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Patients with REM sleep behavior disorder have higher serum levels of allantoin

L. Hasíková, J. Závada, T. Serranová, L. Kotačková, P. Kozlík, K. Kalíková, J. Trnka, D. Zogala, K. Šonka, E. Růžička, P. Dušek

. 2021 ; 90 (-) : 38-43. [pub] 20210730

Language English Country Great Britain

Document type Evaluation Study, Journal Article, Research Support, Non-U.S. Gov't

INTRODUCTION: Rapid eye movement (REM) sleep behavior disorder (RBD) is associated with an increased risk of developing Parkinson's disease (PD). Low uric acid (UA) levels are associated with the risk of development and progression of PD. Allantoin is the major oxidation product of UA and is considered as a biomarker of oxidative stress. We aimed to compare serum levels of UA, allantoin, and allantoin/UA ratio in RBD patients with those in healthy controls, and to examine their associations with clinical severity. METHODS: We evaluated serum levels of UA, allantoin, and allantoin/UA ratio in 38 RBD patients (one female, mean age 66.8 (SD 6.3) years) and in 47 controls (four females, 66.8 (7.6) years). All RBD patients were assessed according to an examination protocol, which included structured interview, Montreal Cognitive Assessment (MoCA), Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS), and dopamine transporter single-photon emission computed tomography (DAT-SPECT). The lower putaminal binding ratio from both hemispheres was used for analysis. RESULTS: Mean serum allantoin concentration and allantoin/UA ratio were significantly increased in the RBD group compared to controls (2.6 (1.8) vs. 1.4 (0.7) μmol/l, p = 0.0004, and 0.008 (0.004) vs. 0.004 (0.002), p < 0.0001, respectively). There were no significant differences in UA levels between the two groups. No significant associations between any biochemical parameter and RBD duration, putaminal binding ratio on DAT-SPECT, MDS-UPDRS, or MoCA score were found. CONCLUSION: Serum allantoin and allantoin/UA ratio are increased in RBD patients in comparison to controls, which may reflect increased systemic oxidative stress in prodromal synucleinopathy.

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$a Hasíková, Lenka $u Institute of Rheumatology, Prague, Czech Republic, Department of Rheumatology, First Faculty of Medicine, Charles University, Prague, Czech Republic
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$a INTRODUCTION: Rapid eye movement (REM) sleep behavior disorder (RBD) is associated with an increased risk of developing Parkinson's disease (PD). Low uric acid (UA) levels are associated with the risk of development and progression of PD. Allantoin is the major oxidation product of UA and is considered as a biomarker of oxidative stress. We aimed to compare serum levels of UA, allantoin, and allantoin/UA ratio in RBD patients with those in healthy controls, and to examine their associations with clinical severity. METHODS: We evaluated serum levels of UA, allantoin, and allantoin/UA ratio in 38 RBD patients (one female, mean age 66.8 (SD 6.3) years) and in 47 controls (four females, 66.8 (7.6) years). All RBD patients were assessed according to an examination protocol, which included structured interview, Montreal Cognitive Assessment (MoCA), Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS), and dopamine transporter single-photon emission computed tomography (DAT-SPECT). The lower putaminal binding ratio from both hemispheres was used for analysis. RESULTS: Mean serum allantoin concentration and allantoin/UA ratio were significantly increased in the RBD group compared to controls (2.6 (1.8) vs. 1.4 (0.7) μmol/l, p = 0.0004, and 0.008 (0.004) vs. 0.004 (0.002), p < 0.0001, respectively). There were no significant differences in UA levels between the two groups. No significant associations between any biochemical parameter and RBD duration, putaminal binding ratio on DAT-SPECT, MDS-UPDRS, or MoCA score were found. CONCLUSION: Serum allantoin and allantoin/UA ratio are increased in RBD patients in comparison to controls, which may reflect increased systemic oxidative stress in prodromal synucleinopathy.
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$a Závada, Jakub $u Institute of Rheumatology, Prague, Czech Republic, Department of Rheumatology, First Faculty of Medicine, Charles University, Prague, Czech Republic
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$a Serranová, Tereza $u Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
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$a Kotačková, Lenka $u Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
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$a Kozlík, Petr $u Department of Analytical Chemistry, Faculty of Science, Charles University, Prague, Czech Republic
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$a Kalíková, Květa $u Department of Physical and Macromolecular Chemistry, Faculty of Science, Charles University, Prague, Czech Republic
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$a Trnka, Jiří $u Institute of Nuclear Medicine, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic
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$a Zogala, David $u Institute of Nuclear Medicine, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic
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$a Šonka, Karel $u Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
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$a Růžička, Evžen $u Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
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$a Dušek, Petr $u Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic; Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Electronic address: petr.dusek@vfn.cz
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