Carl Grunfeld, MD, PhD
Staff Physician, Chief of Metabolism and Endocrine Sections, SFVAMC
Professor of Medicine, UCSF
Email: carl.grunfeld@ucsf.edu
Infection, Inflammation, and Atherosclerosis & HIV Complications
Dr. Grunfeld is the lead investigator in delineating how infection and inflammation can promote atherosclerosis, a major cause of admission to VA hospitals. He has shown that the body reacts to infection by changing how cholesterol and triglycerides travel in the blood - changes that fight infection but also promote atherosclerosis. He also showed that when macrophages are activated by infection or inflammatory signals, they turn into foam cells, the first step in atherosclerosis. Dr. Grunfeld was also the first researcher to show that HIV wasting is primarily due to opportunistic infections and not, as was thought, overwhelming replication of the virus. His group then demonstrated that growth hormone could restore muscle mass and improve function in patients with HIV infection. Dr. Grunfeld defined the metabolic and body fat changes that occur in HIV infection and showed that they would promote atherosclerosis. In addition, he was the first to propose that complications from protease inhibitors - insulin resistance, increased triglycerides and increased cholesterol - were not common to all protease inhibitors. Since the VA population of HIV-infected patients is aging, which predisposes to high triglycerides and diabetes, and many were exposed to Agent Orange, which predisposes to diabetes, the knowledge gained from these studies can help physicians tailor their therapies to optimize outcomes.
Khovidhunkit W, Kim MS, Memon RA, Shigenaga JK, Moser AH, Feingold KR, Grunfeld C. 2004. Effects of infection and inflammation on lipid metabolism: mechanisms and consequences to the host. J Lipid Res 45:1169-96.
Pao V, Lee GA, Grunfeld C. 2008. HIV therapy, metabolic syndrome and cardiovascular risk. Curr Atheroscler Rep 10:61-70.
