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Increased bilirubin levels in de novo Parkinson's disease
Author(s) -
Moccia M.,
Picillo M.,
Erro R.,
Longo K.,
Amboni M.,
Santangelo G.,
Palladino R.,
Allocca R.,
Caporale O.,
Triassi M.,
Pellecchia M. T.,
Barone P.,
Vitale C.
Publication year - 2015
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/ene.12688
Subject(s) - bilirubin , medicine , parkinson's disease , oxidative stress , gastroenterology , direct bilirubin , heme oxygenase , biomarker , disease , heme , enzyme , biochemistry , biology , alkaline phosphatase
Background and purpose Oxidative stress is a central pathogenic mechanism of Parkinson's disease ( PD ), and the heme oxygenase ( HO ) bilirubin pathway is one of the main mammalian antioxidative defences. Indeed, there is growing evidence of HO −bilirubin upregulation from early phases of PD . Our aim was to investigate bilirubin as a possible biomarker of PD diagnosis and progression. Methods A cross‐sectional case−control study was performed to evaluate differences in bilirubin levels between newly diagnosed, drug‐naïve PD subjects and controls. Afterwards, PD subjects were included in a 2‐year longitudinal study to evaluate disease progression in relation to baseline bilirubin levels. Results Seventy‐five de novo PD subjects were selected and matched with 75 controls by propensity score. Analysis of variance showed higher bilirubin levels in PD patients compared with controls ( P < 0.001). Linear regression analysis failed to show a relationship between bilirubin and Unified Parkinson's Disease Rating Scale ( UPDRS ) part III ( P = 0.283) at baseline evaluation. At 2‐year follow‐up, indirect relationships between bilirubin levels and UPDRS part III ( P = 0.028) and between bilirubin levels and levodopa‐equivalent daily dosage ( P = 0.012) were found. Conclusions Parkinson's disease subjects showed higher levels of bilirubin compared with controls. Bilirubin increase might be due to HO overexpression as a compensatory response to oxidative stress occurring from early stages of PD .