Relevance: The most common form of congenital adrenal hyperplasia (CAH) is 21-hydroxylase deficiency, in which a block in cortisol biosynthesis shifts precursors to pathways that make excess adrenal-derived androgens. We report a rare case in which a new diagnosis of CAH due to 21-hydroxylase deficiency occurred in an octogenarian. Clinical case: An 82 year old man presented for evaluation of persistent headache, anorexia, and unintentional weight loss. He was found to have acute worsening of chronic hyponatremia and hyperkalemia with presenting sodium and potassium levels of 121 and 5.8 mEq/L, respectively. He had increased skin pigmentation, but no hypotension or orthostasis. These findings prompted evaluation of his HPA axis. His AM cortisol was 11.9 mcg/dL (6.7-22.6) and ACTH was 1,036 pg/dL (7.2-63.3). After cosyntropin stimulation, his cortisol remained 10.8 at 30 minutes and 10.5 at 60 minutes. DHEA-S was 34.1 mcg/dL (20.8 - 226.4), Renin was 11.5 ng/mL/hr (0.2-5.4) and Aldosterone was < 1.0 ng/dL (0-30). Further hormonal testing showed an AM testosterone 788 ng/dL (264-916), which was higher than expected given the normal age related decline in testosterone. LH was 3.9 mIU/mL (1.2-8.6), FSH was 4.9 mIU/mL (1.3-19.3) and prolactin was 15.4 ng/mL (4.0-15.2). Oral hydrocortisone was initiated: 10mg in the morning and 5mg in the afternoon, in addition to florinef 0.1mg daily. By hospital day 4, his hyperkalemia and hyponatremia had normalized, his headaches resolved, and his appetite improved. Review of a prior CT chest/abdomen/pelvis (done for unintentional weight loss) demonstrated normal adrenal glands with no evidence of malignancy, hemorrhage, enlargement, or atrophy. 21-hydroxylase antibodies were undetectable. On further history, the patient disclosed that adrenarche occurred at age 6. He had short stature in his youth and was treated with growth hormone injections. He and his wife had difficulty conceiving and he was told of low sperm motility but ultimately had three children by natural conception. An insidious presentation of CAH was suspected based on this history and the high normal testosterone levels in this octogenarian. After uninterrupted treatment with hydrocortisone for two weeks, 17-hydroxy progesterone was 800 ng/dL (27-199), his ACTH improved to 660 and his testosterone decreased to 494. A 21-hydroxylase mutational analysis is pending. Conclusions: Classical CAH is typically diagnosed in infancy or youth in the setting of adrenal insufficiency with/without salt wasting, ambiguous genitalia in female infants or virilization. Although atypical to go undiagnosed for decades, non-classic CAH should be considered as a cause of aldosterone and cortisol deficiency, even among elderly patients, who present with signs and symptoms concerning for adrenal insufficiency. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. s presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.