There may be a potential breakthrough in HIV treatment as new research shows that statins may hinder the progression of the worldwide epidemic. Evidence from both clinical trials and basic science studies suggest that statins have anti-inflammatory properties, which may additionally lead to clinical efficacy. Measurement of markers of inflammation such as high sensitivity C-reactive protein in addition to lipid parameters may help identify those patients who will benefit most from statin therapy.
Researchers recruited 24 participants to randomly take either a high dose of Lipitor (atorvastatin) or a placebo. Lipitor, manufactured by Pfizer, by 2003 it had become the best-selling pharmaceutical in history, with Pfizer reporting sales of $12.4 billion in 2008.
Participating patients, in two groups who took no AIDS medications and their cholesterol levels weren’t high enough to require taking statins. Neither group knew which pills they were taking. The drugs didn’t affect levels of HIV in the 22 patients who remained in the study, but the medications did appear to curb their immune systems, reducing the inflammatory response.
Andrew Carr, a professor of medicine at the University of New South Wales in Sydney, Australia stated:
“Persistent inflammation in patients with HIV, especially those on HIV treatment, has been associated with a worse clinical outcome. The cause of this inflammation remains unknown.”
It’s not unusual for HIV patients to take these cholesterol-lowering drugs, because the medications commonly used to combat HIV can cause cholesterol levels to skyrocket. Inflammation caused by the immune system is associated with HIV progression and death, and scientists have long wondered if statins’ anti-inflammatory properties might have benefits for HIV patients besides reducing the risk of cardiovascular disease .
Carr continues:
“For doctors, we should be studying the effects of statins over longer periods in patients with treated HIV disease whose virus is well-controlled but who still have excess inflammation to see if the anti-inflammatory effect of statins is still observed. If so, we would then need to determine if this anti-inflammatory effect improved health outcomes, which would require a long and very large study.”
Statins act by competitively inhibiting HMG-CoA reductase, the first committed enzyme of the HMG-CoA reductase pathway. Because statins are similar to HMG-CoA on a molecular level, they take the place of HMG-CoA in the enzyme and reduce the rate by which it is able to produce mevalonate, the next molecule in the cascade that eventually produces cholesterol, as well as a number of other compounds. This ultimately reduces cholesterol via several mechanisms.
As of 2010, a number of statins are on the market: atorvastatin (Lipitor and Torvast), fluvastatin (Lescol), lovastatin (Mevacor, Altocor, Altoprev), pitavastatin (Livalo, Pitava), pravastatin (Pravachol, Selektine, Lipostat), rosuvastatin (Crestor) and simvastatin (Zocor, Lipex). Several combination preparations of a statin and another agent, such as ezetimibe/simvastatin, sold as Vytorin, are also available.
Most individuals are placed on statins because of high levels of cholesterol. Though reduction of cholesterol is important, heart disease is complex and, as discussed previously, other factors such as inflammation may play a role. Thirty five percent of individuals who develop heart attacks do not have high blood cholesterol levels, yet most of them have atherosclerosis. This means that high levels of cholesterol are not always necessary for atherosclerotic plaques to form.
Source: The Journal of Infectious Diseases
Written by Sy Kraft, B.A.