Although there are several diagnostic tools and measures of disease activity in viral liver diseases, some are invasive while others have limited predictive power. Predicting disease progression, especially in cirrhosis, has proven difficult. Patients respond differently to viral infections, and predicting which patients will progress and when is currently impossible. There is a need for new treatments that can better control or cure viral liver disease. To achieve this, non-invasive tests (NITs) are needed to improve the screening process and the evaluation of treatment efficacy.
The use of non-invasive biomarkers in viral liver diseases can accelerate the drug development process and enable personalized treatment options for the patients at risk of progression to cirrhosis, therefore, preventing end-stage liver disease death.
Viral liver diseases such as hepatitis are characterized by both inflammation and tissue fibrosis. The liver is rich in various collagens, proteoglycans, and matricellular proteins. These proteins are remodeled as part of liver homeostasis and regeneration. During remodeling, proteins are broken down and rebuilt as part of normal tissue repair and maintenance.
In viral liver diseases, the balance between tissue breakdown and rebuilding is disturbed, resulting in net tissue formation leading to fibrosis buildup. Nordic Bioscience's extracellular matrix-based biomarkers for liver fibrosis can quantify this tissue turnover in the liver directly in serological samples. What we offer is an accurate liver fibrosis biomarker panel that gives insight into disease progression.
As the best use of our biomarkers depends on disease severity and specific research questions we are happy to have our team of scientists discuss and understand your aims to select the most appropriate neo-epitope biomarkers that can help answer your research questions.
Nordic Bioscience biomarkers measured in serum differ in hepatitis C (HCV) and have been shown to help identify patients with high urgency of antiviral treatments (Metavir Fibrosis ≥3). Collagen formation (type III collagen; nordicPRO-C3™, type IV collagen; PRO-C4 or P4NP7S) and degradation (type I collagen; C1M, type III collagen; C3M, type IV collagen; C4M, type VI collagen; C6M) biomarkers are remodeled differently when comparing patients with early fibrosis (F0-F2), significant fibrosis (≥F2) and advanced fibrosis (≥F3). The combination of two collagen biomarkers, nordicPRO-C3™, and C4M, together with clinical features (gender, age, BMI) in a multiple-ordered logistic regression model shows improved value for identifying patients with significant (AUC=0.80) and advanced fibrosis (AUC = 0.88), as shown on Figure 1.[1] |  Figure 1. Collagen remodeling biomarkers detect fibrosis in chronic Hepatitis C[1] |
Our biomarker nordicPRO-C3™ measured in serum allows us to quantify the formation of type III collagen in the liver and help predict outcomes in liver disease. In patients with hepatitis C, the levels of serum nordicPRO-C3™ are related to disease outcomes (Figure 2.) Patients with hepatitis C and higher serum levels of nordicPRO-C3™ are more likely to have a sooner outcome than patients with low nordicPRO-C3™.[2]
Figure 2. NordicPRO-C3™ is a predictor of clinical outcome[2]
Baseline levels of nordicPRO-C3™ serve as a predictive factor for alterations in fibrogenesis among hepatitis C patients following treatment. The percentage changes in nordicPRO-C3™, specifically, are contingent upon the initial nordicPRO-C3™ levels. This implies that patients with higher baseline nordicPRO-C3™ might exhibit varying degrees of response to treatment with farglitazar compared to those with lower baseline nordicPRO-C3™ levels. These findings highlight the importance of considering baseline nordicPRO-C3™ levels when assessing the efficacy of farglitazar treatment in individuals with hepatitis C.[3] Baseline nordicPRO-C3™ levels are a reliable predictor of the changes observed in ISHAK score following farglitazar treatment among patients diagnosed with hepatitis C. The extent of alteration in ISHAK score during farglitazar treatment can be attributed to the initial levels of nordicPRO-C3™. Higher baseline nordicPRO-C3™ levels indicate a greater likelihood of significant modifications in ISHAK score following the administration of farglitazar for hepatitis C patients (Figure 3.) |  Figure 3. NordicPRO-C3™ assesses fibrogenesis in liver fibrosis and response to treatment[3] |
Viral liver disease is a generic term for liver damage caused by a viral infection. Hepatitis B and C are the most common viral infections that cause liver damage. Despite the different underlying viral infections, the pathogenesis of fibrosis can be divided into two phases. The acute inflammatory stage is followed by a chronic inflammatory stage with concurrent inflammatory, tissue destruction and repair processes.
How many people have hepatitis?
The prevalence of Hepatitis B and Hepatitis C varies worldwide. In 2015, an estimated 2 billion people worldwide were infected with Hepatitis B, resulting in 650,000 deaths per year. An estimated 71 million people were infected with Hepatitis C in 2015.
How is hepatitis treated?
Treatment of the underlying viral infection is best. Currently, several antiviral drugs (lamivudine, adefovir, entecavir, telbivudine, tenofovir, emtricitabine, standard and PEG-IFN) have shown to delay the progression of cirrhosis but rarely cure the viral infection. In most cases, therefore, lifelong treatment is required.
How is hepatitis diagnosed?
Diagnosis of hepatitis is based primarily on symptoms. Currently, diagnosis is based on the presence of a viral pathogen and blood tests to assess liver function. If blood tests indicate decreased liver function and advanced liver damage, further testing including imaging and liver biopsies may be required.
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