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|Title:||Foveolar hyperplasia: Post prostaglandin therapy|
Heike E. Daldrup-Link
|Citation:||Pearls and Pitfalls in Pediatric Imaging: Variants and Other Difficult Diagnoses. (2012), 222-225|
|Abstract:||© Heike Daldrup-Link and Beverley Newman 2014. Imaging description A five-week-old infant presented with projectile vomiting and failure to thrive. There was a prior history of cyanotic congenital heart disease, treated with prostaglandin therapy. On clinical examination, there was no palpable pyloric mass. An ultrasound demonstrated elongation of the pyloric channel without muscular wall thickening, but with markedly prominent hyperechogenic mucosa of the antrum and pylorus (Fig. 51.1a, b). An upper gastrointestinal (GI) fluoroscopy confirmed gastric outlet obstruction with elongation and narrowing of the pyloric channel (Fig. 51.1c, d). Importance. Prostaglandin therapy can lead to deepening and widening of the gastric fovea (the pits in the mucosa into which gastric glands empty) with hyperplasia and redundancy of the epithelium, especially in the antral and pyloric regions (Figs. 51.1 and 51.2). This “foveolar hyperplasia” can cause obstruction of the gastric outlet, mimicking hypertrophic pyloric stenosis clinically. It is important to differentiate foveolar hyperplasia from hypertrophic pyloric stenosis (Fig. 51.3), since the former is treated conservatively, while the latter is treated with surgical pyloromyotomy.|
|Appears in Collections:||Scopus 2011-2015|
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