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Pharmacological endocrine function tests

Pharmacological endocrine function tests

The reactivity and feedback sensitivity of hormone axes can be tested by administering certain drugs.1

The following presentation is based primarily on Kudielka-Wüst, Wüst, Bertram2 and information from various laboratories.

1. Tests for ADHD and/or depression

The tests compiled here could be suitable for diagnosing ADHD subtypes and determining suitable treatment methods. In practice, these tests have not yet been used in relation to ADHD.

As the HPA axis is hyperactivated or hypoactivated not only in depression and ADHD, but also in other mental disorders, the tests mentioned can only be used to a limited extent to determine which mental disorder is present. Within an identified mental disorder, however, they are very helpful in differentiating it from other disorders and finding a suitable medication.

1.1. Dexamethasone test

  • Measurement of cortisol level (possibly also ACTH) 8 to 9 am or 3 to 4 pm to determine the basal value
  • Administration: Dexamethasone 11 p.m
  • Effect: selective on glucocorticoid receptors (GR).
    Effect on GR 30 times stronger than on mineralocorticoid receptors (MR).
    The GRs (unlike MR, which runs the “day-to-day business”) shut down the HPA axis
    Dexamethasone hardly crosses the blood-brain barrier; therefore hardly any effect on the hypothalamus, strong effect on the pituitary gland
  • Measurement of cortisol level at the same time of day (8 to 9 a.m. or 3 to 4 p.m.) on the following day, possibly midnight after administration of dexamethasone
  • Healthy reaction:
    • Drop in ACTH (= ACTH suppression)
    • Decrease in cortisol (= cortisol suppression)
    • Decrease in IL-1β (= IL-1β suppression)3
  • Not a healthy reaction:
    • Lack of cortisol suppression 15/16 h
      • Suspicion: the shutdown of the HPA axis mediated by glucocorticoid receptors is disturbed
      • Suspected depression, ADHD-HI
    • Elevated cortisol levels at midnight
      • Suspicion of hypercortisolism4
    • No IL-1β suppression
      • Suspicion of depression35
  • Risks, side effects
    • None

Procedure of the DST:6

  • 23:00 In the evening: oral intake of 1 mg dexamethasone
  • 08:00, 16:00, 23:00 following day: measurement of cortisol in blood plasma
  • Due to the impaired negative feedback of the HPA axis or the desensitization of the glucocorticoid receptors on the pituitary gland (here: in melancholic depression)7, the cortisol level decreases only insufficiently after dexamethasone administration (nonsuppression) and remains above 5 µg/dl8

The pure dexamethasone suppression test (DST) is the predecessor of the DEX/CRH test, which is mainly used today. The DST can also detect hypercortisolism of the HPA axis.9 However, the DST proved to be insufficiently sensitive and not specific enough for the diagnosis of depression and was therefore replaced by the dexamethasone/CRH test.10

The probability of distinguishing a depressed subject from a healthy control subject by measuring an elevated cortisol value of > 5 µg/dl cortisol after dexamethasone administration is between 25 and 64 %.111213
In patients with psychotic depression, even 95 % nonsupressors were found.14 Since psychotic depression can, in our opinion, be understood as a “particularly severe melancholic depression” and also correlates with an excessive cortisol stress response, which should actually cause suppression of the HPA axis, this makes it clear that melancholic / psychotic depression is likely to be downregulated or otherwise lacking a response from the glucocorticoid receptors.

Women show a positive test response more frequently than men.15 16 This may support our view that an increased cortisol response of the HPA axis to acute stressors reflects an internalizing stress phenotype, as women are more likely to have an internalizing stress response than men.
The finding that the HPA axis normalizes in men after recovery, but not in women,17 suggests, however, that the correlations are more complex.

The fact that stimulants such as caffeine or nicotine tend to increase ACTH and cortisol levels1816 (especially if they are not used as medication but, like nicotine in tobacco, as intoxicants) is also not surprising from the point of view of ADHD, which is primarily treated with stimulants.

