Herbal Medicines for Parkinson's Disease: A Systematic Review of Randomized Controlled Trials

OBJECTIVE: We conducted systematic review to evaluate current evidence of herbal medicines (HMs) for Parkinson's disease (PD). METHODS: Along with hand searches, relevant literatures were located from the electronic databases including CENTRAL, MEDLINE, EMBASE, CINAHL, AMED, PsycInfo, CNKI, 7 Korean Medical Databases and J-East until August, 2010 without language and publication status. Randomized controlled trials (RCTs), quasi-randomized controlled trials and randomized crossover trials, which evaluate HMs for idiopathic PD were selected for this review. Two independent authors extracted data from the relevant literatures and any disagreement was solved by discussion. RESULTS: From the 3432 of relevant literatures, 64 were included. We failed to suggest overall estimates of treatment effects on PD because of the wide heterogeneity of used herbal recipes and study designs in the included studies. When compared with placebo, specific effects were not observed in favor of HMs definitely. Direct comparison with conventional drugs suggested that there was no evidence of better effect for HMs. Many studies compared combination therapy with single active drugs and combination therapy showed significant improvement in PD related outcomes and decrease in the dose of anti-Parkinson's drugs with low adverse events rate. CONCLUSION: Currently, there is no conclusive evidence about the effectiveness and efficacy of HMs on PD. For establishing clinical evidence of HMs on PD, rigorous RCTs with sufficient statistical power should be promoted in future

The role of sex in the pathophysiology of pulmonary hypertension

Pulmonary arterial hypertension (PAH) is a progressive disease characterised by increased pulmonary vascular resistance and pulmonary artery remodelling as result of increased vascular tone and vascular cell proliferation, respectively. Eventually, this leads to right heart failure. Heritable PAH is caused by a mutation in the bone morphogenetic protein receptor-II (BMPR-II). Female susceptibility to PAH has been known for some time, and most recent figures show a female-to-male ratio of 4:1. Variations in the female sex hormone estrogen and estrogen metabolism modify FPAH risk, and penetrance of the disease in BMPR-II mutation carriers is increased in females. Several lines of evidence point towards estrogen being pathogenic in the pulmonary circulation, and thus increasing the risk of females developing PAH. Recent studies have also suggested that estrogen metabolism may be crucial in the development and progression of PAH with studies indicating that downstream metabolites such as 16α-hydroxyestrone are upregulated in several forms of experimental pulmonary hypertension (PH) and can cause pulmonary artery smooth muscle cell proliferation and subsequent vascular remodelling. Conversely, other estrogen metabolites such as 2-methoxyestradiol have been shown to be protective in the context of PAH. Estrogen may also upregulate the signalling pathways of other key mediators of PAH such as serotonin