Abstract

I read with interest the paper by Drs. Bach and colleagues on the relevance of hyperbilirubinemia in acute and transient psychotic disorders. The authors’ main aim was to replicate previous findings of 2 study groups demonstrating a possible link between hyperbilirubinemia and schizophrenia [1] [2]. The authors, however, do not cite opposite studies, in which schizophrenia was associated with low serum bilirubin levels [3] [4] [5], as well as other endogenous antioxidants [6] [7]. In this regard, it is very curious that the prevalence of hyperbilirubinemia >17 μmol/L in Drs. Bach et al.'s study ranged between 15.7–33% for F2–F9 psychiatric diagnoses (2–4 times higher compared to the general population), especially when the authors admit that the Gilbert syndrome mutation is an unlikely explanation. We have proved, in our own recent study on 137 schizophrenic patients and healthy controls, that schizophrenics display significantly lower serum bilirubin levels regardless of the UGT1A1 genotypes responsible for Gilbert syndrome [8]. In this study, each increase in serum bilirubin by 1 μmol/L was associated with a 19% decrease in the odds for schizophrenia status (P=10−6), suggesting low (and thus not high) serum bilirubin levels to be a significant risk factor for this psychiatric disease.

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