The fact that not all depressive patients have increased or non-decreased ACTH and cortisol levels1916 20 is justified by depression medicine as follows

  • The number of depressive episodes (the fewer episodes, the lower the increase)
  • The severity of the depression
  • The severity of the vegetative symptoms.21

In our opinion, however, the fact that the HPA axis is hypoactive in atypical depression and bipolar depression (bipolar disorder) may be more serious.

1.2. CRH test

  • Administration: CRH
    • Human CRH (D)
    • Ovine CRH (USA, banned in Germany): longer effectiveness
  • Effect: Activation of the pituitary gland
  • Measurement: ACTH and cortisol after 15, 30, 60, 90 minutes
  • Test quality
    • ACTH response to CRH test varies greatly, poor re-test reliability. Results unsatisfactory.
    • Cortisol response to CRH test stable, r = .63
  • Healthy reaction:
    • ACTH increase to 2 times the initial value and higher after 15 min
    • Cortisol increase to 1.5 times the initial value and higher after 30 min
  • Non-healthy reaction22
    • High basal ACTH values, no ACTH increase
      • Conclusion:
        • Suspicion of ACTH production outside the pituitary gland (tumor)
    • Basal ACTH values zero, no ACTH increase, no cortisol increase
      • Conclusion:
        • Suspicion of adrenal Cushing’s syndrome
    • Low basal ACTH values, no ACTH increase, no cortisol increase
      • Conclusion:
        • Suspected pituitary (secondary) adrenal cortical insufficiency
        • CRH receptors could be downregulated10
        • Disruption of ACTH production by the pituitary gland
    • Low basal ACTH levels, delayed and/or prolonged ACTH rise
      • Conclusion:
        • Suspected hypothalamic (tertiary) adrenal cortical insufficiency
        • CRH receptors could be downregulated
        • Disruption of ACTH production by the pituitary gland
    • ACTH increase attenuated, cortisol increase normal
      • Suspicion of depression
  • Risks and side effects
    • Feeling cold
    • Feeling of tightness
    • Tachycardia
    • Shortness of breath
    • Metallic taste sensations
    • Increase in breathing and pulse rate
    • Slight drop in blood pressure

1.3. CRH/vasopressin test

  • Administration: CRH in combination with vasopression
  • Purpose: To check unclear results of the CRH test by optimizing ACTH and cortisol production22
  • Healthy reaction:
    • Increase in ACTH
    • Increase in cortisol
  • Side effects:
    • Feeling of warmth
    • Feeling of tightness
    • Tachycardia
    • Shortness of breath
    • Metallic taste sensations
    • Short-term feeling of cold
    • Increase in breathing and pulse rate
    • Slight drop in blood pressure

1.4. Dexamethasone/CRH test

The DEX/CRH test is a combination of the CRH test and the simple DST.2324 It has replaced the pure dexamethasone test (DST) and is used to predict the success of therapy, to identify relapsed remitted depression patients and family members who are not yet ill but are at risk of developing the disease.10

