Dyslipidemia in Transplant Patients: Which Therapy?

Abstract

Cardiovascular disease is the most important cause of death worldwide in recent years; an increasing trend is also shown in organ transplant patients subjected to immunosuppressive therapies, in which cardiovascular diseases represent one of the most frequent causes of long-term mortality. This is also linked to immunosuppressant-induced dyslipidemia, which occurs in 27 to 71% of organ transplant recipients. The aim of this review is to clarify the pathophysiological mechanisms underlying dyslipidemia in patients treated with immunosuppressants to identify immunosuppressive therapies which do not cause dyslipidemia or therapeutic pathways effective in reducing hypercholesterolemia, hypertriglyceridemia, or both, without further adverse events.

Managing dyslipidemia in solid organ transplant patients

“…Immunosuppressor-mediated dyslipidaemia is characterised by an increase in LDL cholesterol, VLDL cholesterol, and/or an increase in total plasma triglycerides, mainly VLDL triglycerides. 9 , 10 …”

Haematological Drugs Affecting Lipid Metabolism and Vascular Health

“…Despite optimal therapy for dyslipidaemia, many patients (up to 50%) with hyperlipidaemia after mTOR inhibitors therapy do not achieve the cholesterol and triglyceride concentrations recommended by the most prestigious scientific societies. However, the treatment of transplant patients with drug-induced dyslipidaemia was addressed in a recent review [ 81 ]. The other side of the coin is the protective role played by some mTOR inhibitors against atherosclerosis and thrombosis.…”

Lipid management to mitigate poorer postkidney transplant outcomes

“…Data from [8,9,14 ▪ ,15,16,25,26]. ACC, acetyl-coenzyme A carboxylase; HMG-CoA, 3-hydroxy-3-methylglutaryl-coenzyme; LDL, low-density lipoprotein; MAPK, mitogen-activated protein kinase.…”

“…The mechanism of CNI-induced dyslipidemia is somewhat similar to the corticosteroid. CNIs increase FFA formation by enhancing hepatic lipoprotein synthesis in combination with diminishing LPL activity for clearance of circulating triglycerides, particularly from VLDL [14 ▪ ]. The effect on hypercholesterolemia is mediated through lowering bile acid formation and inhibiting mitochondrial 27-hydroxylase (CYP27A1), but the activity of HMG-CoA reductase sustainably increases [15].…”