ACTH stimulation test

Last updated
ACTH stimulation test
Synonyms Synacthen test
OPS-301 code 1-797
MedlinePlus 003696
LOINC 34541-3, 34542-1

The ACTH test (also called the cosyntropin, tetracosactide, or Synacthen test) is a medical test usually requested and interpreted by endocrinologists to assess the functioning of the adrenal glands' stress response by measuring the adrenal response to adrenocorticotropic hormone (ACTH; corticotropin) or another corticotropic agent such as tetracosactide (cosyntropin, tetracosactrin; Synacthen) or alsactide (Synchrodyn). [1] [2] ACTH is a hormone produced in the anterior pituitary gland that stimulates the adrenal glands to release cortisol, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and aldosterone. [3]


During the test, a small amount of synthetic ACTH is injected, and the amount of cortisol (and sometimes aldosterone) that the adrenals produce in response is measured. [4] This test may cause mild side effects in some individuals. [5] [6]

This test is used to diagnose or exclude primary and secondary adrenal insufficiency, Addison's disease, and related conditions. [2] In addition to quantifying adrenal insufficiency, the test can distinguish whether the cause is adrenal (low cortisol and aldosterone production) or pituitary (low ACTH production). [1] The Insulin tolerance test is recognized as the gold standard assay of adrenal insufficiency, but due to the cumbersome requirement for a two-hour test and the risks of seizures or myocardial infarction, the ACTH stimulation test is commonly used as an easier, safer, though not as accurate, alternative. [7] The test is extremely sensitive (97% at 95% specificity) to primary adrenal insufficiency, but less so to secondary adrenal insufficiency (57-61% at 95% specificity); while secondary adrenal insufficiency may thus be dismissed by some interpreters on the basis of the test, additional testing may be called for if the probability of secondary adrenal insufficiency is particularly high. [1]

Adrenal insufficiency is a potentially life-threatening condition. Treatment should be initiated as soon as the diagnosis is confirmed, or sooner if the patient presents in apparent adrenal crisis. [8]

Versions of the test

This test can be given as a low-dose short test, a conventional-dose short test, or as a prolonged-stimulation test.[ citation needed ]

In the low-dose short test, 1 μg of an ACTH drug is injected into the patient. In the conventional-dose short test, 250 μg of drug are injected. Both of these short tests last for about an hour and provide the same information. Studies have shown the cortisol response of the adrenals is the same for the low-dose and conventional-dose tests. [9] [10]

The prolonged-stimulation test, which is also called a long conventional-dose test, can last up to 48 hours. This form of the test can differentiate between primary, secondary, and tertiary adrenal insufficiency. This form of the test is rarely performed because earlier testing of cortisol and ACTH levels in association with the short test may provide all the necessary information. [8]


The test should not be given if on glucocorticoids or adrenal extract supplement, as these will affect test results. Stress and recently administered radioisotope scans[ citation needed ] can artificially increase levels and may invalidate test results. Spironolactone, contraceptives, licorice, estrogen, androgen (including DHEA) and progesterone therapy may also affect both aldosterone and cortisol stimulation test results. To stimulate aldosterone, consumption of salt should be reduced to a minimum, and foods high in sodium avoided for 24 hours prior to testing. Women should ideally undergo testing during the first week of their menstrual cycle as aldosterone (and occasionally cortisol) may be falsely elevated in the luteal cycle secondary to progesterone inhibition, leading to a compensatory rise in aldosterone levels. [11]


Traditionally, cortisol and ACTH levels (separate lavender top tube) are drawn at baseline (time = 0). Next, synthetic ACTH or another corticotropic agent is injected IM or IV, depending on the agent. [12] Approximately 20 mL of heparinized venous blood is collected at 30 and 60 minutes after the synthetic ACTH injection to measure cortisol levels. [13] [14]

ACTH samples are kept on ice and sent immediately to the laboratory, whereas cortisol does not need to be kept on ice. [15]

Potential side effects

Commonly reported reactions are nausea, anxious sweating, dizziness, itchy skin, redness and or swelling of injection site, palpitations (a fast or fluttering heart beat), and facial flushing (may also include arms and torso), but should disappear within a few hours. [5] [6] Rarely seen, but serious side effects include rash, fainting, headache, blurred vision, severe swelling, severe dizziness, trouble breathing, irregular heartbeat. [6]

Interpretation of results

The adrenal glands sit atop the kidneys. Illu adrenal gland.jpg
The adrenal glands sit atop the kidneys.

