Author Interviews, Cost of Health Care, Heart Disease / 19.08.2016
Outpatient Diuretic Protocol Can Keep Some Heart Failure Patients Out of Hospital
MedicalResearch.com Interview with:
[caption id="attachment_27101" align="alignleft" width="198"]
Dr. Leo Buckley[/caption]
Leo F. Buckley, PharmD
Virginia Commonwealth University
Richmond, Virginia
MedicalResearch.com: What is the background for this study?
Response: As the prevalence and costs of heart failure are expected to increase through the year 2030, significant efforts have been devoted towards devising alternatives to inpatient hospitalization for the management of heart failure decompensations. Since loop diuretics are the mainstay of treatment during the majority of hospitalizations, administration of high doses of loop diuretics in the outpatient setting has increased in popularity.
We intended to answer two questions with his study: first, can a patient-specific dosing protocol based on a patient’s usual diuretic dose achieve safe decongestion? and second, does this strategy alter the usual course of heart failure decompensation, which oftentimes culminates in inpatient hospitalization?
Dr. Leo Buckley[/caption]
Leo F. Buckley, PharmD
Virginia Commonwealth University
Richmond, Virginia
MedicalResearch.com: What is the background for this study?
Response: As the prevalence and costs of heart failure are expected to increase through the year 2030, significant efforts have been devoted towards devising alternatives to inpatient hospitalization for the management of heart failure decompensations. Since loop diuretics are the mainstay of treatment during the majority of hospitalizations, administration of high doses of loop diuretics in the outpatient setting has increased in popularity.
We intended to answer two questions with his study: first, can a patient-specific dosing protocol based on a patient’s usual diuretic dose achieve safe decongestion? and second, does this strategy alter the usual course of heart failure decompensation, which oftentimes culminates in inpatient hospitalization?
Prof. Philip Home[/caption]
Professor Philip Home D.M., D.Phil
Professor of Diabetes Medicine
Newcastle University
MedicalResearch.com: What is the background for this study? What are the main findings?
Prof. Home: MK1293 is a biosimilar insulin designed with the same amino acid sequence, manufacturing process and formulation as originator insulin glargine (Lantus). This is the clinical proving study in type 1 diabetes, being a 24-week randomized study in 508 participants between MK1293 and Lantus. The primary efficacy endpoint of non-inferiority of HbA1c was met, as was a secondary of equivalence (difference in change from baseline 0.04 (95% CI -0.11, 0.19) %-units), with other measures including hypoglycaemia, insulin antibodies and adverse events also consistent with similarity.
Dr. Lynda Harris[/caption]
Lynda Harris PhD
Lecturer in Pharmaceutics
University of Manchester
Manchester Pharmacy School
Maternal and Fetal Health Research Centre
Manchester
MedicalResearch.com: What is the background for this study?
Dr. Harris: Pregnancy complications such as pre-eclampsia and fetal growth restriction remain a problem despite advances in antenatal care, and impact heavily on future health: small size at birth is associated with an increased risk of cardiovascular disease and diabetes in later life. Drugs to improve pregnancy outcome are severely lacking, as pregnant women are considered a high risk cohort by drug companies, who fear expensive lawsuits associated with side effects and teratogenicity. The majority of pregnancy complications are caused by a poorly growing or poorly functioning placenta. A number of potential drugs have been identified that enhance placental function in vitro, and improve fetal growth in animal models; however, there is currently no means of restricting their actions to the placenta, and systemic administration of these drugs to pregnant women is not feasible due to the risk of adverse effects in other tissues. To address this issue, we have identified a series of placental “homing peptides” which we have used to create nanocarriers for targeted delivery of drugs to the placenta.
Dr. Victor Serebruany[/caption]
MedicalResearch.com Interview with:
Dr. Anick Bérard[/caption]
MedicalResearch.com Interview with:
Anick Bérard PhD FISPE
Research chair FRQ-S on Medications and Pregnancy
and Director, Réseau Québécois de recherche sur le médicament (RQRM)
and Professor, Research Chair on Medications, Pregnancy and Lactation
Faculty of Pharmacy University of Montreal
and Director, Research Unit on Medications and Pregnancy
Research Center
CHU Ste-Justine
Medical Research: What is the background for this study? What are the main findings?
Dr. Bérard: Paroxetine (one of the most used antidepressant during pregnancy) has been studied extensively over the past 10-12 years. In 2005, a black box warning was put on the Paxil label to caution against use during pregnancy due to the increased risk of cardiac defects. The ACOG 2010 guidelines also suggested switching to other antidepressants during pregnancy. Over the past decade, many studies, including meta-analyses, were performed on on paroxetine use during pregnancy and the risk of cardiac malformations - but results were sometimes statistically significant or not, although a consistent increased risk was observed. It was thought that these variations could be explained by different study designs, patient populations, and because maternal depression was not always taken into account correctly. Hence, we undertook another meta-analysis (the most recent and updated) to quantify the risk of cardiac defects overall as well as specific cardiac defects associated with paoxetine use during pregnancy and to assess the impact of study designs, maternal depression and patient population on the effect of the risk.
We found that women using paroxetine during the first trimester of pregnancy (critical time-window for malformations) were 23% more at risk of having a child with malformations (15 studies combined) - baseline risk of malformation is 3-5% and thus a 23% increased risk is 3.69-6.15% absolute risk; women using paroxetine during the first trimester of pregnancy were 28% more at risk of having a child with cardiac malformations (18 studies combined) - baseline risk of cardiac malformation is 1% and thus a 28% increased risk is 1.28% absolute risk. We found that paroxetine was increasing the risk of many specific cardiac defects as well. Although the estimates varied depending on the comparator group, study design, and malformation detection period, a trend towards increased risk was observed.
Dr. Klessig[/caption]
MedicalResearch.com Interview with:
Prof. Daniel F. Klessig
Boyce Thompson Institute for Plant Research,
Department of Plant Pathology and Plant-Microbe Biology
Cornell University, Ithaca, New York
MedicalResearch: What is the background for this study?
Prof. Klessig: Acetyl salicylic acid, commonly called aspirin, has been the most widely used drug worldwide for more than a century. Currently, 80 million pounds of aspirin are produced worldwide every year and almost 30 billion tablets are consumed annually in the US alone. Long before German pharmacologist Johann Buchner identified the salicylic acid derivative salicin in 1828 as the ingredient in willow bark that is responsible for its therapeutic effects, different cultures throughout the world were, and many still are, using a variety of plants rich in salicylic acid derivatives, such as willow, wintergreen, and meadowsweet, to treat pain, fever, swelling, and other maladies. Aspirin also is used to reduce the risk of heart attack, stroke, and certain cancers.
One might expect that aspirin’s mechanisms of action would be well understood, given its extraordinarily widespread use and the fact that it was first synthesized by the Bayer chemist Felix Hoffmann over 100 years ago. The prevailing view in the biomedical community has been that aspirin works primarily, if not exclusively, by irreversibly inhibiting the enzymatic activities of cyclooxygenases 1 and 2 (COX1 and COX2), thereby disrupting the synthesis of inflammation-inducing prostaglandins. However, this assumption ignores two important facts.