The Autobio Laminin (LN) chemiluminescence immunoassay (CLIA) is intended for the quantitative determination of LN concentration in serum specimens, aiding in the diagnosis, monitoring and prognosis of hepatic fibrosis.
The formation of hepatic fibrosis is resulting from the over produce or deficient degradation, or both, of the extracelular matrix, hence excessive connective tissue builds up in the liver, then fibrosis is in turn formed. Hepatic fibrosis is the common pathological basis for chronic liver disorders. Various chronic liver disorders might gradually progress to hepatic fibrosis.
Various methods exist for the diagnosis of hepatic fibrosis, such as liver biopsy, imaging tests and serologic marker assays. The most reliable means to examine the extent of fibrosis and its activity is still the liver biopsy method. Although it is the Gold standard in hepatic fibrosis diagnosis, liver biopsy has many disadvantages. e.g. it is an invasive test, hence patients are reluctant to take this test and repeated tests are not able to be conducted. It is not possible to monitor the progress of the recovery and effects of the therapy. Fibrosis is characterized by focal inflammation and fibroelastosis, so deviations exist in specimen collection. Consequently, liver biopsy is much limited in clinical practice. Modern medical imaging methods such as type B ultrasound, CT, MRI etc. could observe certain symptoms of hepatic fibrosis. However, these medical imaging methods are yet to be confirmatory and identifiable, not to mention the inability to accurately determine the extent of liver fibrosis. Serological tests are able to identify different stages of liver fibrosis with relative accuracy, which indicates various changes during the development of liver fibrosis. Additionally, the effects of anti-fibrosis therapies could be monitored.
LN is a macromolecular glycoprotein. It is a hetero-trimer composed of α, β and γ 3 polypeptieds, with a molecular weight of more than 800 kD. LN is mainly found in lipocytes, hepatocytes and endothelial cells. It functions with type IV collagen to form basement membrane zone and to stabilize it. With the development of hepatic fibrosis and cirrhosis, LN is synthesized more quickly and deposits within Disse gaps. The binding with type IV collagen forms a continuous basement membrane, influencing the exchange of nutrients and metabolites between blood and tissues and causing hepatocyte failures. Meanwhile, it might be the major material basis for portal vein hypertension. From scientific findings, the worse the liver functions of cirrhosis patients are, the higher the serum LN concentrations would be. Therefore, laminin is a marker of the progression of hepatic sinusoid capillarization and portal liver fibrosis.
