Long-term exposure to excessive cortisol levels in the bloodstream results in Cushing syndrome. Iatrogenic glucocorticoid usage is the most frequent cause of cushingoid characteristics, although several herbal remedies can also raise circulation corticosteroid concentrations, which can result in Cushing’s syndrome.
The terms Cushing syndrome and hypercortisolism are interchangeable. 80 percent of endogenous Cushing’s syndrome is caused by a pituitary gland-dependent Adrenocorticotropic-dependent cortisone excess, which is known as Cushing’s disease.
Epidemiology
Unknowns are the real prevalence and incidence of Cushing’s syndrome. Depending on the frequency and range of medical illnesses needing corticosteroid-based treatment, the prevalence of the illness varies greatly among various cultural and ethnic groups. However, among cases that are known, iatrogenic hypercortisolism outnumbers endogenous sources of the condition.
Of the natural reasons, pituitary gland-mediated Adrenocorticotropic production is responsible for up to 80 percent of instances of hypercortisolism, accompanied by the adrenal glands, an unidentified source, as well as ectopic Adrenocorticotropic release brought on by tumors.
Anatomy
Pathophysiology
The adrenal cortex’s zona fasciculata produces the steroid hormone cortisol. Almost 90 percent of cortisol attaches to this corticosteroid-binding globulin protein when it is produced, resulting in a bioavailability of sixty percent to hundred percent. Cortisol binding protein then transports the cortisol to various regions of the body. Although the bioavailability and efficacy of artificial corticosteroids vary, they all act on the same routes.
A catabolic protein, it is secreted in response to stress. An oversupply of cortisol raises ins insulin tolerance and speeds up glycogenolysis and gluconeogenesis. As a steroid hormone, cortisol has a direct impact on the translation and transcription of enzymatic molecules essential for the metabolism of lipids, glycogen, the synthesis of proteins, and the Krebs cycle. It encourages the body to produce more free glucose, raising blood sugar levels and causing an increase in insulin intolerance.
Peptide acids are produced when proteins are broken down and are utilized in the production of glucose. Prolonged protein catabolism results in osteoporosis, purple scars on the thorax, and poorly heals wounds. Collagen, a protein with 3 amino acids at its base, is used in all of these processes. High levels of cortisol also compromise the immune system because they raise neutrophils and decrease lymphocyte numbers.
Although there is no increased generation of neutrophils, it causes dissociation of the pool of neutrophils in circulation and raises the number of circulatory neutrophils. With fewer lymphocytes and more neutrophils, the normal image of elevated TLC is explained by this process. The downregulation of NF-kappaB, as well as the control of glycogen phosphorylases, AMP kinases, superoxide dismutase, glycogen phosphorylases, and numerous other enzymes, is mediated by the corticosteroids.
Etiology
Exogenous and endogenous hypercortisolism are the two primary etiologies of Cushing’s syndrome. The most frequent cause of Cushing’s syndrome, exogenous (HCH) hypercortisolism, is primarily iatrogenic but also is brought on by using glucocorticoids over an extended period of time.
Endogenous Cushing condition, which can be both Adrenocorticotropic -independent and Adrenocorticotropic -dependent, is brought on by excessive adrenal cortisol production.
The causes of Adrenocorticotropic-dependent Cushing are ectopic Adrenocorticotropic secretion by malignancies and adrenocorticotropic-secreting pituitary adenoma (Cushing syndrome).
Genetics
Prognostic Factors
The standard mortality ratio is comparable to the age-matched community, despite the fact that the early investigations of Cushing’s syndrome revealed a survival rate of 4.6 years with a 5-year survival of just 50 percent.
This is because of recent advancements in treatment. Obesity, hypertension, osteoporosis, diabetes, and heart disease with fractures are the main contributors to the morbidity and mortality of Cushing’s syndrome.
0.2-0.6 mg/kg intravenous for 30-60sec can be used to induce anesthesia and prevent an increase in cortisol production, a hormone associated with stress, for a limited time of 4-8 hours
ICU continuous infusion: 0.04-0.05 mg/kg/hr intravenous
Initial dose: orally 150 mg 2 times daily
Maintenance dose: Titrate the daily dosage by 150 mg, at regular intervals of no more then 2-3 weeks taking into the 24-hour urine free levels of cortisol and the patient's tolerance, until a satisfactory response is attained
Maximum dose: daily dosage is 1200 mg, divided into two equal doses of 600 mg each, Administered two times daily
Initially, take 300 mg of mifepristone Orally every day; may increase to 1200 mg/day as a maximum dose, but not to exceed more than 20 mg/kg in a day
Increases in dosage should not be more than every 2 to 4 weeks. They should be based on evaluating insulin levels, anti-diabetic drug requirements, psychiatric symptoms and glucose control
Dose Adjustments
Dosage Modifications
strong CYP3A inhibitors Coadministration: should not exceed more than 300 mg in a day Hepatic impairment
Mild-moderate: initial dose with no change; limit the maximum dose to 600 mg orally everyday
Severe: not to use Renal impairment: initial dose with no change; limit to 600 mg orally everyday as the maximum dose
Long-term exposure to excessive cortisol levels in the bloodstream results in Cushing syndrome. Iatrogenic glucocorticoid usage is the most frequent cause of cushingoid characteristics, although several herbal remedies can also raise circulation corticosteroid concentrations, which can result in Cushing’s syndrome.
