Diagnostic prediction model for levodopa-induced dyskinesia in Parkinson's disease.


Journal

Arquivos de neuro-psiquiatria
ISSN: 1678-4227
Titre abrégé: Arq Neuropsiquiatr
Pays: Germany
ID NLM: 0125444

Informations de publication

Date de publication:
04 2020
Historique:
received: 13 10 2019
accepted: 10 11 2019
pubmed: 16 4 2020
medline: 10 9 2020
entrez: 16 4 2020
Statut: ppublish

Résumé

There are currently no methods to predict the development of levodopa-induced dyskinesia (LID), a frequent complication of Parkinson's disease (PD) treatment. Clinical predictors and single nucleotide polymorphisms (SNP) have been associated to LID in PD. To investigate the association of clinical and genetic variables with LID and to develop a diagnostic prediction model for LID in PD. We studied 430 PD patients using levodopa. The presence of LID was defined as an MDS-UPDRS Part IV score ≥1 on item 4.1. We tested the association between specific clinical variables and seven SNPs and the development of LID, using logistic regression models. Regarding clinical variables, age of PD onset, disease duration, initial motor symptom and use of dopaminergic agonists were associated to LID. Only CC genotype of ADORA2A rs2298383 SNP was associated to LID after adjustment. We developed two diagnostic prediction models with reasonable accuracy, but we suggest that the clinical prediction model be used. This prediction model has an area under the curve of 0.817 (95% confidence interval [95%CI] 0.77‒0.85) and no significant lack of fit (Hosmer-Lemeshow goodness-of-fit test p=0.61). Predicted probability of LID can be estimated with reasonable accuracy using a diagnostic clinical prediction model which combines age of PD onset, disease duration, initial motor symptom and use of dopaminergic agonists.

Sections du résumé

BACKGROUND
There are currently no methods to predict the development of levodopa-induced dyskinesia (LID), a frequent complication of Parkinson's disease (PD) treatment. Clinical predictors and single nucleotide polymorphisms (SNP) have been associated to LID in PD.
OBJECTIVE
To investigate the association of clinical and genetic variables with LID and to develop a diagnostic prediction model for LID in PD.
METHODS
We studied 430 PD patients using levodopa. The presence of LID was defined as an MDS-UPDRS Part IV score ≥1 on item 4.1. We tested the association between specific clinical variables and seven SNPs and the development of LID, using logistic regression models.
RESULTS
Regarding clinical variables, age of PD onset, disease duration, initial motor symptom and use of dopaminergic agonists were associated to LID. Only CC genotype of ADORA2A rs2298383 SNP was associated to LID after adjustment. We developed two diagnostic prediction models with reasonable accuracy, but we suggest that the clinical prediction model be used. This prediction model has an area under the curve of 0.817 (95% confidence interval [95%CI] 0.77‒0.85) and no significant lack of fit (Hosmer-Lemeshow goodness-of-fit test p=0.61).
CONCLUSION
Predicted probability of LID can be estimated with reasonable accuracy using a diagnostic clinical prediction model which combines age of PD onset, disease duration, initial motor symptom and use of dopaminergic agonists.

Identifiants

pubmed: 32294749
pii: S0004-282X2020005008206
doi: 10.1590/0004-282X20190191
pii:
doi:

Substances chimiques

Antiparkinson Agents 0
Dopamine Agonists 0
Levodopa 46627O600J

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

206-216

Auteurs

Bruno Lopes Santos-Lobato (BL)

Universidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Departamento de Neurociências e Ciências Comportamentais, Ribeirão Preto SP, Brazil.
Universidade de São Paulo, Núcleo de Apoio à Pesquisa em Neurociência Aplicada, São Paulo SP, Brazil.

Artur F Schumacher-Schuh (AF)

Hospital de Clínicas de Porto Alegre, Porto Alegre RS, Brazil.

Carlos R M Rieder (CRM)

Hospital de Clínicas de Porto Alegre, Porto Alegre RS, Brazil.

Mara H Hutz (MH)

Universidade Federal do Rio Grande do Sul, Departamento de Genética, Porto Alegre RS, Brazil.

Vanderci Borges (V)

Universidade Federal de São Paulo, Departamento de Neurologia, São Paulo SP, Brazil.

Henrique Ballalai Ferraz (HB)

Universidade Federal de São Paulo, Departamento de Neurologia, São Paulo SP, Brazil.

Ignacio F Mata (IF)

Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA.
University of Washington, Department of Neurology, Seattle, WA, USA.

Cyrus P Zabetian (CP)

Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA.
University of Washington, Department of Neurology, Seattle, WA, USA.

Vitor Tumas (V)

Universidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Departamento de Neurociências e Ciências Comportamentais, Ribeirão Preto SP, Brazil.
Universidade de São Paulo, Núcleo de Apoio à Pesquisa em Neurociência Aplicada, São Paulo SP, Brazil.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH