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  1. Dexamethasone suppression test measures whether adrenocorticotrophic hormone (ACTH) secretion by the pituitary can be suppressed. How the Test is Performed During this test, you will receive dexamethasone. This is a strong man-made (synthetic) glucocorticoid medicine. Afterward, your blood is drawn so that the cortisol level in your blood can be measured. There are two different types of dexamethasone suppression tests: low dose and high dose. Each type can either be done in an overnight (common) or standard (3-day) method (rare). There are different processes that may be used for either test. Examples of these are described below. Common: Low-dose overnight -- You will get 1 milligram (mg) of dexamethasone at 11 p.m., and a health care provider will draw your blood the next morning at 8 a.m. for a cortisol measurement. High-dose overnight -- The provider will measure your cortisol on the morning of the test. Then you will receive 8 mg of dexamethasone at 11 p.m. Your blood is drawn the next morning at 8 a.m. for a cortisol measurement. Rare: Standard low-dose -- Urine is collected over 3 days (stored in 24-hour collection containers) to measure cortisol. On day 2, you will get a low dose (0.5 mg) of dexamethasone by mouth every 6 hours for 48 hours. Standard high-dose -- Urine is collected over 3 days (stored in 24-hour collection containers) for measurement of cortisol. On day 2, you will receive a high dose (2 mg) of dexamethasone by mouth every 6 hours for 48 hours. Read and follow the instructions carefully. The most common cause of an abnormal test result is when instructions are not followed. How to Prepare for the Test The provider may tell you to stop taking certain medicines that can affect the test, including: Antibiotics Anti-seizure drugs Medicines that contain corticosteroids, such as hydrocortisone, prednisone Estrogen Oral birth control (contraceptives) Water pills (diuretics) How the Test will Feel When the needle is inserted to draw blood, some people feel moderate pain. Others feel only a prick or stinging. Afterward, there may be some throbbing or slight bruising. This soon goes away. Why the Test is Performed This test is done when the provider suspects that your body is producing too much cortisol. It is done to help diagnose Cushing syndrome and identify the cause. The low-dose test can help tell whether your body is producing too much ACTH. The high-dose test can help determine whether the problem is in the pituitary gland (Cushing disease) or from a different site in the body (ectopic). Dexamethasone is a man-made (synthetic) steroid that binds to the same receptor as cortisol. Dexamethasone reduces ACTH release in normal people. Therefore, taking dexamethasone should reduce ACTH level and lead to a decreased cortisol level. If your pituitary gland produces too much ACTH, you will have an abnormal response to the low-dose test. But you can have a normal response to the high-dose test. Normal Results Cortisol level should decrease after you receive dexamethasone. Low dose: Overnight -- 8 a.m. plasma cortisol lower than 1.8 micrograms per deciliter (mcg/dL) or 50 nanomoles per liter (nmol/L) Standard -- Urinary free cortisol on day 3 lower than 10 micrograms per day (mcg/day) or 280 nmol/L High dose: Overnight -- greater than 50% reduction in plasma cortisol Standard -- greater than 90% reduction in urinary free cortisol Normal value ranges may vary slightly among different laboratories. Some labs use different measurements or may test different specimens. Talk to your doctor about the meaning of your specific test results. What Abnormal Results Mean An abnormal response to the low-dose test may mean that you have abnormal release of cortisol (Cushing syndrome). This could be due to: Adrenal tumor that produces cortisol Pituitary tumor that produces ACTH Tumor in the body that produces ACTH (ectopic Cushing syndrome) The high-dose test can help tell a pituitary cause (Cushing disease) from other causes. An ACTH blood test may also help identify the cause of high cortisol. Abnormal results vary based on the condition causing the problem. Cushing syndrome caused by an adrenal tumor: Low-dose test -- no decrease in blood cortisol ACTH level -- low In most cases, the high-dose test is not needed Ectopic Cushing syndrome: Low-dose test -- no decrease in blood cortisol ACTH level -- high High-dose test -- no decrease in blood cortisol Cushing syndrome caused by a pituitary tumor (Cushing disease) Low-dose test -- no decrease in blood cortisol High-dose test -- expected decrease in blood cortisol False test results can occur due to many reasons, including different medicines, obesity, depression, and stress. False results are more common in women than men. Most