Measurement and clinical usefulness of bilirubin in liver disease.

Armando Raúl Guerra Ruiz,Manuel Morales Ruiz,Paula Iruzubieta,Gregori Casals Mercadal,Rosa Maria López Martínez,Marta Lalana Garcés,Bernardo Lavin,Javier Crespo

doi:10.1515/almed-2021-0047

Abstract

Elevated plasma bilirubin levels are a frequent clinical finding. It can be secondary to alterations in any stage of its metabolism: (a)excess bilirubin production (i.e.,pathologic hemolysis); (b)impaired liver uptake, with elevation of indirect bilirubin; (c)impaired conjugation, prompted by a defect in the UDP-glucuronosyltransferase; and (d)bile clearance defect, with elevation of direct bilirubin secondary to defects in clearance proteins, or inability of the bile to reach the small bowel through bile ducts. A liver lesion of any cause reduces hepatocyte cell number and may impair the uptake of indirect bilirubin from plasma and diminish direct bilirubin transport and clearance through the bile ducts. Various analytical methods are currently available for measuring bilirubin and its metabolites in serum, urine and feces. Serum bilirubin is determined by (1) diazo transfer reaction, currently, the gold-standard; (2) high-performance liquid chromatography (HPLC); (3) oxidative, enzymatic, and chemical methods; (4) direct spectrophotometry; and (5) transcutaneous methods. Although bilirubin is a well-established marker of liver function, it does not always identify a lesion in this organ. Therefore, for accurate diagnosis, alterations in bilirubin concentrations should be assessed in relation to patient anamnesis, the degree of the alteration, and the pattern of concurrent biochemical alterations.

Highlights

Bilirubin is an orange-yellow pigment of bile that results from the degradation of various heme-containing proteins, especially from hemoglobin catabolism
It can be secondary to alterations in any stage of its metabolism: (a) excess bilirubin production; (b) impaired liver uptake, with elevation of indirect bilirubin; (c) impaired conjugation, prompted by a defect in the UDP-glucuronosyltransferase; and (d) bile clearance defect, with elevation of direct bilirubin secondary to defects in clearance proteins, or inability of the bile to reach the small bowel through bile ducts
Glucuronic acid is added to unconjugated or indirect bilirubin (UCB) to render it water-soluble; it is either excreted into bile or recirculated back to the bloodstream, where it is filtrated by the kidneys and excreted through urine [1]

Summary

Introduction

Bilirubin is an orange-yellow pigment of bile that results from the degradation of various heme-containing proteins, especially from hemoglobin catabolism. Heme is broken down into biliverdin, which is converted into unconjugated or indirect bilirubin (UCB). UCB is water-insoluble and enters circulation bound to albumin. Glucuronic acid is added to UCB (conjugation) to render it water-soluble (direct bilirubin); it is either excreted into bile or recirculated back to the bloodstream, where it is filtrated by the kidneys and excreted through urine [1]. All liver lesions induce a decrease in the hepatocyte cell count, which may cause hyperbilirubinemia [3]. Hyperbilirubinemia can originate from an alteration in any stage of bilirubin metabolism: excess production, impaired liver uptake, conjugation defects, or biliary excretion defects [4]

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