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|Year : 2012 | Volume
| Issue : 2 | Page : 166
Some embryological facts on ectopic liver tissue in the umbilical cord
Department of Anatomy, Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra, India
|Date of Web Publication||14-Jun-2012|
Department of Anatomy, Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Rajgopal L. Some embryological facts on ectopic liver tissue in the umbilical cord. J Postgrad Med 2012;58:166
The article "Ectopic liver tissue in umbilical cord" was interesting.  I would like to add a few points on the developmental basis of that condition.
During the development and differentiation of a normal liver, there is an epithelial-mesenchymal interaction between the endoderm of the gut and the mesoderm of the septum transversum. With lateral folding of the embryo, there is narrowing of connecting stalk and formation of umbilical ring and cord. At this time, the septum transversum lies close to the umbilical ring. Vitello-intestinal duct (omphalo-mesenteric duct/yolk stalk) which is an endodermal tube connecting the midgut to the definitive yolk sac extends into the umbilical cord at around the same time. Gut endoderm has the potential to form the liver but inhibitors secreted by the neighboring mesoderm, ectoderm and the notochord suppress this. Fibroblast Growth Factor 2 (FGF 2) secreted by the cardiac mesoderm blocks these inhibitors and Bone Morphogenetic Protein (BMP) secreted by the septum transversum makes the endoderm sensitive to FGF 2 and allows differentiation of the endoderm into hepatocytes.  So, in this case, the presence of the mesoderm of septum transversum close to the gut endoderm of vitello-intestinal duct in the umbilical cord could have resulted in ectopic liver tissue.
A search of the literature shows that there are seven cases reported so far and the present case is the eighth one.  Yet, it is unique in the combination of associated defects like hypoplasia of right lung and cardiac anomalies. Embryologically, it is interesting to note that the development of lung buds from the endodermal tracheobronchial diverticulum, septation of the heart and development of hepatic diverticulum from the gut endoderm all happen in the fourth week of intrauterine life. So, an intrauterine incident in the fourth week of pregnancy may explain the combination of defects in this case. Moreover, budding of lung and its differentiation requires the expression of Fibroblast Growth Factor 10 (FGF 10) in the endoderm.  Expression of FGF 8 and FGF 15 are needed for proper development of the outflow tract (OFT) of the heart.  FGF signaling interacts genetically with T-Box transcription 1 (TBX-1) pathways that regulate the development of the OFT of the heart and other endodermal derivatives from the gut tube in a tissue-specific manner. In microdeletion of Chromosome 22 q, the TBX pathways get affected and that could possibly explain the combination of defects of OFT, agenesis of right lung and ectopic liver. 
Unfortunately, this newborn was alive only for a few hours. If karyotyping with G banding had been done, it might have revealed any sporadic mutation of Chromosome 22 and would have helped to counsel the parents regarding future pregnancies.
| :: References|| |
|1.||Vaideeswar P, Yewatkar D, Nanavati R, Bhuiyan P. Ectopic liver tissue in umbilical cord. J Postgrad Med 2011;57:229-30. |
|2.||Sadler TW. Digestive system. In Langman's Medical Embryology. 11 th ed. New Delhi: Wolters Kluwer/Lippincott Williams and Wilkins; 2010. p. 220-2. |
|3.||Lee S, Nam CW, Suh J. Heterotopic liver in the umbilicus: A case report. Basic Appl Pathol 2011;4:30-2. |
|4.||Sakiyama J, Yamagishi A, Kuroiwa A. Tbx4-Fgf10 system controls lung bud formation during chicken embryonic development. Development 2003;130:1225-34. |
|5.||Zhang J, Lin Y, Zhang Y, Lan Y, Lin C, Moon AM, et al. Frs2α-deficiency in cardiac progenitors disrupts a subset of FGF signals required for outflow tract morphogenesis. Development 2008;135:3611-22. |