often, the dexamethasone level in the blood is measured in the morning along with the cortisol level. For the test result to be considered accurate, the dexamethasone level should be higher than 200 nanograms per deciliter (ng/dL) or 4.5 nanomoles per liter (nmol/L). Dexamethasone levels that are lower can cause a false-positive test result. Risks There is little risk involved with having your blood taken. Veins and arteries vary in size from one patient to another, and from one side of the body to the other. Taking blood from some people may be more difficult than from others. Other risks associated with having blood drawn are slight, but may include: Excessive bleeding Fainting or feeling lightheaded Multiple punctures to locate veins Hematoma (blood accumulating under the skin) Infection (a slight risk any time the skin is broken) Alternative Names DST; ACTH suppression test; Cortisol suppression test References Chernecky CC, Berger BJ. Dexamethasone suppression test - diagnostic. In: Chernecky CC, Berger BJ, eds. Laboratory Tests and Diagnostic Procedures. 6th ed. St Louis, MO: Elsevier Saunders; 2013:437-438. Guber HA, Oprea M, Russell YX. Evaluation of endocrine function. In: McPherson RA, Pincus MR, eds. Henry's Clinical Diagnosis and Management by Laboratory Methods. 24th ed. St Louis, MO: Elsevier; 2022:chap 25. Newell-Price JDC, Auchus RJ. The adrenal cortex. In: Melmed S, Auchus RJ, Goldfine AB, Koenig RJ, Rosen CJ, eds. Williams Textbook of Endocrinology. 14th ed. Philadelphia, PA: Elsevier; 2020:chap 15. Review Date 5/13/2021 Updated by: Brent Wisse, MD, Board Certified in Metabolism/Endocrinology, Seattle, WA. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team. From https://medlineplus.gov/ency/article/003694.htm
  2. – AI false positives pose serious danger to patients; cutoff changes recommended by Scott Harris , Contributing Writer, MedPage Today November 15, 2021 share to facebook share to twitter share to linkedin email article This Reading Room is a collaboration between MedPage Today® and: For adrenal insufficiency (AI), reducing false positives means more than reducing resource utilization. Treatments like glucocorticoid replacement therapy can cause serious harm in people who do not actually have AI. Research published in the Journal of the Endocrine Society makes multiple findings that report authors say could help bring down false positive rates for AI. This retrospective study ultimately analyzed 6,531 medical records from the Imperial College Healthcare NHS Trust in the United Kingdom. Sirazum Choudhury, MBBS, an endocrinologist-researcher with the trust, served as a co-author of the report. He discussed the study with MedPage Today. The exchange has been edited for length and clarity. This study ultimately addressed two related but distinct questions. What was the first? Choudhury: Initially the path we were following had to do with when cortisol levels are tested. Cortisol levels follow a diurnal pattern; levels are highest in the morning and then decline to almost nothing overnight. This means we ought to be measuring the level in the morning. But there are logistical issues to doing so. In many hospitals, we end up taking measurements of cortisol in the afternoon. That creates a dilemma, because if it comes back low, there's an issue as to what we ought to do with the result. Here at Imperial, we call out results of <100 nmol/L among those taken in the afternoon. Patients and doctors then have to deal with these abnormal results, when in fact they may not actually be abnormal. We may be investigating individuals who should really not be investigated. So the first aim of our study was to try and ascertain whether we could bring that down to a lower level and in doing so stop erroneously capturing people who are actually fine. What was the second aim of the study? Choudhury: As we went through tens of thousands of data sets, we realized we could answer more than that one simple question. So the next part of the study became: if an individual is identified as suspicious for AI, what's the best way to prove this diagnosis? We do this with different tests like short Synacthen Tests (SST), all with different cutoff points. Obviously, we want to get the testing right, because if you falsely label a person as having AI, the upshot is that treatments will interfere with their cortisol access and they will not do well. Simply put, we would be shortening their life. So, our second goal was to look at all the SSTs we've done at the center and track them to see whether we could do better with the benchmarks. What did you find? Choudhury: When you look at the data, you see that you can bring those benchmarks down and potentially create a more accurate test. First, we can be quite sure that a patient who is tested