Serum Dehydroepiandrosterone Sulfate in the Diagnosis of Adrenal Insufficiency: Ready for Prime Time?

2011 ◽  
Vol 17 (2) ◽  
pp. 167-169 ◽  
Author(s):  
Nicholas Tritos
Keyword(s):  
Adrenal Insufficiency ◽  
Dehydroepiandrosterone Sulfate ◽  
Prime Time

Androgen deficiency in women with adrenal insufficiency. Dehydroepiandrosterone. Review

GYNECOLOGY ◽  
2018 ◽  
Vol 20 (4) ◽  
pp. 35-39
Author(s):  
N F Nuralieva ◽  
M Yu Yukina ◽  
E A Troshina ◽  
N M Platonova
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenal Glands ◽  
Dehydroepiandrosterone Sulfate ◽  
Malignant Neoplasms ◽  
Androgen Deficiency ◽  
Risk Of Death ◽  
Pathological Conditions ◽  
Increased Risk ◽  
Life Threatening

It is known that adrenal insufficiency (AI) is a severe life-threatening disease due to the exceptional role of glucocorticoids and mineralocorticoids in the human body. At the same time, according to some reports, the deficit of androgens synthesized by the adrenal cortex (dehydroepiandrosterone - DHEA and dehydroepiandrosterone sulfate - DHEAS) is associated with an increased risk of death, including increased risk of adverse cardiovascular events, development of osteoporosis, diabetes mellitus and malignant neoplasms. The main source of DHEA and DHEAS in females are adrenal glands, so women with hypocorticism have significantly reduced (down to undetectable) levels of these hormones. However, due to lack of a reliable evidence and, accordingly, clinical recommendations, correction of androgen deficiency in patients with AI is usually not performed. The review discusses the accumulated data on the physiological significance of DHEA and DHEAS, their role in the development of various pathological conditions, as well as safety and efficacy of these drugs.

Serum Dehydroepiandrosterone Sulfate Concentrations in Secondary Adrenal Insufficiency*

1987 ◽  
Vol 65 (3) ◽  
pp. 448-451 ◽  
Author(s):  
TOHRU YAMAJI ◽  
MIYUKI ISHIBASHI ◽  
FUMIMARO TAKAKU ◽  
AKIRA ITABASHI ◽  
SHIGEHIRO KATAYAMA ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Dehydroepiandrosterone Sulfate ◽  
Secondary Adrenal Insufficiency

CLINICAL PRESENTATION AND OUTCOMES OF OPIOID-INDUCED ADRENAL INSUFFICIENCY

2020 ◽  
Vol 26 (11) ◽  
pp. 1291-1297 ◽  
Author(s):  
Taoran Li ◽  
Diane Donegan ◽  
W. Michael Hooten ◽  
Irina Bancos
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenocorticotropic Hormone ◽  
Clinical Manifestations ◽  
Dehydroepiandrosterone Sulfate ◽  
Stimulation Test ◽  
Glucocorticoid Treatment ◽  
Hypothalamic Pituitary Adrenal ◽  
Academic Center ◽  
High Level ◽  
Cosyntropin Stimulation Test

Objective: Opioid-induced adrenal insufficiency (OIAI) may develop in patients treated with chronic opioids due to suppression of the hypothalamic-pituitary-adrenal axis. Our objective was to describe the clinical manifestations, biochemical presentation, and clinical course of OIAI. Methods: A retrospective study of adults diagnosed with OIAI between 2006 and 2018 at an academic center. Opioid daily dose was converted into morphine milligram equivalents (MMEs). Results: Forty patients (women, n = 29 [73%]) taking chronic opioids at a daily median MME dose of 105 (60 to 200) mg and median duration of 60 (3 to 360) months were diagnosed with OIAI. Patients reported fatigue (n = 29, 73%), musculoskeletal pain (n = 21, 53%), and weight loss (n = 17, 53%) for a median of 12 (range, 1 to 132) months prior to diagnosis, and only 7.5% (n = 3) of patients were identified with OIAI through case detection. Biochemical diagnosis of OIAI was based on ( 1) low morning cortisol, baseline adrenocorticotropic hormone and/or dehydroepiandrosterone sulfate in 59% (n = 26) of patients or ( 2) abnormal cosyntropin stimulation test in 41% (n = 14) of patients. With glucocorticoid replacement, 16/23 (70%) patients with available follow-up experienced improvement in symptoms. Opioids were tapered or discontinued in 15 patients, of whom 10 were followed for adrenal function and of which 7 (70%) recovered from OIAI. Conclusion: Minimum daily MME in patients diagnosed with OIAI was 60 mg. OIAI causes significant morbidity, and recognition requires a high level of clinical suspicion. Appropriate glucocorticoid treatment led to improvement of symptoms in 70%. Resolution of OIAI occurred following opioid cessation or reduction. Abbreviations: ACTH = adrenocorticotropic hormone; CST = cosyntropin stimulation test; DHEAS = dehydroepiandrosterone sulfate; HPA = hypothalamic-pituitary-adrenal; MME = morphine milligram equivalent; OIAI = opioid-induced adrenal insufficiency

