What is the pathogenesis of Lymphangiectasia?

• A. Bacteria invade and degrade villi
• B. Dilation and dysfunction of intestinal lacteals → rupture → leakage of protein-rich lymph into lumen → PLE
• C. Autoimmune destruction of enterocytes
• D. Mucus hypersecretion causing malabsorption

Answer: (B)

Lymphangiectasia starts with dilation and dysfunction of the intestinal lacteals inside the villi. When these lymphatic vessels enlarge, pressure builds and lymph—rich in protein and fat—begins to leak into the intestinal lumen. This leakage causes protein-losing enteropathy, leading to hypoalbuminemia, edema, and loss of immunoglobulins, along with impaired fat absorption and steatorrhea because the chyle cannot be properly transported. In some cases, the dilated lacteals can rupture, causing a more rapid or dramatic leakage into the lumen. This mechanism directly explains why protein-rich lymph ends up in the gut and why protein loss occurs, which is the hallmark of lymphangiectasia. Other options describe different disease processes (villous damage from infection, autoimmune enteropathy, or mucus-related malabsorption) that do not center on dilation and leakage of intestinal lymphatics.