In the course of chronic hepatitis, complex pathological or pathophysiological change can be seen. The interrelation of these changes, however, has not fully clarified quantitatively to date. On the other hand, some of these changes in the liver can be evaluated quantitatively as imaging biomarkers such as pharmacokinetic parameters of hemodynamics and hepatocellular uptake function, R2* and fat fraction (FF), apparent diffusion coefficient (ADC), and liver stiffness (LS) using MR imaging ^1-5. The purpose of this study is to clarify the change and interrelation of these quantitative hepatic MR imaging biomarkers in the course of chronic hepatitis.Consecutive 34 patients with variable stage of chronic hepatitis who agreed to be included in this prospective clinical study approved by institutional review board were examined by MR imaging including multi-echo GRE (IDEAL IQ), diffusion weighted imaging (DWI), MR elastography (MRE), and gadoxetate disodium-enhanced MR imaging (EOB-MRI) using 1.5T MR scanner (GE Healthcare, Waukesha, WI, USA). In dynamic study, several concentrations of EOB diluted by normal saline were scanned together in order to evaluate contrast enhancement quantitatively using Differential Sub-sampling with Cartesian Ordering (DISCO) MR imaging that is a newly developed time-resolved MR imaging sequence. Arterial inflow velocity constant (K1a), portal venous inflow velocity constant (K1p), mean transit time (1/k2), distribution volume (Vd), hepatocellular uptake velocity constant (Kh) , concentration of EOB at 20 minutes after administration in extracellular fluid space (E20) and in hepatocytes (H20) were determined by compartment model analysis of EOB-DISCO-MR imaging. R2* and FF were determined from IDEAL IQ. ADC and LS were determined from DWI and MRE, respectively. Correlation coefficients of these hepatic MR biomarkers were statistically examined.Statistically significant correlation was observed in following biomarkers. K1a vs K1p: r = -0.64 (P < 0.001), K1a vs Kh: r = -0.48 (P = 0.004), K1a vs E20: r = 0.37 (P = 0.031), K1a vs H20: r = -0.41 (P = 0.016), K1p vs Kh: r = 0.55 (P = 0.001), K1p vs 1/k2: r = -0.43 (P = 0.012), K1p vs Vd: r = 0.45 (P = 0.008), K1p vs E20: r = -0.49 (P = 0.003), K1p vs H20: r = 0.50 (P = 0.003), K1a vs LS: r = -0.51 (P = 0.002), Kh vs E20: r = -0.64 (P < 0.001), Kh vs H20: r = 0.81 (P < 0.001), Kh vs LS: r = -0.44 (P = 0.010), Vd vs H20: r = 0.38 (P = 0.028), E20 vs FF: r = -0.42 (P = 0.014), E20 vs R2*: r = -0.45 (P = 0.007), H20 vs LS: r = -0.50 (P = 0.003), ADC vs LS: r = -0.35 (P = 0.041).Our results clarified that LS correlates with K1p，Kh, and H20 negatively. This can be explained by that increased interstitial matrix in space of Disse and portal hypertension caused by liver fibrosis may disturb normal membrane transport of EOB and portal venous blood inflow resulting in decrease of EOB concentration in hepatocytes at hepatobiliary phase in EOB-MRI; meanwhile liver fibrosis is considered to be responsible to increase of liver stiffness. On the other hand, K1p correlates with K1a, 1/k2, E20 negatively and positively with Vd. This can be explained by that decreased portal venous blood flow may be compensated by increased arterial blood flow; however, blood flow may be slow and decreased. Therefore, higher concentration of EOB may remain in extracellular fluid space without taken up by hepatocytes compared to normal hemodynamics. ADC was correlated only with LS negatively. Therefore ADC may provide unique information of the liver fibrosis apart from hemodynamics and hepatocellular uptake function; however the correlation was not as strong as pharmacokinetic parameters of EOB-MRI. E20 was negatively correlated with FF and R2*. This kind of correlation has not been reported before. One possible explanation is that the decrease of signal intensity at hepatobiliary phase in EOB-MRI due to fat or iron deposition may be reflected more in extracellular contrast enhancement effect of EOB during compartment model analysis because EOB can produce stronger contrast enhancement effect in hepatocyte than in extracellular fluid space. No significant correlation was seen between the degree of iron or fat content in the liver and liver stiffness.The change and interrelation of pathological and pathophysiological change of the liver in the course of chronic hepatitis can be evaluated quantitatively with use of hepatic MR imaging biomarkers such as pharmacokinetic parameters of EOB, ADC, R2*, Fat fraction, and liver stiffness; this may help non-invasive pathophysiological analysis of the liver disease in the future.