Pharmacological endocrine function tests

By administering certain pharmaceuticals, the reactivity and feedback sensitivity of hormone axes can be tested.¹

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

• 1. Tests for ADHD and/or depression
  • 1.1. Dexamethasone test
  • 1.2. CRH test
  • 1.3. CRH/vasopressin test
  • 1.4. Dexamethasone/CRH test
  • 1.5. ACTH(1-24) test
  • 1.6. Insulin Test (ITT)
  • 1.7. Naloxone test
  • 1.8. Fenfluramine test
  • 1.9. Metyrapone test
  • 1.10. Vasopressin Insulin Test (SAIT)
  • 1.11. Dexamethasone/vasopressin test
  • 1.12. Dexamethasone/insulin test
  • 1.13. Metyrapone/CRH test
• 2. Tests unrelated to ADHD
  • 2.1. Glucose test
  • 2.2. Clonidine test
  • 2.3. L-Dopa test
  • 2.4. GHRH test
  • 2.5. Ghrelin mimetics test
  • 2.6. Vasopressin test (arginine test)
  • 2.7. Metoclopramide test
  • 2.8. TRH test
  • 2.9. GnRH test
• 3. Diagnostic application
  • 3.1. ADHD
  • 3.2. Depression
    • 3.2.1. Melancholic / Psychotic Depression
  • 3.3. Anxiety disorders
  • 3.4. Schizophrenia
  • 3.5. Eating disorders

1. Tests for ADHD and/or depression¶

The tests compiled here could be suitable for diagnosing ADHD subtypes and identifying appropriate treatment methods. In practice, there is no use of these tests in relation to ADHD so far.

Since the HPA axis is hyperactivated or hypoactivated not only in depression and ADHD, but also in other mental disorders, the above-mentioned tests 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 for differentiation from other disorders and for finding a suitable medication.

1.1. Dexamethasone test¶

• Measurement of cortisol level (ACTH, too, if necessary) 8 to 9 a.m. or 3 to 4 p.m. to determine basal level
• Administration: Dexamethasone 23 hrs p.m
• Action: selective on glucocorticoid receptors (GR).
  Effect on GR 30 times stronger than on mineralocorticoid receptors (MR).
  GRs shut down the HPA axis (unlike MR, which does the “day-to-day” business)
  Dexamethasone hardly crosses the blood-brain barrier; therefore, hardly any effect on hypothalamus, strong effect on 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, midnight after dexamethasone administration if necessary
• Healthy response:
  • Drop in ACTH (= ACTH suppression)
  • Drop in cortisol (= cortisol suppression)
  • Drop in IL-1β (= IL-1β suppression)³
• Not healthy reaction:
  • Lack of cortisol suppression 15/16 hrs
    • Suspicion: glucocorticoid receptor-mediated deactivation of the HPA axis is impaired
    • Suspicion: Depression, ADHD-HI
  • Increased cortisol level at midnight
    • Suspicion of hypercortisolism⁴
  • No IL-1β suppression
    • Suspicion of depression³⁵
• Risks, side effects
  • None

Procedure of the DST:⁶

• 23:00 Evening: oral intake of 1 mg dexamethasone
• 08:00, 16:00, 23:00 Following day: measurement of cortisol in blood plasma
• Due to impaired negative feedback of the HPA axis or desensitization of glucocorticoid receptors at 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 dexamethasone-only suppression test (DST) is the precursor of the DEX/CRH test that is primarily used today. The DST can also detect hypercortisolism of the HPA axis.⁹ However, the DST proved to be too insensitive 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 healthy control subjects by measuring an elevated cortisol level on dexamethasone administration of > 5 µg/dl cortisol ranges from 25% to 64%.¹¹¹²¹³
In sufferers with psychotic depression, as much as 95% nonsupressors have been identified.¹⁴ Since psychotic depression, in our opinion, can be understood as a “particularly severe melancholic depression” and also correlates with an excessive cortisol stress response, which should actually cause a suppression of the HPA axis, this illustrates that in melancholic / psychotic depression there is likely to be a downregulation or otherwise lack of response of the glucocorticoid receptors.

Females are more likely to show a positive test response than males.^{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 more often have an internalizing stress response than men.
However, the finding that the HPA axis normalizes after recovery in men but not in women¹⁷ suggests that the relationships are more complex.

That stimulants such as caffeine or nicotine tend to increase ACTH and cortisol levels¹⁸¹⁶ (especially when used as intoxicants rather than drugs, as nicotine is in tobacco) is also not surprising from the perspective of ADHD, which is treated primarily with stimulants.

