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Below is a list of short cases or prompts to highlight a variety of common diagnostic and management dilemmas in the realm of dyslipidemia. For each case, consider what you have done in practice and what you have seen other providers do. Following the case prompt is a brief summary of what our references would recommend in this situation. Like everything in medicine, these dilemmas need to be approached with both science and art as we take care of our patients.
65 yo non-smoking male on HCTZ 25 & ASA 81 was started on Pravastatin 40 qhs for LDL 170 (goal < 130) 3 months ago. LFTs were checked just prior to his visit with you. Both AST & ALT are elevated as below. He feels fine. What should you do?
AST 79 (normal 10-34)
ALT 82 (normal 10-50)
Literature Review:
There is not consensus about how often to follow LFTs in persons taking statins, in fact there is not consensus that any monitoring is necessary. The FDA labeling suggests checking prior to initiating therapy and repeating 3 months after initiation and/or any dose increase. There is a table in the Tarascon pharmacopeia with monitoring recommendations for each statin.
There does appear to be consensus that three times the upper limit of normal of AST or ALT is the level at which discontinuation of a statin is appropriate. (AFP 6/00, UTD). Incidence of this level of transaminitis is about 1-2% of those on statins. Levels should normalize with discontinuation of the medicine.
Bottom Line: No need to change therapy, continue monitoring q 6 months
65 yo non-smoking male on HCTZ 25 & ASA 81 was started on Pravastatin 40 qhs for LDL 170 (goal < 130) 6 months ago. He recently has developed diffuse muscle aching which he believes is due to this medication. You checked a CPK prior to his visit with you and it was normal. What should you do?
Literature Review:
Always take a good history, do a thorough exam and consider a full differential: including arthritis, infectious, PMR, depression, etc.. Consider also checking an ESR or a Rheum panel depending on your findings. (not from lit review – just common sense)
Range of muscle issues associated with statins is from muscle aching with normal CPKs (2-10%) to full blown rhabdomyolysis (0.1%) leading to renal failure. Statins alone (not in combination with other meds) rarely cause a myositis enough to raise CPKs. Even in the face of normal CPKs, muscle symptoms can be due to the statin.
Checking a CPK is debatable, perhaps more useful as a baseline and then with symptoms in the setting of statins and fibrates together. How to proceed with symptoms and normal CPK is completely based on risk-benefit analysis with patient. Patients with liver, renal or thyroid disease are more susceptible to muscle symptoms. Certain medicines combined with statins also predispose to muscle symptoms – fibrates, macrolides, protease inhibitors, alprazolam, tegretol, sertraline, anti-arrythmics and fibrates to name a few.
Pravastatin and fluvastatin have a different molecular make-up and are less likely to cause muscle symptoms (more hydrophilic, less likely to be toxic to muscle cells). In the face of symptoms, it would be reasonable to switch to one of these two meds to see if symptoms improved, but benefit could still be maintained. If symptoms still persist and high perceived benefit of statin, there is anecdotal evidence that CoQ10 supplementation might help symptoms – dose 150-200mg qd. Otherwise, should d/c.
Discontinuing statin should lead to resolution of muscle symptoms in days to weeks.
(Sources: UTD, AFP 6/00)
Bottom Line: Consider switching statins. Weigh risk-benefit of statin treatment in your patient...
55 yo male with past history of MI 6 months ago was started on a statin at hospital discharge. He does not have DM, is not a smoker and is also taking a beta blocker and ACE-I. He is currently taking Atorvastatin (Lipitor) 80mg qhs which is the maximum dose. His LDL on this regimen is 126, HDL 30, TG 174, total cholesterol 197. He is doing “the best he can” with TLC. What medication should be added next?
Literature Review:
Review of his lipid profile shows LDL too high (goal probably < 70 or 100), HDL low (< 40) and TG in a reasonable range. Risks associated with elevated LDL are well known, but note that low HDL is also thought to be an independent risk factor for CHD events.
Adding Niacin would most likely lead to the most improvement in his LDL and HDL profiles. This has risks of multiple side effects including flushing, nausea, headaches, glucose intolerance, and gout. Taking a non-enteric coated aspirin 30 min before the med and using an extended release preparation (Niaspan) can help prevent some of these symptoms.
Revisiting TLC and assuring compliance with current statin dose are also important. Consideration of his interest in other alternative therapies may also be appropriate. If he is unable to tolerate Niaspan, Zetia would be a better-tolerated second choice, although recent studies question true benefit of Zetia. Fibrates would be another choice, but these have greatest benefit with triglyceride lowering and also have risks of GI side effects and interactions with statins.
A nice table summarizing options is on page 11 of the AFP Cholesterol Monograph, 2003.
Bottom Line: Add Niaspan, re-visit TLC and statin compliance.
A 35 yo male presents to establish care with you. He reports a family history of cholesterol problems, but not of CAD that he knows of. He feels fine and takes no medications, does not smoke or have HTN or DM. You check his FLP and find TG 700, total cholesterol 230, HDL 30. You ordered a reflex direct LDL which was 120. What should you do?
Literature Review:First, verify fasting status! If real, then lowering TGs first is a priority. TG > 1000 is associated with a high risk of pancreatitis – he is getting close. First line treatment for moderate to severe hypertriglyceridemia is a fibrate – Tricor or Gemfibrozil.
