Intrahepatic cholestasis of pregnancy (ICP) is the most common multifactorial hepatic disorder of pregnancy, which mainly manifests in the second or third trimester (after 30 weeks). About 1.5%–4% of otherwise healthy pregnancies are affected by intrahepatic cholestasis during pregnancy [1]. It is characterized by intense pruritus without any primary skin rash with elevated levels of bile acid and transaminases with or without increased serum bilirubin in the absence of any alternative cause, and the condition resolves 2–3 weeks after delivery [2]. The maternal outcome is good, but it is associated with very adverse fetal complications like preterm delivery, meconium staining of amniotic fluid, fetal bradycardia, fetal distress, and, most unfortunately, fetal demise, so timely diagnosis and treatment are needed. The deleterious effect on the fetus is directly proportional to the total bile acid (TBA) level with the risk of stillbirth above TBA serum concentration of 100 μmol/L or more. Meta-analysis suggests that most women with IHCP can probably be reassured that the risk of stillbirth is equivalent to that of pregnant women in the general population, as most women have bile acids below this threshold [3]. The therapy’s primary goal is to relieve pruritus, normalize maternal biochemistry, and prevent fetal complications. Ursodeoxycholic acid (UDCA) is used for medical management, but it is advisable to deliver around 37–38 weeks or even earlier if fetal compromise is detected. Pruritus Gravidarum is the term used for pruritus without skin rash occurring in the first trimester of pregnancy [4].