scholarly journals The Postmenopausal Ovary Is Not a Major Androgen-Producing Gland

2001 ◽  
Vol 86 (10) ◽  
pp. 5060-5066 ◽  
Author(s):  
Beatrice Couzinet ◽  
Geri Meduri ◽  
Maria G. Lecce ◽  
Jacques Young ◽  
Sylvie Brailly ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Postmenopausal Women ◽  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Ovarian Tissue ◽  
Dehydroepiandrosterone Sulfate ◽  
Hormonal Changes ◽  
Steroidogenic Enzymes ◽  
Dramatic Decrease ◽  
Androgen Levels

It is currently believed that the postmenopausal ovary remains a gonadotropin-driven, androgen-producing gland. However, the adrenal contribution to circulating androgen levels may explain some conflicting results previously reported. In addition, the steroidogenic potential and gonadotropin responsiveness of the postmenopausal ovary have not been recently reassessed. Plasma T, bioavailable T, free T, androstenedione (Adione), and dehydroepiandrosterone sulfate levels were measured in postmenopausal or ovariectomized women with complete adrenal insufficiency, compared with women with intact adrenals. A stimulation human chorionic gonadotropin test (on d 0, 3, and 6) was performed in postmenopausal women with adrenal insufficiency. Dexamethasone was administered for 4 d in postmenopausal women with intact adrenals. Intraovarian T and androstenedione were also measured in homogenates of ovarian tissue from postmenopausal women. Immunocytochemistry was performed on postmenopausal ovaries and premenopausal controls to detect the presence of steroidogenic enzymes (P-450 aromatase, P-450 SCC, 3β HSD, and P-450 C17) and gonadotropin receptors. Plasma androgen levels were below or close to the limit of the assay in all women with adrenal insufficiency. They were similar in postmenopausal and oophorectomized women with normal adrenals. No hormonal changes were observed after human chorionic gonadotropin injections in women with adrenal insufficiency. In contrast, a dramatic decrease of all steroids was observed after dexamethasone administration in postmenopausal women with intact adrenals. Intraovarian T and androstenedione levels were negligible in postmenopausal ovarian tissue. P-450 aromatase was absent from the 17 ovaries studied, and the enzymes for androgen biosynthesis were either absent (n = 13) or present in very low amounts (n = 4). In all the postmenopausal ovaries, FSH and LH receptors were completely absent. In the absence of adrenal steroids, postmenopausal women have no circulating androgens. This result is consistent with the immunocytochemical studies showing the almost constantly absent steroidogenic enzymes and LH receptors in the postmenopausal ovary. Thus, the climacteric ovary is not a critical source of androgens. The arrest of androgen secretion after menopause may impact significantly on women’s health.

scholarly journals Prevalence of Opioid-Induced Adrenal Insufficiency in Patients Taking Chronic Opioids

2020 ◽  
Vol 105 (10) ◽  
pp. e3766-e3775
Author(s):  
Taoran Li ◽  
Julie L Cunningham ◽  
Wesley P Gilliam ◽  
Larissa Loukianova ◽  
Diane M Donegan ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Dehydroepiandrosterone Sulfate ◽  
Opioid Therapy ◽  
Cross Sectional Study ◽  
Cumulative Exposure ◽  
Case Detection ◽  
Opioid Use ◽  
Cross Sectional ◽  
Chronic Opioid Use ◽  
Made In

