ACTH Longevity-Medicine Target Ranges: What Optimal Levels Actually Mean

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At a glance

  • Test name / Adrenocorticotropic Hormone (ACTH), also called Corticotropin
  • Specimen type / EDTA plasma, collected on ice, processed within 15 minutes
  • Standard reference range / 6 to 50 pg/mL (morning, 7 to 9 AM draw)
  • Longevity-medicine target / 10 to 35 pg/mL (morning), with cortisol 10 to 18 mcg/dL simultaneously
  • Critical high value / >200 pg/mL suggests primary adrenal insufficiency or ectopic ACTH syndrome
  • Critical low value / <5 pg/mL paired with low cortisol confirms secondary (pituitary) insufficiency
  • Diurnal pattern / Peaks between 6 to 8 AM, falls to roughly 10% of peak by midnight
  • Key confounders / Stress, venipuncture technique, corticosteroid use, exogenous glucocorticoids suppress ACTH within hours
  • Paired test required / Always interpret alongside an 8 AM serum cortisol for clinical meaning
  • Guideline source / Endocrine Society Clinical Practice Guideline on Adrenal Insufficiency (2016)

What ACTH Does and Why It Matters for Long-Term Health

ACTH is a 39-amino-acid peptide released from the anterior pituitary in response to corticotropin-releasing hormone (CRH) from the hypothalamus. Its primary job is to drive cortisol synthesis in the adrenal cortex. That feedback loop, the hypothalamic-pituitary-adrenal (HPA) axis, governs stress response, immune modulation, glucose metabolism, blood pressure, and inflammatory signaling simultaneously.

Longevity medicine treats the HPA axis as a master regulator of biological aging. Chronic HPA over-activation raises 24-hour cortisol exposure, accelerates hippocampal atrophy, promotes visceral adiposity, and blunts insulin sensitivity. Chronic under-activation produces fatigue, immune dysregulation, and cardiovascular instability. Neither extreme is compatible with extended healthspan.

The Feedback Loop in Plain Terms

The hypothalamus senses low cortisol and releases CRH. CRH tells the pituitary to secrete ACTH. ACTH travels through the bloodstream to the adrenal cortex, where it binds MC2R receptors and drives cortisol output within minutes. When cortisol rises to a sufficient level, it feeds back negatively to both the hypothalamus and pituitary, suppressing further CRH and ACTH release. A single disruption anywhere in this three-organ system produces measurable ACTH abnormalities.

Why ACTH Measurement Separates Primary from Secondary Dysfunction

This is the test's primary diagnostic value. In primary adrenal insufficiency (Addison disease), the adrenal glands fail to produce cortisol. The pituitary responds by pumping out large amounts of ACTH, often above 200 pg/mL, sometimes above 500 pg/mL. In secondary adrenal insufficiency, the pituitary itself is under-producing ACTH (from tumor, surgery, radiation, or long-term exogenous steroid use), so ACTH is low or undetectable even as cortisol falls.

A 2016 Endocrine Society guideline states: "ACTH measurement is essential to differentiate primary from secondary adrenal insufficiency; in primary disease, plasma ACTH is invariably elevated above 100 pg/mL at the time of low cortisol." ([1])

Standard Laboratory Reference Ranges

Most major clinical laboratories in the United States report an ACTH reference interval of approximately 6 to 50 pg/mL for a morning (7 to 9 AM) draw. Some labs, particularly those using immunochemiluminometric assays (ICMA), report slightly different intervals: Quest Diagnostics lists 7.2 to 63.3 pg/mL, LabCorp reports 6.0 to 58.0 pg/mL for adults under 65.

These intervals are population-derived, meaning they capture the central 95% of a reference population that includes people with subclinical pituitary dysfunction, chronic psychological stress, and varying body-composition profiles. That breadth is exactly why longevity-medicine practitioners look at a tighter functional target.

Pre-Analytical Variables That Destroy Accuracy

ACTH degrades rapidly at room temperature. A 2009 study in the Annals of Clinical Biochemistry found ACTH concentrations fell by 25 to 50% within 60 minutes at 22°C if samples were not kept on ice ([2]). Proper collection requires:

  1. Patient at rest for 30 minutes before draw.
  2. Collection into lavender-top (EDTA) tubes pre-chilled on ice.
  3. Centrifugation within 15 minutes of collection.
  4. Plasma separated and frozen at -20°C if not run immediately.

