Weller Clive, Charlett André, Oxlade Norman L, Dobbs Sylvia M, Dobbs R John, Peterson Dale W, Bjarnason Ingvar T
Section of Clinical Neuropharmacology, Institute of Psychiatry, London, UK.
Helicobacter. 2005 Aug;10(4):288-97. doi: 10.1111/j.1523-5378.2005.00329.x.
Eradicating Helicobacter may convert rapidly progressive idiopathic parkinsonism to quieter disease, however only a minority of probands have evidence of current infection.
To explore the cross-sectional fit of parkinsonism as an extra-alimentary consequence of Helicobacter pylori, using the serum antibody profile.
A discriminant index for parkinsonism was based on the Western Blot pattern of IgG antibodies against electrophoretically separated H. pylori antigens in 124 subjects with idiopathic parkinsonism, 196 without. In parkinsonism, association was assessed between index and 1, anthropometric measures; 2, current and 3, increase over 4 years in hypokinetic and psychomotor/psychometric disability; and 4, a global score of current severity.
Predicted probability of being labeled parkinsonian was greatest with cytotoxin-associated-gene-product (CagA) positivity and vacuolating-toxin negativity (p = .03 and .004, respectively, for antibody-age interactions), and urease-B negativity (p = .03, irrespective of age). In this circumstance, the odds for parkinsonism increased fivefold by age 80 years (p = .001). Helicobacter status, according to anti-urease enzyme-linked immunosorbent assay (ELISA), did not complement the model. Gradients, of clinically relevant size, were found between index and disease burden, despite the potentially confounding effect of antiparkinsonian medication. The higher the index 1, the worse was posture, as gauged by forward displacement of occiput (p = .04), 2, the shorter mean stride-length (p = .003), longer reaction time (= .002) and lesser cognitive efficiency (= .03), 3, the greater their deterioration (p = .006, .002, and .03 respectively), and 4, the greater the overall severity of parkinsonism (< .001).
The apparent importance of H. pylori in the etiology/pathogenesis of idiopathic parkinsonism is not confined to those with evidence of current infection.
根除幽门螺杆菌可能会使快速进展性特发性帕金森病转变为病情较稳定的疾病，然而只有少数先证者有当前感染的证据。
利用血清抗体谱探讨帕金森病作为幽门螺杆菌一种消化道外后果的横断面拟合情况。
帕金森病的判别指数基于124例特发性帕金森病患者和196例非帕金森病患者针对经电泳分离的幽门螺杆菌抗原的IgG抗体的免疫印迹模式。在帕金森病患者中，评估指数与以下各项之间的关联：1.人体测量指标；2.当前情况；3.4年内运动减少及精神运动/心理测量功能障碍的增加情况；4.当前严重程度的总体评分。
细胞毒素相关基因产物（CagA）阳性且空泡毒素阴性时（抗体与年龄的相互作用分别为p = 0.03和0.004）以及尿素酶B阴性时（无论年龄如何，p = 0.03），被判定为帕金森病的预测概率最高。在这种情况下，到80岁时患帕金森病的几率增加了五倍（p = 0.001）。根据抗尿素酶酶联免疫吸附测定（ELISA）得出的幽门螺杆菌状态并不能完善该模型。尽管抗帕金森病药物可能存在混杂效应，但在指数与疾病负担之间发现了具有临床相关性的梯度。指数越高，1.枕部向前移位所衡量的姿势越差（p = 0.04），2.平均步幅越短（p = 0.003）、反应时间越长（p = 0.002）且认知效率越低（p = 0.03），3.病情恶化越严重（分别为p = 0.006、0.002和0.03），4.帕金森病的总体严重程度越高（p < 0.001）。
幽门螺杆菌在特发性帕金森病病因/发病机制中的明显重要性并不局限于有当前感染证据的患者。
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