Abstract Context Chronic opioid use may lead to adrenal insufficiency because of central suppression of the hypothalamic-pituitary-adrenal axis. However, the prevalence of opioid-induced adrenal insufficiency (OIAI) is unclear. Objective To determine the prevalence of OIAI and to identify predictors for the development of OIAI in patients taking opioids for chronic pain. Design Cross-sectional study, 2016-2018. Setting Referral center. Patients Adult patients taking chronic opioids admitted to the Pain Rehabilitation Center. Main outcome measure Diagnosis of OIAI was considered if positive case detection (cortisol < 10 mcg/dL, ACTH < 15 pg/mL, and dehydroepiandrosterone sulfate < 25 mcg/dL), and confirmed after endocrine evaluation. Daily morphine milligram equivalent (MME) was calculated. Results In 102 patients (median age, 53 years [range, 22-83], 67% women), median daily MME was 60 mg (3-840), and median opioid therapy duration was 60 months (3-360). Abnormal case detection testing was found in 11 (10.8%) patients, and diagnosis of OIAI was made in 9 (9%). Patients with OIAI were on a higher daily MME (median, 140 [20-392] mg vs 57 [3-840] mg, P = 0.1), and demonstrated a 4 times higher cumulative opioid exposure (median of 13,440 vs 3120 mg*months, P = 0.03). No patient taking <MME of 20 mg/day developed OIAI (sensitivity of 100% for MME > 20 mg); however, specificity of MME cutoff >20 mg was only 19%. After opioid discontinuation, 6/7 patients recovered adrenal function. Conclusion The prevalence of OIAI was 9%, with MME cumulative exposure being the only predictor for OIAI development. Patients on MME of 20 mg/day and above should be monitored for OIAI.

scholarly journals Testosterone Use and Adrenal Hemorrhage

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A160-A160
Author(s):  
Moin U Sattar ◽  
Priyanka L Mahali ◽  
Natalia Chamorro-Pareja ◽  
Nisha Suda ◽  
Noah Bloomgarden
Keyword(s):  
Adrenal Insufficiency ◽  
Antiphospholipid Syndrome ◽  
Immunoglobulin Therapy ◽  
Dehydroepiandrosterone Sulfate ◽  
International Normalized Ratio ◽  
Adrenal Hemorrhage ◽  
Critically Ill Patient ◽  
Primary Adrenal Insufficiency ◽  
Intravenous Immunoglobulin Therapy ◽  
History Of

Abstract Background: Testosterone supplementation has been associated with a variety of side effects, such as polycythemia, and can potentially increase the risk of cardiovascular disease. Testosterone use has also been associated with increased thrombotic events, especially in patients with underlying hypercoagulable state. Clinical Case: A 57-year-old man presented with abdominal pain and distention. He had history of previous intramuscular (IM) and oral testosterone use for ten years. For 8 weeks prior to initial presentation, he reported using weekly IM 500mg Testosterone injections. Computed Tomography (CT) of the abdomen and pelvis revealed multiple thrombi of the portal, splenic, superior mesenteric and inferior mesenteric veins. He was started on Warfarin and discharged home. A few weeks later, he presented with similar symptoms with labs now showing an International Normalized Ratio (INR) of 10.2. Repeat CT was significant for presence of bilateral adrenal hemorrhage, measuring 2.9cm on the right and 2.4cm on the left, which were not seen on previous imaging done one week prior. During the hospital course, he was found to be hypotensive with low platelet count so Intravenous Immunoglobulin therapy was initiated for suspected catastrophic antiphospholipid syndrome (CAPS). Morning cortisol was 5.82 ug/dL (6.2–29.0) so this critically-ill patient was started on stress dose hydrocortisone, which was subsequently tapered to physiological dose after clinical improvement. Cosyntropin stimulation test was performed after withholding the prior dose of hydrocortisone. The baseline cortisol was 0.88 ug/dL (6.20–29.00ug/dL), after administration of 250mcg of Cosyntropin 30- and 60-minute cortisol levels were 1.5 ug/dL (4.3–22.4ug/dL) and 1.6 ug/dL (4.3–22.4ug/dL) respectively. Baseline ACTH of 121.0 pg/mL (7.2–63.3pg/mL), consistent with primary adrenal insufficiency. Dehydroepiandrosterone Sulfate (DHEA-S) level was 15.7 ug/dL (80.0–560.0ug/dL). Hypercoagulability workup was significant for the presence of lupus anticoagulant and antibodies positive for heparin induced thrombocytopenia, so patient was diagnosed with Antiphospholipid syndrome. Conclusion: This is a case of hypercoagulability in a patient with history of anabolic steroid misuse who developed extensive intraabdominal venous thrombosis, adrenal hemorrhage, and primary adrenal insufficiency. Adrenal vein thrombosis and hemorrhage can be life threatening sequalae of testosterone misuse and should be considered in the differential for patients with history of testosterone misuse and adrenal insufficiency.