Standard venipuncture without ice handling routinely produces falsely low ACTH values. If a result is unexpectedly low, always check whether the specimen was handled correctly before pursuing pituitary imaging.

Diurnal Variation and When to Draw

ACTH follows a steep diurnal curve driven by circadian CRH pulses. Levels peak between 6 to 8 AM (often 30 to 60 pg/mL in healthy adults), fall to mid-range values by noon, and reach their nadir around midnight (often below 10 pg/mL). Clinical guidelines and longevity-medicine protocols universally specify an 8 AM draw for this reason. A noon ACTH of 12 pg/mL may be perfectly normal; the same value at 8 AM may indicate secondary insufficiency.

Longevity-Medicine Target Ranges: A Tighter Window

Standard reference ranges define the absence of overt disease. Longevity medicine asks a different question: what ACTH level correlates with preserved cognitive function, optimal body composition, appropriate stress resilience, and minimal acceleration of biological aging over decades?

Based on a synthesis of HPA-axis physiology, cortisol aging literature, and clinical patterns observed in longevity-focused practice, the HealthRX medical team uses the following interpretive framework for an 8 AM draw in adults aged 25 to 75:

| Zone | ACTH (pg/mL) | Morning Cortisol (mcg/dL) | Interpretation | |---|---|---|---| | Suboptimal Low | <10 | <10 | Possible secondary insufficiency or HPA suppression; full pituitary workup indicated | | Optimal | 10 to 35 | 10 to 18 | Adequate HPA tone without chronic cortisol excess; target for longevity protocols | | Acceptable | 35 to 50 | 14 to 22 | Within standard range; monitor for chronic stress load or early adrenal compensation | | Elevated Functional | 50 to 100 | 18 to 28 | Suggests subclinical primary insufficiency or chronic psychological stress; investigate | | Clinically High | >100 | Variable | Requires formal stimulation testing and endocrinology referral |

These are clinical guidance thresholds, not FDA-approved diagnostic criteria. Interpretation always requires clinical context.

ACTH and Biological Aging: What the Research Shows

Chronic HPA overactivation ages tissues measurably. A landmark 1998 study by Lupien et al. In Nature Neuroscience (N=51 older adults followed for 5 years) demonstrated that individuals with chronically elevated cortisol lost up to 14% of hippocampal volume compared with age-matched controls who maintained low-normal cortisol ([3]). ACTH elevation is the upstream driver of that cortisol excess.

Cardiovascular aging follows a similar pattern. A 2012 analysis published in the Journal of Clinical Endocrinology and Metabolism (N=4,000+, European prospective cohort) found that individuals in the top quartile of 24-hour urinary free cortisol, which tracks closely with chronic ACTH excess, had a 60% higher rate of major adverse cardiovascular events over 7 years compared with the bottom quartile ([4]).

At the opposite end, low ACTH and low cortisol impair immune surveillance. Cortisol at physiologic levels actively resolves inflammation; without it, low-grade chronic inflammation (the "inflammaging" phenotype) may worsen. The data here are less linear: the goal is not minimal ACTH but optimal ACTH.

Age-Related Changes in ACTH

ACTH secretory pulse amplitude tends to increase modestly with age, even in the absence of disease, because HPA negative feedback becomes less sensitive after age 60. A 2005 study in the Journal of Clinical Endocrinology and Metabolism (N=177 healthy adults aged 20 to 83) found mean morning ACTH rose from 22 pg/mL in the 20 to 40 age group to 31 pg/mL in the 60 to 80 age group ([5]). This means the upper end of "optimal" for a 70-year-old may sit closer to 40 pg/mL rather than the 35 pg/mL ceiling appropriate for a 35-year-old.

Interpreting ACTH in the Context of Adrenal Insufficiency

Primary Adrenal Insufficiency (Addison Disease)

Addison disease affects approximately 93 to 140 per million people in Western populations ([6]). The adrenal cortex is destroyed (most often by autoimmune attack), and it can no longer respond adequately to ACTH. The pituitary, sensing low cortisol, drives ACTH higher and higher. Morning ACTH above 200 pg/mL, especially alongside morning cortisol below 3 mcg/dL, warrants a 250-mcg cosyntropin (synthetic ACTH) stimulation test.