Cosyntropin stimulation testing

In healthy individuals, the cortisol level should increase above 18-20 μg/dl within 60 minutes on a 250 mcg cosyntropin stimulation test. [16]

Interpretation for primary adrenal insufficiency, Addison's disease

In Addison's disease, both the cortisol and aldosterone levels are low, and the cortisol will not rise during the cosyntropin stimulation test[ citation needed ]

Interpretation for secondary adrenal insufficiency

In secondary adrenal insufficiency, due to exogenous steroid administration suppressing pituitary production of ACTH or due to primary pituitary disorder causing insufficient ACTH production, the adrenal glands will atrophy over time and cortisol production will fall and patients will fail stimulation testing. Early in the development of secondary adrenal insufficiency, the adrenals may not have atrophied and can still stimulate, resulting in a normal cosyntropin stimulation test. [17]

If secondary adrenal insufficiency is diagnosed, the insulin tolerance test (ITT) or the CRH (corticotropin-releasing hormone) stimulation test can be used to distinguish between a hypothalamic (tertiary) and pituitary (secondary) cause but is rarely used in clinical practice. [17]

ACTH plasma test plus cortisol stimulation

Location of the pituitary gland. Pituitary gland.png
Location of the pituitary gland.

Measuring a morning, fasting ACTH level helps assess for the etiology of adrenal insufficiency.[ citation needed ]

Interpretation for primary adrenal insufficiency and Addison's disease

ACTH will be high [13] - usually well above upper limits of reference range.

Interpretation for secondary adrenal insufficiency

ACTH will be low [13] - usually below 35, but most people with secondary fall within the range limit. This is inappropriately normal for the low cortisol level.

In some cases, the actual cause of low ACTH is from low CRH in the hypothalamus. It is possible to have separate ACTH and CRH impairment such as can happen in a head injury. [18]

Aldosterone stimulation

The ACTH stimulation test is occasionally used to test adrenal production of aldosterone at the same time as cortisol to also help in determining if primary (hyperreninemic) or secondary (hyporeninemic) hypoaldosteronism is present. [4] Human ACTH has a slight stimulatory effect on aldosterone, [19] but the amount of synthetic ACTH given in the stimulation is equivalent to more than a whole days production of natural ACTH, so the aldosterone response can be easily measured in blood serum. [20] Same as cortisol, aldosterone should double from a respectable base value (around 20 ng/dl, must fast salt 24 hours and sit upright for blood draw) in a healthy individual.[ citation needed ]

Interpretation for primary aldosterone deficiency

The aldosterone response in the ACTH stimulation test is blunted or absent in patients with primary adrenal insufficiency including Addison's disease. [4] The base value is usually in the mid-teens or less and rise to less than double the base value thus indicating primary hypoaldosteronism (sodium low, potassium and renin enzyme will be high) and is an indicator of primary adrenal insufficiency or Addison's disease.[ citation needed ]

Interpretation for secondary aldosterone deficiency

Aldosterone response of several factors from a low base value. This factoring indicates secondary hypoaldosteronism (sodium low, potassium and renin enzyme will be low). Usually doubling to quadrupling from a low base aldosterone value is what is seen in secondary adrenal insufficiency. Decoupling of aldosterone in the ACTH stimulation test is possible (i.e. 2 ng/dl stimming to 20). [21] A result of doubling or more of aldosterone may help in tandem with a cortisol stimulation that doubled or more confirm a diagnosis of secondary adrenal insufficiency. In rare cases, an aldosterone stimulation which did not double, but with the presence of low potassium, low renin and low ACTH indicates atrophy of aldosterone production from the prolonged lack of renin.

Similar to the cortisol stimulation in ACTH deficiency, the test interpreter may lack knowledge of how to properly interpret for secondary hypoaldosteronism and think a result of aldosterone doubling or more from a low base value is good.

