Increased bilirubin levels in de novo Parkinson's disease.
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| Title: | Increased bilirubin levels in de novo Parkinson's disease. |
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| Authors: | 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. |
| Source: | European Journal of Neurology. Jun2015, Vol. 22 Issue 6, p954-959. 6p. 1 Chart, 3 Graphs. |
| Subjects: | Bilirubin, Parkinson's disease, Bile pigments, Extrapyramidal disorders, Oxidative stress |
| Abstract: | 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. [ABSTRACT FROM AUTHOR] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | 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. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 13515101 |
| DOI: | 10.1111/ene.12688 |
