Diet, physical inactivity and the prevalence of constipation throughout and after pregnancy

Few studies appear to have investigated the prevalence of constipation for all three trimesters of the gestative period, or indeed after birth. Using a prospective 4- to 7-day weighed food diary, International Physical Activity Questionnaire and 7-day bowel habit diary, dietary factors, physical activity levels and bowel habit parameters were assessed and examined concurrently at weeks 13, 25, 35 of pregnancy and 6 weeks post-partum. Ninety-four primiparous pregnant women were initially recruited, and 72, 59, 62 and 55 completed the first, second, third trimester and post-partum study stages, respectively. Key dietary factors and physical activity levels were compared between the constipated and non-constipated groups from each of the three trimesters and after parturition. Compared with non-constipated mothers-to-be, constipated participants consumed statistically significantly less water in the first trimester (P = 0.04), more food in the second trimester (P = 0.04), and less iron (P = 0.02) and food (P = 0.04) in the third trimester and after birth, respectively. No statistically significant differences were identified between light, moderate and vigorous physical activity levels when groups were compared. This study demonstrates that dietary factors may play a role in terms of preventing, or alleviating, bowel habit perturbations both throughout and after pregnancy. Further research is required to investigate the interrelationship between physical activity and constipation during and after pregnancy

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.)