| Diabetes |
Common contributor to dyslipidemia. Abnormal lipids are seldom normalized by glycemic control alone. |
| Hypothyroidism |
Thyroid hormone regulates multiple steps in lipid metabolism including LDL receptor expression and LPL activity. |
| Alcohol |
Can cause hypertriglyceridemia in susceptible patients but mild intake linked to decreased risk of vascular disease. |
| Renal disease |
Increased LDL in nephrotic syndrome, hypertriglyceridemia in end-stage renal disease. |
| Obstructive liver disease |
Can be associated with very high cholesterol levels. Some evidence that diseases such as primary biliary cirrhosis not associated with increased vascular events despite dyslipidemia. |
| Diuretics |
Increased LDL with high doses. Current practice of using low doses of thiazides decreases vascular events and has minimal effect on lipids. |
| β-Adrenergic receptor blockers |
Increased triglycerides/decreased HDL probably by inhibiting LPL. |
| Anabolic steroids |
Can result in very low HDL (<10 mg/dL). |
| Estrogens |
Exacerbate hypertriglyceridemia when given orally. This effect is not seen with topical estrogen therapy. |
| Protease inhibitors |
Increased triglycerides/decreased HDL especially in setting of HIV-associated lipodystrophy. |
| Glucocorticoid excess |
Increased triglycerides/decreased HDL probably related to exacerbation of insulin resistance. |
| Antipsychotics |
Increased triglycerides/decreased HDL probably related to increased adiposity and insulin resistance. |
| Retinoids |
Increased triglycerides. |
| Systemic lupus erythematosus |
Chronic inflammation may increase risk of vascular disease independent of effects on lipid metabolism. |
| Acute intermittent porphyria |
Many agents used to treat lipid disorders reported to provoke episodes of abdominal pain. |