Biochemical markers, extracellular components in liver fibrosis and cirrhosis.
Liver fibrosis and cirrhosis are common sequelae to diverse liver injuries in the tropics or Nigeria. The development of hepatic fibrosis or cirrhosis is due to increased synthesis, deposition, and possibly reduced degradation of hepatic extracellular matrix components, especially collagens, such as interstitial type I and III, basement membrane type IV, microfibrillar type VI, and pericellular type V, non-collagenous proteins, such as laminin, fibronectin, undulin, etc., and various types of proteoglycans, such as hyaluronan, etc. In Nigeria, the common approach for diagnosing or assessing the activity of connective tissue in this organ is the histological examination of a biopsy, if one is performed by a specialist physician. The liver biopsy provides a static picture of the changes that have already taken place in the liver. Another possible method is (where the facilities are available) a quantitative assessment of the liver biopsy by biochemical determination of total collagen via hydroxyproline. Biopsy is an invasive method and cannot be repeated often enough in the bid to ensuring an intensive follow-up of the changes taking place during the course of antifibrotic treatment or therapy. Thus, serum or other biological fluid assays for connective tissue proteins, such as the aminoterminal propeptide of type III Procollagen PIIINP, or the dimeric carboxyterminal domain of type IV collagen known as NCl or PIVCP, laminin, and others are essentially non-invasive and can be carried out repeatedly. In addition, the measurement of certain enzymes of connective tissue proteins in serum may the reflect activity of liver fibrogenesis. They offer the potential for diagnosis and therapeutic control. However, it is very important to note that circulating biochemical markers of fibrogenesis, fibrolysis or both may not reflect hepatic fibrosis or cirrhosis, since they are not liver-specific. Thus, the best diagnostic approach would be the identification and measurement in serum of the driving force of fibrogenic process.
Bolarin
D M
DM
Department of Chemical Pathology, College of Medical Sciences, University of Calabar, Calabar, Nigeria.
Azinge
E C
EC
D015415:Biomarkers / Q000032:analysis* / Q000378:metabolism*; D001706:Biopsy; D003094:Collagen / Q000378:metabolism; D017364:Collagenases / Q000378:metabolism; D004150:Dipeptidases / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism; D005353:Fibronectins / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D006821:Hyaluronoglucosaminidase / Q000378:metabolism; D006909:Hydroxyproline / Q000378:metabolism; D007797:Laminin / Q000378:metabolism; D008103:Liver Cirrhosis / Q000175:diagnosis* / Q000209:etiology / Q000378:metabolism*; D020782:Matrix Metalloproteinases / Q000378:metabolism; D009549:Nigeria; D010446:Peptide Fragments / Q000378:metabolism; D011347:Procollagen / Q000378:metabolism; D011509:Proteoglycans / Q000378:metabolism; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity
D015415:Biomarkers; D005353:Fibronectins; D006023:Glycoproteins; D007797:Laminin; D010446:Peptide Fragments; D011347:Procollagen; D011509:Proteoglycans; C041876:procollagen Type III-N-terminal peptide; C042813:procollagen type I carboxy terminal peptide; D003094:Collagen; D006821:Hyaluronoglucosaminidase; D004150:Dipeptidases; C022449:proline dipeptidase; D017364:Collagenases; D020782:Matrix Metalloproteinases; D006909:Hydroxyproline