Protein-induced Motor Fluctuations Despite Continuous Subcutaneous Foslevodopa/Foscarbidopa Infusion: A Case Report
Objective:
This is the first case report regarding the interaction between protein intake and foscarbidopa/foslevodopa (fCD/fLD) subcutaneous infusion, leading to worsening of parkinsonism in a patient with advanced Parkinson’s disease.
Background:
In patients with advanced Parkinson’s disease who are experiencing motor fluctuations refractory to standard carbidopa-levodopa treatment, fCD/fLD infusion by pump offers a therapeutic advantage as it administers levodopa subcutaneously and then directly into the bloodstream, bypassing gastrointestinal tract absorption. Protein intake should not affect levodopa absorption in Parkinson’s patients using fCD/fLD pump.
Design/Methods:
Case report.
Results:
A 41-year-old right-handed male with young-onset Parkinson’s disease diagnosed at age 35 was switched over to fCD/fLD pump due to increasing wearing off fluctuations after failing best medical treatment with immediate-release carbidopa/levodopa (IR CD/LD) and extended-release carbidopa/levodopa (Rytary and Crexont). The total maximum calculated levodopa dose per day was 1,050 mg prior to switching to fCD/fLD pump. At two-week post-pump initiation, patient reported increased ON time however, he still noted interference after eating, experiencing worsening symptoms, requiring him to take an extra dose of IR CD/LD as needed. We brought the patient back to the office for motor MDS-UPDRS OFF-ON testing on fCD/LD pump and then repeated motor MDS-UPDRS one hour and two hours after the consumption of 4 protein bars (total 40 g protein). Baseline motor MDS-UPDRS scores were 42 and 9 during OFF and ON, and 27 and 47 after 1hr and 2hr post-protein intake.
Conclusions:
Even though fCD/fLD pump is a subcutaneous levodopa infusion, it seems that oral protein interferes with its central effect. We propose that amino acids, the products of protein breakdown, may compete with levodopa for transport into the central nervous system at the L-type amino-acid transporter 1 (LAT1) protein located in the blood-brain barrier.
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