Abstract
Idiopathic unconjugated hyperbilirubinemia (Gilberts syndrome, GS) is a relatively common congenital hyperbilirubinemia occurring in 3-7% of the world 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 was reported that uncojugated bilirubin had neurotoxicity in the developing nervous system. The ‘neurodevelopmental hypothesis’ of schizophrenia was proposes that a yet-unidentified event occurring in utero or early postnatal life. We have observed that patients suffering from schizophrenia frequently present an increased unconjugated bilirubin plasma concentration when admitted to the hospital. Therefore, we had notice the relation between unconjugated bilirubin and the etiology and vulnerability of schizophrenia. Our reported findings suggest that there are significant biological and clinical character differences between schizophrenic patients with GS and without GS. From the viewpoint of heterogeneity of schizophrenia, there may be poor outcome for the subtype of schizophrenia with GS. Keywords: Schizophrenia, (Gilbert's Syndrome), Hyperbilirubinemia, liver disease, neurodevelopmental hypothesis, etiology, heterogeneity
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