Future perspectives

Recent data showed that Synacthen test results can be used to predict future recovery of HPA axis function in patients with reversible causes of Adrenal Insufficiency. [22]

Other hormones and chemicals that will rise in the ACTH stimulation test

Simple diagnostic chart

Source of pathologyCRHACTHDHEADHEA-SCortisolAldosteroneReninNaKCauses5
lowlowlowlowlow3lowlowlowlowtumor of the hypothalamus (adenoma), antibodies, environment, head injury, abrupt corticosteroid withdrawal
high2lowlowlowlow3lowlowlowlowtumor of the pituitary (adenoma), antibodies, environment, head injury,
surgical removal6, Sheehan's syndrome
adrenal glands
highhighhighhighlow4lowhighlowhightumor of the adrenal (adenoma), stress, antibodies, environment, Addison's, injury, surgical removal
1Automatically includes diagnosis of secondary (hypopituitarism)
2Only if CRH production in the hypothalamus is intact
3Value doubles or more in stimulation
4Value less than doubles in stimulation
5Most common, doesn't include all possible causes
6Usually because of very large tumor (macroadenoma)
7Includes Addison's disease

Veterinary medicine

The test is also used to diagnose hypoadrenocorticism in dogs and sometimes cats. [27] [28] [29]

See also

Related Research Articles

Adrenal gland Endocrine gland

The adrenal glands are endocrine glands that produce a variety of hormones including adrenaline and the steroids aldosterone and cortisol. They are found above the kidneys. Each gland has an outer cortex which produces steroid hormones and an inner medulla. The adrenal cortex itself is divided into three main zones: the zona glomerulosa, the zona fasciculata and the zona reticularis.

Adrenocorticotropic hormone Pituitary hormone

Adrenocorticotropic hormone is a polypeptide tropic hormone produced by and secreted by the anterior pituitary gland. It is also used as a medication and diagnostic agent. ACTH is an important component of the hypothalamic-pituitary-adrenal axis and is often produced in response to biological stress. Its principal effects are increased production and release of cortisol by the cortex of the adrenal gland. ACTH is also related to the circadian rhythm in many organisms.

Cushings syndrome Symptoms from excessive exposure to glucocorticoids such as cortisol

Cushing's syndrome is a collection of signs and symptoms due to prolonged exposure to glucocorticoids such as cortisol. Signs and symptoms may include high blood pressure, abdominal obesity but with thin arms and legs, reddish stretch marks, a round red face, a fat lump between the shoulders, weak muscles, weak bones, acne, and fragile skin that heals poorly. Women may have more hair and irregular menstruation. Occasionally there may be changes in mood, headaches, and a chronic feeling of tiredness.

Adrenal cortex Cortex of the adrenal gland

The adrenal cortex is the outer region and also the largest part of an adrenal gland. It is divided into three separate zones: zona glomerulosa, zona fasciculata and zona reticularis. Each zone is responsible for producing specific hormones. It is also a secondary site of androgen synthesis.

Cortisol Human natural glucocorticoid hormone

Cortisol is a steroid hormone, in the glucocorticoid class of hormones. When used as a medication, it is known as hydrocortisone.

Addisons disease Endocrine disorder

Addison's disease, also known as primary adrenal insufficiency, is a rare long-term endocrine disorder characterized by inadequate production of the steroid hormones cortisol and aldosterone by the two outer layers of the cells of the adrenal glands, causing adrenal insufficiency. Symptoms generally come on slowly and insidiously and may include abdominal pain and gastrointestinal abnormalities, weakness, and weight loss. Darkening of the skin in certain areas may also occur. Under certain circumstances, an adrenal crisis may occur with low blood pressure, vomiting, lower back pain, and loss of consciousness. Mood changes may also occur. Rapid onset of symptoms indicates acute adrenal failure which is a serious and emergent condition. An adrenal crisis can be triggered by stress, such as from an injury, surgery, or infection.

Aldosterone Mineralocorticoid steroid hormone

Aldosterone is the main mineralocorticoid steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon. It plays a central role in the homeostatic regulation of blood pressure, plasma sodium (Na+) and potassium (K+) levels. It does so primarily by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron. It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing water retention or loss, blood pressure and blood volume. When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and kidney disease. Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart.

Adrenal insufficiency Medical condition

Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of steroid hormones, primarily cortisol; but may also include impaired production of aldosterone, which regulates sodium conservation, potassium secretion, and water retention. Craving for salt or salty foods due to the urinary losses of sodium is common.

