SUN-433 - A Subtle Presentation of Primary Adrenal Insufficiency in A Patient with Tuberculosis

Background:
Tuberculosis (TB) is a leading cause of infectious adrenalitis. We present a case of adrenal tuberculosis precipitating subclinical primary adrenal insufficiency (AI).

Clinical

Case:
A 24-year-old male with HIV, disseminated TB with pulmonary, gastrointestinal, and lymph node involvement presented with nausea and emesis, which was thought to be due to recent TB treatment. He was found febrile, tachycardic, and hypotensive. CT abdomen and pelvis showed bilateral enlarged adrenal glands with nodular infiltration, which were normal on imaging eight months prior. Multiphasic CT of adrenals showed bilateral adrenal enlargement with peripheral enhancement and central hypoattenuation, consistent with adrenal TB. Labs showed sodium 131 (135-145 mmol/L), potassium 3.5 (3.5-5.1 mmol/L), morning cortisol 15.6 (4.8-19.5 mcg/dL), DHEA sulfate 56 (74-617 mcg/dL), aldosterone < 1 (supine 3-6 ng/dL), and plasma renin 0.15 (0.25-5.82 ng/mL/hr). Despite a random cortisol level of 17.2 (6-10AM 4.8-19.5 mcg/dL, 4-8PM 2.5-11.9 mcg/dL), ACTH level at the time was 223 (6-50 pg/mL), which was concerning for subclinical primary AI. Stress-dose hydrocortisone was started for persistent hypotension, titrated to physiologic dosing upon discharge.

Discussion:
Adrenal TB accounts for 7-20% of cases of AI in those with active TB via hematogenous or lymphatic spread. Imaging commonly shows bilateral adrenal enlargement in active TB, whereas chronic or inactive TB infection results in calcification and atrophy of the adrenal glands. While most cases are asymptomatic, nonspecific symptoms such as nausea, emesis, and fatigue can occur when at least 90% of adrenal tissue is affected. Although our patient initially had a normal morning cortisol level, worsening clinical status with an elevated ACTH and bilateral adrenal enlargement seen on imaging pointed towards a diagnosis of subclinical primary AI. Subclinical AI is defined as biochemical changes that show signs of adrenal function impairment, such as elevated ACTH and decreased adrenal responsiveness to ACTH, with a normal basal cortisol level. Subclinical AI has been described in adrenal TB such as our patient. The mainstay treatment for adrenal TB is to treat the underlying infection. In our case, significant improvement was seen upon initiation of stress dose steroids. With appropriate treatment of the underlying infection, there can be recovery of adrenal function and eventual discontinuation of steroids, but this has not been consistently demonstrated and remains an area of future study.

Conclusion:
In patients with active TB and clinical decompensation, it is important to initiate prompt treatment with steroids and antituberculosis medications if there is suspicion for adrenal involvement. In these patients, subclinical AI is a common finding, so careful evaluation of the hypothalamic-pituitary-adrenal axis is recommended.

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