<prompt> Please answer with one of the option in the bracket. Write reasoning in between . Write answer in between .Q:An otherwise healthy 13-year-old boy is brought to the physician for the evaluation of severe acne for the last 3 years. Topical retinoic acid and oral tetracycline did not improve his symptoms. He shaves his chin and mustache area every few days. His parents report that he grew 5 cm 2 in during the last year. The onset of pubic hair growth was at age 8. He is at the 95th percentile for height and weight. Vital signs are within normal limits. Examination shows several pimples and pustules along the skin of the cheeks, chin, and neck. Genitals are Tanner stage 4 and pubic hair is Tanner stage 5. Early morning serum laboratory studies drawn 30 minutes after administration of ACTH show:Sodium 137 mEqLPotassium 3.8 mEqLCortisol 0800 h 4 μgdLAldosterone 10 ngdL N 73017OH-Progesterone 230 ngdL N 390Deoxycorticosterone 2.7 ngdL N 3.511.5Androstenedione 350 ngdL N 80240Dehydroepiandrosterone sulfate DHEAS 420 μgdL N 29412Which of the following is the most likely underlying cause of this patients symptoms?? A: Leydig-cell tumor production of androgens, B: Exposure to exogenous steroids, C: 21β-hydroxylase deficiency, D: Constitutive activation of adenylyl cyclase, E: 17α-hydroxylase deficiency,  <response>: This is a clinical vignette describing a 13-year-old boy with severe acne, early puberty, rapid growth, and lab results showing elevated 17-hydroxyprogesterone and androstenedione with low cortisol and aldosterone. This pattern is most consistent with 21-hydroxylase deficiency, which is the most common cause of congenital adrenal hyperplasia. It leads to a buildup of progesterone precursors like 17-hydroxyprogesterone that are shunted into the androgen synthesis pathway, causing virilization. The low cortisol and aldosterone are due to impaired synthesis. The other choices can be ruled out based on the lab results and clinical presentation.C: 21β-hydroxylase deficiency 