005). By multivariable logistic regression, after controlling for age, sex, race, BMI, liver disease diagnosis, and alcohol intake, the relationship Fulvestrant mouse between caffeine intake and reduced fibrosis persisted both for the group as a whole (OR, 0.25; 95% CI, 0.09-0.67; P = 0.006) and for those with HCV infection (OR, 0.19; 95% CI: 0.05-0.66; P = 0.009) (Fig. 2). Age also remained significant by multivariable analysis, with increasing age increasing the risk of advanced fibrosis (OR, 1.06; 95% CI: 1.02-1.10; P = 0.001). In keeping with the reduced fibrosis on liver biopsy, patients with
greater caffeine consumption also had lower aspartate aminotransferase (51 versus 74 U/L; P = 0.01), alkaline phosphatase (66 versus 81 U/L; Selleckchem EPZ-6438 P = 0.005), and direct bilirubin (0.14 versus 0.19 mg/dL; P = 0.006) levels, and increased levels of serum albumin (3.99 versus 3.78 g/dL; P = 0.005). Because white patients consumed greater than twice the amount of caffeine as nonwhite patients, the effect
of race on the caffeine–fibrosis relationship was explored. Adjustment for race had no effect on the OR of advanced fibrosis for patients in the highest quartile of caffeine consumption (OR, 0.33; 95% CI, 0.13-0.83). The association between fibrosis and caffeine consumption above 308 mg/day was similar for white patients as for the group as a whole (OR, 0.30; 95% CI, 0.11-0.82; P = 0.018). A similar analysis for nonwhite patients revealed a nonsignificant protective association (OR, 0.62; 95% CI, 0.06-3.33; P = 0.69); however, only four (6%) nonwhite patients consumed more than 308 mg caffeine daily. When nonwhite patients were analyzed, using caffeine as either a continuous variable or above the 75th percentile for nonwhite patients only (130 mg/day), there was no apparent benefit to increasing caffeine intake and a nonsignificant trend toward an association with a greater risk of advanced fibrosis (OR,
>130 mg/day, 1.49; 95% CI, 0.48-4.6; P = 0.49). When caffeine intake was categorized by coffee-cup equivalents or compared selleck chemicals by quartiles of consumption, there appeared to be a threshold effect on fibrosis. Greater than 2–coffee-cup equivalents of caffeine was associated with lower rates of advanced fibrosis (20%), but the protective association was not linear with similar rates of advanced disease among those consuming 0 to 1 (31%) and 1 to 2 (45%) coffee-cup equivalents of caffeine (Supporting Table 1). This pattern was again more pronounced in patients with HCV (>2 cups/day, 16%; 1-2 cups/day, 48%; <1 cup/day, 33%; P = 0.035) (Supporting Table 2).
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