SAT-436 - Adrenal Crisis Precipitated by Severe Hypothyroidism in Polyglandular Autoimmune Syndrome Type II

Background:
Polyglandular autoimmune syndrome (PAS) may initially present with vague symptoms, especially in young adults with known autoimmune thyroid disease. Adrenal insufficiency can be overlooked when abdominal pain dominates the clinical picture. This case highlights adrenal crisis unmasked by worsening hypothyroidism in a patient with Hashimoto’s thyroiditis.

Case Presentation:
A 21‑year‑old woman with recently diagnosed Hashimoto’s thyroiditis and poor adherence to levothyroxine presented with progressive weakness, nausea, vomiting, and abdominal pain. She reported inability to stand for long periods, minimal oral intake except water, lethargy, and decreased urine output. Initial vitals showed BP 90/50 mmHg and HR 110 bpm. Electrolytes were normal, and CT abdomen revealed no acute pathology. She was discharged but returned within 48 hours with worsening hypotension requiring vasopressors.
Repeat evaluation showed BP 80/50 mmHg with persistent tachycardia. Labs demonstrated sodium 130 mmol/L, potassium 5.1 mmol/L, glucose 32 mg/dL, high anion gap metabolic acidosis, leukocytosis 19,000/µL, creatinine 1.17 mg/dL, and β‑hydroxybutyrate 5 mmol/L. TSH had risen dramatically from 4.23 µIU/mL on her first admission to 10,957 µIU/mL.
Given refractory hypotension and hypoglycemia, adrenal insufficiency was suspected. Morning cortisol was 8.3 µg/dL. Cosyntropin stimulation testing showed inadequate responses of 6.0, 5.2, and 5.1 µg/dL. She was started on IV hydrocortisone with rapid hemodynamic improvement and transitioned to oral therapy. Levothyroxine was restarted after steroid coverage. Her abdominal pain, metabolic derangements, and weakness resolved.

Discussion:
This presentation is consistent with PAS type II, with Hashimoto’s thyroiditis preceding primary adrenal insufficiency. The misleading abdominal pain and initially normal electrolytes contributed to delayed recognition. Severe hypothyroidism, reflected by the extreme TSH elevation, likely worsened adrenal decompensation. Hypoglycemia, high anion gap acidosis, and vasopressor‑dependent shock were key clues to adrenal crisis. Early glucocorticoid therapy is lifesaving and must precede thyroid hormone replacement to avoid precipitating further adrenal collapse.

Conclusion:
In young patients with autoimmune thyroid disease, persistent hypotension, abdominal pain, and hypoglycemia should prompt evaluation for adrenal insufficiency. Early recognition of PAS prevents life‑threatening adrenal crisis and guides safe initiation of thyroid hormone therapy.

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