The fact that increased or non-decreased ACTH and cortisol levels are not found in all depressed patients^{1916 20} is justified by depression medicine as follows

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

In our opinion, however, the fact that hypoactivity of the HPA axis is present in atypical depression as well as in bipolar depression (bipolar disorder) is probably more serious.

1.2. CRH test¶

• Administration: CRH
  • Human CRH (D)
  • Ovine CRH (USA, banned in D): longer efficacy
• Effect: Activation of the pituitary gland
• Measurement: ACTH and cortisol after 15, 30, 60, 90 minutes
• Test quality
  • ACTH response to CRH test varies widely, poor re-test reliability. Results unsatisfactory.
  • Cortisol response to CRH test stable, r = .63
• Healthy response:
  • ACTH increase to 2 times baseline and higher after 15 min
  • Cortisol increase to 1.5 times baseline and higher after 30 min
• Not healthy reaction²²
  • High basal ACTH levels, 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 levels, no ACTH increase, no cortisol increase
    • Conclusion:
      • Suspicion of pituitary (secondary) adrenocortical insufficiency
      • CRH receptors might be downregulated¹⁰
      • Disruption of ACTH production by the pituitary gland
  • Low basal ACTH levels, delayed and/or prolonged ACTH surge
    • Conclusion:
      • Suspected hypothalamic (tertiary) adrenocortical insufficiency
      • CRH receptors might be downregulated
      • Disruption of ACTH production by the pituitary gland
  • ACTH increase attenuated, cortisol increase normal
    • Suspicion of depression
• Risks and side effects
  • Cold feeling
  • 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 verify unclear results of CRH test by optimizing ACTH and cortisol production²²
• Healthy response:
  • Increase in ACTH
  • Cortisol increase
• Side effects:
  • Warm feeling
  • Tightness
  • Tachycardia
  • Shortness of breath
  • Metallic taste sensations
  • Short-term cold feeling
  • 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 remitted depression patients at risk of relapse and family members not yet ill who are at risk of developing the disease.¹⁰

• Administration: 1st stage: dexamethasone 11 pm evening, 2nd stage: CRH after cortisol measurement at 3 to 4 pm
• Effect: see dexamethasone test
• 1. Stage: Measurement: Cortisol at 15:00 to 16:00 on the following day
• Healthy response:
  • Decrease in cortisol blood level to below 5 µg/dl
• Not 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 glucocorticoid receptors on the pituitary gland (here: in melancholic depression)⁷
    • Note: normal supression in ADHD-I, despite cortisol stress response elevated as in melancholic depression²⁵ Therefore, probably no desensitization of GR / overexpression of MR at pituitary in ADHD-I
• 2. Step: Injection 100 µg human CRH
• 2. Stage: Measurement CRH and ACTH in blood plasma every 15 minutes
• Not healthy reaction:
  • Possibly markedly increased ACTH response to CRH administration compared to healthy subjects and high blood cortisol levels²⁶
    Sarubin explains one possible explanation²⁷:
  • GR have a very high binding affinity for artificial glucocorticoids such as dexamethasone and cause the negative feedback at the pituitary gland in healthy subjects. However, the cited study refers to the hippocampus.²⁷
  • Dexamethasone leads to decreased ACTH secretion in depressed patients only in the short term, as the brain attempts to compensate by increased secretion of CRH-synergistic hormones such as vasopressin²⁸²⁹ .
  • CRH injection leads to an interaction of increased vasopressin concentration with the injected CRH. This not only cancels the partial ACTH suppression at the pituitary gland, but on the contrary leads to increased ACTH release in depressed subjects.³⁰³¹
  • Cortisol and ACTH levels decreased by dexamethasone were not raised by subsequent single administration of either CRH or vasopressin in another study. Only subsequent joint administration of CRH and vasopressin increased the cortisol and ACTH levels reduced by dexamethasone again.³⁰

