In an open pilot study, doses of safinamide (100, 150, and 200 mg once a day, higher than previously tested) were administered to 13 parkinsonian patients along with a stable dose of dopamine (DA) agonist, causing a significant progressive improvement in motor performance as evaluated by the Unified Parkinson Disease Rating Scale (UPDRS) part III over an 8-week period (4.2 points; P < 0.001). In association with levodopa, the same doses of safinamide in another group of patients (N = 11) induced a significant decrease in motor fluctuations (UPDRS part IV, 2.1 points; P < 0.001), accompanied by a dose-proportional increase of the levodopa AUC, up to 77% from baseline. Because MAO-B was fully inhibited (95%) at all doses tested, we suggest that these biochemical and symptomatic dose-dependent effects must be related to additional mechanisms of action, such as inhibition of glutamate release, increased dopamine release, or inhibition of dopamine re-uptake. These hypotheses are under investigation and will pursue confirmation in controlled clinical trials.

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Cardiovascular events are the main cause of death in hemodialysis patients. Nevertheless, acute myocardial infarction may be misdiagnosed in uremic patients, because typical markers have a high rate of false positivity. A recent two-year prospective study showed that predialytic high serum concentrations of troponin T and CK-MB mass were associated with high mortality, cardiac mortality, myocardial infarction and unstable angina (MACEs). We studied 16 uremic patients (13 M; 3 W) on standard HD and 6 patients (4 M; 2 W) on on-line HDF, who had been taking folic acid for at least three months. Patients who suffered from acute or chronic cardiac ischemic disease were excluded. Anthropometric parameters, pre and post-dialytic pH, HCO3 and electrolytes did not differ between the two groups. Kt/V and URR % were lower in conventional HD vs on-line HDF (p<0.04; p<0.04). ORR % was strongly elevated in on-line HDF compared with HD (p<0.005). In conventional HD, ORR % was directly correlated with Kt/V and URR% (r = 0.49, p<0.04; r = 0.48, p<0.04, respectively). Even in on-line HDF ORR % was directly correlated with Kt/V and URR % (r = 0.79, p<0.04; r = 0.76, p<0.05, respectively). Troponin I and CK-MB mass were not significantly different in pre vs post-dialysis, both in standard HD and on-line HDF. Nevertheless, in standard HD postdialytic troponin I correlated with serum sodium concentration (r = 0.93, p < 0.000), potassium (r = 0.67, p < 0.004) and serum chlorine (r = 0.92, p < 0.92, p < 0.000). CK-MB mass showed a correlation with serum chlorine (r = 0.49, p < 0.05). Postdialytic CK-MB mass correlated with serum potassium in on-line HDF (r = 0.83, p < 0.03). Our data suggest that hemodialytic treatments, both standard HD and on-line HDF, do not modify serum troponin I and CK-MB mass. Consequently, we can use these parameters for the diagnostic approach in acute or chronic ischemic heart disease in hemodialysis patients.