Lipid management
د. حسين محمد جمعةاختصاصي الامراض الباطنة
البورد العربي
كلية طب الموصل
2010
Key points
Consensus guidelines exist for lipid managementDifferences in use of tests between doctors are large
Secondary causes for lipid disorders are common and are easily diagnosed
Predisposing factors for adverse reaction to lipid lowering drugs can be identified
Introduction
This module presents two typical patients seen in a district hospital lipid clinic. Laboratories differ in the profiles of tests they offer, and some will add tests where considered appropriate. However, most laboratory testing is driven by the request which arrives on the laboratory form. In the case of lipid disorders, this process can lead to delayed or missed diagnosis and inappropriate or even dangerous treatment.Case 1
A 64 year old man was referred with hyperlipidaemia resistant to treatment with atorvastatin 40 mg. He had had a myocardial infarction in 2002 and started taking atorvastatin six months before referral. Before this, his total cholesterol concentration was 8.1 mmol/l, triglycerides 1.5 mmol/l, and high density lipoprotein cholesterol 1.4 mmol/l. On treatment his total cholesterol was 6.8 mmol/l, triglycerides 1.3 mmol/l, and HDL cholesterol 1.4 mmol/l. He seemed healthy and reported no specific complaints. His body mass index was 28.Liver enzymes three months before were normal, and no creatine kinase measurement was available. Retesting confirmed the previous lipid results but showed a creatine kinase activity of 3460 IU/l, alanine aminotransferase activity of 30 IU/l, and aspartate aminotransferase of 108 IU/l (raised). Urea and creatinine were within normal limits and a subsequent urine screen for myoglobinuria was negative. Random blood glucose was 5.8 mmol/l.
What would you do in this circumstance? How urgently would you do it?
The atorvastatin was stopped and the patient's renal function and creatine kinase were monitored every three days for two weeks, after which the creatine kinase had fallen to 2400 IU/l; it was the same a week later. When he returned to the clinic after this three week period the creatine kinase activity had not fallen further and a simple battery of tests was organised to exclude other causes for his myopathy (autoantibodies, erythrocyte sedimentation rate, thyroid function). Although he was clinically euthyroid, his thyroid stimulating hormone concentration was 52 mIU/l and his free T4 was 4 pmol/l.What would you do in this circumstance?
He was started on thyroxine. Two months later he reported feeling generally fitter; his cholesterol was 5.4 mmol/l and creatine kinase was within the normal range, and he was restarted uneventfully on a statin.Learning bite
Non-fasting results can produce higher triglycerides and lower high density lipoprotein cholesterol concentration.Non-fasting measurements slightly overestimate CHD risk but are regarded as sufficiently accurate to use in screening and are more convenient for patients. Routine use of a tourniquet has no significant effect on lipid measurements.
Learning bite - special circumstances
You can give statins to patients who have received a renal transplant, but you should do so cautiously. Some drugs such as ciclosporin can interact with statins. The maximum dose of rosuvastatin that you can give to patients of South Asian origin is 20 mg daily.Testing lipids
How often should patients' lipids be tested after starting lipid lowering treatment?A review of the international literature suggests intervals of:
8 (±4) weeks after starting drug treatment
8 (±4) weekly after adjustments to treatment until within the target range.
The 2008 NICE lipid modification guideline however proposed a "fire and forget" policy for primary prevention in the absence of severe lipid disorders. This view has, however, been controversial particularly in higher risk primary prevention patients, and many specialists advocate treating to targets of 5 and 3 mmol/l (total and LDL cholesterol respectively) or 4 and 2 mmol/l in higher risk and diabetic patients.
How often should cholesterol or lipids be tested once a patient has reached target or optimal cholesterol?
Annually (unless there is a specific reason for more frequent reviews)
How often should liver enzymes be routinely measured in patients taking statins?
Measure alanine aminotransferase:Before treatment with a statin
Eight weeks after starting a statin or after any dose increase.
What if liver enzymes become raised in a person taking a statin?
If ≤3 x upper limit of normal:Continue statin
Recheck liver enzymes in 4-6 weeks
No extra monitoring required unless values rising.
If ≥3 x upper limit of normal (depending on magnitude of rise):
Stop statin or reduce dose, recheck liver enzymes within 4-6 weeks
Cautious reintroduction of statin may be considered (for example at a lower dose).
How often should creatine kinase be measured in patients taking statins?
Pre-treatmentBefore starting treatment with a statin
If the baseline creatine kinase level is >5 times the upper limit of normal, do not start statin.
Monitoring
Risk factors for myopathy absent:
Routine monitoring of creatine kinase is not necessary
Check creatine kinase if patient develops myalgia.
Risk factors for myopathy present:
Balance risk/benefit of treatment with a statinIf a statin is prescribed: check creatine kinase within 8 weeks of commencing statin, after any dosage increase or if patient develops myalgia.
What if creatine kinase becomes raised in a person taking a statin?
If ≥5 x upper limit of normal:Stop treatment, check renal function, and monitor creatine kinase fortnightly
Consider secondary causes of myopathy if creatine kinase remains elevated.
If ≤5 x upper limit of normal:
If no muscle symptoms, continue statin (patients should be alerted to report symptoms; consider further checks of creatine kinase)If muscle symptoms, monitor symptoms and creatine kinase regularly if creatine kinase continues to rise.
