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Side-effects of long-term prostaglandin E(1) treatment in neonates
Gyula Tálosi1, Márta Katona, Sándor Túri
1Department of Paediatrics, University of Szeged, Szeged, Hungary. talosigy@pedia.szote.u-szeged.hu
Insights
Prolonged Prostaglandin E1 (PGE1) therapy in neonates may cause adverse effects like feeding issues and hyperostosis. Fluid-electrolyte balance and pseudo-Bartter syndrome are dose-dependent risks requiring frequent monitoring.
Area of Science:
- Neonatal Cardiology
- Pediatric Pharmacology
Background:
- Prostaglandin E1 (PGE1) therapy is sometimes necessary for neonates with ductus arteriosus-dependent congenital heart defects for over two weeks.
- PGE1 analogues can lead to various adverse effects.
Purpose of the Study:
- To evaluate the adverse effects and clinical outcomes of prolonged Prostaglandin E1 (PGE1) treatment in neonates.
- To identify potential dose-dependent relationships between PGE1 therapy duration and adverse events.
Main Methods:
- Retrospective analysis of nine neonates receiving PGE1 treatment for more than 14 days.
- Monitoring of leukocyte counts, clinical symptoms, and biochemical parameters, including electrolytes and bicarbonate levels.
Main Results:
- Persistent high leukocyte and neutrophil counts were observed.
- Two patients experienced feeding difficulties and abdominal distension, with possible gastric-outlet obstruction.
- Three patients developed cortical hyperostosis and a pseudo-Bartter syndrome-like condition, particularly with higher cumulative PGE1 doses.
- Significant correlations were found between PGE1 dose and serum K+ levels (r=-0.770) and blood bicarbonate levels (r=0.889).
Conclusions:
- Frequent monitoring of fluid-electrolyte parameters is crucial for neonates on PGE1 therapy exceeding two weeks.
- Fluid-electrolyte disturbances and pseudo-Bartter syndrome appear to be more dose-dependent than cortical hyperostosis.
- Individual susceptibility, dose, and therapy length are important factors in adverse event development.
Background:
In some neonates suffering from ductus arteriosus dependent congenital heart defect, a Prostaglandin E(1) (PGE1) therapy longer than 2 weeks may be needed. However, PGE1 analogue compounds may produce several adverse effects.
Methods:
The authors retrospectively analyzed the data of nine patients who underwent a PGE1 treatment lasting longer than 14 days.
Results:
The leukocyte count of the patients remained high throughout the treatment period, and the proportion of neutrophils was over 50%. Transient feeding difficulty and abdominal distension, and possible signs of gastric-outlet obstruction, were observed in two cases. In the case of three patients, cortical hyperostosis developed after different cumulative doses (1584, 3384 and 4320 microg). Significant correlations were found between the doses of PGE1 and serum K(+) levels (r=-0.770, P < 0.05) and between the blood standard bicarbonate levels and PGE1 doses (r= 0.889, P < 0.01). Bartter syndrome-like condition developed in those three patients who received the largest cumulative doses.
Conclusions:
Fluid-electrolyte parameters must be controlled frequently in the case of each patient treated with PGE1 for longer than 2 weeks. Although the dose, the length of the therapy and individual susceptibility may be equally important, fluid-electrolyte disturbances and the development of pseudo-Bartter syndrome seem to be more dose-dependent than cortical hyperostosis.
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