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Depending on the genetic mutations, 46,XX infants can show enlarged clitoris, incomplete labial fusion and genital hyperpigmentation [30]. In contrast, some girls can have normal external genitalia which may delay diagnosis and they can subsequently present with adrenal crisis [31]. Older girls and women with genetically confirmed non-SW 3βHSD2D can present with androgen symptoms of hirsutism, premature pubarche or menstrual disorders including oligomenorrhea and primary amenorrhea [16, 32]. Several deleterious mutations in the HSD3B2 gene have been described that can cause SW during the first few weeks of life and may be fatal if not treated adequately [31, 32]. Biochemical findings include hyponatremia, hyperkalemia, metabolic acidosis and hypoglycemia [15, 33]. On the other hand, missense mutations in the coding region of HSD3B2 gene is associated with non-SW form due to the presence of some residual enzymatic activity, about 10%, is sufficient to prevent aldosterone deficiency [16, 24, 32, 34, 35]. Recurrent episodes of hypoglycemia were reported to be a presenting feature in a suspected case of 3βHSD2D but the genotype was not performed to confirm the diagnosis [36]. Another patient presented during second day of life with hypoglycemia, later on, the molecular genetics confirmed 3βHSD2D [31].
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