case report
Ten years of depression and agoraphobia. The problem was adrenal insufficiency.
2026-06-23
Ten years of depression and agoraphobia. The problem was adrenal insufficiency.
Ten years of depression
A 48-year-old Japanese man had been living under a diagnosis of depression for ten years. He was prescribed 60 mg of duloxetine daily. Over time, his condition grew more restrictive; due to agoraphobia, he stopped seeing his doctor in person and instead had his mother collect his psychiatric medication for him.
Six days before he was hospitalized, his physical health began to mirror his mental decline. He developed a fever, malaise, and severe nausea. He stopped urinating. After he began struggling to speak and his consciousness wavered, he was brought to the hospital by ambulance.
The limits of psychiatry
Upon arrival, his Glasgow Coma Scale score was 8 out of 15. He could open his eyes to the sound of a voice but was unable to speak. While he was hemodynamically stable, his laboratory results revealed a body in profound chemical crisis. His sodium was dangerously low at 108 mmol/L, and his plasma was hypotonic.
His symptoms—nausea, impaired consciousness, and low sodium—initially suggested a syndrome of inappropriate antidiuretic hormone secretion (SIADH). However, further testing revealed the source was not psychiatric or a simple fluid imbalance. His serum cortisol was nearly undetectable at less than 0.05 µg/dL, and his ACTH was low at 2.0 pg/mL. The diagnosis was secondary adrenal insufficiency.
The pituitary thread
A brain MRI provided the missing link. The scan showed slight swelling and enhancement of the pituitary infundibulum, suggesting hypophysitis—an inflammation of the pituitary gland. This inflammation had effectively shut down his body’s ability to produce cortisol.
The lack of cortisol had triggered a chain reaction: it stimulated the release of vasopressin, which kept his body from excreting water and drove his sodium levels to life-threatening lows. It also suppressed his appetite by affecting neurons in the hypothalamus, explaining his severe nausea and lack of intake.
A dangerous recovery
Treatment began with a continuous infusion of hydrocortisone. However, in undiagnosed adrenal insufficiency, the cure can be as hazardous as the disease. Within six hours of receiving the hormone his body lacked, his vasopressin levels plummeted. His kidneys suddenly began flushing out massive amounts of diluted urine—reaching a rate of 930 mL per hour.
This "autocorrection" caused his blood sodium to spike from 110 mmol/L to 120 mmol/L in just ten hours. Such a rapid rise puts the brain at risk for osmotic demyelination syndrome (ODS), a permanent and devastating neurological condition. Doctors had to quickly administer large doses of 5% dextrose and desmopressin to force the sodium back down and protect his brain.
Refeeding and resolution强化
By the second day, the patient regained consciousness. By the third, his appetite returned as the hydrocortisone took effect. But this sudden return of hunger led to a second pitfall: refeeding syndrome. As he began to eat, his phosphorus levels crashed to 1.2 mg/dL. On the sixth night, his consciousness deteriorated again, his speech became slurred, and his lactate levels rose.
After receiving intravenous sodium phosphate, his consciousness finally returned to normal on day eight. He was discharged on day 23 with a maintenance dose of hydrocortisone. Sixteen months later, a follow-up MRI showed the pituitary swelling had resolved. The man who had spent a decade under a psychiatric label for depression was now managed with a simple daily hormone replacement.
The medical picture
Serum Sodium
108 mmol/L
Serum Cortisol
< 0.05 µg/dL
Adrenocorticotropic hormone (ACTH)
2.0 pg/mL
Plasma Osmolality
229 mOsm/kg
Urine Sodium
125 mmol/L
Adapted faithfully from the open-access case report: Journal of Medical Case Reports (PMC13064267). DOI: 10.1186/s13256-026-05924-0. Read the original at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13064267/.