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I saw a patient for follow-up recently, 30 yr old WM with a significant history of both depression/anxiety and Type IIb hyperlipidemia. I've never seen such an ugly cholesterol profile before in someone trying so hard to improve it. The guy got down to a BMI of 21, indicates exercise (aerobic and anaerobic) every day, following the AHA dietary guidelines for hyperlipidemia to the letter, and his lipid profile is still horrible. LDL was 300+, HDL was <20, TriG were 500+ (which makes calc. the LDL difficult). Obviously, this is a genetic case.
The patient detailed a long history (since age 18) of PMDs and specialists denying mono or polytherapy for the hyperlipidemia despite consistently very poor lipid profiles, all 1st degree relatives (mother/father/brother) having the same condition (mother and father are both currently being treated successfully with pharmacological polytherapy), and 2nd degree relatives with similar history, including significant morbidity and mortality. Patient indicated that previous physicians said he was "too young" to be concerned about his lipid profile and that once he started therapy he would have to be on it for the rest of his life and they didn't want to do that.
My resident agreed with the assessment of the previous PMDs/specialists, saying that despite his lipid profile his Framingham score was only 4, indicating a 1% 10-year risk. Despite the Framingham score, I asked my attending to review the case (he tends to be a bit more aggressive with treatment). The attending agreed that while his Framingham score was low, the case was obviously genetic it origin and that no amount of patient initiated modification was going to change his lipid profile and that while his 10-year risk is excellent, the foundation for future vascular problems has to be considered. Based on his conclusion he put the patient on pravastatin, 40mg QD and told him to get a repeat lipid profile & LFT in 6 weeks, and return for follow-up in 8 weeks.
When we got the results the lipid profile was significantly improved and his LFT's were nominal, so we are on the right track, but on his follow-up appointment he indicated that his depression and anxiety had recently returned at a low level, despite no aggravating factors and remission of symptoms for 3+ years with continuing treatment of sertraline, 100mg QD.
My resident says it's the pravastatin and that statin therapy should be discontinued, despite the improved lipid profile, because the depression/anxiety is unlikely to resolve on its own and increasing the sertraline to combat the side-effect is inappropriate. The attending indicated that he also believed it was the pravastatin but with the lipid profile improvement he was hesitant to pull the medication, but he also didn't want to unnecessarily increase the sertraline either. I was told by my resident to research the subject and report back with what I found.
What do you guys think? I have read a few papers that Statins can cause relapse in those with a history of depression as well as trigger it in those who are predisposed with no previous history, but none of them seemed to indicate whether it persist for the duration of statin therapy or whether it is transitory as a result of adjustment to the statin. If it is persistent would it be more appropriate to try and adjust the sertraline to compensate or yank the statin?
The patient detailed a long history (since age 18) of PMDs and specialists denying mono or polytherapy for the hyperlipidemia despite consistently very poor lipid profiles, all 1st degree relatives (mother/father/brother) having the same condition (mother and father are both currently being treated successfully with pharmacological polytherapy), and 2nd degree relatives with similar history, including significant morbidity and mortality. Patient indicated that previous physicians said he was "too young" to be concerned about his lipid profile and that once he started therapy he would have to be on it for the rest of his life and they didn't want to do that.
My resident agreed with the assessment of the previous PMDs/specialists, saying that despite his lipid profile his Framingham score was only 4, indicating a 1% 10-year risk. Despite the Framingham score, I asked my attending to review the case (he tends to be a bit more aggressive with treatment). The attending agreed that while his Framingham score was low, the case was obviously genetic it origin and that no amount of patient initiated modification was going to change his lipid profile and that while his 10-year risk is excellent, the foundation for future vascular problems has to be considered. Based on his conclusion he put the patient on pravastatin, 40mg QD and told him to get a repeat lipid profile & LFT in 6 weeks, and return for follow-up in 8 weeks.
When we got the results the lipid profile was significantly improved and his LFT's were nominal, so we are on the right track, but on his follow-up appointment he indicated that his depression and anxiety had recently returned at a low level, despite no aggravating factors and remission of symptoms for 3+ years with continuing treatment of sertraline, 100mg QD.
My resident says it's the pravastatin and that statin therapy should be discontinued, despite the improved lipid profile, because the depression/anxiety is unlikely to resolve on its own and increasing the sertraline to combat the side-effect is inappropriate. The attending indicated that he also believed it was the pravastatin but with the lipid profile improvement he was hesitant to pull the medication, but he also didn't want to unnecessarily increase the sertraline either. I was told by my resident to research the subject and report back with what I found.
What do you guys think? I have read a few papers that Statins can cause relapse in those with a history of depression as well as trigger it in those who are predisposed with no previous history, but none of them seemed to indicate whether it persist for the duration of statin therapy or whether it is transitory as a result of adjustment to the statin. If it is persistent would it be more appropriate to try and adjust the sertraline to compensate or yank the statin?
