Table 4.
Causes of secondary hypertriglyceridaemia.
| Causes | Mechanism |
|---|---|
| Obesity, IR, and metabolic syndrome phenotype | Increased production of VLDL due to increased flux of FFA from the expanded adipose tissue mass. |
| Suboptimal diabetes control | Increased VLDL production and reduced chylomicron and VLDL clearance |
| Alcohol | Increased chylomicron and VLDL production, increased lipolysis-free fatty acid fluxes from adipose tissue to the liver |
| Pregnancy | Increased chylomicron and VLDL synthesis, reduced HL and LPL activity, relative IR |
| Chronic renal failure | Downregulation of LPL and LDLR activity |
| Hypothyroidism | Reduced LPL and LDLR activity |
| High-Fat and High-GI food | Increased production of chylomicron and VLDL particles |
| Multiple myeloma | Reduced clearance of TRL particles and reduced function of LPL secondary to paraproteins binding with them |
| SLE | Reduced LPL activity due to endothelial damage and antibodies against LPL |
| Drugs | |
| Thiazide diuretics and beta blockers | Reduced LPL activity |
| Oral Oestrogen, Tamoxifen, Clomiphene | Increased VLDL production |
| Corticosteroids | Increased VLDL production due to IR |
| Protease Inhibitors | Increased VLDL production and reduced LPL activity |
| First- and second-generation antipsychotics and tetracyclic antidepressants | Increased IR and VLDL production and reduced LPL activity |
| Cyclosporin, sirolimus, and everolimus | Increased ApoC3 levels and inhibited LPL |
| Isotretinoin | Increased ApoC3 levels |
| Propofol | Formulated in a 10% oil-in-water lipid emulsion rich in TG and PL and, hence, increased fat delivery |
FFA: free fatty acids; GI: glycaemic index; HL: hepatic lipase; IR: insulin resistance; LDLR: low-density lipoprotein receptor; LPL: lipoprotein lipase; PL: phospholipids; SLE: systemic lupus erythematosus; TRL: triglyceride-rich lipoproteins; VLDL: very-low-density lipoprotein.