycaemia and hyper tension are the most significant cardiovascular adverse effects resulting from glucocorticoid therapy, [6] but mechanistic insights are incomplete. Documented changes in human lipid profiles on varying doses of prednisone [7][8][9][10] include elevated VLDL, TG and LDL cholesterol, and either increased or decreased HDL cholesterol.…”
Section: Reverse Cholesterol Transportmentioning
confidence: 99%
“…Sustained glucocorticoid treatment is known to promote hypertension, dyslipidemia, and glucose intolerance. 15 The impact of corticosteroids on the cardiovascular system has been well documented for patients undergoing transplants, 26 as well as for patients with systemic lupus and rheumatoid arthritis. 27,28 Souverein and colleagues 29 recently investigated the risk for CVD and cerebrovascular disease development in a large cohort of patients treated with glucocorticoids.…”
Section: Commentmentioning
confidence: 99%
“…The levels of LDL-cholesterol and triglycerides begin to increase in the second postoperative week and reach a peak around the 3 rd to the 6 th month. Immunosuppressants, mainly cyclosporine and corticosteroids, seem to directly contribute to posttransplantation dyslipidemia [33][34][35][36][37] . Prednisone works by increasing the hepatic production of apolipoprotein B, predisposing the patient to insulin resistance, reducing the activity of the lipoprotein lipase, and decisively contributing to the weight gain observed in patients in the postoperative period 38 .…”
mentioning
confidence: 99%