title: The effect of levodopa benserazide hydrochloride on homocysteinemia levels in patients with Parkinson's disease and treatment of hyperhomocysteinemia.
abstract: This study aims to investigate hyperhomocysteinemia (HHcy) resulted from treatment in patients with Parkinson's disease (PD) and to evaluate the therapeutic outcome of HHcy.
  
  
  
  Ninety-three newly diagnosed PD patients were divided into Madopar group (treated with Madopar) and non-Madopar group (not treated with Madopar). Plasma Hcy levels were measured. Five months later, 67 patients presenting with HHcy were randomly divided into treatment group (n = 34) (receiving methylcobalamin 500 µg, tid, and folic acid 50 mg, tid, orally) and control group (n = 33).  Madopar dosage was maintained in both groups. MRI examination was performed to detect cerebral ischemia and patients were evaluated by Webster's rating scale. Plasma Hcy levels were measured at 3-month follow-up. Webster's scores and MRI were performed at 6-month follow-up.
  
  
  
  At the initial visit, Hcy levels of patients of Madopar group were significantly higher than those of non-Madopar group  (18.52 ± 6.48 µmol/L) vs. (15.78 ± 3.42), p < 0.05]. At 5-month follow-up, patients of the non-Madopar group presented significantly increased Hcy levels (18.97 ± 7.42 µmol/L) compare with pre-treatment Hcy levels (p < 0.05), whereas Hcy levels were slightly increased in patients of Madopar group (20.61 ± 7.87 µmol/L, p > 0.05). In the treatment group, serum Hcy levels were significantly decreased after 3-month treatment with methylcobalamin and folic acid (p < 0.01). However, serum Hcy levels were not significantly changed in patients of the control group. In addition, in the treatment group, no patient presented ischemic stroke with clinical symptoms and four patients were confirmed with new cerebral ischemic and lacunar lesions by MRI examination. However, in the control group, two ischemic strokes with clinical symptoms and 11 new cerebral ischemic and lacunar lesions were detected. Significant differences were observed between two groups (p < 0.05). Furthermore, post-treatment modified Webster scores were significantly decreased than pre-treatment scores for both groups. However, no significant differences were found between groups (p > 0.05).
  
  
  
  Oral administration of Levodopa in the treatment of PD can cause HHcy, which can result in increased occurrence of ischemic stroke. Supplementation of methylcobalamin and folic acid can effectively reduce Hcy level and thereby prevent the occurrence of ischemic stroke.
authors.affiliation: Department of Neurology, The First People's Hospital of Zhangjiagang, Zhangjiagang, China. qiuyi1028@sohu.com.
authors.forename: G
authors.initials: G
authors.lastname: Guo
authors.forename: S
authors.initials: S
authors.lastname: Xu
authors.forename: L-D
authors.initials: LD
authors.lastname: Cao
authors.forename: Q-Y
authors.initials: QY
authors.lastname: Wu
mesh_terms: D000978:Antiparkinson Agents / Q000009:adverse effects* / Q000627:therapeutic use; D001545:Benserazide / Q000009:adverse effects* / Q000627:therapeutic use; D015259:Dopamine Agents / Q000009:adverse effects* / Q000627:therapeutic use; D004338:Drug Combinations; D006710:Homocysteine / Q000032:analysis; D006801:Humans; D020138:Hyperhomocysteinemia / Q000139:chemically induced*; D007980:Levodopa / Q000009:adverse effects* / Q000627:therapeutic use; D010300:Parkinson Disease / Q000188:drug therapy*
chemical_list: D000978:Antiparkinson Agents; D015259:Dopamine Agents; D004338:Drug Combinations; C005177:benserazide, levodopa drug combination; D006710:Homocysteine; D007980:Levodopa; D001545:Benserazide