in the afternoon and whose cortisol level is >234 does not have AI. If their level is <53.5 then further investigation is needed There were similar findings for SSTs, which in our case were processed using a platform made by Abbott. For this platform, we concluded that the existing cut-offs should be dropped down to 367 at 30 minutes or 419 at about 60 minutes. Did anything surprise you about the study or its findings? Choudhury: If you look at the literature, the number of individuals who fail at 30 minutes but pass at 60 minutes is around 5%. But I was very surprised to see that our number at Imperial was about 20%. This is a key issue because, as I mentioned, if individuals are wrongly labelled adrenally insufficient, you're shortening their life. It's scary to think about the number of people who might have been given steroids and treated for AI when they didn't have the condition. What do you see as the next steps? Choudhury: I see centers unifying their cutoffs for SST results and making sure we're all consistent in the way we treat these results. From a research perspective, on the testing we're obviously talking about one specific platform with Abbott, so research needs to be done on SST analyzers from other manufacturers to work out what their specific cutoffs should be. Read the study here and expert commentary on the clinical implications here. The study authors did not disclose any relevant relationship with industry. Primary Source Journal of the Endocrine Society Source Reference: Ramadoss V, et al "Improving the interpretation of afternoon cortisol levels and SSTs to prevent misdiagnosis of adrenal insufficiency" J Endocrine Soc 2021; 5(11): bvab147. From https://www.medpagetoday.com/reading-room/endocrine-society/adrenal-disorders/95661
  3. Patients with subclinical hypercortisolism, i.e., without symptoms of cortisol overproduction, and adrenal incidentalomas recover their hypothalamic-pituitary-adrenal (HPA) axis function after surgery faster than those with Cushing’s syndrome (CS), according to a study. Moreover, the researchers found that an HPA function analysis conducted immediately after the surgical removal of adrenal incidentalomas — adrenal tumors discovered by chance in imaging tests — could identify patients in need of glucocorticoid replacement before discharge. Using this approach, they found that most subclinical patients did not require treatment with hydrocortisone, a glucocorticoid taken to compensate for low levels of cortisol in the body, after surgery. The study, “Alterations in hypothalamic-pituitary-adrenal function immediately after resection of adrenal adenomas in patients with Cushing’s syndrome and others with incidentalomas and subclinical hypercortisolism,” was published in Endocrine. The HPA axis is the body’s central stress response system. The hypothalamus releases corticotropin-releasing hormone (CRH) that acts on the pituitary gland to release adrenocorticotropic hormone (ACTH), leading the adrenal gland to produce cortisol. As the body’s defense mechanism to avoid excessive cortisol secretion, high cortisol levels alert the hypothalamus to stop producing CRH and the pituitary gland to stop making ACTH. Therefore, in diseases associated with chronically elevated cortisol levels, such as Cushing’s syndrome and adrenal incidentalomas, there’s suppression of the HPA axis. After an adrenalectomy, which is the surgical removal of one or both adrenal glands, patients often have low cortisol levels (hypocortisolism) and require glucocorticoid replacement therapy. “Most studies addressing the peri-operative management of patients with adrenal hypercortisolism have reported that irrespective of how mild the hypercortisolism was, such patients were given glucocorticoids before, during and after adrenalectomy,” the researchers wrote. Evidence also shows that, after surgery, glucocorticoid therapy is administered for months before attempting to test for recovery of HPA function. For the past 30 years, researchers at the University Hospitals Cleveland Medical Center have withheld glucocorticoid therapy in the postoperative management of patients with ACTH-secreting pituitary adenomas until there’s proof of hypocortisolism. “The approach offered us the opportunity to examine peri-operative hormonal alterations and demonstrate their importance in predicting need for replacement therapy, as well as future recurrences,” they said. In this prospective observational study, the investigators extended their approach to patients with subclinical hypercortisolism. “The primary goal of the study was to examine rapid alteration in HPA function in patients with presumably suppressed axis and appreciate the modulating impact of surgical stress in that setting,” they wrote. Collected data was used to decide