1.5. ACTH(1-24) test¶

• Administration: ACTH(1-24) (Synacthen, an artificial ACTH made of 24 amino acids instead of the 35 in natural ACTH)
• Effect: stimulation of the adrenal cortex
• Measurement: cortisol, aldosterone if necessary, 1 hour after ACTH injection (ACTH short test)
• Healthy response:
  • 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 Rise
  • Progesterone increase less than 2.5 ng/ml
• Not healthy reaction:
  • No / lower cortisol increase
    • Suspicion of adrenal 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: Do ACTH long tests. The background to this is that after a prolonged ACTH deficit, the adrenal cortex does not immediately produce cortisol again after the first ACTH administration, but must first slowly ramp up cortisol production again.
        • Reappearance of cortisol increase after several days of ACTH(1-24) administration (ACTH long test)
          • Suspicion of secondary NNRI
        • Failure to increase cortisol after several days of ACTH/1-24) administration (ACTH long test)
          • Suspicion of primary NNRI
  • Increased cortisol
    • Suspicion of depression
  • Lack of aldosterone increase
    • Suspected deficient addressing of mineralocorticoid receptors
  • Progesterone increase by more than 2.5 ng/ml to max. 15 ng/m and cortisol increase 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
  • Other measured values indicate rare defects⁴⁴
• Risks, side effects
  • None

1.6. Insulin Test (ITT)¶

• Must be performed as an inpatient
• Tests 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 glucose (hypoglycemia)
• Healthy response:
  • Increase of 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 goodness: moderate reliability in men (± 41%), very poor reliability in 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 Rise
    • By less than 3 µg/l / 20 mU/L to less than 10 ng/ml
      • Suspicion of partial growth hormone deficiency
    • To less than 5 ng/ml
      • Suspicion of severe growth hormone deficiency
  • Cortisol level
    • 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; if necessary, cortisol administration might be necessary (only) in case of severe diseases or stress
    • Increases by less than 170 nmol/L
      • Suspicion of Cushings Syndrome
  • ACTH level does not reach 1.5 to 2 times the original value
    • Suspicion of adrenocorticotropic insufficiency
• Contraindications
  • Seizures
  • Epilepsy
  • Cardiovascular problems
  • Ischemic heart disease
  • Severe panhypopituitarism
  • Hypoadrenalism
  • Hypothyroidism
• Risks and side effects
  • Hypoglycemic shock
  • Test is therefore very rarely performed 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
  • Cortisol increase
• Risks and side effects
  • None

1.8. Fenfluramine test¶

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

• Administration: Fenfluramine
• Healthy response: prolactin release
• Non-healthy response: suppressed prolactin secretion
  • Suspicion of: Depression¹⁰

1.9. Metyrapone test¶

• Administration: metyrapone (metopirone) after measurement of basal cortisol levels
• Action: 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 of cortisol to 8 µg/100 ml / zero
  • Increase in blood 11-deoxycortisol to 5 - 15 µg/100ml
  • Increase of ACTH in the blood to > 200 pg/ml
  • Increase in tetrahydro-11-deoxycortisol in urine
  • Drop in aldosterone
• Not healthy reaction⁴⁷
  • Drop in cortisol to no more than 60% of basal level or higher; and
    Increase in blood 11-deoxycortisol to 1100 - 3300 µg/100ml
    • Suspicion of Cushings Syndrome
  • Increase of 11-deoxycortisol in the blood lower
    • Suspicion of secondary or tertiary adrenocortical insufficiency
  • No changes in value
    • Suspicion of 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 risk of gastrointestinal symptoms
  • Dizziness
  • Headache
  • Drowsiness
  • Blood pressure drop
  • Allergic skin reactions
  • Contraindications:
    • For newborns to toddlers
    • In case of manifest primary adrenal insufficiency (risk of Addisonian crisis)
    • Drugs that cause enzyme induction in the liver should be discontinued,
      e.g.:
      • Phenobarbital
      • Phenytoin
      • Carbamazepine
      • Rifampicin

1.10. Vasopressin Insulin Test (SAIT)¶

This should be viewed critically due to low benefits 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 healthy sober value:
  • Plasma glucose 100 - 125 mg/dl (5.6 to 6.9 mmol/l)
    • Suspicion of prediabetes (not in pregnant women)
  • Plasma glucose ≥ 126 mg/dl (≥ 7.0 mmol/l)
    • Suspicion of manifest diabetes (also in pregnant women)
• Administration: Glucose
• Healthy response:
  • Of somatostatin (growth hormone inhibition hormone)
  • Increase in blood glucose level
    • 2-h value < 140 mg/dl (< 7.8 mmol/l)(not in pregnant women)⁴⁹
  • Growth hormone decrease
• Not healthy reaction:
  • Increase in blood glucose 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
• Action: Clonidine is an alpha-2-adrenoceptor agonist and inhibits catecholamine production via it
• Healthy response:
  • Increase in growth hormone releasing hormone (GHRH)¹
  • Increase in growth hormone (GH)¹
  • Drop in somatostatin (?)¹
  • 50% drop in catecholamines
    • Dopamine
    • Norepinephrine
    • Adrenalin
• Not healthy reaction⁵⁰
  • Decreased decrease in catecholamine levels and metanephrine levels
    • Suspicion of primary hypertension
  • Unchanged or increased 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
    • Suspected decreased alpha-2 adrenergic receptors
      • Thereby reduced inhibitory inhibition of the noradrenaline system

