INTRODUCTION
Congenital Adrenal Hyperplasia (CAH) is a group of inherited disorders caused by genetic defects that hinder the production of adrenal hormones, cortisol, and aldosterone, either completely or at their normal rate. It may be caused by a deficiency of one of the five enzymes responsible for cortisol synthesis. These enzymes include 21α-hydroxylase, 11β-hydroxylase and 17α-hydroxylase/17,20-lyase, cholesterol 20,22 desmolase and 3β-hydroxysteroid dehydrogenase [1]. Adrenal steroidogenesis occurs by a series of steps facilitated by the zone-specific enzyme expression and different types of CAH interrupt this process at distinct branch points. Furthermore, there is a substitute pathway for the endogenous synthesis of androgens, which also plays a significant role in the causation of CAH [2,3]. CAH is further categorized into two types - Classic & Non-Classic. Classic CAH, although a more severe form, is rare and is usually detected at birth and is associated with the life-threatening adrenal crisis in both sexes and virilization of the external genitalia in 46, XX patients. Non-Classic CAH is a more common form that has a milder phenotype in which clinical problems are not obvious during the neonatal period or childhood and generally develops during adolescence or adulthood [4,5]. In Classic CAH, the findings usually visible at birth include ambiguous genitalia in females due to excess male androgens, whereas in males no overt abnormality of the external genitalia is present. In 95% of the cases of CAH, the identified deficiency is of 21α-hydroxylase enzyme [6]. This leads to impairment of cortisol and aldosterone production with excess production of androgens that leads to the aforementioned findings. We present a case of a four-month-old male child who presented with Classic CAH with signs of dehydration, malnutrition, and failure to thrive.