  • Administration: 1st stage: dexamethasone 23:00 in the evening, 2nd stage: CRH after cortisol measurement at 15:00 to 16:00
  • Effect: see dexamethasone test
    1. Stage: Measurement: Cortisol at 15:00 to 16:00 on the following day
  • Healthy reaction:
    • Decrease in the cortisol blood level to below 5 µg/dl
  • Not a healthy reaction:
    • Cortisol blood level remains above 5 µg/dl (nonsupression)
      • Disturbed negative feedback of the HPA axis
      • Suspicion of melancholic (internalizing) depression8
      • Desensitization of the glucocorticoid receptors on the pituitary gland (here: for melancholic depression)7
      • Attention: normal suppression in ADHD-I, despite the increased cortisol stress response as in melancholic depression25 Therefore probably no desensitization of the GR / overexpression of MR at the pituitary gland in ADHD-I
    1. Stage: Injection of 100 µg human CRH
    1. Stage: measurement of CRH and ACTH in blood plasma every 15 minutes
  • Not a healthy reaction:
    • Possibly significantly increased ACTH response to CRH administration compared to healthy subjects and high cortisol blood levels26
      Sarubin explains one possible explanationERROR_UNKNOWN_FOOTNOTE:
    • GR have a very high binding affinity for artificial glucocorticoids such as dexamethasone and cause negative feedback at the pituitary gland in healthy volunteers. However, the cited study refers to the hippocampus.27
    • Dexamethasone only leads to a short-term reduction in ACTH secretion in depressed patients, as the brain tries to compensate for this by increasing the release of CRH-synergistic hormones such as vasopressin2829 .
    • The CRH injection leads to a combination of increased vasopressin concentration with the injected CRH. This not only cancels out the partial ACTH suppression at the pituitary gland, but on the contrary leads to increased ACTH release in depressed subjects.3031
    • In another study, the cortisol and ACTH levels reduced by dexamethasone were not increased by subsequent single administration of CRH or vasopressin. Only a subsequent joint administration of CRH and vasopressin increased the cortisol and ACTH levels reduced by dexamethasone again.30

Details of the DEX/CRH test

The combined DEX/CRH test can distinguish32 (melancholic) depressives from healthy subjects with a certainty of 80 to 90 %3334 and is the standard neuroendocrinological test for depressive patients worldwide.3536

However, the combined DEX/CRH test can only be used diagnostically if the expected cortisol response of the disorder to be tested is known. The cortisol responses of severe melancholic (or psychotic) depression on the one hand and (atypical depression or) bipolar disorder on the other differ in both remitted and non-remitted states.37
This is in line with our other presentations in this article, which indicate that the cortisol reactions of mental disorders are merely a reflection of a disorder of the HPA axis, but are not directly linked to a specific disorder in their manifestation.

The DEX/CRH test should allow conclusions to be drawn about the relationship between mineralocorticoid receptors (MR) and glucocorticoids (GR). Administration of the MR antagonist spironolactone increases the basal and mean cortisol levels3839 40 41 as well as the cortisol response to the DEX/CRH test.42

The effect of MR antagonists on the HPA axis is clearly measurable but small, suggesting that mineralocortoid receptors modulate but do not regulate HPA axis activity.38

A high cortisol response (cortisol nonsupression) to the DEX/CRH test - as is common in melancholic depression and is then around 10 times higher than in healthy people43 - is likely to indicate a low number of MR in relation to GR, while a low cortisol response (suppression) indicates a high number of MR in relation to GR.

1.5. ACTH(1-24) test

  • Administration: ACTH(1-24) (Synacthen, an artificial ACTH consisting of 24 amino acids instead of the 35 in natural ACTH)
  • Effect: Stimulation of the adrenal cortex
  • Measurement: cortisol, possibly aldosterone, 1 hour after ACTH injection (ACTH short test)
  • Healthy reaction:
    • Cortisol increase of more than 15 ng/ml44 or of ≥ 180-200 μg/l (500-550 nmol/l) after ACTH stimulation or doubling or more after ACTH stimulation45
      • Test quality: stable reliability (± 12 %)
    • Aldosterone increase
    • Progesterone increase less than 2.5 ng/ml
  • Not a healthy reaction:
    • No / lower increase in cortisol
      • Suspected adrenal cortical insufficiency (= weakness) (NNRI),
        • Primary NNRI, adrenal gland itself is impaired in hormone production
        • Secondary NNRI, caused by pituitary gland
        • Tertiary NNRI, caused by hypothalamus
        • To find out which of these problems exists: Long-term ACTH tests. The background to this is that the adrenal cortex does not immediately produce cortisol again after a long-lasting ACTH deficit following the first ACTH administration, but has to slowly ramp up cortisol production again.
          • Cortisol rises again after several days of ACTH (1-24) administration (ACTH long test)
            • Suspicion of secondary NNRI
          • No increase in cortisol after several days of ACTH/1-24) administration (ACTH long test)
            • Suspicion of primary NNRI
    • Increased increase in cortisol
      • Suspicion of depression
    • Lack of aldosterone increase
      • Suspicion of inadequate addressing of the mineralocorticoid receptors
    • Progesterone increase of more than 2.5 ng/ml up to max. 15 ng/m and cortisol increase of less than 15 ng/ml
      • Suspicion of heterozygous 21-hydroxylase deficiency44
    • 17-alpha-hydroxyprogesterone increases to over 15 ng/ml to 100ng//ml
      • Suspected non-classical or late-onset AGS/21-hydroxylase deficiency due to CYP21A2 gene defect
    • Further measured values indicate rare defects44
  • Risks, side effects
    • None