2.3. L-Dopa test¶

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

2.4. GHRH test¶

• Administration: Growth Hormone Releasing Hormone (GHRH)
• Healthy response:
  • Increase in growth hormone (GH)
• Side effect:
  • Heat sensations
  • Taste and smell sensations changed
  • Headache
  • Paleness

2.5. Ghrelin mimetics test¶

• Administration: ghrelin mimetics (e.g. macimorelin)
• Effect: Ghrelin receptor agonist
• Healthy response:
  • 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 healthy reaction:
  • Growth hormone rise delayed
    • Suspicion of deficiency of growth hormone in the hypothalamus

2.7. Metoclopramide test¶

• Administration: metoclopramide
• Effect: Metoclopramide is a dopamine antagonist
• Healthy response:
  • Dopamine decrease
  • Increase in prolactin
• Side effects:
  • Diarrhea
  • Fatigue
  • Drowsiness
  • Extrapyramidal disorders
  • Cardiovascular disorders

2.8. TRH test¶

Used to test the hypothalamic-pituitary-gonadal axis.
Has little significance in view of modern blood value measurement methods.

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 HPA axis nonsuppression in ADHD-HI

One large study (n = 2307) found reduced cortisol suppression to dexamethasone in hyperactivity/impulsivity (ADHD-HI), whereas inattention (ADHD-I) showed no correlation with nonsuppression.²⁵ This is consistent with the results of a smaller study that found nonsuppression in only a portion of ADHD sufferers and found that nonsuppression correlated with higher levels of hyperactivity.⁵² In contrast, another small study, but involving only 9 ADHD-affected children, 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 individuals.⁵⁴
In SHR rats, which serve as animal models of ADHD-HI (with hyperactivity), dexamethasone causes a reduction in ADHD-HI symptoms.⁵⁵⁵⁶ SHR genetically have excessive expression of mineralocorticoid receptors (MR) and normal expression of glucocorticoid receptors (GR).⁵⁷

Dexamethasone acts selectively as a GR agonist, i.e., MR are addressed 30 times more weakly than GR.⁵⁸ Whether prednisone is also a selective GR agonist is debatable. There are voices for it⁵⁸ as against it⁵⁹

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

For an account of possible treatment for ADHD-HI sufferers in whom the dexamethasone suppression test (DST) shows suppression, that is, in whom there is a reduction in cortisol levels on dexamethasone, see ⇒ Dexamethasone in ADHD.

3.2. Depression¶

3.2.1. Melancholic / Psychotic Depression¶

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

Causes:

• Excessive endocrine stress response HPA axis (not in atypical depression)
• Increased CRH release (hypersecretion)
• Decreased CRH receptors in the PFC
• Disruption of the HPA axis

Tests:

• ACTH (1-24) test:
  • Cortisol secretion increased
• CRH test
  • ACTH reaction flattened¹⁰
  • Cortisol response normal
• Metyrapone/CRH test:
  • Normalization of the decreased ACTH response
• DST
  • Lack of suppression of cortisol release
  • However, DST is too unspecific and too insensitive, therefore replaced today by dexamethasone/CRH test¹⁰
• DST/CRH test
  • Dexamethasone causes cortisol suppression
  • CRH, given afterward, causes cortisol to rise in depressives (stops cortisol suppression)¹⁰
• TRH test:
  • Inconsistent findings of the PRL reaction
• Clonidine test:
  • Reduced increase in growth hormone
    • Suspicion of depression¹⁰
    • Suspected decreased alpha-2 adrenergic receptors
      • 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

Causes:

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

Tests:

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

3.4. Schizophrenia¶

Illustration based on Kudielka-Wüst, Wüst, Bertram²

Causes:

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

Tests:

Inconsistent findings due to heterogeneous disorder pattern

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

3.5. Eating disorders¶

Bulimia, anorexia

Causes:

• Basal hypercortisolism due to impaired shutdown of the HPA axis

Tests:

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