Hypercortisolism Definition, Symptoms, Causes, Treatment
Cardinal manifestation of prolonged hypercortisolism is cushing's syndrome, which may include not only obesity but also connected with hypertension, hyperglycemia, osteoporosis and female hirsutism.
Hypercortisolism has a number of effects on bone metabolism, and there is suppression of osteoblast activity with increased bone matrix protein resorption. Increased renal excretion of calcium combined with decreased absorption of calcium from intestinal results in hypocalcemia. This hypocalcemia is offset by slightly increased secretion of PTH. At the same time, PTH increases the activity of osteoclasts.
The overall effect is marked osteopenia. Since hypercortisolism reduces growth hormone and IGF-1 secretion, over time, marked linear growth retardation. Thinning of the skin and the formation of purple strips on the abdomen, thighs, buttocks are associated with a hypercortisol effect on the collagen metabolism. Hypercortisolism increases gastric acid secretion, which is considered to be associated with a high incidence of peptic ulcers.
Primary hypercortisolism, where cortisol hyper-secretion is autonomous and usually depends on ACTH. This is due to either adenoma or rarely, adrenal gland cancer. Circulating plasma cortisol inhibits the release of the ACTH, so that the levels of the trophic hormone are low. Tumor usually develops unilaterally and the contralateral gland atrophies are due to the lack of ACTH.
Secondary hypercortisolism results in hyperplasia of gland dependent on pituitary secretion. Secondary hypercortisolism may be associated with a small anterior pituitary adenoma (about 15% of cases, a Nelson syndrome) or derangement in the mechanism controlling ACTH release, which may include hypothalamus CRF and factors that control it. However, ACTH production is not independent because it can still be inhibited by high doses of glucocorticoid.
Some commonly reported symptoms of Hypercortisolism are given below
Exact underlying cause of hypercortisolism depends upon number of factors. However, in many cases tumor of adrenal gland is main cause which leads increase secretion of cortisol. Similarly, administration of high doses of exogenous corticosteroids result in exogenous hypercotisolism. Conditions in which high doses of corticosteroids are administered include arthritis, asthma and some autoimmune diseases.
Treatment of hypercortisolism highly depends upon root cause treatment. e.g if hypercortisolism occurs due to high dose corticosteroids then their use must discontinue or dose should be adjusted to make it tolerable for body. Similarly, if cortisol is overproducing then cortisol inhibitory drugs would be mainstay. Tumor induce hypercortisolism can managed via cytotoxic drugs.
Hypercortisolism has a number of effects on bone metabolism, and there is suppression of osteoblast activity with increased bone matrix protein resorption. Increased renal excretion of calcium combined with decreased absorption of calcium from intestinal results in hypocalcemia. This hypocalcemia is offset by slightly increased secretion of PTH. At the same time, PTH increases the activity of osteoclasts.
The overall effect is marked osteopenia. Since hypercortisolism reduces growth hormone and IGF-1 secretion, over time, marked linear growth retardation. Thinning of the skin and the formation of purple strips on the abdomen, thighs, buttocks are associated with a hypercortisol effect on the collagen metabolism. Hypercortisolism increases gastric acid secretion, which is considered to be associated with a high incidence of peptic ulcers.
Primary hypercortisolism, where cortisol hyper-secretion is autonomous and usually depends on ACTH. This is due to either adenoma or rarely, adrenal gland cancer. Circulating plasma cortisol inhibits the release of the ACTH, so that the levels of the trophic hormone are low. Tumor usually develops unilaterally and the contralateral gland atrophies are due to the lack of ACTH.
Secondary hypercortisolism results in hyperplasia of gland dependent on pituitary secretion. Secondary hypercortisolism may be associated with a small anterior pituitary adenoma (about 15% of cases, a Nelson syndrome) or derangement in the mechanism controlling ACTH release, which may include hypothalamus CRF and factors that control it. However, ACTH production is not independent because it can still be inhibited by high doses of glucocorticoid.
Hypercortisolism Symptoms
Some commonly reported symptoms of Hypercortisolism are given below
- Central Obesity
- Hypertension
- Memory Problems
- Weakness
- Loss of energy
- Redness on skin
- Fat depots around neck and shoulders
- Difficulty in focusing
- Delayed healing
- Depression
- Hair loss
- Swelling around feet and legs
Hypercortisolism Causes
Exact underlying cause of hypercortisolism depends upon number of factors. However, in many cases tumor of adrenal gland is main cause which leads increase secretion of cortisol. Similarly, administration of high doses of exogenous corticosteroids result in exogenous hypercotisolism. Conditions in which high doses of corticosteroids are administered include arthritis, asthma and some autoimmune diseases.
Hypercortisolism Treatment
Treatment of hypercortisolism highly depends upon root cause treatment. e.g if hypercortisolism occurs due to high dose corticosteroids then their use must discontinue or dose should be adjusted to make it tolerable for body. Similarly, if cortisol is overproducing then cortisol inhibitory drugs would be mainstay. Tumor induce hypercortisolism can managed via cytotoxic drugs.
Hypercortisolism Definition, Symptoms, Causes, Treatment
Reviewed by Simon Albert
on
September 08, 2019
Rating:
Reviewed by Simon Albert
on
September 08, 2019
Rating:
