Correlations of Hepatic Hemodynamics, Liver Function, and Fibrosis Markers in Nonalcoholic Fatty Liver Disease: Comparison with Chronic Hepatitis Related to Hepatitis C Virus

Abstract

The progression of chronic liver disease differs by etiology. The aim of this study was to elucidate the difference in disease progression between chronic hepatitis C (CHC) and nonalcoholic fatty liver disease (NAFLD) by means of fibrosis markers, liver function, and hepatic tissue blood flow (TBF). Xenon computed tomography (Xe-CT) was performed in 139 patients with NAFLD and 152 patients with CHC (including liver cirrhosis (LC)). The cutoff values for fibrosis markers were compared between NAFLD and CHC, and correlations between hepatic TBF and liver function tests were examined at each fibrosis stage. The cutoff values for detection of the advanced fibrosis stage were lower in NAFLD than in CHC. Although portal venous TBF (PVTBF) correlated with liver function tests, PVTBF in initial LC caused by nonalcoholic steatohepatitis (NASH-LC) was significantly lower than that in hepatitis C virus (C-LC) (p = 0.014). Conversely, the liver function tests in NASH-LC were higher than those in C-LC (p < 0.05). It is important to recognize the difference between NAFLD and CHC. We concluded that changes in hepatic blood flow occurred during the earliest stage of hepatic fibrosis in patients with NAFLD; therefore, patients with NAFLD need to be followed carefully.

Black Phosphorus Quantum Dots Gated, Carbon‐Coated Fe3O4 Nanocapsules (BPQDs@ss‐Fe3O4@C) with Low Premature Release Could Enable Imaging‐Guided Cancer Combination Therapy

“…The biochemical indices containing total bilirubin (TB), aspartate aminotransferase (AST), serum creatinine (Cr) and alanine aminotransferase (ALT) were investigated;ALT,AST,a nd Cr are closely correlated with liver and kidneys functions. [37] Briefly,s imilari ndicator levels were found in BPQDs (Figures 3B) EGFR was conjugated to the surface of BPQDs@DOX@ss-Fe 3 O 4 @C NPs to examinet he NPs targeting ability in vivo, using dualM R/fluorescence imaging device.E GFR is al arge family of receptor tyrosine kinases (TK) expressed in several types of cancer,i ncluding,l ung, breast, esophageal,a nd head and neck. [38] In this study,t he level of EGFR was tested in normalc ells (H522 and MCF-10A) and cancerc ell lines (A549 and MCF-7;F igure 3D,aand Figure S11A); compared to normalc ells, EGFR was highly expressed in cancer cell lines.…”

Quantitative Proteomics and Mechanistic Modeling of Transporter‐Mediated Disposition in Nonalcoholic Fatty Liver Disease

“…Collectively, the quantitative proteomics‐informed PBPK analysis complement the notion of increased MRP3‐mediated basolateral and decreased MRP2‐mediated canalicular efflux clearance in NASH. Additional factors such as a change in hepatic hemodynamics (e.g., liver blood flow and microvasculature) in NAFLD—which are challenging to capture in the current PBPK framework due to limited knowledge—may contribute to deviation from the model simulations. Overall, the transporter expression differences may contribute significantly to the PK variability in NASH, although the magnitude of such PK changes could typically be less than twofold on the basis of the quantitative proteomics data and the available clinical PK data.…”

The Relationship between Serum Bilirubin and Elevated Fibrotic Indices among HBV Carriers: A Cross-Sectional Study of a Chinese Population

“…All of them were obtained according to the published formula, as previously described [46,47,48]. $\text{FIB}-4=\frac{\text{Age} \left(\text{years}\right)\times \text{AST} \left(\mathrm{normalU}/\mathrm{normalL}\right)}{\text{Platelet count} \left(\frac{{10}^9}{\mathrm{L}}\right)\times {\left[\text{ALT} \left(\mathrm{normalU}/\mathrm{normalL}\right)\right]}^{1/2}}$ $\text{APRI}=\frac{\text{AST} \left(/\text{ULN}\#\right)}{\text{Platelet count} \left(\frac{{10}^9}{\mathrm{L}}\right)}\times 100$ (# where ULN = upper limit of normal for that laboratory, the upper limit of normal for both AST and ALT was 40 U/L).…”