The Role of Vitamins Deficiency in the Development of Hydatidiform Moles: Mechanism and Function

Hydatidiform mole is characterized by the swelling of the placental villi, trophoblastic hyperplasia, and the absence or abnormal presence of an embryonic element which is one of the emergency conditions in pregnancy that can endanger the lives of women (۱). Its prevalence varies by geographical region, and the incidence is higher in Asia, the Middle East, and Africa (۲). Studies have shown that nutritional deficiencies such as reduced dietary intake of animal fats and carotene, which are precursors to vitamin A production, can also increase the risk of molar pregnancy, and women who consumed more carotene-containing foods were ۴۰% less likely to have a molar pregnancy (۳). In the human body, vitamin A or its precursor is metabolized to retinol, and in the next step, retinol is metabolized to retinoic within the cells. Finally, the retinoic complex and the retinoic receptor led to apoptosis and terminated the cell cycle (۴). Increased apoptosis can reduce the risk of malignant trophoblastic disease, thus activating and inducing apoptosis and ending the cell cycle with retinoic acid may be effective as a treatment to prevent malignant trophoblastic disease. In fact, low levels of retinol in the liver and blood of patients with hydatidiform mole reduce retinoic acid in the cell and lead to the uncontrolled proliferation of trophoblastic cells and reduced apoptosis, increasing the risk of hydatidiform conversion (۵).