1.6. Insulin test (ITT)

  • Must be performed on an inpatient basis
  • Tests the overall stress response, as hypoglycemia is a strong stressor that activates the HPA axis
  • Administration: Insulin
  • Effect: massive stress reaction due to drop in blood sugar (hypoglycemia)
  • Healthy reaction:
    • Increase in ACTH by at least 1.5 to 2.5 times46 starting from 10 - 48 pg/ml
    • Increase in cortisol by at least 3 µg/l46
      • Test quality: stable reliability ± 10 %
    • Increase in prolactin
    • Increase in growth hormone by at least 3 µg/l / 20 mU/L, to at least 10 ng/ml
      • Test quality: moderate reliability for men (± 41 %), very poor reliability for women (± 104 %)
    • Drop in blood sugar (hypoglycemia) by 50 % or to below 2.2 mmol/l46 = 40 mg/dl
    • Patient sweats
  • Unhealthy reaction
    • Growth hormone increase
      • By less than 3 µg/l / 20 mU/L to less than 10 ng/ml
        • Suspected partial growth hormone deficiency
      • To less than 5 ng/ml
        • Suspicion of severe growth hormone deficiency
    • Cortisol levels
      • Does not reach 1.5 to 2 times the original value, at least 550 nmol/L
        • Suspicion of hypocortisolism
      • Reaches between 400 and 550 nmol/L
        • Mild hypocortisolism; cortisol administration may (only) be necessary in cases of severe illness or stress
      • Increases by less than 170 nmol/L
        • Suspicion of Cushing’s syndrome
    • ACTH level does not reach 1.5 to 2 times the original value
      • Suspected adrenocorticotropic insufficiency
  • Contraindications
    • Seizures
    • Epilepsy
    • Cardiovascular problems
    • Ischemic heart disease
    • Severe panhypopituitarism
    • Hypoadrenalism
    • Hypothyroidism
  • Risks and side effects
    • Hypoglycemic shock
    • Test is therefore only very rarely carried out today

1.7. Naloxone test

  • Administration: Naloxone
  • Mode of action: selective opioid receptor antagonist
    e.g. emergency medication for opioid overdose
  • Healthy reaction
    • Increase in ACTH
    • Increase in cortisol
  • Risks and side effects
    • None

1.8. Fenfluramine test

Used to test the serotonergic response in relation to the HPA axis.