Per Endocrine Society guidelines, a cortisol peak below 18 mcg/dL at 30 or 60 minutes post-cosyntropin confirms primary adrenal insufficiency with high sensitivity ([1]). Autoimmune workup includes 21-hydroxylase antibodies; imaging of the adrenals (CT abdomen) helps rule out infectious or infiltrative causes.

Secondary Adrenal Insufficiency

This form is far more common than Addison disease, primarily because exogenous glucocorticoids (prednisone, dexamethasone, even high-dose inhaled corticosteroids used long-term) suppress pituitary ACTH secretion. When a patient uses 20 mg prednisone daily for 3 weeks and abruptly stops, morning ACTH may remain below 5 pg/mL for weeks to months while the pituitary axis recovers.

ACTH below 10 pg/mL alongside morning cortisol below 10 mcg/dL should prompt a low-dose (1-mcg) cosyntropin stimulation test or insulin tolerance test under endocrine supervision. The key clinical point: the adrenal glands themselves are structurally normal in secondary insufficiency; they simply lack the ACTH signal to function.

Subclinical Adrenal Dysfunction in Longevity Medicine

Most patients presenting to longevity clinics do not have overt Addison disease or pituitary tumors. They arrive with fatigue, sleep disruption, body-composition resistance, and mood dysregulation. ACTH in the 50 to 80 pg/mL range alongside cortisol in the 20 to 25 mcg/dL range suggests the HPA axis is running hot. The cause is almost always chronic psychosocial stress, sleep deprivation, or undisclosed exogenous stimulant use rather than primary adrenal pathology.

Addressing the modifiable inputs, specifically sleep architecture (targeting 7 to 9 hours with documented slow-wave sleep), cortisol-lowering behavioral practices (mindfulness-based stress reduction has reduced morning cortisol by 12 to 15% in randomized trials ([7])), and correcting nutritional deficiencies that impair HPA regulation (magnesium, vitamin C, B5), often normalizes ACTH within 8 to 12 weeks without pharmaceutical intervention.

ACTH and Related Biomarkers: Building a Complete Adrenal Panel

Interpreting ACTH in isolation is rarely sufficient. The following panel provides adequate clinical resolution for both disease exclusion and longevity optimization:

The Minimum Interpretable Adrenal Panel

  • 8 AM ACTH (plasma, on ice): Assess HPA drive.
  • 8 AM serum cortisol: Assess adrenal response to that drive.
  • 24-hour urinary free cortisol (UFC): Assess integrated cortisol exposure; values above 50 mcg/24h in the setting of elevated ACTH suggest hypercortisolism workup.
  • DHEA-S: The adrenal cortex secretes both cortisol and DHEA-S under ACTH stimulation. DHEA-S falls with age and blunted adrenal reserve. A cortisol-to-DHEA-S ratio above 10:1 (when cortisol is in mcg/dL and DHEA-S in mcg/dL) may indicate adrenal aging or exhaustion.
  • Aldosterone and plasma renin activity (PRA): Aldosterone is not directly regulated by ACTH (it responds to angiotensin II and potassium), but primary adrenal insufficiency affects aldosterone production as well; hyponatremia and hyperkalemia in a fatigued patient prompt this add-on.

The Cortisol Awakening Response as a Functional Complement

The cortisol awakening response (CAR), measured with salivary cortisol at wake, +30 minutes, and +60 minutes, reflects HPA reactivity rather than baseline output. A blunted CAR (less than 50% rise from wake to +30 minutes) correlates with burnout, chronic fatigue syndrome, and reduced stress resilience across multiple prospective cohort studies ([8]). Combining a morning plasma ACTH with a salivary CAR gives both the pituitary signal strength and the adrenal reactivity in a single morning protocol.

Ectopic ACTH Syndrome and Cushing Disease: When ACTH Goes Very High

Markedly elevated ACTH, above 200 to 500 pg/mL, alongside clinical signs of hypercortisolism (central obesity, purple striae, proximal muscle weakness, hypertension, diabetes), points to either Cushing disease (pituitary corticotroph adenoma) or ectopic ACTH syndrome (small-cell lung cancer, carcinoid tumors, medullary thyroid carcinoma).

Cushing disease carries a significant mortality burden. A 2015 meta-analysis in the European Journal of Endocrinology (N=3,525 across 21 studies) found standardized mortality ratios of 2.0 to 5.0 in patients with untreated or incompletely treated Cushing disease compared to age-matched controls ([9]). This is not a clinical scenario to optimize through lifestyle alone. MRI of the pituitary (with gadolinium, 3-mm cuts) and inferior petrosal sinus sampling (IPSS) for lateralization remain the diagnostic standard.

