Adrenal disorders

Clinical information

The function of the adrenal cortex is to synthesise numerous steroid hormones. These are divided into glucocorticoids (e.g. cortisol), mineralocorticoids (e.g. aldosterone) and sex hormones (e.g. androgens). The amount and timing of the hormone production is primarily regulated by the adrenocorticotropic hormone (ACTH) which is produced by the pituitary gland. ACTH in turn is controlled by the corticotropin-releasing hormone (CRH).

Synthesis of aldosterone, the main regulator of salt and water in the body, is also controlled by the amount of sodium and potassium in the blood and by the renin-angiotensin-aldosterone system (RAAS).

Hormone production in the adrenal cortex can be impaired by different diseases, resulting in a hormone over- or underproduction. This leads to hypo- or hyperfunction of different endocrinal organs and to various diseases.

Diagnostics

Hyperfunction of the adrenal cortex is associated with Conn’s syndrome, Cushing’s syndrome and adrenogenital syndrome.

A chronic surplus in cortisol is also referred to as hypercortisolism. It may cause symptoms that are referred to as Cushing’s syndrome. Possible causes may be found outside the adrenal glands, e.g. overproduction of ACTH due to a tumour of the anterior pituitary (Cushing’s disease), or in the adrenal glands.  Cushing’s syndrome can also be caused by an excess of cortisol-like components from medication. To diagnose Cushing’s syndrome, measurement of cortisol in blood, saliva and urine, as well as ACTH determination are recommended.

Aldosterone overproduction results in hyperaldosteronism. The most common symptom is high blood pressure. Up to ten percent of all cases of hypertension are caused by primary hyperaldosteronism (Conn’s syndrome). In Conn’s syndrome, the renin concentration is simultaneously decreased, while the secondary form of hyperaldosteronism is a result of overstimulation of the RAAS. In suspected cases of hyperaldosteronism, determination of the aldosterone-renin concentration is recommended.

In adrenogenital syndrome, cortisol production is impaired by congenital enzyme defects. Increased amounts of cortisol precursors (e.g. 17-OH progesterone) are produced, however, not the functional hormone. Due to the lack of negative feedback, the accumulation of precursors leads to increased production of androgens.

Hypofunction of the adrenal cortex causes adrenal cortex insufficiency. The most frequent cause of primary adrenal cortex insufficiency is Addison’s disease. Because of the autoimmune-induced destruction of hormone-producing cells of the adrenal cortex, it can no longer synthesise hormones. Diagnostics is based on the combined measurement of cortisol and ACTH.

Techniques

Method
Parameter
Substrate
Species
IIFT
adrenal cortex
adrenal gland
monkey
ELISA
cortisol
determination in saliva
antibody-coated microplate wells
ChLIA
IDS Cortisol 1
Antibody-coated magnetic particles
ChLIA
IDS Salivary Cortisol 1
Antibody-coated magnetic particles
ChLIA
IDS Urinary Cortisol 1
Antibody-coated magnetic particles
ChLIA
IDS Cortisol Calibrator Set 1
1 x 1.0mL Calibrator 1/2/3/4/5/6
ChLIA
IDS Urinary Cortisol Calibrator Set 1
1 x 1.0mL Calibrator 1/2/3/4/5/6
ChLIA
IDS Cortisol Control Set 1
3 x 1.0mL Control 1/2/3
ChLIA
IDS Urinary Cortisol Control Set 1
3 x 1.0mL Control 1/2
ChLIA
IDS Salivary Cortisol Control Set 1
4 x 2.0mL Control 1/2/3
ELISA
aldosterone
antibody-coated microplate wells
ChLIA
IDS Aldosterone 1
Antibody-coated magnetic particles
ChLIA
IDS Aldosterone Control Set 1
6 x 1.0mL Control 1/2/3
ChLIA
IDS ACTH II 1
Antibody-coated magnetic particles
ChLIA
IDS ACTH II Calibrator Set 1
2 x 1.0mL Calibrator 1/2/3/4/5
ChLIA
IDS ACTH II Control Set 1
6 x 1.0mL Control 1/2
ELISA
17-OH-progesterone
antibody-coated microplate wells
ChLIA
IDS 17-OH Progesterone 1
Antibody-coated magnetic particles
ChLIA
IDS 17-OH Progesterone Control Set 1
2 x 1.0mL Control 1/2/3
ChLIA
IDS Direct Renin 1
Antibody-coated magnetic particles
ChLIA
IDS Direct Renin Control Set 1
6 x 1.0mL Control 1/2/3
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