Hyperlipidaemia

Aetiology/Causes

Primary Causes:

• Genetic predispositions (e.g., familial hypercholesterolaemia)

Secondary Causes:

• Excessive alcohol intake: Raises TG levels

• Diabetes: Poorly controlled diabetes often results in elevated TG

• Hypothyroidism

• Nephrotic syndrome

• Cholestatic or chronic liver disease

• Obesity

• Certain medications (e.g., thiazide diuretics, beta-blockers, oral oestrogens, atypical antipsychotics)

Pathophysiology

Elevated LDL-C and triglycerides contribute to the formation of atherosclerotic plaques, increasing the risk of coronary artery disease, stroke, and peripheral vascular disease. Low HDL-C further exacerbates CVD risk due to its role in reverse cholesterol transport.

Symptoms and Examination Findings

Symptoms:

• Generally asymptomatic

• Severe hypertriglyceridaemia (>10 mmol/L) may cause pancreatitis

Examination Findings:

• Xanthelasma: Yellowish deposits on the eyelids

• Arcus cornealis: Greyish-white ring around the cornea

• Tendon xanthomas: Nodules on tendons (Achilles, hands) indicating familial hypercholesterolaemia

Differential Diagnosis

• Primary lipid disorders

• Hypothyroidism

• Uncontrolled diabetes

• Alcohol-related liver disease

Investigations

Lipid Profile Testing:

• Measures total cholesterol, HDL-C, LDL-C, and TG

• Use fasting sample to accurately assess TG if elevated

Other Tests:

• Thyroid function tests (TFTs) to rule out hypothyroidism

• Liver function tests (LFTs) for underlying liver disease

• Renal function tests to evaluate nephrotic syndrome

• HbA1c for diabetes screening

Management Algorithm

1. Exclude Secondary Causes:

   • Identify and manage conditions contributing to elevated lipids

2. Assess Absolute CVD Risk:

   • Estimate the 5-year CVD risk to guide treatment intensity

3. Pharmacological Management:

   • Statins: First-line therapy for CVD risk reduction

     • High-Intensity Doses: Atorvastatin (40–80 mg) or Rosuvastatin (20–40 mg)

     • Indications: All patients with established CVD or high CVD risk

   • Ezetimibe (10 mg daily): Add-on if LDL-C targets are unmet with statin monotherapy

   • PCSK9 Inhibitors (e.g., Evolocumab): For familial hypercholesterolaemia or uncontrolled lipid levels on other therapies

   • Fibrates: Effective for lowering TG, particularly when >4 mmol/L

     • Dosage Adjustment: Based on renal function (eGFR)

     • Combination Therapy: Use with statins when TG remains elevated

   • Fish Oils: 2–4 g/day for TG reduction in severe cases

   • Bile Acid Binding Resins: Avoid in high TG due to risk of further elevation

4. Non-Pharmacological Management:

   • Dietary Changes:

     • Increase intake of plant sterols

     • Reduce saturated fats; replace with monounsaturated or polyunsaturated fats

     • Soluble fibre (e.g., oats, psyllium)

   • Exercise: At least 30 minutes, five times weekly

   • Weight Loss: Particularly if overweight or obese

   • Limit Alcohol Consumption: Reduces TG levels

   • Smoking Cessation

Treatment Targets

• LDL-C: <2.0 mmol/L (primary prevention); <1.8 mmol/L (secondary prevention)

• Non-HDL-C: <2.5 mmol/L

• TG: <2.0 mmol/L

• HDL-C: >1.0 mmol/L

Complications

• Cardiovascular events (e.g., myocardial infarction, stroke)

• Pancreatitis with high triglycerides

• Atherosclerosis

Prognosis

• Long-term outcomes are significantly improved with adequate lipid management and lifestyle changes, reducing the risk of cardiovascular events.

Notes

• Diabetes and Hypertriglyceridaemia: Control of diabetes can rapidly reduce TG levels

• Statin Use in High TG: Statins can be used in combination with fibrates to lower CVD risk, even if TG reduction is modest

• Monitoring: No routine CK