A critical clinical distinction: ACTH-dependent Cushing (pituitary or ectopic source) shows high or high-normal ACTH alongside high cortisol; ACTH-independent Cushing (adrenal adenoma or carcinoma) shows suppressed ACTH (often <5 pg/mL) alongside high cortisol, because the autonomous adrenal tumor suppresses the pituitary by negative feedback.

Medications and Supplements That Affect ACTH

Several drugs commonly used in hormone-optimization medicine alter ACTH or its interpretation:

  • Exogenous glucocorticoids (prednisone, hydrocortisone, dexamethasone, high-dose inhaled fluticasone): Suppress ACTH dose-dependently. Even 5 mg prednisone daily suppresses the HPA axis measurably within 2 weeks of continuous use ([10]).
  • Metyrapone: Blocks cortisol synthesis, causing ACTH to rise steeply; used diagnostically in the metyrapone stimulation test for secondary insufficiency.
  • Mitotane: Adrenolytic drug used in adrenocortical carcinoma; destroys adrenal tissue, sending ACTH very high.
  • Phosphodiesterase inhibitors and DHEA supplementation: Do not materially affect ACTH in standard doses.
  • Mifepristone (RU-486): Blocks glucocorticoid receptors, eliminating negative feedback and causing ACTH and cortisol to rise paradoxically; confounds interpretation.

Always document all steroid use, including topical and inhaled formulations, before ordering ACTH.

Monitoring Frequency and Protocol in Longevity Practice

For a patient without known adrenal or pituitary disease, the HealthRX medical team recommends the following surveillance cadence:

  • Baseline: 8 AM ACTH and cortisol drawn at initial evaluation, paired with DHEA-S, CBC, CMP, and fasting lipid panel.
  • Annual monitoring: Repeat 8 AM ACTH and cortisol once per year if values are in the optimal zone and no new clinical concerns arise.
  • Every 6 months: Indicated if baseline ACTH is outside the 10 to 35 pg/mL target, if the patient is using any exogenous corticosteroid, or if symptoms of fatigue, weight gain, or blood pressure instability emerge.
  • Immediate re-draw: Required if clinical presentation changes acutely, or if a specimen was not handled on ice and results are unexpectedly low.

Patients who have been on long-term testosterone replacement therapy (TRT) do not typically show ACTH suppression from TRT alone; the adrenal axis and the gonadal axis are largely independent at the pituitary level. Thyroid hormone replacement similarly does not directly alter ACTH, though untreated hypothyroidism slows cortisol clearance and can modestly raise steady-state cortisol.

Special Populations

Women on Hormone Therapy

Oral estrogen increases cortisol-binding globulin (CBG), which raises total cortisol but not free cortisol. ACTH itself is not directly altered by oral estradiol at standard replacement doses. However, when using total serum cortisol to assess adrenal response, a woman taking oral estrogen may show a falsely reassuring cortisol even with partial adrenal insufficiency, because total cortisol is artificially elevated. Transdermal estradiol has minimal effect on CBG and is preferred when accurate cortisol interpretation is needed.

Older Adults (Age 65+)

As noted above, morning ACTH tends to run higher in older adults due to reduced HPA negative feedback sensitivity. The longevity-medicine upper bound of "optimal" shifts to approximately 40 pg/mL for patients over 65, provided cortisol remains below 20 mcg/dL. Periodic DHEA-S measurement becomes particularly informative in this population because adrenal androgen output declines steeply with age even when ACTH remains adequate.

Patients Recovering from Critical Illness

Critical illness-related corticosteroid insufficiency (CIRCI), previously called relative adrenal insufficiency, is a well-described entity in ICU patients. These patients may have ACTH values in the normal or high-normal range but still fail to mount adequate cortisol responses to stress due to end-organ receptor resistance. The 2017 Society of Critical Care Medicine (SCCM) and European Society of Intensive Care Medicine (ESICM) joint guidelines recommend against routine ACTH stimulation testing in septic shock management and instead focus on clinical response to empiric hydrocortisone 200 mg/day for 7 days in vasopressor-dependent patients ([11]).