  • Administration: Fenfluramine
  • Healthy reaction: prolactin release
  • Non-healthy reaction: Suppressed prolactin secretion
    • Suspicion of: Depression10

1.9. Metyrapone test

  • Administration: Metyrapone (Metopirone) after measurement of basal cortisol levels
  • Effect: Metyrapone inhibits adrenal 11-beta-hydroxylase, which is required for the conversion of 11-deoxycortisol (substance S) to cortisol in the adrenal cortex and which is thereby blocked.47
  • Healthy reaction47
    • Drop in cortisol to 8 µg/100 ml / zero
    • Increase in 11-deoxycortisol in the blood to 5 - 15 µg/100ml
    • Increase in ACTH in the blood to > 200 pg/ml
    • Increase in tetrahydro-11-deoxycortisol in the urine
    • Drop in aldosterone
  • Non-healthy reaction47
    • Drop in cortisol to a maximum of 60% of the basal value or higher and
      Increase in 11-deoxycortisol in the blood to 1100 - 3300 µg/100ml
      • Suspicion of Cushing’s syndrome
    • Lower increase in 11-deoxycortisol in the blood
      • Suspicion of secondary or tertiary adrenal insufficiency
    • No changes in value
      • Suspected androgen-producing tumor of the adrenal gland
    • Drop in cortisol to a maximum of 8 µg/100 ml
      • Suspicion of accelerated metyrapone degradation
  • Side effects47
    • Gastrointestinal complaints
      • Vomiting
      • Abdominal pain
      • Nausea
      • Countermeasure: simultaneous food intake significantly reduces the risk of gastrointestinal complaints
    • Dizziness
    • Headache
    • Drowsiness
    • Drop in blood pressure
    • Allergic skin reactions
    • Contraindications:
      • For newborns to infants
      • With manifest primary adrenal cortical insufficiency (risk of an Addisonian crisis)
      • Medication that causes enzyme induction in the liver should be discontinued,
        • Phenobarbital
        • Phenytoin
        • Carbamazepine
        • Rifampicin

1.10. Vasopressin insulin test (SAIT)

This should be viewed critically due to its low benefit and high side effects.48

1.11. Dexamethasone/vasopressin test

1.12. Dexamethasone/insulin test

1.13. Metyrapone/CRH test

2. Tests unrelated to ADHD

2.1. Glucose test

  • Healthy sober value:
    • Plasma glucose < 100 mg/dl (< 5.6 mmol/l)
    • In pregnant women < 90 mg/dl (< 5 mmol/l)
  • Not a healthy sober value:
    • Plasma glucose 100 - 125 mg/dl (5.6 to 6.9 mmol/l)
      • Suspected prediabetes (not in pregnant women)
    • Plasma glucose ≥ 126 mg/dl (≥ 7.0 mmol/l)
      • Suspected manifest diabetes (also in pregnant women)
  • Administration: Glucose
  • Healthy reaction:
    • Of somatostatin (growth hormone inhibiting hormone)
    • Increase in blood sugar level
      • 2-h value < 140 mg/dl (< 7.8 mmol/l)(not for pregnant women)49
    • Drop in growth hormone
  • Not a healthy reaction:
    • Increase in blood sugar level
    • For pregnant women:
      • 1-h value ≥ 180 mg/dl (≥ 10.0 mmol/l) or
      • 2-h value ≥ 155 mg/dl (≥ 8.6 mmol/l)
        • Suspicion of gestational diabetes49
    • 2-h value 140-199 mg/dl (7.8-11.0 mmol/l)
      • Suspected prediabetes with increased cardiovascular risk49
  • Side effects:
    • None

2.2. Clonidine test

  • Administration: Clonidine
  • Effect: Clonidine is an alpha-2-adrenoceptor agonist and thus inhibits catecholamine production
  • Healthy reaction:
    • Increase in growth hormone releasing hormone (GHRH)1
    • Increase in growth hormone (GH)1
    • Drop in somatostatin (?)1
    • 50 % drop in catecholamines
      • Dopamine
      • Noradrenaline
      • Adrenalin
  • Non-healthy reaction50
    • Reduced drop in catecholamine and metanephrine levels
      • Suspicion of primary hypertension
    • Unchanged or elevated catecholamine levels and metanephrine levels
      • Suspected pheochromocytoma = disease of the chromaffin cells of the adrenal medulla (occurrence: 1/100,000 persons/year).
      • Suspected genetic causes, e.g. multiple endocrine neoplasia type 2
    • Reduced increase in growth hormone
      • Suspicion of depression10
      • Suspicion of reduced alpha-2 adrenoceptors
        • Thereby reduced inhibitory inhibition of the noradrenaline system

