Wednesday, April 4, 2018

Exploring the Intra-tracheal route for Bronchopulmonary Dysplasia Therapy in Extreme Preterms


Exploring the Intra-tracheal route for Bronchopulmonary Dysplasia Therapy in Extreme Preterms


Abin Chandrakumar, Pharm.D
MS Pharmacology & Therapeutics Student | University of Manitoba, Canada
Graduate Research Assistant | Children’s Hospital Research Institute of Manitoba ,
Canada.

Having decided to pursue academics further, I was in the quest of graduate student positions in labs focusing on clinical studies during the Pharm.D internship period at Al Shifa College of Pharmacy. Halfway through my internship, I was offered a funded graduate student position by Dr. Geert W‘t Jong at his clinical research unit at the University of Manitoba. I joined the Department of Pharmacology & Therapeutics as agraduate student under the supervision of Dr.‘t Jong and has been associated with his team in several studies this year. The studies that I am currently part of includes a Phase I/II clinical trial and a large provincial database study.For the former, I was able to work in close collaboration with pharma-industry, receiving extensive training in regulatory submissions and clinical trial management. Through this article, I would like to share the background of the trial, which I anticipate will help the readership of Shifa ClinPharm to get an overview of the topic and plan novel collaborative research in this area.
Background:
Preterm infants, defined as those born at less than 37 weeks gestational age, have lungs which are not structurally and functionally developed completely. The surfactantis lipoproteins secreted by type II pneumocytes (specialized alveolar epithelial cells) and helps prevent thecollapse of smaller alveoli due to high surface pressure by reducing the surface tension. Infants who are born preterm might not have sufficient surfactant in terms of biochemical quality and quantity which combined with the structural immaturity of the lung precipitates neonatal respiratory distress syndrome (formerly known as hyaline membrane disease). The lack of surfactants can lead to atelectasis, a condition characterized by the non-uniform filling of the terminal airways leading to alveolar collapse. Infants born in the initial stages of thesaccular stage of lung development still have incompletely developed alveoli as well as immature type II pneumocytes and therefore require surfactant administration to maintain the terminal airway patency. Many of these infants require oxygen supplementation and/or mechanical ventilation to sustain life. Although these strategies have helped reduce mortality of infants as premature as 24 weeks gestational age, the long-term sequelae associated with the barotrauma and volutrauma of this supplemental therapies lead to the development of permanent lung injury called as the Bronchopulmonary Dysplasia (BPD). The definition of BPD has evolved over time and the currentdiagnostic criteria differentiate between infants born before and after 32 weeks gestational age.Although not all infants who receive the supplemental oxygenation and ventilation develop these conditions, those children who develop this condition can have reduced quality of life with developmental delay and recurrent pulmonary complications.
Steroids in Bronchopulmonary Dysplasia Prevention:
Steroids were found to reduce theincidence and severity of BPD when administered systemically to preterm infants receiving oxygen supplementation. In addition to reducing the underlying inflammatory response associated with BPD, steroids also increase surfactant production, accelerates lung cell differentiation, reduces vascular permeability, and increases lung fluid resorption. Regardless of the mechanism, corticosteroids have positive results in the treatment of preterm infants with BPD. However, the systemic use of steroids in this population can lead to neurodevelopmental and cognitive adversities. In the light of emerging short term and long term adverse outcomes, American Academy of Pediatrics and the Canadian Pediatric Society discouraged post-natal use of steroids in 2002. It was recommended that the therapy should only be used under exceptional circumstances and only with the understanding and agreement of parents outside randomized trials. This lead to a drastic reduction in both studies and clinical use of postnatal corticosteroids. Further studies shifted their attention to alternatives like Vitamin A, macrolides, leukotriene receptor antagonists, pulmonary vasodilators etc.whichalthough demonstrated potential, lacked definitive evidence of therapeutic efficacy.Furthermore, administration of steroids locally into the lungs as an inhalation to prevent the long-term adversities associated with the systemic drug exposure was considered in several studies. But, this method is technically challenging in this age group and there are concerns over the distribution of the drug to the terminal region of the respiratory tract where the drug needs to act.
