Severe Medication Induced Dyslipidemia in an Adult with Breast Cancer

Background/Synopsis

A 57 year-old woman with recently diagnosed breast cancer receiving weekly neoadjuvant paclitaxel and biweekly doxorubicin and cyclophosphamide therapy with dexamethasone is referred to lipid clinic to evaluate for genetic testing for hyperlipidemia. Her other medications included loperamide, metformin, omeprazole, ondansetron, prochlorperazine, cyclobenzaprine, hydroxyzine, ibuprofen, tramadol, metoprolol, and olanzapine. The abnormal laboratory results were incidentally noted by her oncologist on routine blood work, and included a total cholesterol (TC) of 964 mg/dL, triglycerides (TG) of 5,031 mg/dL, and HDL-C of 31 mg/dL. She denies a history of dyslipidemia, abdominal pain, or pancreatitis. Family history is notable for her father who died of a myocardial infarction in his 40s. Examination revealed no xanthelasmas, tendinous xanthomas, achilles tendon thickening, hepatomegaly, or corneal arcus.

Objective/Purpose

To demonstrate the severity of iatrogenic dyslipidemia that may result from the combination of atypical antipsychotics and steroids.

Methods

Retrospective review of electronic medical records and literature review.

Results

Echocardiogram was unremarkable and recent CT chest suggested no coronary artery calcification. Repeat lipid panel showed TC of 1,043 mg/dL, TG of 4,593 mg/dL, and HDL-C of 26 mg/dL. TSH was 0.8 MIU/L and hemoglobin A1C was 9.6%. Her serum was noted to be cloudy. Prior lipid panel from PCP was requested and it showed TC, TG, and HDL-C levels of 238, 538, and 34 mg/dL, respectively just weeks prior to steroid and antipsychotic initiation. Given the history and temporal correlation, her hyperglycemia and dyslipidemia were attributed to the combination of olanzapine and dexamethasone and less likely due to genetic causes. After lifestyle modification counseling, atorvastatin 40 mg, icosapent ethyl 1 g, and fenofibrate 145 mg were initiated. Olanzapine was changed to another agent for symptom control. Urgent endocrinology referral also prompted maximization of her metformin dose and initiation of insulin therapy with home glucose monitoring. Repeat lipid panel showed improvement of TC and TG levels to 102 mg/dL and 190 mg/dL, respectively.

Conclusions

While atypical antipsychotics and steroids are known culprits of dyslipidemia and metabolic syndrome, the severity of dyslipidemia seen in this case is atypical. Cancer patients undergoing active therapy are particularly vulnerable. Identification of iatrogenic dyslipidemia should therapy alteration or discontinuation, if possible. Lifestyle modifications and aggressive lipid-lowering therapy remain indicated. Very high TG levels should prompt early initiation of multiple agents, including fibrates and omega-3 fatty acids, to prevent pancreatitis.