Xanthelasma

Published on 02/04/2015 by admin

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Last modified 22/04/2025

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170 Xanthelasma

Instruction

Examine this patient’s eyes.

Salient features

History

• Jaundice, generalized pigmentation, itching (primary biliary cirrhosis)

• Family history of hyperlipidaemia

• History of diabetes, hypertension.

• Symptoms of hypothyroidism (p. 516)

• History of oral contraceptives.

Examination

• Xanthelasmata (flat yellow nodules or plaques) seen on eyelids and around both eyes, particularly on the inner canthus (Fig. 170.1)

• Look for the following signs:

• Corneal arcus
• Jaundice, generalized pigmentation, scratch marks (primary biliary cirrhosis)
• Tendon xanthomata
• Palmar xanthomata.

• Tell the examiner that you would like to check the following:

• Urine sugar
• Blood pressure
• Pulse and ankle jerks (hypothyroidism).
image

Fig. 170.1 Xanthelasma. Multiple, soft, yellow plaques involving the eyelid.

Remember: Blood lipids can often be normal.

Diagnosis

This patient has xanthelasmata on the eyelids (lesions) and I would like to test serum lipids to exclude an underlying lipid disorder (aetiology).

Advanced-level questions

In which conditions are xanthelasmata seen?

Those in which there is an increase in serum cholesterol (see Fig. 173.1C–E):

• Type IIb hyperlipidaemia: increased cholesterol and triglycerides

• Type IIa hyperlipidaemia: increased cholesterol only

• Type III hyperlipidaemia: equal increase in cholesterol and triglycerides.

Mention a few secondary causes of hyperlipidaemia

Diabetes mellitus, hypothyroidism, nephrotic syndrome, cholestatic jaundice, excess alcohol intake, oral contraceptives.

How would you manage a patient with hyperlipidaemia?

• Lifestyle advice

• Dietary modification (usually adequate for those whose cholesterol level is in the range 6.5–8 mmol/l)

• Avoidance of alcohol, smoking, oestrogens and thiazides

• Exercise

• Control of hypertension and diabetes

• Lipid-lowering drugs.

Mention a few lipid-lowering drugs

• Ion exchange resin: colestyramine

• Fibrates: bezafibrate, gemfibrozil

• Sitostanol-ester margarine (a plant sterol that reduces serum cholesterol concentration by inhibiting cholesterol absorption)

• Hydroxymethylglutaryl (HMG) coenzyme A (CoA) reductase inhibitors: simvastatin, pravastatin, lovastatin. These drugs block the endogenous synthesis of cholesterol and reduce levels of LDL cholesterol

• Nicotinic acid derivatives: nicotinic acid, probucol.

Are HMG CoA reductase inhibitors useful in patients with hypercholesterolaemia and coronary heart disease?

Yes, the Scandinavian Simvastatin Survival Study (the 4S trial) demonstrated a survival benefit from lowering cholesterol with simvastatin in patients with coronary disease (Lancet 1994;344:1383–9). In the LIPID study (Long-Term Intervention with Pravastatin in Ischemic Heart Disease), a major secondary prevention trial, pravastatin administered to 9000 patients with unstable angina or acute myocardial infarction significantly reduced total mortality by 23%, coronary heart disease mortality by 24%, the need for coronary revascularization, the number of admissions to hospitals (Lancet 2000;355:1871–5) and the risk of stroke by 20% (N Engl J Med 2000;343:317–26). The Lescol in Severe Atherosclerosis (LISA) study evaluated fluvastatin in patients with coronary artery disease and hypercholesterolaemia and found that it reduced cardiac events by 71%.

What is the role of HMG CoA reductase inhibitors in patients with hypercholesterolaemia and no signs of coronary heart disease?

A study from Scotland showed that treatment with pravastatin significantly reduced the incidence of myocardial infarction (30% reduction) and death from cardiovascular causes (33% reduction) without adversely affecting the risk of death from non-cardiovascular causes in men with moderate hypercholesterolaemia and without a history of myocardial infarction (N Engl J Med 1995;333:1301–1307).

What is the role of HMG CoA reductase inhibitors in patients with coronary artery disease and ‘average’ cholesterol levels?

The CARE study (Cholesterol and Recurrent Events Trials Investigators) found that pravastatin lowered rates of coronary events (including fatal events and non-fatal myocardial infarction) in majority of the patients with coronary disease who have average cholesterol levels (N Engl J Med 1996;335:1001–9).

What is the effect of statins on elevated triglyceride concentrations?

Serum triglyceride concentrations are reduced by all statins with atovastatin and simvastatin having the greatest effect. Higher the baseline concentration of triglycerides, greater is the reduction induced by statin therapy.

Mention some adverse effects of statins?

• Common: GI upset, myalgias and hepatitis

• Rare: rash, myopathy, peripheral neuropathy, insomnia, bad dreams, difficulty in sleeping or concentrating.

What is the effect of meals on statin absorption?

Lovastatin is better absorbed when taken with food whereas pravastatin is best taken on an empty stomach or at bedtime. Food has less of an effect on the absorption of other statins.

Why are all statins best given in the evening?

Because the rate of endogenous cholesterol synthesis is higher at night.

In a patient with hypercholesterolaemia on treatment with statins who requires further lowering of LDL cholesterol, what second drug would you add if the patient’s serum HDL is low?

Nicotinic acid is the preferred second drug. Nicotinic acid usually increases serum HDL concentrations by 30%, fibrates by 10–15%, statins by 5–10% and bile acid resins by 1–2% (N Engl J Med 1999;341:498–511). The ARBITER 6–HALTS (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol 6–HDL and LDL Treatment Strategies) trial compared the effects of two combination therapies—either niacin or ezetimibe added to long-term statin therapy—on carotid intima–media thickness over a 14-month period. Addition of extended-release niacin caused significant regression in thickness that was superior to that seen with ezetimibe (N Engl J Med 2009; 361:2113–22). The two much-anticipated outcome studies for niacin are AIM-HIGH, due out in 2011, and HPS2-THRIVE, which is expected to be completed in 2013.

What is the role of statins in patients with elevated low density lipoproteins and LDL and high-sensitivity C-reactive protein?

In the JUPITER trial (Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin), rosuvastatin significantly reduced the primary end-point (a composite of non-fatal myocardial infarction, non-fatal stroke, hospitalization for unstable angina, arterial revascularization, or confirmed death from cardiovascular causes) in apparently healthy people with LDL cholesterol levels of <1.3 g/l (3.4 mmol/l) but with elevated high-sensitivity C-reactive protein levels of ≥2.0 mg/l (N Engl J Med 2008;359:2195–207).

James Scott, FRS contemporary Professor and Chairman of the Department of Medicine at Hammersmith Hospital, London, is a physician, biochemist and molecular biologist. He has made a considerable contribution to lipid and cardiovascular research.

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