2.3. L-Dopa test

  • Administration: L-Dopa
  • Healthy reaction:
    • Increase in growth hormone releasing hormone (GHRH)
    • Increase in growth hormone (GH)

2.4. GHRH test

  • Administration: growth hormone releasing hormone (GHRH)
  • Healthy reaction:
    • Increase in growth hormone (GH)
  • Side effect:
    • Feelings of warmth
    • Taste and odor sensations altered
    • Headache
    • Pallor

2.5. Ghrelin mimetics test

  • Administration: ghrelin mimetics (e.g. macimorelin)
  • Effect: Ghrelin receptor agonist
  • Healthy reaction:
    • Increase in the growth hormone somatotropin

2.6. Vasopressin test (arginine test)

  • Administration: Vasopressin
  • Effect: Stimulation of growth hormone production through
    • Alpha-adrenergic stimulation
    • Serotonergic stimulation
    • Somatostatin suppression.
  • Test quality
    • Pathological results should be confirmed by a second test51
  • Healthy reaction
    • Growth hormone increase to over 8 ng/ml within 30 - 60 minutes
    • IGF-I
    • IGFBP-3
  • Not a healthy reaction:
    • Growth hormone increase delayed
      • Suspected growth hormone deficiency in the hypothalamus

2.7. Metoclopramide test

  • Administration: Metoclopramide
  • Effect: Metoclopramide is a dopamine antagonist
  • Healthy reaction:
    • Drop in dopamine
    • Increase in prolactin
  • Side effects:
    • Diarrhea
    • Tiredness
    • Drowsiness
    • Extrapyramidal disorders
    • Cardiovascular disorders

2.8. TRH test

Used to test the hypothalamic-pituitary-gonadal axis.
In view of modern blood value measurement methods, this is hardly relevant any more.

2.9. GnRH test

Used to test the hypothalamic-pituitary-gonadal axis.

3. Diagnostic application

Endocrine function tests are used as diagnostic tools for various disorders. Unfortunately, this is not yet the case for ADHD.

3.1. ADHD

Studies on the nonsuppression of the HPA axis in ADHD-HI

One large study (n = 2307) found reduced cortisol suppression to dexamethasone in hyperactivity/impulsivity (ADHD-HI), while inattention (ADHD-I) showed no correlation to nonsuppression.25 This is consistent with the results of a smaller study that found nonsuppression in only a proportion of ADHD sufferers and found that nonsuppression correlated with higher levels of hyperactivity.52 In contrast, another small study, in which only 9 children with ADHD were involved, found suppression in ADHD.53 Another study found nonsuppression in 22.7% of ADHD-HI sufferers (with hyperactivity), which is 4-fold higher than the 5.7% in healthy people.54
In SHR rats, which serve as an animal model for ADHD-HI (with hyperactivity), dexamethasone causes a reduction in ADHD-HI symptoms.5556 SHR have a genetically determined excessive expression of mineralocorticoid receptors (MR) and a normal expression of glucocorticoid receptors (GR).57

Dexamethasone acts selectively as a GR agonist, i.e. the MR are addressed 30 times weaker than GR.58 Whether prednisone is also a selective GR agonist is disputed. There are voices in favor58 as well as against59

The results suggest that nonsuppression of the HPA axis is more common in ADHD-HI, but may not always be present.

A description of a possible treatment for ADHD-HI sufferers in whom the dexamethasone suppression test (DST) shows suppression, i.e. in whom a reduction in cortisol levels occurs in response to dexamethasone, can be found at Dexamethasone for ADHD.

