Challenges of phototherapy for neonatal hyperbilirubinemia (Review)

Juan Wang, Genxin Guo, Aimin Li, Wen-Qi Cai, Xianwang Wang, Juan Wang, Genxin Guo, Aimin Li, Wen-Qi Cai, Xianwang Wang

Abstract

Phototherapy is universally recognized as the first option for treating neonatal jaundice due to its unparalleled efficiency and safety in reducing the high serum free bilirubin levels and limiting its neurotoxic effects. However, several studies have suggested that phototherapy may elicit a series of short- and long-term adverse reactions associated with pediatric diseases, including hemolysis, allergic diseases, DNA damage or even cancer. The aim of the present review was to summarize the etiology, mechanism, associated risks and therapeutic strategies for reducing high neonatal serum bilirubin levels. In order to shed light on the negative effects of phototherapy and to encourage implementation of a reasonable and standardized phototherapy scheme in the clinic, the present review sought to highlight the current understanding of the adverse reactions of phototherapy, as it is necessary to further study the mechanism underlying the development of the adverse effects of phototherapy in infants in order to explore novel therapeutic alternatives.

Keywords: adverse reaction; hyperbilirubinemia; jaundice; neonatal; phototherapy.

Copyright: © Wang et al.

Figures

Figure 1
Figure 1
Schematic illustration of bilirubin metabolism. Aging red blood cells are recognized and phagocytosed by mononuclear macrophages in the circulation, which then release hemoglobin. The released hemoglobin is catabolized to produce heme, which is then reduced and oxidized to bilirubin. Bilirubin formed by this process first binds to plasma albumin and is then transported to the liver as a bilirubin-albumin complex. Next, bilirubin is first separated from albumin and then taken up by hepatocytes. Subsequently, it is combined with ligandins (Y and Z proteins) to form a bilirubin-ligand complex, and is then transported to the smooth endoplasmic reticulum of the hepatocyte, where is conjugated with glucuronic acid to form conjugated bilirubin. Conjugated bilirubin is then released into the intestine with bile, hydrolyzed and reduced to generate bilinogen, the majority of which is excreted with the feces, while a small quantity of bilinogen is reabsorbed into the circulation by intestinal mucosal cells. The majority (~90%) of the reabsorbed bilinogen is discharged into the intestinal cavity with bile, forming the enterohepatic circulation of bilinogen, whereas only a small amount (~10%) enters the systemic circulation, passes through the kidneys and is excreted in the urine.
Figure 2
Figure 2
Mechanism of action of phototherapy for neonatal hyperbilirubinemia. Upon exposure to light, non-polar unconjugated bilirubin (Z,Z-bilirubin) in the skin is converted into water-soluble bilirubin isomers, including Z,E-bilirubin, E,Z-bilirubin, E,E-bilirubin, E,Z-cyclobilirubin and E,E-cyclobilirubin.

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