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1. Secondary Adrenal Insufficiency
By Ashley B. Grossman, MD, FRCP, FMedSci
Secondary adrenal insufficiency is adrenal hypofunction due to a lack of ACTH.
Symptoms are the same as for Addison disease, but there is usually less hypovolemia
(see Addison Disease : Symptoms and Signs). Diagnosis is clinical and by laboratory
findings, including low plasma ACTH with low plasma cortisol. Treatment depends
on the cause but generally includes hydrocortisone.
Secondary adrenal insufficiency may occur in panhypopituitarism
(A state in which the secretion of all anterior pituitary hormones is inadequate or absent. ) , in
isolated failure of ACTH production, in patients receiving corticosteroids (by any route,
including high doses of inhaled, intra-articular, or topical corticosteroids), or after
corticosteroids are stopped. Inadequate (adj) thiếu hụt ( too low in quality or too small in
amount; not enough) ACTH can also result from failure of the hypothalamus to stimulate
pituitary ACTH production, which is sometimes called tertiary adrenal insufficiency(n)
sự thiếu,sự không đủ
Panhypopituitarism (see Symptoms and Signs) may occur secondary to pituitary
tumors, various tumors, granulomas, and, rarely, infection or trauma that
destroys pituitary tissue. In younger people, panhypopituitarism may occur
secondary to a craniopharyngioma
craniopharyngioma
A brain tumour affecting mainly children and arising from persistent primitive cells in the
region of the pituitary gland. It causes headaches, visual field loss and delayed physical and
mental development.Treatment is by surgical removal.
. Patients receiving corticosteroids for > 4 wk may have insufficient ACTH secretion
during metabolic stress to stimulate the adrenals to produce adequate quantities of
corticosteroids, or they may have atrophic adrenals that are unresponsive to ACTH.
These problems may persist for up to 1 yr after corticosteroid treatment is stopped.
Symptoms and Signs
Symptoms and signs are similar to those of Addison disease (see Addison
Disease : Symptoms and Signs). Differentiating clinical or general
laboratory features include the absence of
hyperpigmentation(Hyperpigmentation is the increase in the natural color of the skin.)
and relatively normal electrolyte and BUN levels; hyponatremia, if it occurs, is
usually dilutional.
Patients with panhypopituitarism have depressed thyroid and gonadal function and
hypoglycemia. Coma (s hôn mê)may supervene(x y ra không ng ) when symptomaticự ả ờ
secondary adrenal insufficiency occurs. Adrenal crisis(c n) is especially likely if a patient isơ

2. treated for a single endocrine gland problem, particularly with thyroxine, without
hydrocortisone replacement.
Diagnosis
• Serum cortisol
• Serum ACTH
• ACTH stimulation testing
• CNS imaging
Tests to differentiate primary and secondary adrenal insufficiency are
discussed under Addison disease (see Addison Disease : Diagnosis).
Patients with confirmed secondary adrenal insufficiency should have CT
or MRI of the brain to rule out a pituitary tumor or atrophy. Adequacy(sự
toàn v n) of the hypothalamic- pituitary-adrenal axis during taperingẹ or
after stopping long-term corticosteroid treatment can be determined by
injecting cosyntropin 250 mcg IV or IM. After 30 min, serum cortisol
should be > 20 g/dL (>μ 552 nmol/L); specific levels vary somewhat(1
chút) depending on the laboratory assay in use. An insulin stress test to
induce hypoglycemia and a rise in cortisol is the standard for testing
integrity of the hypothalamic- pituitary-adrenal axis.
Cosyntropin là 1 corticotropin t ng h p ( corticotropin HM c bài ti t b i thùy tr c of tuy nổ ợ đượ ế ở ướ ế
yên)=>kích thích v th ng th n bài ti t hormones (corticosterone) nêunh sau tiêmỏ ượ ậ ế ư
cosyntropin mà cortisol không t ng ch ng t th ng th n có v n .ă ứ ỏ ượ ậ ấ đề
corticotropin
[kor″tĭ-ko-tro´pin]
1. a hormone secreted by the anterior lobe of the PITUITARY
GLAND that stimulates the cortex of the ADRENAL
GLAND to secreteits hormones, including CORTICOSTERONE. If production of corticotropin falls below
normal, the adrenal cortex decreases insize, and production of the cortical hormones declines.
cosyntropin
(kō′sĭn-trō′pĭn)
n.
A synthetic corticotropin.
Insulin tolerance test
From Wikipedia, the free encyclopedia

3. An insulin tolerance test (ITT) is a medical diagnostic procedure during which insulin is
injected into a patient's vein to assess pituitary function, adrenal function, and sometimes for
other purposes. An ITT is usually ordered and interpreted by endocrinologists.
Insulin injections are intended to induce extreme hypoglycemia below 2.2 mmol/l (40 mg/dl).
In response, adrenocorticotropic hormone (ACTH) and growth hormone (GH) are released as
a part of the stress mechanism. ACTH elevation causes the adrenal cortex to
release cortisol. Normally, both cortisol and GH serve as counterregulatory hormones,
opposing the action of insulin, i.e. acting against the hypoglycemia.[1]
The corticotropin-releasing hormone (CRH) test can be used to distinguish between
hypothalamic and pituitary causes but is rarely used in clinical practice. After administration of
CRH 100 mcg (or 1 mcg/kg) IV, the normal response is a rise of serum ACTH of 30 to 40
pg/mL; patients with pituitary failure do not respond, whereas those with hypothalamic
disease usually do.
Treatment
• Hydrocortisone or prednisone
• Fludrocortisone not indicated
• Dose increase during intercurrent illness
Glucocorticoid replacement is similar to that described for Addison disease. Each case varies
regarding (gi i t : i v i..v n ..)the type and degree of specific hormoneớ ừ đố ớ ấ đề
deficiencies. Fludrocortisone is not required because the intact adrenals produce
aldosterone . During acute febrile illness or after trauma, patients receiving corticosteroids for
non endocrine disorders may require supplemental doses to augment their endogenous
hydrocortisone production. In panhypopituitarism, other pituitary deficiencies should be treated
appropriately (see Selective Pituitary Hormone Deficiencies).
Key Points
• Secondary adrenal insufficiency involves ACTH deficiency due to pituitary or,
less often, hypothalamic causes (including suppression by long-term corticosteroid
use).
• Other endocrine deficiencies (eg, hypothyroidism, growth hormone deficiency) may
coexist(cùng t n t i)ồ ạ
• Unlike in Addison disease, hyperpigmentation does not occur and serum Na and K
levels are relatively normal.
• ACTH and cortisol levels both are low.
Glucocorticoid replacement is required but mineralocorticoids
(eg, fludrocortisone) are not necessary.
mineralocorticoids
• Hormones from the outer layer (cortex) of the adrenal gland that promote retention of
sodium and excretion of potassium in the urine. ALDOSTERONE is the most powerful
mineralocorticoid. Compare GLUCOCORTICOIDS.
Last full review/revision May 2014 by Ashley B. Grossman, MD, FRCP, FMedSci