3.2. Depression

3.2.1. Melancholic / psychotic depression

Modified representation, based on Kudielka-Wüst, Wüst, Bertram2


  • Excessive endocrine stress response HPA axis (not in atypical depression)
  • Increased CRH release (hypersecretion)
  • Reduced CRH receptors in the PFC
  • Switch-off of the HPA axis disrupted


  • ACTH (1-24) test:
    • Increased release of cortisol
  • CRH test
    • ACTH reaction flattened10
    • Cortisol response normal
  • Metyrapone/CRH test:
    • Normalization of the reduced ACTH response
  • DST
    • Lack of suppression of cortisol release
    • However, DST is too unspecific and too insensitive, so today it has been replaced by the dexamethasone/CRH test10
  • DST/CRH test
    • Dexamethasone causes cortisol suppression
    • CRH, given afterwards, causes an increase in cortisol in depressives (prevents cortisol suppression)10
  • TRH test:
    • Inconsistent findings of the PRL reaction
  • Clonidine test:
    • Reduced increase in growth hormone
      • Suspicion of depression10
      • Suspicion of reduced alpha-2 adrenoceptors
        • Thereby reduced inhibitory inhibition of the noradrenaline system

3.3. Anxiety disorders

Panic disorder, phobia, obsessive-compulsive disorder, PTSD

Modified representation, based on Kudielka-Wüst, Wüst, Bertram2


  • Central dysregulation and adaptation of CRH receptors in the pituitary gland


  • CRH test
    • ACTH response flattened or excessive
    • Cortisol output values unchanged
  • DST/CRH test
    • CRH causes reduced cortisol suppression
  • TRH test
    • Normal TSH reaction
  • GHRH test
    • Suppressed growth hormone reaction
  • Clonidine test
    • Normal growth hormone reaction

3.4. Schizophrenia

Illustration based on Kudielka-Wüst, Wüst, Bertram2


  • Hypersensitivity of central dopamine receptors
  • Change in HPA axis function


Inconsistent findings due to heterogeneous disorder pattern

  • ITT test
    • Inconspicuous and normal basal ACTH and cortisol reactions
  • CRH test
    • Inconspicuous and normal basal ACTH and cortisol reactions
  • DST
    • Frequent cortisol suppression
  • DST/CRH test
    • CRH prevents cortisol suppression
  • TRH test
    • TSH response normal or suppressed
    • PRL reaction normal
  • GHRH test
    • Normal growth hormone reactions

3.5. Eating disorders

Bulimia, anorexia


  • Basal hypercortisolism due to impaired deactivation of the HPA axis


  • CRH test
    • Suppressed ACTH reaction
    • Normal cortisol response
  • Naloxone test
    • Reduced hormone response
  • DST
    • Pronounced nonsuppression of cortisol release
  • TRH test
    • Normal TSH increase
  • GnRH test
    • Reduced gonadotropin reaction

  1. Ehlert: Das endokrine System, in: Ehlert, von Känel (2011): Psychoendokrinologie und Psychoimmunologie, Seiten 4-36

  2. Kudielka-Wüst, Wüst, Bertram (2007): Methoden der Psychoneuroendokrinologie, Forschungsorientierte Vertiefung: Psychoneuroendokrinologie, Universität Trier, Download

  3. Maes, Bosmans, Suy, Vandervorst, DeJonckheere, Raus (1991): Depression‐related disturbances in mitogen‐induced lymphocyte responses and interleukin‐1β and soluble interleukin‐2 receptor production. Acta Psychiatrica Scandinavica, 84: 379-386. doi:10.1111/j.1600-0447.1991.tb03163.x

  4. Bioscientia: Dexamethason-Kurztest

  5. Maes, Bosmans, Meltzer, Scharpé, Suy (1993): Interleukin-1β: A putative mediator of HPA axis hyperactivity in major depression? American Journal of Psychiatry, 150(8), 1189-1193.