whether to start glucocorticoid therapy. The analysis included 14 patients with Cushing’s syndrome and 19 individuals with subclinical hypercortisolism and an adrenal incidentaloma. All participants had undergone surgical removal of a cortisol-secreting adrenal tumor. “None of the patients received exogenous glucocorticoids during the year preceding their evaluation nor were they taking medications or had other illnesses that could influence HPA function or serum cortisol measurements,” the researchers noted. Glucocorticoid therapy was not administered before or during surgery. To evaluate HPA function, the clinical team took blood samples before and at one, two, four, six, and eight hours after the adrenalectomy to determine levels of plasma ACTH, serum cortisol, and dehydroepiandrosterone sulfate (DHEA-S) — a hormone produced by the adrenal glands. Pre-surgery assessment of both groups showed that patients with an incidentaloma plus subclinical hypercortisolism had larger adrenal masses, higher ACTH, and DHEA-S levels, but less serum cortisol after adrenal function suppression testing with dexamethasone. Dexamethasone is a man-made version of cortisol that, in a normal setting, makes the body produce less cortisol. But in patients with a suppressed HPA axis, cortisol levels remain high. After the adrenalectomy, the ACTH concentrations in both groups of patients increased. This was found to be negatively correlated with pre-operative dexamethasone-suppressed cortisol levels. Investigators reported that “serum DHEA-S levels in patients with Cushing’s syndrome declined further after adrenalectomy and were undetectable by the 8th postoperative hour,” while incidentaloma patients’ DHEA-S concentrations remained unchanged for the eight-hour postoperative period. Eight hours after surgery, all Cushing’s syndrome patients had serum cortisol levels of less than 2 ug/dL, indicating suppressed HPA function. As a result, all of these patients required glucocorticoid therapy for several months to make up for HPA axis suppression. “The decline in serum cortisol levels was slower and less steep [in the incidentaloma group] when compared to that observed in patients with Cushing’s syndrome. At the 6th–8th postoperative hours only 5/19 patients [26%] with subclinical hypercortisolism had serum cortisol levels at ≤3ug/dL and these 5 were started on hydrocortisone therapy,” the researchers wrote. Replacement therapy in the subclinical hypercortisolism group was continued for up to four weeks. Results suggest that patients with an incidentaloma plus subclinical hypercortisolism did not have an entirely suppressed HPA axis, as they were able to recover its function much faster than the CS group after surgical stress. From https://cushingsdiseasenews.com/2018/10/11/most-subclinical-cushings-patients-dont-need-glucocorticoids-post-surgery-study/?utm_source=Cushing%27s+Disease+News&utm_campaign=a881a1593b-RSS_WEEKLY_EMAIL_CAMPAIGN&utm_medium=email&utm_term=0_ad0d802c5b-a881a1593b-72451321
  4. (HealthDay News) – A number of factors, including the duration of glucocorticoid exposure, older age at diagnosis, and preoperative adrenocorticotropic hormone (ACTH) concentration, are associated with a higher risk of mortality in patients treated for Cushing's disease (CD), according to research published online Feb. 7 in the Journal of Clinical Endocrinology & Metabolism. In an effort to identify predictors of mortality, cardiovascular disease, and recurrence with long-term follow-up, Jessica K. Lambert, MD, of the Mount Sinai Medical Center in New York City, and colleagues performed a retrospective chart review of 346 patients with CD who underwent transsphenoidal adenectomy. The researchers found that the average length of exposure to glucocorticoids was 40 months. The risk of death was higher for those patients who had a longer duration of glucocorticoid exposure, older age at diagnosis, and higher preoperative ACTH concentration. For patients who achieved remission, depressed patients had a higher risk of death. The risk of cardiovascular disease was highest for men, older people, and those with diabetes or depression. "Our study has identified several predictors of mortality in patients with treated CD, including duration of exposure to excess glucocorticoids, preoperative ACTH concentration, and older age at diagnosis. Depression and male gender predicted mortality among patients who achieved remission," the authors write. "These data illustrate the importance of early recognition and treatment of CD. Long-term follow-up, with management of persistent comorbidities by an experienced endocrinologist, is needed even after successful treatment of CD." Abstract Full Text (subscription or payment may be required)
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