Addison’s disease is caused by a significant decrease in cortisol production – the stress hormone – by the adrenal glands. Know the many problems it causes.
Addison’s disease results from a significant reduction of cortisol production by the adrenal glands. The same is a chronic adrenocortical insufficiency, more than 90% destruction of both adrenal glands.
Cortisol is also known as the ‘ stress hormone ‘since it performs essential actions, such as maintaining glucose levels in the blood and the nervous and cardiovascular systems’ functioning. It is also responsible for protecting the body from self-injurious mechanisms, such as excessive inflammatory and immune responses.
The general cause of chronic adrenal insufficiency is the destruction of both adrenal glands – located above both kidneys – due to bleeding, tumor metastases, or infections such as, for example, tuberculosis; but, at present, most cases are caused by immune mechanisms.
Addison’s disease manifests as tiredness, loss of appetite (anorexia), nausea, vomiting, low blood pressure (hypotension), and low blood glucose (hypoglycemia). The color of people’s skin with Addison’s disease is very characteristic, which is brown – this disease was once known as the ‘ tanned disease, ‘although this term is in disuse. Also, the mucous membranes, especially the gums and the inside of the cheeks, have dark blue spots.
In blood is usually low levels of glucose and sodium and high potassium; Also, there are low levels of two hormones produced in the adrenal gland: cortisol and aldosterone. There may also be very low levels of androgen in women, which are also produced in the adrenal gland.
Addison’s disease can be associated with other endocrine diseases of immune origin. Patients need to receive the contribution of hormones that they do not have, cortisol and aldosterone.
Other names for Addison’s disease include:
- Primary adrenocortical insufficiency.
- Chronic adrenocortical insufficiency.
- Primary adrenocortical insufficiency.
- Chronic adrenocortical insufficiency.
- Addison’s syndrome (an infrequently used term).
Secondary and tertiary adrenal insufficiency
Also, there is secondary and tertiary adrenal insufficiency, which are not Addison’s diseases. Secondary adrenal insufficiency is due to inadequate secretion of the hormone that stimulates the production of glucocorticoids by the adrenal; This hormone is adrenocorticotropic or ACTH, which is released into the blood from the pituitary gland, an organ that produces various hormones that, in turn, act on various hormone-producing organs (endocrine organs). Since ACTH is the hormone that induces glucocorticoid production, its deficiency leads to insufficient cortisol production by the adrenal.
In tertiary adrenal insufficiency, the deficit is in the hormone that stimulates ACTH production, known as a corticotropin-releasing hormone or CRH (which is produced in the brain, in an area called the hypothalamus).
Causes of Addison’s disease
Possible causes of primary adrenal insufficiency or Addison’s disease are:
- Autoimmune adrenal gland atrophy is the most common cause and accounts for 75% of Addison’s disease cases. It can be an isolated condition associated with an autoimmune disorder of other endocrine glands called a pluriglandular syndrome.
- Among the infections, the most frequent cause is tuberculosis (20% of Addison’s disease cases). This can affect the adrenal cortex and medulla (in which case there will be additional symptoms caused by a lack of catecholamines) because the tuberculosis bacteria spread in both adrenal gland areas. Other causes are some fungal infections ( mycosis ) and syphilis.
- Vascular disorders of the adrenal gland can be caused by bleeding in the adrenal glands (adrenal stroke) and metastases.
- Certain AIDS-related conditions, such as Kaposi’s sarcoma or cytomegalovirus or cryptococcal infections.
- Metabolic diseases such as hemochromatosis, amyloidosis, and adrenoleukodystrophy.
- Other causes of Addison’s disease can be drugs that interfere with cortisol synthesis, congenital underdevelopment of the adrenal gland (called congenital adrenal hypoplasia), or a lack of response to ACTH (in this case, there is ACTH hormone, but it is not capable of producing its effect on the adrenal gland, that is, it does not induce the production of cortisol by adrenal cells due to a defect in its receptors).
The inflammation of the adrenal gland (suprarrenalitis) of immune origin leads to the destruction of the adrenal cortex and conserving the adrenal medulla. Due to this, the production of catecholamines ( adrenaline and noradrenaline), which are hormones produced in the marrow, is preserved, with a more or less critical reduction in the production of the adrenal cortex’s hormones: cortisol, aldosterone, and androgens.
In autoimmune or atrophic adrenalitis, there is a genetic predisposition, in many cases, which is associated with the presence of certain types of HLA ( Human Leukocyte Antigen, the system of molecules involved in immune recognition): HLA-B8, HLA-D3, and HLA-D4. Also, most patients (65%) have antibodies to the enzymes involved in synthesizing adrenal steroids (cortisol, aldosterone, and testosterone ). The incidence is the same in both sexes under 30 years of age. After this age, it is more frequent in women. Atrophic adrenalitis is only an isolated process in 40% of cases. In the rest, it is part of pluriglandular syndrome.