  6. Serubin (2012): Der Einfluss von Escitalopram und Quetiapin Prolong auf die Hypothalamus – Hypophysen – Nebennierenrinden – Achsenaktivität bei depressiven Patienten; Dissertation, Seite 19

  7. Amsterdam, Winokur, Abelman, Lucki, Rickels (1983): Cosyntropin (ACTH alpha 1-24) stimulation test in depressed patients and healthy subjects. American Journal of Psychiatry 140: 907-909

  8. Carroll, Curtis, Mendels (1976): Neuroendocrine regulation in depression. I. Limbic systemadrenocortical dysfunction. Archives of General Psychiatry 33: 1039-1044

  9. Carroll, Feinberg, Greden, Tarika, Albala, Haskett, James, Kronfol, Lohr, Steiner, de Vigne, Young (1981): A specific laboratory test for the diagnosis of melancholia. Standardization, validation, and clinical utility. Archives of General Psychiatry 38:15-22

  10. Heim, Miller: Depression, in: Ehlert, von Känel (2011): Psychoendokrinologie und Psychoimmunologie, Seiten 365-382

  11. Nelson, Davis (1997): DST studies in psychotic depression: a meta-analysis. American Journal of Psychiatry 154: 1497-1503

  12. Heuser, Yassouridis, Holsboer (1994): The combined dexamethasone/CRHTest: A refined laboratory test for psychiatric disorders. J Psychiatr Res 28: 341-356

  13. Sarubin (2012): Der Einfluss von Escitalopram und Quetiapin Prolong auf die Hypothalamus – Hypophysen – Nebennierenrinden – Achsenaktivität bei depressiven Patienten; Promotion, Seite 19

  14. Juruena, Bocharova, Agustini, Young (2018): Atypical depression and non-atypical depression: Is HPA axis function a biomarker? A systematic review. J Affect Disord. 2018 Jun;233:45-67. doi: 10.1016/j.jad.2017.09.052. Epub 2017 Oct 6.

  15. Zobel, Nickel, Sonntag, Uhr, Holsboer, Ising (2001): Cortisol response in the combined dexamethasone/CRH test as predictor of relapse in patients with remitted depression: a prospective study. J Psychiatr Res, 2001 Mar-Apr; 35: 83–94

  16. Künzel, Binder, Nickel, Ising, Fuchs, Majer, Pfennig, Ernst, Kern, Schmid, Uhr, Holsboer, Modell (2003): Pharmacological and nonpharmacological factors influencing hypothalamic-pituitary-adrenocortical axis reactivity in acutely depressed psychiatric in-patients, measured by the DEX-CRH test. Neuropsychopharmacology 28: 2169-2178

  17. Binder, Künzel, Nickel, Kern, Pfennig, Majer, Uhr, Ising, Holsboer (2009): HPA-axis regulation at in-patient admission is associated with antidepressant therapy outcome in male but not in female depressed patients. Psychoneuroendocrinology 34 (1): 99-109

  18. Matta, Fu, Valentine, Sharp (1998): Response of the hypothalamo-pituitary-adrenal axis to nicotine. Psychoneuroendocrinology 23: 103–113

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  20. Strickland, Deakin, Percival, Dixon, Gater, Goldberg (2002): Bio-social origins of depression in the community. Interactions between social adversity, cortisol and serotonin neurotransmission. British Journal of Psychiatry 180: 168-173

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  43. Holsboer (2000): The corticosteroid receptor hypothesis of depression, Neuropsychopharmacology 23: 477–501

  44. Biosientia: ACTH-Test

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  47. Bioscientia: Metopiron-Test

  48. Schoof, Nazli, Marx, Dörr (1999): Sequentialer Arginin-Insulin-Test (SAIT). Eine sinnvolle Alternative zum isolierten Insulintoleranztest und Arginintest? Monatsschrift Kinderheilkunde, January 1999, Volume 147, Issue 1, pp 27–31

  49. Laborverbund Dr. Kramer & Kollegen: Glukosetoleranztest

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