Frequently asked questions

›What is the optimal ACTH range for longevity and healthy aging?
Longevity-medicine practitioners target 10 to 35 pg/mL on an 8 AM draw, always interpreted alongside a morning cortisol of 10 to 18 mcg/dL. This window reflects adequate HPA tone without the tissue-aging effects associated with chronically elevated cortisol. Adults over age 65 may reasonably target up to 40 pg/mL given age-related changes in HPA feedback sensitivity.
›What is the normal ACTH range on a standard lab report?
Most US clinical labs report a reference interval of roughly 6 to 50 pg/mL for a morning draw, though specific cutoffs vary: LabCorp lists 6.0 to 58.0 pg/mL and Quest Diagnostics lists 7.2 to 63.3 pg/mL. These intervals represent the central 95% of a broad reference population and are wider than the functional targets used in longevity medicine.
›What does a high ACTH level mean?
Elevated ACTH, above 100 pg/mL, most commonly indicates primary adrenal insufficiency (Addison disease), in which failing adrenal glands force the pituitary to overproduce ACTH. Very high ACTH above 200 pg/mL alongside signs of hypercortisolism raises concern for Cushing disease (pituitary adenoma) or ectopic ACTH syndrome from a tumor such as small-cell lung cancer. Formal cosyntropin stimulation testing and endocrinology referral are required.
›What does a low ACTH level mean?
ACTH below 5 to 10 pg/mL, especially when paired with low morning cortisol, suggests secondary adrenal insufficiency. The most common cause in clinical practice is prior or ongoing use of exogenous corticosteroids (prednisone, dexamethasone, high-dose inhaled steroids) that suppress pituitary function. Pituitary tumors, prior pituitary surgery, and head trauma are structural causes. The adrenal glands are structurally normal in secondary insufficiency but lack the ACTH signal to produce cortisol.
›Does time of day affect ACTH results?
Yes, significantly. ACTH follows a steep diurnal curve, peaking between 6 and 8 AM (often 30 to 60 pg/mL) and falling to near-nadir levels by midnight (often below 10 pg/mL). All clinical reference ranges and longevity targets are specified for an 8 AM draw. A result drawn at noon or in the evening cannot be compared against morning reference intervals and may be misinterpreted as low.
›How is ACTH collected correctly?
ACTH degrades rapidly at room temperature. Blood must be drawn into a pre-chilled EDTA (lavender-top) tube, kept on ice immediately after collection, centrifuged within 15 minutes, and the plasma separated and frozen if not processed promptly. Failure to follow this cold-chain protocol is a leading cause of falsely low ACTH results. If an unexpectedly low value is returned, always verify specimen handling before ordering further workup.
›Should ACTH always be drawn with cortisol?
Yes. ACTH alone rarely provides enough information for clinical decisions. An 8 AM serum cortisol must be drawn at the same time to allow paired interpretation. ACTH tells you how hard the pituitary is driving the adrenal gland; cortisol tells you how well the adrenal gland is responding. Only the combination distinguishes primary from secondary adrenal dysfunction and guides the next diagnostic step.
›Can stress or poor sleep raise ACTH?
Yes. Acute psychological stress, sleep deprivation, and even the stress of the venipuncture itself can transiently raise ACTH. Patients should rest quietly for at least 30 minutes before the draw. Chronically elevated ACTH in the 50 to 80 pg/mL range without structural pituitary or adrenal pathology often reflects sustained psychosocial stress or sleep disruption rather than primary disease. Addressing sleep and stress can normalize ACTH within 8 to 12 weeks in many patients.
›Do exogenous steroids affect ACTH?
Yes, profoundly. Any exogenous glucocorticoid, including oral prednisone, inhaled fluticasone at high doses, topical steroids over large skin areas, and epidural or intra-articular corticosteroid injections, suppresses pituitary ACTH secretion via negative feedback. Even 5 mg of prednisone daily for 2 weeks measurably suppresses the HPA axis. Always disclose all corticosteroid use, including over-the-counter formulations, before ACTH testing.
›How does ACTH relate to DHEA and aging?
Both cortisol and DHEA-S are produced by the adrenal cortex in response to ACTH, but they follow opposite aging trajectories. Cortisol tends to remain stable or rise slightly with age; DHEA-S falls by roughly 80% between age 25 and age 75. A rising cortisol-to-DHEA-S ratio is considered a marker of adrenal aging and adverse metabolic risk in longevity medicine. Monitoring DHEA-S alongside ACTH and cortisol adds important context to HPA-axis assessment.
›What is Cushing disease and how does ACTH help diagnose it?
Cushing disease is hypercortisolism caused by a pituitary corticotroph adenoma that secretes excess ACTH. ACTH is high or high-normal (often 50 to 200 pg/mL) while cortisol is clearly elevated and fails to suppress on a 1-mg overnight dexamethasone suppression test. It must be distinguished from ectopic ACTH syndrome (from tumors outside the pituitary) and from ACTH-independent hypercortisolism (adrenal adenoma), in which ACTH is suppressed below 5 pg/mL because the autonomous adrenal tumor overrides pituitary feedback.
›How often should ACTH be monitored in a longevity protocol?
For patients with values in the optimal 10 to 35 pg/mL range and no symptoms, annual repeat testing is appropriate. If ACTH falls outside the target, if the patient uses any corticosteroid regularly, or if fatigue, weight changes, or blood pressure instability emerge, re-testing every 6 months is preferred. A single out-of-range result should be confirmed with a repeat draw to rule out specimen-handling error before pursuing imaging or stimulation testing.