The terms Cushing syndrome and hypercortisolism are interchangeable. 80 percent of endogenous Cushing’s syndrome is caused by a pituitary gland-dependent Adrenocorticotropic-dependent cortisone excess, which is known as Cushing’s disease.
Unknowns are the real prevalence and incidence of Cushing’s syndrome. Depending on the frequency and range of medical illnesses needing corticosteroid-based treatment, the prevalence of the illness varies greatly among various cultural and ethnic groups. However, among cases that are known, iatrogenic hypercortisolism outnumbers endogenous sources of the condition.
Of the natural reasons, pituitary gland-mediated Adrenocorticotropic production is responsible for up to 80 percent of instances of hypercortisolism, accompanied by the adrenal glands, an unidentified source, as well as ectopic Adrenocorticotropic release brought on by tumors.
The adrenal cortex’s zona fasciculata produces the steroid hormone cortisol. Almost 90 percent of cortisol attaches to this corticosteroid-binding globulin protein when it is produced, resulting in a bioavailability of sixty percent to hundred percent. Cortisol binding protein then transports the cortisol to various regions of the body. Although the bioavailability and efficacy of artificial corticosteroids vary, they all act on the same routes.
A catabolic protein, it is secreted in response to stress. An oversupply of cortisol raises ins insulin tolerance and speeds up glycogenolysis and gluconeogenesis. As a steroid hormone, cortisol has a direct impact on the translation and transcription of enzymatic molecules essential for the metabolism of lipids, glycogen, the synthesis of proteins, and the Krebs cycle. It encourages the body to produce more free glucose, raising blood sugar levels and causing an increase in insulin intolerance.
Peptide acids are produced when proteins are broken down and are utilized in the production of glucose. Prolonged protein catabolism results in osteoporosis, purple scars on the thorax, and poorly heals wounds. Collagen, a protein with 3 amino acids at its base, is used in all of these processes. High levels of cortisol also compromise the immune system because they raise neutrophils and decrease lymphocyte numbers.
Although there is no increased generation of neutrophils, it causes dissociation of the pool of neutrophils in circulation and raises the number of circulatory neutrophils. With fewer lymphocytes and more neutrophils, the normal image of elevated TLC is explained by this process. The downregulation of NF-kappaB, as well as the control of glycogen phosphorylases, AMP kinases, superoxide dismutase, glycogen phosphorylases, and numerous other enzymes, is mediated by the corticosteroids.
Exogenous and endogenous hypercortisolism are the two primary etiologies of Cushing’s syndrome. The most frequent cause of Cushing’s syndrome, exogenous (HCH) hypercortisolism, is primarily iatrogenic but also is brought on by using glucocorticoids over an extended period of time.
Endogenous Cushing condition, which can be both Adrenocorticotropic -independent and Adrenocorticotropic -dependent, is brought on by excessive adrenal cortisol production.
The causes of Adrenocorticotropic-dependent Cushing are ectopic Adrenocorticotropic secretion by malignancies and adrenocorticotropic-secreting pituitary adenoma (Cushing syndrome).
The standard mortality ratio is comparable to the age-matched community, despite the fact that the early investigations of Cushing’s syndrome revealed a survival rate of 4.6 years with a 5-year survival of just 50 percent.
This is because of recent advancements in treatment. Obesity, hypertension, osteoporosis, diabetes, and heart disease with fractures are the main contributors to the morbidity and mortality of Cushing’s syndrome.