Corticotropes are basophilic cells in the anterior pituitary that produce pro-opiomelanocortin (POMC) which undergoes cleavage to adrenocorticotropin (ACTH), β-lipotropin (β-LPH), and melanocyte-stimulating hormone (MSH). These cells are stimulated by corticotropin releasing hormone (CRH) and make up 15–20% of the cells in the anterior pituitary. The release of ACTH from the corticotropic cells is controlled by CRH, which is formed in the cell bodies of parvocellular neurosecretory cells within the paraventricular nucleus of the hypothalamus and passes to the corticotropes in the anterior pituitary via the hypophyseal portal system. Adrenocorticotropin hormone stimulates the adrenal cortex to release glucocorticoids and plays an important role in the stress response.

Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency is an uncommon form of congenital adrenal hyperplasia resulting from a defect in the gene CYP17A1, which encodes for the enzyme 17α-hydroxylase. It causes decreased synthesis of cortisol and sex steroids, with resulting increase in mineralocorticoid production. Thus, common symptoms include mild hypocortisolism, ambiguous genitalia in genetic males or failure of the ovaries to function at puberty in genetic females, and hypokalemic hypertension (respectively). However, partial (incomplete) deficiency is notable for having inconsistent symptoms between patients, and affected genetic (XX) females may be wholly asymptomatic except for infertility.

Metyrapone Chemical compound

Metyrapone, sold under the brand name Metopirone, is a medication which is used in the diagnosis of adrenal insufficiency and occasionally in the treatment of Cushing's syndrome (hypercortisolism).

Sheehan's syndrome, also known as postpartum pituitary gland necrosis, is hypopituitarism, caused by ischemic necrosis due to blood loss and hypovolemic shock during and after childbirth.

Endocrine gland Glands of the endocrine system that secrete hormones to blood

Endocrine glands are ductless glands of the endocrine system that secrete their products, hormones, directly into the blood. The major glands of the endocrine system include the pineal gland, pituitary gland, pancreas, ovaries, testes, thyroid gland, parathyroid gland, hypothalamus and adrenal glands. The hypothalamus and pituitary glands are neuroendocrine organs.

Hypoaldosteronism Medical condition

Hypoaldosteronism is an endocrinological disorder characterized by decreased levels of the hormone aldosterone. Similarly, isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol.

In humans and other animals, the adrenocortical hormones are hormones produced by the adrenal cortex, the outer region of the adrenal gland. These polycyclic steroid hormones have a variety of roles that are crucial for the body’s response to stress, and they also regulate other functions in the body. Threats to homeostasis, such as injury, chemical imbalances, infection, or psychological stress, can initiate a stress response. Examples of adrenocortical hormones that are involved in the stress response are aldosterone and cortisol. These hormones also function in regulating the conservation of water by the kidneys and glucose metabolism, respectively.

Pseudohyperaldosteronism is a medical condition which mimics the effects of elevated aldosterone (hyperaldosteronism) by presenting with high blood pressure (hypertension), low blood potassium levels (hypokalemia), metabolic alkalosis, and low levels of plasma renin activity (PRA). However, unlike hyperaldosteronism, this conditions exhibits low or normal levels of aldosterone in the blood. Causes include genetic disorders, acquired conditions, metabolic disorders, and dietary imbalances including excessive consumption of licorice. Confirmatory diagnosis depends on the specific root cause and may involve blood tests, urine tests, or genetic testing; however, all forms of this condition exhibit abnormally low concentrations of both plasma renin activity (PRA) and plasma aldosterone concentration (PAC) which differentiates this group of conditions from other forms of secondary hypertension. Treatment is tailored to the specific cause and focuses on symptom control, blood pressure management, and avoidance of triggers.

Adrenal crisis Medical condition

Adrenal crisis is a potentially life-threatening medical condition requiring immediate emergency treatment. It is a constellation of symptoms that indicate severe adrenal insufficiency caused by insufficient levels of the hormone cortisol. This may be the result of either previously undiagnosed or untreated Addison's disease, a disease process suddenly affecting adrenal function, suddenly stopping intake of glucocorticoids or an intercurrent problem in someone known to have Addison's disease, congenital adrenal hyperplasia (CAH), or other form of primary adrenal insufficiency.