References

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  2. Aardal-Eriksson E, Karlberg BE, Holm AC. Salivary cortisol: an alternative to serum cortisol determinations in dynamic function tests. Clin Chem Lab Med. 1998;36(4):215-222. Referenced alongside: Ellis MJ, Livesey JH, Comparison of ACTH stability in EDTA plasma at varying temperatures. Ann Clin Biochem. 2009. https://pubmed.ncbi.nlm.nih.gov/7691482/
  3. Lupien SJ, de Leon M, de Santi S, et al. Cortisol levels during human aging predict hippocampal atrophy and memory deficits. Nat Neurosci. 1998;1(1):69-73. https://pubmed.ncbi.nlm.nih.gov/10195112/
  4. Whitworth JA, Williamson PM, Mangos G, Kelly JJ. Cardiovascular consequences of cortisol excess. Vasc Health Risk Manag. 2005;1(4):291-299. See also: Vogelzangs N et al, urinary cortisol and cardiovascular events, J Clin Endocrinol Metab 2012. https://pubmed.ncbi.nlm.nih.gov/16276948/
  5. Van Cauter E, Leproult R, Kupfer DJ. Effects of gender and age on the levels and circadian rhythmicity of plasma cortisol. J Clin Endocrinol Metab. 1996;81(7):2468-2473. https://pubmed.ncbi.nlm.nih.gov/8675562/
  6. Napier C, Pearce SH. Current and emerging therapies for Addison's disease. Curr Opin Endocrinol Diabetes Obes. 2014;21(3):147-153. https://pubmed.ncbi.nlm.nih.gov/24755997/
  7. Turakitwanakan W, Mekseepralard C, Busarakumtragul P. Effects of mindfulness meditation on serum cortisol of medical students. J Med Assoc Thai. 2013;96 Suppl 1:S90-95. https://pubmed.ncbi.nlm.nih.gov/23724462/
  8. Wust S, Wolf J, Hellhammer DH, et al. The cortisol awakening response: normal values and confounds. Noise Health. 2000;2(7):79-88. https://pubmed.ncbi.nlm.nih.gov/12689474/
  9. Clayton RN, Raskauskiene D, Reulen RC, Jones PW. Mortality and morbidity in Cushing's disease over 50 years in Stoke-on-Trent, UK: audit and meta-analysis of literature. J Clin Endocrinol Metab. 2011;96(3):632-642. See also: Ntali G, Grossman A. European Journal of Endocrinology 2015 meta-analysis. https://pubmed.ncbi.nlm.nih.gov/21159838/
  10. Dinsen S, Baslund B, Klose M, et al. Why glucocorticoid withdrawal may sometimes be as dangerous as the treatment itself. Eur J Intern Med. 2013;24(8):714-720. https://pubmed.ncbi.nlm.nih.gov/24054881/
  11. Annane D, Pastores SM, Rochwerg B, et al. Guidelines for the Diagnosis and Management of Critical Illness-Related Corticosteroid Insufficiency (CIRCI) in Critically Ill Patients (Part I): Society of Critical Care Medicine (SCCM) and European Society of Intensive Care Medicine (ESICM) 2017. Crit Care Med. 2017;45(12):2078-2088. https://pubmed.ncbi.nlm.nih.gov/28938253/