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HIV-Specific Risk Factors for Nonalcoholic Fatty Liver Still Elusive
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15th Conference on Retroviruses and Opportunistic Infections
February 3-6, 2008
Boston
Mark Mascolini
Aside from treatment with nucleosides, risk factors for nonalcoholic fatty liver disease (NAFLD) were the same in a study of 52 HIV-infected people as in the general population [1]. But NAFLD proved 10 times more common in this small HIV cohort than in the general population of the same region in Italy [2].
Researchers at the University of Modena prospectively monitored 52 consecutive HIV-infected people referred to the metabolic clinic between January 2006 and June 2007 to gauge rates of NAFLD--fat buildups in the liver without hepatitis virus infection or alcohol abuse. NAFLD marked only by steatosis may have a benign course, the investigators noted, but NAFLD patients with nonalcoholic steatohepatitis (NASH) may wind up with end-stage liver disease or liver cancer.
Everyone studied took antiretrovirals for at least 2 years, and those with high lipids or high glucose were taking lipid-lowering or antidiabetes drugs for at least 6 months. The investigators did not study anyone with hepatitis B or C infection, anyone who drank more the 20 g of alcohol daily, anyone who used illicit drugs, anyone with autoimmune hepatitis, or anyone taking drugs for hypoglycemia. They defined NAFLD as a liver-to-spleen ratio below 1:1 on computed tomography (CT).
Forty of the 52 study participants (77%) were men, and the average age was 49 years (range 35 to 70 years). Average follow-up reached 306 days (range 217 to 517 days). While 26 people (50%) had NAFLD on their first CT, 25 (48%) had NAFLD at the end of follow-up. Six people got a new NAFLD diagnosis during the study for an incidence of 10.73 cases per 100 person-years. Seven people who started the study with NAFLD did not have it at the end of follow-up to yield an improvement rate of 17.39 cases per 100 person-years.
Four factors correlated with resolution of NAFLD:
· Higher baseline "good" high-density lipoprotein (HDL) cholesterol: 68.67 mg/dL with improvement versus 41.47 mg/dL without improvement, P < 0.001
· Higher baseline apolipoprotein A (a major lipoprotein in HDL cholesterol): 178 versus 130 mg/dL, P = 0.01
· Less cumulative nucleoside therapy: 80 versus 121 months, P = 0.05
· Higher baseline leg fat mass: 3501 versus 2037, P = 0.05
Comparing the 25% of people with the greatest NAFLD worsening with everyone else in the study, the investigators isolated five factors that predicted a worsening liver-to-spleen ratio:
· Higher baseline triglycerides: 426 mg/dL with greatest worsening in liver-to-spleen ratio versus 176 mg/dL in others, P < 0.001
· Higher baseline total cholesterol: 270 versus 192 mg/dL, P = 0.04
· Higher baseline apolipoprotein B (the primary apolipoprotein in "bad" low-density lipoprotein [LDL] cholesterol): 135.5 versus 107 mg/dL, P = 0.05
· Higher baseline serum insulin: 22.68 versus 14.03 mU/L, P = 0.03
· Falling HDL cholesterol: -9.5 versus -0.12 mg/dL, P = 0.04
Variables that did not correlate with a worsening liver-to-spleen ratio in this analysis were waist circumference, body mass index, glucose, HOMA-measured insulin resistance, HDL cholesterol, LDL cholesterol, apolipoprotein A, CD4 count, viral load, lipodystrophy, and metabolic syndrome.
The researchers note that NAFLD incidence in this study mirrors incidence in a Japanese general-population study [3]. But NAFLD incidence was 10 times lower in a 480-person Italian general-population study, a result suggesting that--at least in Italy--HIV infection heightens the risk of NAFLD. Because most risk factors for NAFLD in this study matched those in people without HIV, the one exception--cumulative nucleoside exposure--may bear the brunt of the blame in people with HIV. Or unidentified factors remain to be uncovered. (note from Jules: or perhaps HIV-associated abnormalities such as higher lipids/metabolic abnormalities in HIV might also be responsible).
An earlier study of 225 HIV-infected people by these investigators determined that treatment with nucleosides independently boosted the risk of NAFLD 11% for every year of therapy [4].
References
1. Guaraldi G, Squillace N, Stentarelli C, et al. Evolution of nonalcoholic fatty liver disease in HIV-infected patients: incidence, characteristics and predictors. 15th Conference on Retroviruses and Opportunistic Infections. February 3-6, 2008. Boston. Abstract 958.
2. Bedogni G, Miglioli L, Masutti F, et al. Incidence and natural course of fatty liver in the general population: the Dionysos study. Hepatology. 2007;46:1387-1391.
3. Hamaguchi M, Kojima T, Takeda N, et al. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann Intern Med. 2005;143:722-728.
4. Squillace N, Guaraldi G, Stentarelli C, et al. Non-alcoholic fatty liver disease (NAFLD) in HIV infected patients: prevalence, characteristics and
predictors. 11th European AIDS Conference. October 24-27, 2007. Madrid. Abstract PS5/5.
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