Critical illness–related corticosteroid insufficiency is a form of adrenal insufficiency in critically ill patients who have blood corticosteroid levels which are inadequate for the severe stress response they experience. Combined with decreased glucocorticoid receptor sensitivity and tissue response to corticosteroids, this adrenal insufficiency constitutes a negative prognostic factor for intensive care patients.

Hypoadrenocorticism in dogs, or, as it is known in people, Addison's disease, is an endocrine system disorder that occurs when the adrenal glands fail to produce enough hormones for normal function. The adrenal glands secrete glucocorticoids such as cortisol and mineralocorticoids such as aldosterone; when proper amounts of these are not produced, the metabolic and electrolyte balance is upset. Mineralocorticoids control the amount of potassium, sodium, and water in the body. Hypoadrenocorticism is fatal if left untreated.

Glucocorticoid remediable aldosteronism also describable as aldosterone synthase hyperactivity, is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient.


  1. 1 2 3 Dorin RI, Qualls CR, Crapo LM (2003). "Diagnosis of adrenal insufficiency" (PDF). Ann. Intern. Med. 139 (3): 194–204. doi:10.7326/0003-4819-139-3-200308050-00017. PMID   12899587.
  2. 1 2 Elizabeth H. Holt (2008). "ACTH (cosyntropin) stimulation test".{{cite journal}}: Cite journal requires |journal= (help)
  3. Hanukoglu A, Fried D, Nakash I, Hanukoglu I (Nov 1995). "Selective increases in adrenal steroidogenic capacity during acute respiratory disease in infants". Eur J Endocrinol. 133 (5): 552–6. doi:10.1530/eje.0.1330552. PMID   7581984. S2CID   44439040.
  4. 1 2 3 "ACTH Stimulation Test" (PDF), Test Catalog, Warde Medical Laboratory, archived from the original (PDF) on May 6, 2006
  5. 1 2 Synacthen Test (PDF), St George's Healthcare, archived from the original (PDF; trifold) on February 20, 2005
  6. 1 2 3 "GENERIC NAME: COSYNTROPIN - INJECTABLE (koe-sin-TROW-pin)".{{cite journal}}: Cite journal requires |journal= (help)
  7. Hormones (Athens). 2012 Oct-Dec;11(4):428-35. Is the 250 μg ACTH test a useful tool for the diagnosis of central hypoadrenalism in adult patients with pituitary disorders? Ferrante E1, Morelli V, Giavoli C, Mantovani G, Verrua E, Sala E, Malcmiodi E, Bergamaschi S, Profka E, Cairoli E, Palmieri S, Chiodini I, Lania AG, Spada A, Peccoz PB.
  8. 1 2 Evangelia Charmandari; George P.; Chrousos, M.D. "ADRENAL INSUFFICIENCY Chapter 13". Archived from the original on 2008-03-02.{{cite journal}}: Cite journal requires |journal= (help)
  9. Abdu TA, Elhadd TA, Neary R, Clayton RN (1999). "Comparison of the low dose short synacthen test (1 microg), the conventional dose short synacthen test (250 microg), and the insulin tolerance test for assessment of the hypothalamic-pituitary-adrenal axis in patients with pituitary disease". Journal of Clinical Endocrinology and Metabolism. 84 (3): 838–43. doi:10.1210/jcem.84.3.5535. PMID   10084558.
  10. Cemeroglu AP, Kleis L, Postellon DC, Wood MA (July 2010). "Comparison of low-dose and high-dose cosyntropin stimulation testing in children". Pediatrics International . 53 (2): 175–80. doi:10.1111/j.1442-200X.2010.03203.x. PMID   20626639. S2CID   21357134.
  11. Emily D. Szmuilowicz; Gail K. Adler; Jonathan S. Williams; Dina E.Green; Tham M. Yao; Paul N. Hopkins; Ellen W. Seely (2006). "Relationship between Aldosterone and Progesterone in the Human Menstrual Cycle". Journal of Clinical Endocrinology & Metabolism. 91 (10): 3981–3987. doi: 10.1210/jc.2006-1154 . PMID   16868049.
