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Fatty Liver Is Worse in HIV
"IMPACT of HIV COINFECTION on the DEVELOPMENT of STEATOSIS (FATTY LIVER) in PATIENTS with Chronic HCV Infection"
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Reported by Jules Levin
There were a number of presentations at DDW May 2005 on fatty liver & studies finding that fatty liver can be associated with accelerating HCV disease to fibrosis. The study presented in a poster at DDW by McGovern finds ART & nukes were associated with fatty liver. Elevations in lipids & insulin resistance have been found to be associated with fatty liver in HCV monoinfected individuals. Thee ‘triple hit’ combination of having HCV, metabolic syndrome, fatty liver may accelerate liver disease; the “double-hit” combination of HCV plus fatty liver may accelerate liver disease. Several studies presented at DDW & in previous literature have found that pioglitazone improved fatty liver & had a beneficial effect on fibrosis and imflamation. Numerous previous studies find that fatty liver can accelerate liver disease in HCV monoinfected individuals. Is there any reason to think this does not occur in coinfected patients? I don’t think so, but this question has not been studied by HIV researchers. Fatty liver may significantly contribute to the lower SVR rates to PegIFN/RBV therapy in coinfected patients. And perhaps therapy to improve fatty liver with pioglitazone & perhaps selecting HAART regimens less likely to cause metabolic syndrome could reduce fatty liver in coinfected patients & improve SVR rates. For HIV+ individuals, you don’t have to be HCV or HBV infected to have fatty liver & fatty liver by itself can cause liver disease.
Authors I Gaslightwala & EJ Bini reported study results at DDW finding that fatty liver (steatosis) is more common, more severe, & more likely to be a mixed pattern of microsteatosis & macrosteatosis in HCV/HIV coinfected patients than in those with HCV monoinfection. Among coinfected patients, steatosis was more common (72% vs 52%), and was more common in those with severe immunosuppression (<350 CD4 cells) (83% vs 64%). Future investigations to determine the impact of steatosis on fibrosis progression in coinfected patients are needed.
The authors provided this background. Although steatosis is common in HCV-infected individuals, the impact of HIV infection on the development of steatosis in these individuals in not known. The aims of this study were to determine the prevalence of steatosis in HIV/HCV coinfected patients & to evaluate whether steatosis is associated with HIV viral load, CD4 count, or treatment with HAART.
Consecutive patients who were scheduled for liver biopsy were prospectively identified & were interviewed by a research assistant who obtained detailed demographic & clinical data. Fibrosis was scored on a scale of 0 to 4; steatosis was scored according to the percent of hepatocytes involved: 0 (no steatosis); 1 (<33%); 2 (33% to 66%); or 3 (>66%) using the Brunt system.
RESULTS
707 patients (mean age 51.4) were enrolled, including 154 with HCV/HIV & 554 with HCV alone.
There were no differences between the groups with regard to age & gender, although coinfected patients were more likely to be Black (71.7% vs 40.1%, p<0.001) & weighed less (79.2 vs 88.4 kg, p<0.001).
Among coinfected patients, the median CD4 count was 429 cells/mm3, 50.6% had undetectable HIV RNA, & 84.4% were taking HAART.
Stage 3-4 fibrosis (43.6% vs 30.0%, p<0.001) & steatosis (72.1% vs 52.0%, p<0.001) were more common in coinfected patients.
The steatosis score (0, 1, 2, 3) in coinfected patients (27.9%, 24%, 37%, 11%) was significantly more severe (p<0.0001) than in those with HCV (48%, 31.8%, 17.1%, 3.1%).
Of patients with steatosis, the type of steatosis (micro, macro, or mixed) in HCV/HIV coinfected patients (18%, 36%, 45.9%) & HCV monoinfected (1.4%, 88.9%, 9.7%) differed significantly (p<0.001).
Among coinfected patients, the prevalence of steatosis was more common in patients with CD4 counts <350 (83% vs 64%, p=0.009) but did not differ between patients with undetectable vs detectable HIV RNA (75% vs 68%, p=0.32) or bwteen those who were & were not taking HAART (73.8% vs 62.5%, p=0.26).
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