MON-155 - A Rare Case of Reversible Male Hypogonadism Due to Statin Therapy

Statin therapy is a cornerstone for both primary and secondary risk reduction of cardiovascular disease. Statins exert their action by blocking HMG-CoA reductase, which is the rate limiting enzyme in cholesterol biosynthesis. Cholesterol is a precursor in steroid hormone synthesis, thus mechanistically the use of statin therapy may reduce testosterone levels causing hypogonadism. The current literature demonstrates marginal reductions in testosterone with statins without clinical relevance. We describe a rare case of symptomatic hypogonadism with reversal upon statin discontinuation.



A 64-year-old male with coronary artery disease status post prior percutaneous coronary intervention is evaluated for hypogonadism with complaints of lethargy, fatigue, loss of muscle mass, low libido, and erectile dysfunction. He denied opioid use, prior radiation therapy, testicular infection or injuries. His initial fasting 8am testing showed a total testosterone level of 167 ng/dL (250-1110) and free testosterone of 26.9 pg/mL (35-155). On his follow up encounter to repeat testing to confirm hypogonadism, he reported self-discontinuation of atorvastatin due to concerns of statin therapy and hypogonadism. Repeat testing two months later showed improvement in testosterone levels with total testosterone 256 ng/dL (250-1110), free testosterone 46 pg/mL (35-155), sex hormone binding globulin of 26.19 nmol/L (17.33-71.5), and LH 2.03 mIU/mL (1.5-9.3). He had no weight changes, lifestyle modifications, or other medication adjustments during this time. He reported an improvement in symptoms correlating with testosterone level normalization. He was referred to cardiology to assist in tailoring his lipid lowering medication.



We describe a rare case of symptomatic hypogonadism associated with high dose statin therapy that reversed upon medication discontinuation. There are many implications of this described phenomenon including the clinical decision to consider testosterone replacement versus seeking alternative lipid lowering therapies. There is some data to describe a dose dependent testosterone effect which may give clinicians reason to continue statin therapy at lower doses when indicated prior to discontinuing all together. Other alternative lipid lowering medications such as bempedoic acid and ezetimibe can be considered. PCSK9 inhibitors have the potential to lower testosterone levels however the current literature reports that the effects are negligible. We describe this rare occurrence with hopes to further discussions on optimal treatment plans for patients with possible hypogonadism needing lipid lowering therapy.

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