Endocrine Abstracts

Background: HDL is a plasma lipid-protein complex of lipids and alphalipoproteins (apolipoproteins A-I and A-II). It is involved in reverse transport of cholesterol from peripheral tissue to liver, allowing cholesterol degradation. HDL cholesterol (HDL-C) levels are inversely associated with cardiovascular risk. HDL-C levels can be elevated due to genetic causes or drugs. We present a case where significantly raised HDL levels caused some concern at the outset.

Case: A 66-year-old female was referred to lipid clinic for elevated cholesterol. She had epilepsy, well-controlled on carbamazepine. There were no peripheral stigmata of hyperlipidaemia. She had no family history of premature coronary artery disease; calculated cardiovascular risk was low. Full fasting lipid profile showed total cholesterol 9.7 mmol/l (3.5–5.0), triglycerides 2.1 mmol/l (0.8–1.8), LDL 5.2 mmol/l (1.5–4.0), and HDL 3.5 mmol/l (1.0–2.10). The total cholesterol:HDL ratio was 2.8 mmol/l (0–4.5). Apolipoprotein A-I was raised at 3.65 g/l (1.25–2.15). Separate cardiology review for chest pain resulted in coronary angiogram and transthoracic echocardiogram, confirming normal coronary arteries, and preserved ventricular function. Hepatology review and Fibroscan for abnormal liver function tests ruled out liver pathology. Repeat lipid profile revealed a similar picture and no lipid-lowering treatment was instituted.

Discussion: Hyperalphalipoproteinemia (HALP) is a condition where HDL-C levels are elevated raising total cholesterol values. LDL-cholesterol may be normal or elevated. Peripheral stigmata of hyperlipidaemia are usually absent. HALP can result from primary causes due to familial genetic defects or can be secondary to drugs, alcohol, or primary biliary cirrhosis. Most patients are incidentally diagnosed. Medical therapy is rarely required. Carbamazepine is well documented to cause elevated HDL-C, attributed to its enzyme inducing effect leading to increased hepatic synthesis of alphalipoproteins. Careful clinical and biochemical evaluation is essential in patients presenting with lipid abnormalities. Statin therapy is not a panacea for all hypercholesterolaemia patients.