For his age and risks, LDL is actually fine. LDL goal is < 160.
His HDL is low, but this should be re-checked and then re-addressed after TGs lower.
TLC should also be discussed and instituted simultaneously with fibrate tx.Finally, thought should be given to secondary causes and familial disorders. DM, thyroid, kidney and liver dx should be ruled out. He should abstain from alcohol until levels are improved. A more detailed FH should be obtained for type of lipid d/o and assurance that no-one has early CAD. Physical exam looking for xanthomas should be done. Consider referral to lipid specialist if any concern for a familial disorder. Nice review of possible familial TG disorders is in NEJM - Hypertriglyceridemia, 9/07.
Bottom Line: Start TLC and fibrates. Think about secondary, familial causes.
60 yo male diabetic with HTN – both well controlled – without history of MI. He does have documented claudication and a past history of smoking, having successfully quit 2 years ago. You have checked his cholesterol a few times over the last 10 years, most recently last week - total cholesterol 200, TG 250, HDL 25, LDL 125. In the past he has refused a cholesterol medicine citing that his levels are “not that bad” and he is already on “too many pills”. He eats a fairly “normal” diet – not daily fast food, but also not watching his fat intake closely. His primary exercise is walking his terrier for 30 minutes each day.
Literature Review:
Depending on your interpretation of the literature, his LDL goal is at least < 100 and perhaps < 70. There is also data that suggests that all diabetics would benefit from statin therapy regardless of LDL level. Both the 70 target and the “all diabetics” assertion arise from results of The Heart Protection Study.
A nice summary of that study is in the ATP3 update: Page 228.
The brief summary of the HPS study is that this was an RCT of people without known CAD but with the other “equivalent” risks – DM, PVD, Stroke – who were randomized to 40mg pravastatin qd or not regardless of LDL. Treated patients had decreased all-cause mortality, mortality from CHD events, and less CHD events no matter what their baseline LDL was. There are some questions about the sub-group analysis process which is why these are suggested as “reasonable” practice rather than being completely adopted as new guidelines.
Anyway, I personally think there are several reasons why this particular patient should be on a statin.
The real point of this question is to think about how to engage patients in their treatment – either meds or lifestyle change. Some ideas include exploring their “life priorities” – grandkids, fishing, whatever and linking that to their health; exploring their worries about the therapy, or their perception of barriers to lifestyle change.
There are models of behavior change – the Diclemente precontemplative, contemplative, etc. circle is used commonly. There is also a model about assessing readiness for change which you may be familiar with.
Bottom Line: Should be on a statin, LDL < 70-100. It's all about the art of medicine.
45 yo female non-smoker otherwise healthy presents for follow-up from work-place health evaluation. She had a non-fasting fingerstick total cholesterol 240 and HDL 46 and is interested in having a fasting lab in follow-up for the elevated total cholesterol. Fasting results are: total cholesterol 220, TG 332, HDL 42, LDL 111.
What are the abnormalities in this lipid panel and what should you / she do about it?
Literature Review:
This woman’s 10 yr Framingham risk of cardiac events is 1%, therefore her LDL goal is < 160.
Her LDL and HDL are fine. Her primary abnormality is hyperTG – this is in a moderately high range.
If her TG were over 500, she should be put on a fibrate given the risk of complications.
However, at this level (332), TLC is the primary intervention of choice – particularly a low fat diet.The ATP3 guidelines use the concept of a “non-HDL goal” as a secondary target for patients with normal LDL and high TGs > 200.
Non-HDL is total cholesterol – HDL. In this patient non-HDL = 220-42 = 178.
The non-HDL goal is always 30 more than the LDL goal. In this patient the non-HDL goal = 190.Since her non-HDL is also at its goal, she really doesn’t need a medicine at this time.
Obviously TLC will be beneficial to her both in terms of lowering her TG and her general healthIf her non-HDL was not at goal, then use of a fibrate or niacin would be appropriate.
Bottom Line: You don’t have to treat every TG between 200-500 with medicine if both LDL and non-HDL are at goal. TLC is where it's at.
45 yo female smoker with BP 135/90 and FH of MI in father at 61 yo presents as new patient to your practice. Her FLP shows total cholesterol 262, LDL 170, TG 275, HDL 35. (Same case as at start of the day.) Her BMI is 32 and a fasting glucose is 116.
Literature review:
She likely has abdominal obesity, although we didn't measure
She has the high TG and the low HDL and
She has elevated BP and elevated fasting glucose.
A thorough, but long and complex review of metabolic syndrome is in Circulation, 2005.
Interventions for her include:
**Of note, the ATP3 guidelines would normally put people with a 10 yr risk of 10-20% with an LDL goal of < 130, but in their “update” they suggest that having a risk of 10-20% AND metabolic syndrome might be enough to lower the goal to < 100.
So in this patient, if she quit smoking, technically her goal would be < 160, but maybe we should think of managing her more aggressively due to the perceived risk associated with the metabolic syndrome.
** The point being once the LDL is at goal, you might not be finished yet.
Bottom Line: The key point about making the diagnosis of metabolic syndrome is recognizing the significant risk associated with having “mild” abnormalities across the board. 40% of Americans of 40 yo have this constellation – ubiquitous!