Cushing's syndrome is characterized by a series of systemic complications that increase cardiovascular (heart and blood vessel) risk and cause severe atherosclerotic (hardening of the arteries) damage that develops together with an acquired metabolic syndrome. Short-term remission from hypercortisolism improves metabolic and vascular damages, but long-term remission from Cushing's syndrome seems to be associated with similar or worse metabolic and vascular damage, probably because of persistent abdominal obesity or insulin resistance years after normalization of cortisol secretion. Study results suggest that an increased cardiovascular risk also may persist in patients who undergo treatment with exogenous glucocorticoids after therapy withdrawal.
Screening studies in high-risk populations have suggested that Cushing's syndrome is more common than previously appreciated. Patients who have specific signs and symptoms or clinical diagnoses known to be associated with high cortisol should be considered for screening.
Cushing disease is the most common form of Cushing syndrome.
Cushing's disease diagnosis
The measurement of late-night salivary cortisol provides the most sensitive method for screening, and urine-free cortisol and low-dose dexamethasone suppression testing may be used for confirmation of the diagnosis of endogenous hypercortisolism.
Another opinion - Diagnostic tests used to screen for Cushing's syndrome include 24-hour urine cortisol, the 1 mg dexamethasone suppresion test, and late night salivary cortisol. A normal screening test excludes the diagnosis of Cushing's. Patients with an abnormal screening test should be referred to an endocrinologist for complete evaluation of the pituitary-adrenal axis.
Cushing's Syndrome treatment, therapy
The successful treatment of Cushing syndrome depends on specific therapy directed against the cause of hypercortisolism. In addition to surgical procedures, various drugs have been employed in the management of this difficult disease. Compounds with neuromodulatory properties have been effective in only a limited number of cases. These agents include serotonin antagonists (cyproheptadine, ketanserin, ritanserin), dopamine agonists (bromocriptine, cabergoline), GABA agonists (valproic acid [sodium valproate]), and somatostatin analogs (octreotide).
Cushing's syndrome results from prolonged exposure to excess glucocorticoids. Patients may develop multiple metabolic problems including obesity, hyperglycemia, hypertension, depression, low bone mass, muscle atrophy, and hypogonadism. Cutaneous manifestations of hypercortisolism include skin atrophy, excessive bruising, purple striations, poor wound healing, facial plethora, vellous hypertrichosis and hirsutism.
I about 12 years ago I was bush hogging a field and was attacked by a swarm of yellow jackets and had an anaphylactic reaction to the stings. I started seeing a physician who tested my sensitivity to bee stings and noted that I developed across reactivity to every kind of bee and started me on bee venom therapy for about six months. Three years later I had to go to the minor emergency care center for a UTI and was diagnosed with type 2 DM. I was perplexed because I had no family history and just attributed it to poor eating habits and started taking metformin, victoza and Zocor under the guidance of my endo. Is it possible that the bee venom injections elevated cortisol levels and I could have Cushing's syndrome instead of metabolic syndrome? I haven't brought this up tomy endo as I am trying to educate myself. Have you encountered other patients with this?
A. I have not yet encountered such a relationship.