Histogenesis and Gross Morphometric Evaluation of the Human Foetal Liver: A Descriptive Observational Study

Background: The hepatocytes and bile duct epithelium originate from foregut endoderm as a ventral diverticulum near the anterior intestinal portal by the third week of intrauterine life. The connective tissue and sinusoidal endothelium of liver arise from the mesodermal septum transversum, while Kupffer cells derive from mesenchymal precursors. Hematopoietic stem cells initially arise from the yolk sac and later from the aorta-gonad-mesonephros (AGM) region. Endoderm–mesenchyme interactions shape the liver’s architecture which is crucial for segmental resection and regeneration. Hence, a detailed study of foetal liver architecture was undertaken. The aim is to measure the morphometric parameters (length and breadth) of the human liver in aborted foetuses of all gestational age (excluding anomalies) and analyse their growth trends. To examine the sequential histological changes in the developing liver, including the appearance and maturation of vascular structures, hepatocyte cords, hemopoietic activity, connective tissue elements, and glycogen deposition. To correlate the observed developmental stages with potential implications for neonatal and adult hepatic disorders. Material and Methods: 42 aborted foetuses (formalin fixed) from 12 weeks to 35 weeks were taken. Liver dimensions and histological features with routine Haematoxylin and Eosin staining was done. Results: There is a progressive increase in length and breadth of the liver with respect to advancing gestational age from week 14 onwards till 26 weeks. But beyond that, the growth is slower. The length of liver grows faster than the breadth. Appearance of central vein, sinusoids, cords of hepatocytes and hemopoiesis noted at 12 weeks. Connective tissue elements noted from 14 weeks, with formation of incomplete lobulation. Proper portal triad established at 16-17 weeks. Kupffer cells are noted in the sinusoidal walls from 21 weeks. Glycogen vacuolation in hepatocytes noted from 26 weeks. Conclusion: Delayed or disrupted hemopoiesis, sinusoid formation, Kupffer cell appearance and portal triad formation could lead to potential architectural disarray in newborns and subsequently result in defects in adult life such as neonatal hemochromatosis, congenital hepatic fibrosis, extrahepatic biliary atresia, glycogen storage diseases, hepatoblastoma etc. Sometimes, these conditions are one of the causes of stillbirth or neonatal demise.

Keywords: Foetal liver, Hepatogenesis, Histogenesis, Kupffer cells, Portal triad, Hemopoiesis.