ABSTRACT
Low dose buprenorphine initiation (LDBI) is a dosing strategy used to transition patients from full opioid agonists to buprenorphine. The purpose of LDBI is to circumvent obstacles associated with disruption in analgesia, precipitated withdrawal, and prerequisite opioid withdrawal prior to initiating buprenorphine, as not all patients are able to tolerate physical withdrawal symptoms recommended by national guidelines. No literature exists directly comparing traditional buprenorphine initiation to LDBI. Until information on long-term outcomes is available, these dosing strategies should be reserved for patients unable to tolerate traditional buprenorphine initiation. Available published research suggests LDBI strategies will allow some patients to successfully transition to buprenorphine with minimal or no symptoms of withdrawal. Ensuring access to pharmacotherapy during hospital admission is a crucial time for potential intervention and should be considered when appropriate. This narrative review discusses the background of LDBI strategies as well as practical clinical and operational considerations for the inpatient clinician.
ABSTRACT
OBJECTIVE: Patent ductus arteriosus is a common morbidity associated with preterm birth. The incidence of patent ductus arteriosus increases with decreasing gestational age to approximately 70% in infants born at 25 weeks' gestation. Our major goal was to determine if genetic risk factors play a role in patent ductus arteriosus seen in preterm infants. METHODOLOGY: We investigated whether single-nucleotide polymorphisms in genes that regulate smooth muscle contraction, xenobiotic detoxification, inflammation, and other processes are markers for persistent patency of ductus arteriosus. Initially, 377 single-nucleotide polymorphisms from 130 genes of interest were evaluated in DNA samples collected from 204 infants with a gestational age of <32 weeks. A family-based association test was performed on genotyping data to evaluate overtransmission of alleles. RESULTS: P values of <.01 were detected for genetic variations found in 7 genes. This prompted additional analysis with an additional set of 162 infants, focusing on the 7 markers with initial P values of <.01, and 1 genetic variant in the angiotensin II type I receptor previously shown to be related to patent ductus arteriosus. Of the initial positive signals, single-nucleotide polymorphisms in the transcription factor AP-2 beta and tumor necrosis factor receptor-associated factor 1 genes remained significant. Additional haplotype analysis revealed genetic variations in prostacyclin synthase to be associated with patent ductus arteriosus. An angiotensin II type I receptor polymorphism previously reported to be associated with patent ductus arteriosus after prophylactic indomethacin administration was not associated with the presence of a patent ductus arteriosus in our population. CONCLUSIONS: Overall, our data support a role for genetic variations in transcription factor AP-2 beta, tumor necrosis factor receptor-associated factor 1, and prostacyclin synthase in the persistent patency of the ductus arteriosus seen in preterm infants.
