Abstract
Background: Duodenal atresia is the most common type of intestinal atresia. Pathogenesis of duodenal atresia can be explained by an embryological theory that involves persistent physiologic epithelial occlusion (“epithelial plug”), first published in 1900. Tandler’s developmental arrest theory has been accepted by the majority of recognized modern textbooks to date. The aim of the presented study is to re-evaluate the relevance of Tandler’s observations. Method: Tandler’s paper was reviewed retrospectively and discussed from the point of view of subsequent research. Results and Discussion: Local epithelial proliferation, vacuolization failure and mesenchyme ingrowth may continuously serve as a partly convincing but incomplete embryologic model to explain membranous duodenal atresia. Tandler’s theory has some weak points regarding the epithelial-mesenchymal interaction, the predisposition of the post-ampullary region, the association of duodenal atresia with other malformations and trisomy 21, and familial occurrence. Shrinkage artifacts, misinterpretation of a three-dimensional problem investigated with a two-dimensional tool (light microscope), animal studies, and the lack of apoptosis call the real existence of a solid stage in early duodenal embryology into question. Conclusion: More sophisticated morphologic, genetic and molecular-biological investigations revealed new insights regarding endoderm to mesoderm signaling as an important key to the pathogenesis of duodenal atresia.
Highlights
Duodenal atresia is the most common intestinal atresia with a prevalence of 0.9 per 10,000 births
Pathogenesis of duodenal atresia can be explained by an embryological theory that involves persistent physiologic epithelial occlusion (“epithelial plug”), first published in 1900
Misinterpretation of a three-dimensional problem investigated with a two-dimensional tool, animal studies, and the lack of apoptosis call the real existence of a solid stage in early duodenal embryology into question
Summary
Duodenal atresia is the most common intestinal atresia with a prevalence of 0.9 per 10,000 births. Until Tandler’s report in 1902, theories were mainly based on the assumption that intestinal atresia would generally result from late fetal intrauterine events or “catastrophes” [1]. Membranous obstruction (duodenal septum, web or diaphragm) is noted in 9 of 10 cases. Calder described the first case of congenital duodenal obstruction in 1733, and Vidal reported the first successful treatment by gastrointestinal bypass anastomosis in 1905. Persistence of the temporary embryonic epithelial occlusion of the duodenum serves as an explanation for the pathogenesis of duodenal atresia. Tandler’s developmental arrest theory was an outstanding hypothesis that was accepted by the scientific community of his time. The suitability of the epithelial plug theory to explain atresia of other parts of the gastrointestinal tract should be discussed
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