Reduced L-dopa absorption and increased clinical fluctuations in Helicobacter pylori-infected Parkinson's disease patients

被引:71
作者
Pierantozzi, M
Pietroiusti, A
Sancesario, G
Lunardi, G
Fedele, E
Giacomini, P
Frasca, S
Galante, A
Marciani, MG
Stanzione, P [1 ]
机构
[1] Univ Roma Tor Vergata, Neurol Clin, Rome, Italy
[2] IRCCS Fdn S Lucia, I-00179 Rome, Italy
[3] Univ Roma Tor Vergata, Dept Internal Med, Rome, Italy
[4] IST, Lab Pharmacol & Toxicol, Pharmacol & Neurosci Serv, Genoa, Italy
[5] Dept Expt Med, Sect Pharmacol & Toxicol, Genoa, Italy
[6] Univ Rome La Sapienza, Nervous & Mental Disorders Clin, Rome, Italy
[7] Univ Roma Tor Vergata, Dept Anesthesiol & Reanimat, Rome, Italy
关键词
D O I
10.1007/s100720170061
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
We report that the area under the curve of L-dopa plasma concentration, following the administration of a single 250 mg L-dopa dose, is augmented after Helicobacter pylori (HP) eradication in six Parkinson's disease (PD) patients showing high IgG antibody titer against HP. A prolongation of L-dopa clinical benefit was also observed. We suggest that HP infection-activated gastric alterations may be responsible, at least in pare, for the reported erratic efficacy of oral L-dopa therapy in some advanced PD patients. Given the high percentage of HP-positivity in the age cohorts including the largest prevalence of PD patients, we propose that HP eradication be recommended in all PD patients under L-dopa therapy.
引用
收藏
页码:89 / 91
页数:3
相关论文
共 8 条
[1]  
Calam J, 1999, YALE J BIOL MED, V72, P195
[2]   Reactive oxygen species activity and lipid peroxidation in Helicobacter pylori associated gastritis:: relation to gastric mucosal ascorbic acid concentrations and effect of H-pylori eradication [J].
Drake, IM ;
Mapstone, NP ;
Schorah, CJ ;
White, KLM ;
Chalmers, DM ;
Dixon, MF ;
Axon, ATR .
GUT, 1998, 42 (06) :768-771
[3]  
Fahn S., RECENT DEV PARKINSON, V2, P153, DOI DOI 10.1002/ANA.410220556
[4]   PARKINSONISM - ONSET PROGRESSION AND MORTALITY [J].
HOEHN, MM ;
YAHR, MD .
NEUROLOGY, 1967, 17 (05) :427-&
[5]  
Malfertheiner P, 1997, GUT, V41, P8
[6]  
Miyaji H, 1999, ALIMENT PHARM THERAP, V13, P1303
[7]  
Thor P, 1996, J PHYSIOL PHARMACOL, V47, P469
[8]   Helicobacter pylori activates the histidine decarboxylase promoter through a mitogen-activated protein kinase pathway independent of pathogenicity island-encoded virulence factors [J].
Wessler, S ;
Höcker, M ;
Fischer, W ;
Wang, TC ;
Rosewicz, S ;
Haas, R ;
Wiedenmann, B ;
Meyer, TF ;
Naumann, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (05) :3629-3636