Mark R. Goldstein, MD

To the Editor: We read the interesting paper by Dr. Susan Rehm on the recently changing epidemiology and increasing incidence of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia.¹ We feel these trends may be related in part to the increasing use of statin therapy in both outpatient and hospital settings.

In a case-control study,² skin and soft tissue infections as the source of bacteremia were significantly more prevalent among patients treated with statins compared with patients not receiving statin therapy. Additionally, there have been isolated reports of recurrent community-acquired MRSA skin infections in subjects on therapy with high-dose statins and no obvious risk factors for skin infection.³

The epidermis is a very active site of cholesterol synthesis, and after barrier disruption in the murine model, there is a brisk increase in epidermal cholesterol synthesis.⁴ Moreover, if the increase in epidermal cholesterol synthesis is inhibited by the topical application of statins, barrier function is impaired.⁴

Therefore, it is plausible that systemic statin therapy alters epidermal cholesterol homeostasis, resulting in barrier inadequacy and impaired innate immune function of the skin,⁵ leaving it more vulnerable to external pathogens and resulting bacteremia. Importantly, this needs to be investigated, particularly in light of the increasing and widespread use of high-dose statin therapy.

To the Editor: We read the interesting paper by Dr. Susan Rehm on the recently changing epidemiology and increasing incidence of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia.¹ We feel these trends may be related in part to the increasing use of statin therapy in both outpatient and hospital settings.

In a case-control study,² skin and soft tissue infections as the source of bacteremia were significantly more prevalent among patients treated with statins compared with patients not receiving statin therapy. Additionally, there have been isolated reports of recurrent community-acquired MRSA skin infections in subjects on therapy with high-dose statins and no obvious risk factors for skin infection.³

The epidermis is a very active site of cholesterol synthesis, and after barrier disruption in the murine model, there is a brisk increase in epidermal cholesterol synthesis.⁴ Moreover, if the increase in epidermal cholesterol synthesis is inhibited by the topical application of statins, barrier function is impaired.⁴

Therefore, it is plausible that systemic statin therapy alters epidermal cholesterol homeostasis, resulting in barrier inadequacy and impaired innate immune function of the skin,⁵ leaving it more vulnerable to external pathogens and resulting bacteremia. Importantly, this needs to be investigated, particularly in light of the increasing and widespread use of high-dose statin therapy.

To the Editor: We read the interesting paper by Dr. Susan Rehm on the recently changing epidemiology and increasing incidence of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia.¹ We feel these trends may be related in part to the increasing use of statin therapy in both outpatient and hospital settings.

In a case-control study,² skin and soft tissue infections as the source of bacteremia were significantly more prevalent among patients treated with statins compared with patients not receiving statin therapy. Additionally, there have been isolated reports of recurrent community-acquired MRSA skin infections in subjects on therapy with high-dose statins and no obvious risk factors for skin infection.³

The epidermis is a very active site of cholesterol synthesis, and after barrier disruption in the murine model, there is a brisk increase in epidermal cholesterol synthesis.⁴ Moreover, if the increase in epidermal cholesterol synthesis is inhibited by the topical application of statins, barrier function is impaired.⁴

Therefore, it is plausible that systemic statin therapy alters epidermal cholesterol homeostasis, resulting in barrier inadequacy and impaired innate immune function of the skin,⁵ leaving it more vulnerable to external pathogens and resulting bacteremia. Importantly, this needs to be investigated, particularly in light of the increasing and widespread use of high-dose statin therapy.