Assessment of the environmental fate and effects of azilsartan, a selective antagonist of angiotensin II type 1.

In this paper the results of a thorough evaluation of the environmental fate and effects of azilsartan are presented. Azilsartan medoxomil is administered as a pro-drug for the treatment of patients with essential hypertension. The pro-drug is converted by hydrolysis to the active pharmaceutical ingredient azilsartan. Laboratory tests to evaluate the environmental fate and effects of azilsartan medoxomil were conducted with azilsartan and performed in accordance with OECD test guidelines. The predicted environmental concentration (PEC) in surface water was estimated at 0.32 µg L(-1) (above the action limit of 0.01 µg L(-1)), triggering a Phase II assessment. Azilsartan is not readily biodegradable. Results of the water sediment study demonstrated significant shifting of azilsartan metabolites to sediment. Based on the equilibrium partitioning method, metabolites are unlikely to pose a risk to sediment-dwelling organisms. Ratios of the predicted environmental concentrations (PECs) to the predicted-no-effect concentrations (PNECs) did not exceed the relevant triggers, and the risk to aquatic, sewage treatment plant (STP), groundwater and sediment compartments was concluded acceptable. A terrestrial assessment was not triggered. Azilsartan poses an acceptable risk to the environment.

Assessment of guided tissue regeneration procedures in intrabony defects with bioabsorbable and non-resorbable barriers.

THE PURPOSE OF THIS STUDY was to assess periodontal regenerative techniques in intrabony defects utilizing a bioabsorbable, polylactic acid (PLA) barrier or the non-resorbable, expanded polytetrafluoroethylene (ePTFE) barrier. Thirty patients (26 to 64 years old) each with one radiographically evident intrabony periodontal lesion of probing depth > or = 6 mm participated in a 12-month controlled clinical trial. The subjects were randomly divided into two independent groups. The test group (n = 16) received a PLA barrier. The control group (n = 14) received an ePTFE barrier. Plaque index (PI), gingival index (GI), probing depth (PD), clinical attachment level (CAL), and bone fill were recorded by a single calibrated examiner not involved with the surgical treatment prior to surgery, and at 6, 9, and 12 months postsurgery. The treatment results were statistically analyzed utilizing two sets of data. The "averaged-site" data set consisted of values computed from the averaging of measurements from all sites encompassing the defect. The second data set was comprised of only the deepest measurement of the defect. Statistical tests used to analyze these data sets included the t-test and paired t-test for parametric data and the Wilcoxon rank sum test and the Wilcoxon signed rank test for non-parametric data. Analyses with both the averaged-site data and deepest-site data resulted in significant improvements in PD reductions, CAL, and bone fill, after 12 months of healing with both the PLA and ePTFE barrier devices. Comparisons of healing response between treatments found no significant differences when the averaged-site data were analyzed. When only the deepest site of the defect was considered, the control group resulted in significantly more attachment gain (ePTFE, 3.36 mm; PLA, 1.75 mm; P < 0.02) and shallower probing depths (ePTFE, 3.29 mm; PLA, 4.69 mm; P < 0.01) than the test group. In intrabony defects, the use of PLA or ePTFE barriers in GTR procedures yielded comparable clinical results; however, in this study, data analysis using the deepest site of the defect found, after 12 months of healing, significantly more attachment gain and shallower probing depths with ePTFE.