Provided is a model for evaluating the degree of liver fibrosis constructed based on bile acids. A plurality of bile acids are simultaneously detected by a liquid chromatography-tandem mass spectrometer to further improve the accuracy in combination with other liver indicators; moreover, a multiple regression analysis method is applied to establish a grading diagnosis model for the degree of liver fibrosis caused by a chronic liver disease, which can significantly improve the sensitivity and specificity of the existing non-invasive diagnosis of liver fibrosis. When the model is used to evaluate the degree of liver fibrosis of a patient, the highest AUC is up to 0.9278; the sensitivity is up to 86.79%; and the specificity is up to 89.01%. The detection results are completely consistent with the pathological results of clinical liver biopsy. Therefore, patients need not receive a liver biopsy.

The present application provides compositions and methods for determining a disease or condition in a subject. The method comprises contacting a body fluid with a molecule comprising a reporter thereof and the reported is cleaved by an agent in the body fluid. Diseases and conditions that can be determined by the method are also described.

Methods, compositions, and kits for determining whether a subject has a liver condition, including hepatic steatosis, hepatic inflammation, hepatocellular ballooning, and/or hepatic fibrosis, are provided. In various embodiments, the subject's liver condition includes non-alcoholic steatohepatitis (NASH).

The present invention relates to a method for diagnosis, prediction and/or prognosis of an active autoimmune pathology in a subject, comprising detecting the co-expression of PD-1 and CD38 proteins at the surface of T lymphocytes in a biological sample from the subject.

The present invention also relates to a use of the pool of PD-1 (Programmed cell death 1) and CD38 protein as biomarkers for diagnosis, prediction and/or prognosis of an active autoimmune pathology in a subject.

The present invention further relates to a test device for detecting the co-expression of PD-1 and CD38 in a sample from a subject, comprising: (i) optionally means for obtaining a sample from the subject, and (ii) means for detecting the co-expression of PD-1 and CD38 at the surface of the T lymphocytes in said sample, and (iii) means for determining the frequency of co-expression of PD-1 and CD38 in the sample

Provided herein are methods for treating a patient having NASH who has been determined to have a particular threshold level of serum Pro-C3 (e.g., greater than 10 ng/ML) by administering to the patient a modified Fibroblast growth factor 21 (FGF-21) in an amount and with a frequency sufficient to treat NASH. Also provided are methods for monitoring responsiveness of a patient having NASH to treatment with a modified FGF-21, the method comprising: determining the serum Pro-C3 level in a blood sample from the patient obtained during or after treatment, wherein: a decreased serum Pro-C3 level in the blood sample from the patient obtained during or after treatment, as compared to the serum Pro-C3 level in a blood sample from the patient obtained prior to treatment with the modified FGF-21, indicates that the patient is responsive to treatment with the modified FGF-21.

Biomarkers of NASH, NAFLD, and fibrosis and methods for diagnosis (or aiding in the diagnosis) of NAFLD, NASH and/or fibrosis are described herein. Additionally, methods of distinguishing between NAFLD and NASH, methods of classifying the stage of fibrosis, methods of determining the severity of liver disease, methods of determining the severity of liver disease or fibrosis, and methods of monitoring progression/regression of NASH, NAFLD, and/or fibrosis are described herein.

Disclosed herein is a method for detecting liver disease in a patient. Also, disclosed are methods of isolating EVs derived from hepatocytes. Methods of assessing effectiveness of liver therapies are also disclosed. Methods involve isolating or otherwise obtaining EVs derived from hepatocytes and analyzing the content of the EVs.

Methods for diagnosing non-alcoholic steatohepatitis (NASH) and NASH with or without advanced liver fibrosis in a subject are provided, such methods including the detection of levels of a variety of biomarkers diagnostic of NASH versus simple steatosis and NASH with advanced liver fibrosis versus NASH without advanced liver fibrosis. The invention also provides methods treating NASH (e.g., NASH with or without advanced liver fibrosis) by administering a biomarker or an agent that modulates a biomarker of NASH or fibrosis. Compositions in the form of kits and panels of reagents for detecting the biomarkers of the invention are also provided.

Provided herein are methods for treating cholestasis in a subject having a liver disease. The method includes administering to the subject an Apical Sodium-dependent Bile Acid Transporter (ASBTI). More specifically, the present invention relates to methods for treating cholestasis in a subject where the method includes administering an ASBTI to a subject at a dose of at least 10 .Math.g/kg/day.

The present invention relates generally to methods treating cholestatic liver disease by administering an ileal bile acid transporter inhibitor (IBAT inhibitor), wherein the treatment results in increased event-free survival (EFS). The present invention relates also to methods for providing a prediction of response to an IBAT inhibitor therapy for treatment of cholestatic liver disease by predicting EFS.