Possible adrenal crisis? Use your prescribed emergency plan and seek emergency medical care. Adrenal crisis

03 Tertiary

Tertiary and steroid-induced adrenal insufficiency

When hypothalamic signaling or long-term glucocorticoid (steroid) exposure can suppress the HPA axis.

What this type is

Tertiary adrenal insufficiency is often described as a problem in hypothalamic signaling—the part of the brain that helps start the message to the pituitary. The hypothalamus releases corticotropin-releasing hormone (CRH). CRH tells the pituitary to release ACTH. ACTH tells the adrenal glands to make cortisol.

People also use “steroid-induced” or “glucocorticoid-induced” when prolonged glucocorticoid (steroid) medicines have suppressed that HPA axis. The body may make less of its own CRH, ACTH, and cortisol while it is exposed to outside glucocorticoids. How long that lasts, and whether a medicine should change, is a decision for the prescribing clinician.

Primary AI / Addison’s disease begins in the adrenal glands. Secondary AI is a pituitary–ACTH pathway. Tertiary / steroid-induced AI involves hypothalamic CRH signaling or HPA-axis suppression related to glucocorticoid exposure. Clinicians sometimes use “secondary” and “tertiary” in overlapping ways; ask your team which language they use for you.

How this type is typically acquired

The most common pathway is suppression of hypothalamic CRH and the rest of the HPA axis after prolonged glucocorticoid medicines from outside the body. Your clinician judges what counts as prolonged in your case.

Glucocorticoids can be given in several ways:

Oral glucocorticoid tablets or liquids
Injected glucocorticoids (into a joint, muscle, vein, or other site)
High-dose inhaled glucocorticoids
Topical (skin) glucocorticoids in some circumstances, especially when a large area is treated, the skin barrier is altered, or potent products are used for a long time
Other glucocorticoid products the clinician identifies (for example rectal or nasal preparations when they think exposure is relevant)

Not every person who takes a glucocorticoid develops adrenal insufficiency. Dose, duration, potency, how the medicine is taken, other health conditions, and how the medicine is stopped all matter. Your clinician weighs those factors.

If glucocorticoids need to be reduced, that taper must be clinician-guided. Stopping suddenly can be dangerous.

Other hypothalamic causes matter when CRH signaling is impaired without the pituitary being the original problem. Teams may consider tumors, surgery, radiation, trauma, infiltrative disease, or other hypothalamic injury. Those stories overlap with secondary AI in practice; ask your clinician which name they use.

Science: the HPA axis when CRH or outside steroids lead

The HPA axis is a loop with feedback. Cortisol (and glucocorticoid medicines that act like cortisol) signal the hypothalamus and pituitary to ease off CRH and ACTH. After long exposure to outside glucocorticoids, that “ease off” can persist. The adrenal glands may make less cortisol because they are not being asked. As with secondary AI, mineralocorticoid (aldosterone) production is often relatively preserved compared with primary AI, because aldosterone is driven more by renin–angiotensin than by ACTH. Your team still decides whether salt, fluids, or extra medicines are part of your plan.

Recovery of the axis, if it happens, does not follow a single timeline. Your clinician follows that. People can still face adrenal crisis during illness, injury, or if glucocorticoids are stopped too quickly. Crisis education lives on the adrenal crisis page.

Testing your team may discuss

Your team may discuss tests such as:

A careful history of glucocorticoid exposure (what, how it was taken, for how long, and how it was changed)—documentation matters here
A morning cortisol blood test
An ACTH level, often discussed together with cortisol
Cosyntropin (ACTH stimulation) testing
Imaging of the hypothalamus or pituitary when the clinician is evaluating a structural cause rather than medicine-related suppression
Additional specialist tests if the team needs more information after first-line evaluation

Your clinician interprets labs and decides when, or whether, a steroid can be reduced.

Questions to ask your medical team

Bring these to your visit:

Do I have tertiary or steroid-induced adrenal insufficiency, or another type, and what supports that description?
Which of my glucocorticoid medicines (oral, injected, inhaled, topical, or other) do you want documented, and should any of them change—only under your direction?
If a taper is appropriate, who will write it, how will we watch for symptoms, and what should I do if I become ill during a taper?
What is my sick-day or stress-dosing plan for fever, vomiting, injury, or a procedure?
Will you train me (and a caregiver) on an emergency glucocorticoid injection, and what belongs in my kit?
What should I tell emergency responders and the ER, including that I have been on glucocorticoids?
Should I wear medical identification, and what wording do you recommend?
Which other medicines should you know about?
How will we follow recovery of my HPA axis, if that is a goal, and who is responsible for follow-up?