Physical Compatibility of Medications Used in Critically Ill Patients with Balanced Fluid Solutions.

Using balanced fluids for resuscitation in patients with septic shock may lead to improved patient outcomes. However, compatibility data on co-administering balanced fluids via y-site connector with other intravenous medications is lacking. The purpose of this study was to examine the physical compatibility of frequently used intravenous medications for patients with septic shock with balanced fluids, Plasma-Lyte A, and Lactated Ringers, using a simulated y-site. Medications studied were acyclovir, amiodarone, ampicillin, aztreonam, cefepime, ceftriaxone, ciprofloxacin, heparin, hydrocortisone, gentamicin, levofloxacin, meropenem, piperacillin-tazobactam, tobramycin, and vancomycin. All medications were assessed with Plasma-Lyte A; amiodarone, ampicillin, cefepime, hydrocortisone, and levofloxacin were also assessed for compatibility with Lactated Ringers, based on missing or conflicting compatibility data. The medications were diluted to maximum concentrations used for patient administration and mixed with the balanced fluid solution in equal volumes. Physical compatibility was determined by assessing samples visually against light and dark backgrounds and using a laboratory turbidimeter. Assessments occurred at time of mixing and at 15-minute intervals up to one hour. Amiodarone demonstrated turbidimetric incompatibility when combined with Plasma- Lyte A or Lactated Ringers and should not be co-administered with either of these fluids via y-site connector. Each remaining study drug displayed visible and turbidimetric compatibility with the assessed balanced fluid. Acyclovir, ampicillin, aztreonam, cefepime, ceftriaxone, ciprofloxacin, gentamicin, heparin, hydrocortisone, levofloxacin, meropenem, piperacillin-tazobactam, tobramycin, and vancomycin exhibited physical compatibility with Plasma- Lyte A in a simulated y-site for up to one hour. Ampicillin, cefepime, hydrocortisone, and levofloxacin were also physically compatible with Lactated Ringers.

Clinical potential of liraglutide in cardiovascular risk reduction in patients with type 2 diabetes: evidence to date.

Metformin is the first-line therapy for the management of type 2 diabetes. After 3 months of metformin, add-on therapy can be considered if an individual's glycemic control has not been achieved for hemoglobin A1c, fasting blood glucose levels, and postprandial blood glucose levels. Liraglutide is a potential second-line option for the management of type 2 diabetes mellitus, particularly for those who are or may be at a high risk of cardiovascular disease. It can also be used an add-on therapy for those individuals with established cardiovascular disease. Liraglutide has additional benefits, such as no to minimal risk of hypoglycemia and promotion of weight loss through its mechanism of action. This particular article summarizes evidence on cardiovascular biomarkers and surrogate endpoints, along with macrovascular events, with liraglutide therapy. Overall, liraglutide has extensive cardiovascular evidence based on which it could be used as a desirable agent for glycemic control while lowering the risk of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, and hospitalization from heart failure.

Cytotoxicity of 2-chlorodeoxyadenosine and arabinosylcytosine in leukaemic lymphoblasts from paediatric patients: significance of cellular nucleoside transporter content.

2-chlorodeoxyadenosine (2-CdA) and arabinosylcytosine (araC) are nucleoside drugs that are used to treat various leukaemias, although 2-CdA has not been tested extensively in children with acute lymphoblastic leukaemia (ALL). Nucleoside cytotoxicity depends on the conversion of these agents to 5'-phosphate derivatives, following drug entry into cells via nucleoside transport (NT) processes. This study compared es nucleoside transporter content, determined using a flow cytometric assay with SAENTA [5'-S-(2-aminoethyl)-N6-(4-nitrobenzyl)-5'-thioadenosine] fluorescein, and cytotoxicities of 2-CdA and araC in fresh lymphoblasts from previously untreated paediatric ALL patients and the human T-lymphoblast cell line, CCRF-CEM. Lymphoblast samples from individual patients ranged widely in sensitivity to both 2-CdA (IC50, 6 nmol/l to > 5 micromol/l; mean = 418 nmol/l; n = 8) and araC (IC50, 59 nmol/l to > 5 micromol/l; mean = 1050 nmol/l; n = 7), although IC50 values for the two drugs were correlated (r = 0.78, P = 0.032, n = 7). Cellular es nucleoside transporter content varied more than 35-fold among samples from 10 patients. The correlation between es nucleoside transporter content and drug sensitivity was statistically significant for araC (r = -0.93, P = 0.023, n = 5), but not for 2-CdA (r = -0.57, P = 0.23, n = 6). Exposure of CCRF-CEM cells to araC resulted in a substantial araC concentration-dependent increase in the relative survival of es transporter-deficient cells, whereas the increase was slight following exposure to 2-CdA. We conclude that, in ALL lymphoblasts, es nucleoside transporter content is a determinant of araC sensitivity and that a deficiency in NT may impart resistance to araC.