Gastric foveolar hyperplasia and gastric outlet obstruction caused by long-term prostaglandin use

A male neonate, who was born in an external center from the second pregnancy of an 18-year-old mother, was diagnosed with transposition of the great arteries on the 4th day after birth. Prostaglandin, milrinone and dopamine treatments were started, and the neonate was referred to our neonatal clinic. On postnatal day 9, angiographic balloon atrial septostomy was performed and prostaglandin infusion was discontinued during follow-up. Prostaglandin infusion was restarted for the neonate as desaturation developed on the 13th postnatal day. A stent was placed in the patent ductus arteriosus of the neonate who was admitted for angiography for the second time. The chest X-ray performed on the 22nd day because of postpartum abdominal distension showed irregularity in the stomach contours and no gas passage to the distal part of the stomach (Fig. 1). Abdominal ultrasonography was performed for further imaging (Fig. 2). Please share your thoughts on the neonate radiological images presented below.Fig. 22a. Transverse ultrasound image of the antropyloric region showing marked antral mucosal hypertrophy. 2b. Longitudinal ultrasound image of the pyloric diameter. The pyloric muscle thickness measurements are indicated by the white marker.View Large Image Figure ViewerDownload Hi-res image Download (PPT) -Gastric foveolar hyperplasia occurred due to long-term prostaglandin use.-Transient gastric outlet obstruction occurred secondary to gastric foveolar hyperplasia. One of the long-term adverse effects of prostaglandin E1 (PGE1 treatment for ≥120 hours) is gastric outlet obstruction (measured through the ultrasound findings of elongated and thickened pyloric musculature or marked antral mucosal hypertrophy) [1Perme T. Mali S. Vidmar I. Gvardijančič D. Blumauer R. Mishaly D. et al.Prolonged prostaglandin E1 therapy in a neonate with pulmonary atresia and ventricular septal defect and the development of antral foveolar hyperplasia and hypertrophic pyloric stenosis.Ups J Med Sci. 2013; 118: 138-142Crossref PubMed Scopus (17) Google Scholar,2Akkinapally S. Hundalani S.G. Kulkarni M. Fernandes C.J. Cabrera A.G. Shivanna B. et al.Prostaglandin E1 for maintaining ductal patency in neonates with ductal-dependent cardiac lesions.Cochrane Database Syst Rev. 2018; 27: CD011417Google Scholar]. Gastric outlet tract obstruction may occur after >5 days of PGE1 treatment. In our case, Prostaglandin E1 had complex effects on the gastrointestinal tract by the 3rd week. PGE1 induces proliferation of the gastrointestinal mucosa, especially in the antral region of the stomach, where the gastric pits (foveolae) are typically the longest. Additionally, PGE1 relaxes the circular muscles of the gastrointestinal tract and the cardia. These changes are predominantly caused by the elongation and dilatation of the gastric pits [3Peled N. Dagan O. Babyn P. Silver M.M. Barker G. Hellmann J. et al.Gastric-outlet obstruction induced by prostaglandin therapy in neonates.N Engl J Med. 1992; 327: 505-510Crossref PubMed Scopus (87) Google Scholar]. Collectively, these findings show that prolonged use of PGE1 infusion in neonates with congenital heart disease may cause transient gastric obstruction. Therefore, the clinical and radiological features of gastric obstruction are relieved after stopping PGE1 infusion [4Soyer T. Yalcin S. Bozkaya D. Yiğit S. Tanyel F.C. Transient hypertrophic pyloric stenosis due to prostoglandin infusion.J Perinatol. 2014; 34: 800-801Crossref PubMed Scopus (9) Google Scholar]. In our case, the clinical and radiological findings of gastric outlet obstruction resolved 4 days after discontinuation of PGE1 treatment. The male neonate tolerated full feeding on the 5th day after the discontinuation of treatment. Permission was obtained from parents for case image. None.