An Audit of Brivaracetam in Patients With Drug-Resistant Epilepsy and Psychiatric Comorbidities

BACKGROUND: Epilepsy mostly affects children in sub-Saharan Africa. However, little is known about the therapeutic itinerary of these children living with epilepsy (CWE). This study aimed to describe the therapeutic itinerary of CWE in Kinshasa and to analyze its relationships with clinical features, behavioral problems, and cognitive impairment. METHODS: This hospital-based study has included 104 CWE aged 6 to 17  years. The features of their therapeutic itinerary and their relationship with clinical features, behavioral problems, and cognitive impairment were analyzed. RESULTS: The vast majority of CWE (87%) has started their therapeutic itinerary by the Western medicine. The first source of information about epilepsy as well as the type of antiepileptic treatment varied with the socioeconomic status of families of CWE. The total duration of the therapeutic itinerary was shorter for the CWE who were living with both their parents (P = .038), who had generalized seizures (P = .0073) or who had no family history of epileptic seizures (P = .019). The CWE who had total behavioral problem, compared with the others, were putting more time (P = .021) to reach the Centre de Santé Mentale Telema (CSMT) after the suspicion or the diagnostic of epilepsy. The total duration of CWE who had cognitive impairment (P = .021) was longer than that of CWE who had not cognitive impairment. CONCLUSION: The therapeutic itinerary of CWE in Kinshasa began with Western medicine. The remainder of this therapeutic itinerary looks like what is described in sub-Saharan literature with the majority of CWE seeking the healing based on beliefs. This study also shows that the therapeutic itinerary of CWE was associated with socioeconomic conditions, clinical features, behavioral problems, and cognitive impairment

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)