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Editorial |

Targeting the Host to Control an Infection Disorder

Kasturi Haldar, PhD
Arch Intern Med. 2008;168(19):2067-2068. doi:10.1001/archinte.168.19.2067.
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Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, which catalyzes the production of mevalonate from HMG CoA, the first and rate-limiting step in cholesterol biosynthesis in mammalian cells. Inhibition of HMG CoA reductase in the liver induces production of low-density lipoprotein receptors and, thus, clearance of circulating low-density lipoprotein, resulting in lower cholesterol levels.1,2 Historically, the use of statins revolutionized cholesterol management and reduction of cardiovascular risk.3 However, in addition to their cholesterol-lowering effects and benefit in preventing stroke, coronary heart disease, myocardial infarction, and peripheral artery disease, statins also seem to reduce inflammation in patients with cancer, dementia, severe infection, and pulmonary hypertension.4 In this issue of the Archives, Thomsen et al5 present evidence that statin use is associated with an improved prognosis after severe pneumonia. These data suggest a substantial decrease in mortality with statin use. C-reactive protein levels were lower in statin users compared with nonusers, which suggests that statins reduce inflammation.

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Figure.

Pathway of cholesterol biosynthesis. CoA indicates coenzyme A; HMG CoA, 3-hydroxy-3-methylglutaryl CoA.

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