Correlation between Serum Zinc Levels and Levodopa in Parkinson’s Disease

Abstract

Long-term intake of potential zinc-chelating drugs may cause zinc deficiency. We postulated that zinc deficiency in Parkinson’s disease (PD) patients was related to the intake of drugs such as levodopa. We investigated the relationship between zinc levels and levodopa administration period, dosage, and symptoms of zinc deficiency in PD patients. We measured serum zinc levels and analyzed correlations between serum zinc levels, the levodopa oral administration period, dosage, dosing frequency, and zinc deficiency symptoms including taste disorders. Data analyses were performed using Spearman’s rank correlation coefficient. The mean serum zinc level was 60.5 ± 11.6 μg/dL. The mean administration period for levodopa was 8.0 ± 5.5 years, mean administration frequency 3.4 ± 0.9 times/d, and mean administration dose 420.6 ± 237.1 mg/d. Negative correlations between zinc levels and levodopa dosage and dosing frequency were found. Multiple regression analysis showed a significant correlation with the frequency of levodopa (β = −0.360, p = 0.007). No significant change in clinical symptoms was observed after zinc administration, but anxiety tended to improve. Our results indicated that frequent levodopa administration strongly influenced serum zinc levels which may have alleviating effects on psychiatric symptoms; therefore, preventing zinc deficiency can be important during PD treatment.

Efficacy of the iron‐chelating agent, deferiprone, in patients with Parkinson's disease: A systematic review and meta‐analysis

“…37 Other studies argued that zinc deficiency could be related to Levodopa administration in PD patients. Matsuyama et al 38 investigated the relationship between levodopa administration period, dosage, and zinc level in PD patients. They indicated that levodopa strongly influenced serum zinc levels which might have alleviating effects on psychiatric symptoms and recommended preventing zinc deficiency as an important step in PD treatment.…”

“…Other studies argued that zinc deficiency could be related to Levodopa administration in PD patients. Matsuyama et al 38 . investigated the relationship between levodopa administration period, dosage, and zinc level in PD patients.…”

Serum zinc deficiency is a potential risk factor for the occurrence of levodopa-induced dyskinesia in drug-naïve Parkinson’s disease

“…Second, low serum Zn levels could be associated with a higher dose of L-DOPA, which is a strong indicative factor of LID development. Matsuyama et al revealed that serum Zn levels were negatively associated with levodopa dosage and frequency (Matsuyama et al, 2021). Zn deficiency could be triggered by inadequate Zn intake, insufficient absorption, and increased need and excretion, which refers to continuous use of chelating drugs such as levodopa (Tomita and Yoshikawa, 2002;Szewczyk, 2013;Matsuyama , 2021).…”

“…Matsuyama et al revealed that serum Zn levels were negatively associated with levodopa dosage and frequency (Matsuyama et al, 2021). Zn deficiency could be triggered by inadequate Zn intake, insufficient absorption, and increased need and excretion, which refers to continuous use of chelating drugs such as levodopa (Tomita and Yoshikawa, 2002;Szewczyk, 2013;Matsuyama , 2021). Therefore, there is a possibility that the Zn-L-DOPA interaction could affect the total LEDD, which leads to a shortening of LID development.…”

“…L-3,4-dihydroxyphenylalanine (L-DOPA) is currently the best choice for managing Parkinson's disease (PD) and the most effective option for ameliorating motor symptoms of PD and maintaining quality of life (Thanvi et al, 2007;Connolly and Lang, 2014). However, long-term application of L-DOPA is known to be associated with various motor complications, such as motor fluctuation and dyskinesia (Ahlskog and Muenter, 2001;Matsuyama et al, 2021). Levodopainduced dyskinesia (LID) consists of involuntary movement such as choreic movement, dystonia, or a combination of various movement phenomena; this complication can be disabling and worsen quality of life in PD patients (Thanvi et al, 2007).…”