Local Administration of Steroids: Evidence of Safety
Infants who develop respiratory distress are administered with exogenous surfactants (usually obtained from bovine and porcine sources)  via endotracheal tubes and my current research focuses on administering steroidvia this route (intratracheal) in combination with exogenous surfactants. This strategy not only uses a common route for achieving therapeutic goals, but the drugs supplement each other's action. The terminal airways if collapsed, will prevent the budesonide from reaching the distal regions and can lead to therapeutic failure. The surfactant clears the way for steroid by opening the terminal airway by reducing the surface tension and thus provides a larger area for the steroid to act. The steroid helps in the maturation of type II pneumocytes and thereby increase the endogenous surfactant production, thus supplementing the exogenously administered one. Although there were earlier concerns regarding alteration of the surfactant properties when combined with budesonide, especially thecholesterol containing surfactants (eg: BLES, Survanta), the surfactometry studies were mostly done using diluted surfactants with phospholipid concentration of 1mg/mL. However, the clinical phospholipid concentration of surfactants is different from each other and much higher than the concentration used in the surfactometry studies (27mg/mL for BLES, 76mg/mL for Curosurf, 25mg/mL for Survanta). This was tested in astudy by Yeh et al, where he determined the surface activity of Survanta in combination with Budesonide at both low and high concentration of surfactant phospholipid concentration. He found that the budesonide and surfactants when combined together at clinical concentrations, did not alter the surface activity. Two clinical trials in preterm infants were conducted using the surfactant Survanta in combination with Budesonide (0.25mg/kg of Budesonide) by Tsu F. Yeh. The results of the studies were promising with BPD reduction and absence of any major adverse effects of glucocorticoid therapyin the budesonide/surfactant group. The study is still in progress and preliminary data of the 2-4 year follow-up group did not show any long-term impairments in growth, neuromotor or cognitive function. In comparison to the control group. Another study in preterm lamb model also found that there was negligible systemic exposure when budesonidewas used in combination with a surfactant. However, the drawback associated with the clinical trial conducted by Yeh et al is that there has been no explanation regarding why the dose of 0.25mg/kg was administered in the clinical trial. There have been no PK-PD studies done in infants to determine the optimal dose that will provide maximum benefit and reduce the systemic exposure simultaneously.
Our Current Research: BITS Study
Our clinical research unit plans to do a Phase I/II clinical trial in preterm infants less than 29 weeks gestational age to determine the optimal dosage of the combination. The study which has been abbreviated as BITS (Budesonide with Intra-Tracheal Surfactants) has received conditional Institutional Ethics Board clearance and is currently waiting for Health Canada Division V clinical trial approval. The study is a single dose escalation study using the combination of varying concentrations of Budesonide with bovine lipid extract surfactant. The pharmacokinetic and pharmacodynamics behavior of the drug will be estimated with respect to fixed and random effect parameters using nonlinear mixed-effect modeling. Sensitivity analysis will be used in combination with the nonlinear mixed effect modeling to reduce the influence of any confounders that could alter the study results and substantiate the findings. This study is done in collaboration between University of Manitoba (Winnipeg, Canada), University of Toronto (Toronto, Canada; tentatively included) and University of Utah (Salt Lake City, USA). The study is funded by academic grants from Manitoba Institute of Child Health and for-profit sponsors. The anticipated duration of this study is 16 months and we anticipate that the study will help us establishthe platform for a large-scale Phase III clinical trial in the near future.
It is indelible that the clinical exposure I received at KIMS Al Shifa Hospital during my 6 years at Al Shifa College of Pharmacy has immensely helped me in blending in with the clinical team here. Also, the Pharm D curriculum, which was taught to me during the 4th and 5th year comprising of Applied Pharmacokinetics, biostatistics, Pharmacoepidemiology and research methodology had given me the theoretical background which helped me with a smooth transition.  Also, I am thankful to Dr. T.N.K Suriyaprakash and Dr. Dilip.C for their continuous support that helped me gain acceptance to the University previous year and also achieve the prestigious provincial scholarship of Research Manitoba Graduate Studentship this year.

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