Chloasma is a required hypermelanosis of sun-exposed areas occurred during pregnancy and it can affect 50-70% of pregnant women. It presents as symmetric hyperpigmented macules, which can confluent or punctuate. The most common locations are the cheeks, the upper lip, the chin and the forehead. The exact mechanism by which pregnancy affects the process of melanogenesis is unknown. Estrogen, progesterone, and melanocyte-stimulating hormone (MSH) levels are normally increased during the third trimester of pregnancy. However, nulliparous patients with chloasma have no increased levels of estrogen or MSH. In addition, the occurrence of melasma with estrogen- and progesterone-containing oral contraceptive pills has been reported. The observation that postmenopausal woman who are given progesterone develop melasma, while those who are given only estrogen do not, implicates progesterone as playing a critical role in the development of melasma. UV-B, UV-A, and visible light are all capable of stimulating melanogenesis. The condition is self-limited; however spontaneous resolution is time-consuming and may take months to resolve normal pigmentation. Therefore, it is worthwhile to prevent the onset of chloasma, by strict photoprotection. Prudent measures to avoid sun exposure include hats and other forms of shade combined with the application of a broad-spectrum sunscreen at least daily. Sunscreens containing physical blockers, such as titanium dioxide and zinc oxide, are preferred over chemical blockers because of their broader protection. Chloasma can be difficult to treat. Quick fixes with destructive modalities (eg, cryotherapy, medium-depth chemical peels, lasers) yield unpredictable results and are associated with a number of potential adverse effects. The mainstay of treatment remains topical depigmenting agents. Hydroquinone (HQ) is most commonly used.