Idiopathic unconjugated
hyperbilirubinemia (
Gilbert's syndrome, or GS) is a relatively common congenital
hyperbilirubinemia occurring in 3-7% of the world's population. It has been recognized as a benign familial condition in which
hyperbilirubinemia occurs in the absence of structural
liver disease or
hemolysis, and the plasma concentration of conjugated
bilirubin is normal. Recently, it has been reported that unconjugated
bilirubin exhibited neurotoxicity in the developing nervous system. The 'neurodevelopmental hypothesis' of
schizophrenia proposes that an as-yet-unidentified event occurs in utero or during early postnatal life. We have observed that patients suffering from
schizophrenia frequently present with an increased unconjugated
bilirubin plasma concentration when admitted to the hospital. As a result, we noticed a relationship between unconjugated
bilirubin and the etiology of, and vulnerability to,
schizophrenia. Our reported findings suggest that there are significant biological and clinical character differences between schizophrenic patients with and without GS. From the viewpoint of the heterogeneity of
schizophrenia, there may be a poor outcome for the subtype of
schizophrenia with GS.