0.2-0.6 mg/kg intravenous for 30-60sec can be used to induce anesthesia and prevent an increase in cortisol production, a hormone associated with stress, for a limited time of 4-8 hours
ICU continuous infusion: 0.04-0.05 mg/kg/hr intravenous
Initial dose: orally 150 mg 2 times daily
Maintenance dose: Titrate the daily dosage by 150 mg, at regular intervals of no more then 2-3 weeks taking into the 24-hour urine free levels of cortisol and the patient's tolerance, until a satisfactory response is attained
Maximum dose: daily dosage is 1200 mg, divided into two equal doses of 600 mg each, Administered two times daily
Initially, take 300 mg of mifepristone Orally every day; may increase to 1200 mg/day as a maximum dose, but not to exceed more than 20 mg/kg in a day
Increases in dosage should not be more than every 2 to 4 weeks. They should be based on evaluating insulin levels, anti-diabetic drug requirements, psychiatric symptoms and glucose control
Dose Adjustments
Dosage Modifications
strong CYP3A inhibitors Coadministration: should not exceed more than 300 mg in a day Hepatic impairment
Mild-moderate: initial dose with no change; limit the maximum dose to 600 mg orally everyday
Severe: not to use Renal impairment: initial dose with no change; limit to 600 mg orally everyday as the maximum dose
250 mg orally every 6 times a day; should not exceed more than 6 g/day
https://www.ncbi.nlm.nih.gov/books/NBK470218/
medtigo
Cushing Syndrome
Updated :
September 5, 2023
Long-term exposure to excessive cortisol levels in the bloodstream results in Cushing syndrome. Iatrogenic glucocorticoid usage is the most frequent cause of cushingoid characteristics, although several herbal remedies can also raise circulation corticosteroid concentrations, which can result in Cushing’s syndrome.
The terms Cushing syndrome and hypercortisolism are interchangeable. 80 percent of endogenous Cushing’s syndrome is caused by a pituitary gland-dependent Adrenocorticotropic-dependent cortisone excess, which is known as Cushing’s disease.
Unknowns are the real prevalence and incidence of Cushing’s syndrome. Depending on the frequency and range of medical illnesses needing corticosteroid-based treatment, the prevalence of the illness varies greatly among various cultural and ethnic groups. However, among cases that are known, iatrogenic hypercortisolism outnumbers endogenous sources of the condition.
Of the natural reasons, pituitary gland-mediated Adrenocorticotropic production is responsible for up to 80 percent of instances of hypercortisolism, accompanied by the adrenal glands, an unidentified source, as well as ectopic Adrenocorticotropic release brought on by tumors.
The adrenal cortex’s zona fasciculata produces the steroid hormone cortisol. Almost 90 percent of cortisol attaches to this corticosteroid-binding globulin protein when it is produced, resulting in a bioavailability of sixty percent to hundred percent. Cortisol binding protein then transports the cortisol to various regions of the body. Although the bioavailability and efficacy of artificial corticosteroids vary, they all act on the same routes.
A catabolic protein, it is secreted in response to stress. An oversupply of cortisol raises ins insulin tolerance and speeds up glycogenolysis and gluconeogenesis. As a steroid hormone, cortisol has a direct impact on the translation and transcription of enzymatic molecules essential for the metabolism of lipids, glycogen, the synthesis of proteins, and the Krebs cycle. It encourages the body to produce more free glucose, raising blood sugar levels and causing an increase in insulin intolerance.
Peptide acids are produced when proteins are broken down and are utilized in the production of glucose. Prolonged protein catabolism results in osteoporosis, purple scars on the thorax, and poorly heals wounds. Collagen, a protein with 3 amino acids at its base, is used in all of these processes. High levels of cortisol also compromise the immune system because they raise neutrophils and decrease lymphocyte numbers.
Although there is no increased generation of neutrophils, it causes dissociation of the pool of neutrophils in circulation and raises the number of circulatory neutrophils. With fewer lymphocytes and more neutrophils, the normal image of elevated TLC is explained by this process. The downregulation of NF-kappaB, as well as the control of glycogen phosphorylases, AMP kinases, superoxide dismutase, glycogen phosphorylases, and numerous other enzymes, is mediated by the corticosteroids.
Exogenous and endogenous hypercortisolism are the two primary etiologies of Cushing’s syndrome. The most frequent cause of Cushing’s syndrome, exogenous (HCH) hypercortisolism, is primarily iatrogenic but also is brought on by using glucocorticoids over an extended period of time.
Endogenous Cushing condition, which can be both Adrenocorticotropic -independent and Adrenocorticotropic -dependent, is brought on by excessive adrenal cortisol production.
The causes of Adrenocorticotropic-dependent Cushing are ectopic Adrenocorticotropic secretion by malignancies and adrenocorticotropic-secreting pituitary adenoma (Cushing syndrome).
The standard mortality ratio is comparable to the age-matched community, despite the fact that the early investigations of Cushing’s syndrome revealed a survival rate of 4.6 years with a 5-year survival of just 50 percent.
This is because of recent advancements in treatment. Obesity, hypertension, osteoporosis, diabetes, and heart disease with fractures are the main contributors to the morbidity and mortality of Cushing’s syndrome.
https://www.ncbi.nlm.nih.gov/books/NBK470218/
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