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Dr. Stephen Daniels (Colorado) teaches us about screening for obesity-related dyslipidemia, the prevalence of familial dyslipidemia, when to order fasting lipid panels, and how to feel confident about starting that statin!
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Dyslipidemia can be diagnosed based on various components of the lipid panel. The following values are used as cutoffs for what is considered borderline versus abnormal.
LDL: A calculated value using the Friedewald formula. Dr. Daniels reminds us, when triglycerides are elevated (greater than 400), the calculation breaks down. Consider ordering a directly measured LDL in this case. Note that the normative values above are also based on calculated LDLs, not measured.
Non-HDL Cholesterol: Total cholesterol minus HDL. Found to be a sensitive screening tool for dyslipidemia.
TG: A measured value of triglycerides. This is sensitive to whether the patient has eaten recently.
Apoprotein B (Not on Chart): a particularly atherogenic lipoprotein. This is not on a standard lipid panel and should not be routinely used to screen patients.
Lipoprotein a (Not on Chart): a lipoprotein that also influences the development of atherosclerosis and acute embolic events. This is used to risk stratify patients rather than diagnose dyslipidemia. Dr. Daniels recommends testing lipoprotein a in patients with a strong family history of atherosclerotic heart disease. If this is elevated, you should be very rigorous in controlling other risk factors (hypertension, tobacco exposure). Note that because this is genetically determined, you only need to test once. Different lab sites have different normal values!
Universal screening is recommended for all children with a lipid panel between 9-11 years old and then again around 18-21 years old. The initial lipid panel does NOT have to be fasting. Studies have shown that there is a minimal clinical difference between nonfasting and fasting lipid panels. However, if abnormal, Dr. Daniels does recommend repeating a fasting lipid panel to confirm values.
In terms of timing, you can think of it as “one before and one after puberty”. Puberty will decrease both LDL and HDL. In females, LDL and HDL will increase again post puberty. In males, just LDL will increase again. Screening is timed pre-pubertal to catch lipid levels before these changes happen. Moreover, the atherosclerotic process typically starts around 9-11 years old even in familial hypercholesterolemia. By screening at this age, you will catch dyslipidemia before significant damage can happen.
Although more specific classifications exist, Dr. Daniels believes distinguishing between these categories may not be that helpful at the primary care level. Instead, he divides dyslipidemia into the following buckets.
When dyslipidemia is secondary to a lifestyle that results in an elevated BMI, you will typically see an elevated TG and low HDL. The LDL is often normal.
Familial Hypercholesterolemia is an abnormality of the LDL receptor; either the receptor is defective or there are too few receptors. There are two forms of familial hypercholesterolemia: 1) homozygous and 2) heterozygous. Homozygous familial hypercholesterolemia is a more severe and rapidly progressive form of the disease. Patients have LDLs in the 300 to 500s and can have coronary artery disease or aortic valve disease in their teens. It is crucial to identify these patients early and intervene. This is not very common though; the prevalence is estimated at 1:300,000. In comparison, patients with heterozygous familial hypercholesterolemia have LDLs > 190 OR LDLs 160-190 and a strong family history. This is the most common form of genetic dyslipidemia and is seen in 1 out of every 250 children. It is important to know that patients can live at a normal height and weight. NOT ALL DYSLIPIDEMIA IS RELATED TO OBESITY.
After diagnosing a patient with dyslipidemia, Dr. Daniels recommends ruling out secondary causes such as liver, thyroid, and renal disease. Consider obtaining a lipoprotein a to risk stratify your patients and determine whether more aggressive treatment is needed. If a patient has familial hyperlipidemia, remember to counsel on screening for their family members.
Management of dyslipidemia always begins with lifestyle modifications. Even if a child is diagnosed with familial dyslipidemia, dietary modifications are important. Patients should decrease saturated fat and cholesterol in their diet.
Counseling on lifestyle modifications can be difficult. Remember that lifestyle changes are a gradual process and take patience. Start by asking the patient and family first! What types of changes do you think you are capable of making? Talk about behaviors rather than BMI. When behaviors change, the lipid profile and BMI will follow. If your clinic has the resources, it can be helpful to involve a dietician.
Statins should be considered for patients who’s 1) LDL is greater than 190 OR 2) LDL is 160-190 AND have an additional risk factor for atherosclerosis (ex. hypertension). Dr. Daniels starts with a higher intensity statin (rosuvastatin or atorvastatin), but at a lower dose like 10 mg.
When starting statins, patients should have a repeat lipid panel in 6-8 weeks. Once their lipids are in a steady range, labs can be spaced to every 3-6 months. Common side effects to monitor for are myalgias, liver damage, and teratogenicity. Obtain liver enzymes intermittently for patients on statins and ensure that if they are female and sexually active, that they are on birth control. Myalgia with progression to rhabdomyolysis is rare. If patients report myalgias, Dr. Daniels recommends measuring a creatine kinase (CK). If the CK is more than 10 times the upper limit of normal, this is considered a clinically significant myopathy. Stop the statin and see if symptoms resolve. In the future, you can retry the same statin or a different statin.
Ideally, after starting a statin, the LDL will be less than 130. However, LDL less than 160 or a 30-50% decrease is a reasonable goal. Dr. Daniels points out that the higher you go up on a statin, there are diminishing returns and higher risk of side effects. The decision to intensify medical treatment should be a shared one between patient and provider. If you are still not meeting goals on a statin alone, consider bile acid sequestrants (but note that they can be difficult to tolerate due to GI side effects). PCSK9-inhibitors can also be used, but these are typically reserved for homozygous FH (at this point, consult your local cardiologist).
It’s important to remember that triglycerides are the most sensitive to the patient’s diet. An accurate measurement of triglycerides requires a fasting panel. The management of hypertriglyceridemia is similar to hypercholesterolemia. If that panel returns with TG greater than 150, consider the same lifestyle interventions as for patients with hypercholesterolemia (regular aerobic exercise and reduce simple sugars and saturated fats). If the TG are severely elevated, consider pharmacologic treatment with fibrates and omega-3 fatty acid. This is to prevent pancreatitis rather than atherosclerosis.
Though FH has been traditionally thought to be most prevalent in white individuals, there remains a significant gap in our understanding of the burden of dyslipidemia among minoritized populations. While individual patients vary genetically, there is no genetic basis to race, and so solutions to decrease HLD risk lie in restructuring our healthcare system to mitigate inequities. It is important that counseling is culturally appropriate to different diets and body images.
Listeners will learn to screen and manage dyslipidemia.
After listening to this episode listeners will be able to …
Dr. Daniels reports no relevant financial disclosures. The Cribsiders report no relevant financial disclosures.
Park J, Daniels S, Lee N, Masur S, Chiu C, Berk J. “#41: The Good, the Bad, and the Fasting: Dyslipidemia with Dr. Stephen Daniels”. The Cribsiders Pediatric Podcast. https:/www.thecribisders.com/ December 22, 2021
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