scholarly journals No Postoperative Adrenal Insufficiency in a Patient with Unilateral Cortisol-Secreting Adenomas Treated with Mifepristone before Surgery

2016 ◽  
Vol 9 ◽  
pp. CMED.S39997 ◽  
Author(s):  
Rachel M. Saroka ◽  
Michael P. Kane ◽  
Lawrence Robinson ◽  
Robert S. Busch
Keyword(s):  
Adrenal Gland ◽  
Adrenal Insufficiency ◽  
Hpa Axis ◽  
Reference Range ◽  
Dehydroepiandrosterone Sulfate ◽  
Dexamethasone Suppression Test ◽  
Normal Range ◽  
Free Cortisol ◽  
Suppression Test ◽  
Dexamethasone Suppression

Background Glucocorticoid replacement is commonly required to treat secondary adrenal insufficiency after surgical resection of unilateral cortisol-secreting adrenocortical adenomas. Here, we describe a patient with unilateral cortisol-secreting adenomas in which the preoperative use of mifepristone therapy was associated with recovery of the hypothalamic–pituitary–adrenal (HPA) axis, eliminating the need for postoperative glucocorticoid replacement. Case Presentation A 66-year-old Caucasian man with type 2 diabetes mellitus, hyperlipidemia, hypertension, and obesity was hospitalized for Fournier's gangrene and methicillin-resistant Staphylococcus aureus sepsis. Abdominal computed tomography scan revealed three left adrenal adenomas measuring 1.4, 2.1, and 1.2 cm and an atrophic right adrenal gland. Twenty-four-hour urinary free cortisol level was elevated (237 µg/24 hours, reference range 0–50 µg/24 hours). Hormonal evaluation after resolution of the infection showed an abnormal 8 mg overnight dexamethasone suppression test (cortisol postdexamethasone 14.5 µg/dL), suppressed adrenocorticotropic hormone (ACTH; <5 pg/mL, reference range 7.2–63.3 pg/mL), and low-normal dehydroepiandrosterone sulfate (50.5 µg/dL, male reference range 30.9–295.6 µg/dL). Because of his poor medical condition and uncontrolled diabetes, his Cushing's syndrome was treated with medical therapy before surgery. Mifepristone therapy was started and, within five months, his diabetes was controlled and insulin discontinued. The previously suppressed ACTH increased to above normal range accompanied by an increase in dehydroepiandrosterone sulfate levels, indicating recovery of the HPA axis and atrophic contralateral adrenal gland. The patient received one precautionary intraoperative dose of hydrocortisone and none thereafter. Two days postoperatively, ACTH (843 pg/mL) and cortisol levels (44.8 µg/dL) were significantly elevated, reflecting an appropriate HPA axis response to the stress of surgery, and two weeks postoperatively, ACTH was within normal range and a repeat dexamethasone suppression test was normal. Six months postoperatively, ACTH was within normal limits and cortisol was approaching normal. The patient has exhibited no postoperative signs or symptoms of adrenal insufficiency in 12 months. Conclusion Preoperative mifepristone therapy was associated with apparent recovery of the HPA axis prior to unilateral adrenalectomy in a patient with unilateral adrenal adenomas. Postoperatively, the patient experienced no signs or symptoms of adrenal insufficiency and no glucocorticoid replacement was required.

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