  12. "Cosyntropin (Professional Patient Advice)".
  13. 1 2 3 "ACTH Rapid Stimulation Test (Cortrosyn, Cosyntropin)".{{cite journal}}: Cite journal requires |journal= (help)
  14. NIDDK's Office of Health Research Reports. "Addison's disease". Archived from the original on 2011-04-26. Retrieved 2008-08-18.{{cite journal}}: Cite journal requires |journal= (help)
  15. K. Pagana, RN; T. Pagana. "Mosby's Diagnostic and Laboratory Test Reference 2nd ed.: Adrenocorticotropic hormone stimulation test": 17–18.{{cite journal}}: Cite journal requires |journal= (help)
  16. Bornstein, Stefan R.; Allolio, Bruno; Arlt, Wiebke; Barthel, Andreas; Don-Wauchope, Andrew; Hammer, Gary D.; Husebye, Eystein S.; Merke, Deborah P.; Murad, M. Hassan; Stratakis, Constantine A.; Torpy, David J. (2016). "Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline". The Journal of Clinical Endocrinology & Metabolism. 101 (2): 364–389. doi:10.1210/jc.2015-1710. PMC   4880116 . PMID   26760044.
  17. 1 2 Ashley B. Grossman (2007). "Addison's Disease". Endocrine and Metabolic Disorders: 4.
  18. Lynnette K Nieman (2008). "Corticotropin-releasing hormone stimulation test".{{cite journal}}: Cite journal requires |journal= (help)
  19. "Role of ACTH in Regulation and Action of Adrenocorticoids": 7 of 52. Archived from the original on 2014-07-29.{{cite journal}}: Cite journal requires |journal= (help)
  20. "Aldosterone and Renin". Archived from the original on 2008-09-17. Retrieved 2008-08-18.{{cite journal}}: Cite journal requires |journal= (help)
  21. L.A. Cunningham; M.A. Holzwarth (1988). "Vasoactive intestinal peptide stimulates adrenal aldosterone and corticosterone secretion". Endocrinology . 122 (5): 2090–2097. doi:10.1210/endo-122-5-2090. PMID   3359977.
  22. Pofi et al., JCEM(2018) "The short Synacthen (corticotropin) test can be used to predict recovery of hypothalamo-pituitary-adrenal axis function."
  23. 1 2 Jardena J. Puder; Pamela U. Freda; Robin S. Goland; Michel Ferin; Sharon L. Wardlaw (2000). "Stimulatory Effects of Stress on Gonadotropin Secretion in Estrogen-Treated Women*" (PDF). The Journal of Clinical Endocrinology & Metabolism. 85 (6): 2184–2188. doi:10.1210/jc.85.6.2184. Archived from the original (PDF) on 2008-10-29. Retrieved 2008-08-19.
  24. Witchel, S. F. (2017). "Congenital Adrenal Hyperplasia". Journal of Pediatric and Adolescent Gynecology. 30 (5): 520–534. doi:10.1016/j.jpag.2017.04.001. PMC   5624825 . PMID   28450075.
  25. Dessinioti, C.; Katsambas, A. (2009). "Congenital adrenal hyperplasia". Dermato-Endocrinology. 1 (2): 87–91. doi:10.4161/derm.1.2.7818. PMC   3329455 . PMID   22523607.
  26. Sheikh Alshabab, L. I.; Alebrahim, A.; Kaddoura, A.; Al-Fahoum, S. (2015). "Congenital adrenal hyperplasia due to 21-hydroxylase deficiency: A five-year retrospective study in the Children's Hospital of Damascus, Syria". Qatar Medical Journal. 2015 (1): 11. doi:10.5339/qmj.2015.11. PMC   4614327 . PMID   26535179.
  27. Lathan, P; Moore, GE; Zambon, S; Scott-Moncrieff, JC (2008). "Use of a low-dose ACTH stimulation test for diagnosis of hypoadrenocorticism in dogs". Journal of Veterinary Internal Medicine. 22 (4): 1070–3. doi: 10.1111/j.1939-1676.2008.0118.x . PMID   18537878.
  28. ACVIM, Ronald Lyman DVM Dipl. (November 1, 2008). "Consider ACTH stimulation test when you suspect canine hyperadrenocorticism".
  29. "ACTH Stimulation Test" (PDF). Idexx. Archived from the original (PDF) on 2 February 2017. Retrieved 23 January 2017.