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Prostaglandin-induced antral hyperplasia in neonates: clinical experience and dose-response characteristics
1Department of Radiology, Hospital for Sick Children, Toronto, Ont., Canada.
Insights
Prostaglandin (PG) therapy can cause antral hyperplasia (AH) in infants. Lower doses of PG were linked to less severe AH symptoms, and stopping PG treatment resolved the condition.
Area of Science:
- Pediatric Gastroenterology
- Neonatal Cardiology
- Pharmacology
Background:
- Prostaglandins (PG) are crucial for maintaining ductal patency in infants with cyanotic heart disease.
- Antral hyperplasia (AH) is a potential adverse drug reaction associated with PG administration.
- Previous reports identified AH in infants receiving PG for congenital heart defects.
Purpose of the Study:
- To characterize the dose-response relationship of prostaglandin-induced antral hyperplasia (AH).
- To analyze the clinical course and optimal management strategies for AH in infants.
- To investigate the variability in clinical presentation and obstruction severity related to AH.
Main Methods:
- Retrospective analysis of 14 infants diagnosed with AH (sonographically or pathologically).
- Correlation of cumulative prostaglandin dose with clinical presentation (gastric aspirates, palpable mass).
- Assessment of clinical and sonographic resolution after prostaglandin discontinuation.
Main Results:
- Infants with AH and large gastric aspirates received significantly lower cumulative PG doses (1,633 ± 1,266 µg/kg) compared to those with a palpable mass (3,458 ± 1,703 µg/kg) (p < 0.01).
- Clinical toxicity generally correlated with PG dose, but hyperplasia location influenced obstruction severity.
- Discontinuation of PG led to resolution of clinical and sonographic findings in all cases.
- Nasojejunal tube placement was successful in several cases, avoiding surgery.
Conclusions:
- Antral hyperplasia is a dose-related adverse effect of prostaglandins in infants.
- Management involves PG discontinuation, with potential for nasojejunal tube placement to avoid surgery.
- Variability in hyperplasia location can affect the degree of gastric outlet obstruction.
Abstract:
Antral hyperplasia (AH) induced by prostaglandins (PG) has been described by us recently in 5 infants with cyanotic heart disease receiving the drug. The purpose of the present study was to analyze 14 infants diagnosed as having AH either sonographically or pathologically in an attempt to characterize the dose-response characteristics of this adverse drug reaction, its clinical course and its optimal management. Infants with AH exhibiting large gastric aspirates have received a significantly lower cumulative dose (1,633 +/- 1,266 micrograms/kg) than those presented also with a palpable mass (3,458 +/- 1,703 micrograms/kg), (p < 0.01). While in general there is a dose-related clinical toxicity, variability in the location of the hyperplasia can explain cases of no apparent obstruction despite large cumulative doses of PG. In asymptomatic cases the antral hyperplasia, although visualized, it did not result in gastric outlet obstruction. In all cases followed by us to date, discontinuation of the PG has resulted in resolution of the clinical and sonographic findings. Nasojejunal tube was successfully attempted in several cases, preventing surgery in these very-high-risk infants.