Salivary cortisol levels by tandem mass spectrometry during high dose ACTH stimulation test for adrenal insufficiency in children

Endocrine ◽  
2019 ◽  
Vol 67 (1) ◽  
pp. 190-197 ◽  
Author(s):  
Christina S. Chao ◽  
Run-Zhang Shi ◽  
Rajiv B. Kumar ◽  
Tandy Aye
2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Lara Albert ◽  
Joaquím Profitós ◽  
Jordi Sánchez-Delgado ◽  
Ismael Capel ◽  
José Miguel González-Clemente ◽  
...  

Purpose. The prevalence of adrenal insufficiency (AI) in patients with decompensated liver cirrhosis is unknown. Because these patients have lower levels of cortisol-binding carrier proteins, their total serum cortisol (TSC) correlates poorly with free serum cortisol (FC). Salivary cortisol (SaC) correlates better with FC. We aimed to establish SaC thresholds for AI for the 250 μg intravenous ACTH test and to estimate the prevalence of AI in noncritically ill cirrhotic patients. Methods. We included 39 patients with decompensated cirrhosis, 39 patients with known AI, and 45 healthy volunteers. After subjects fasted ≥8 hours, serum and saliva samples were collected for determinations of TSC and SaC at baseline 0’(T0) and at 30-minute intervals after intravenous administration of 250 μg ACTH [30’(T30), 60’(T60), and 90’(T90)]. Results. Based on the findings in healthy subjects and patients with known AI, we defined AI in cirrhotic patients as SaC-T0< 0.08 μg/dL (2.2 nmol/L), SaC-T60 < 1.43 μg/dl (39.5 nmol/L), or ΔSaC<1 μg/dl (27.6 nmol/L). We compared AI determination in cirrhotic patients with the ACTH test using these SaC thresholds versus established TSC thresholds (TSC-T0< 9 μg/dl [248 nmol/L], TSC-T60 < 18 μg/dl [497 nmol/L], or ΔTSC<9 μg/dl [248 nmol/L]). SaC correlated well with TSC. The prevalence of AI in cirrhotic patients was higher when determined by TSC (48.7%) than by SaC (30.8%); however, this difference did not reach statistical significance. AI was associated with sex, cirrhosis etiology, and Child-Pugh classification. Conclusions. Measuring SaC was more accurate than TSC in the ACTH stimulation test. Measuring TSC overestimated the prevalence of AI in noncritically ill cirrhotic patients.


Author(s):  
Didem Turgut ◽  
Serhan Vahit Pişkinpaşa ◽  
Havva Keskin ◽  
Kemal Agbaht ◽  
Ezgi Coşkun Yenigün

Objective: Systemic amyloidosis may affect many organs, and may cause endocrinologic problems which may result in adrenal insufficiency. However, assessment of adrenocortical reserve is challenging in amyloidosis patients with renal involvement. We aimed to evaluate adrenocortical reserve with various methods of cortisol measurement to determine any occult clinical condition. Methods: Patients with renal amyloidosis and healthy subjects were evaluated in this cross-sectional study. Basal cortisol, corticosteroid-binding globulin (CBG), and albumin levels were measured. Serum free cortisol (cFC) level was calculated. Cortisol response tests performed after ACTH stimulation test (250 μg, intravenously) were evaluated, and free cortisol index (FCI) was calculated. Results: Twenty renal amyloidosis patients, and 25 healthy control subjects were included in the study. Patients and control subjects had similar median serum baseline cortisol levels [258 (126-423) vs 350 (314-391) nmol/L, p=0.169)] whereas patients’ stimulated cortisol levels at the 60th minute were lower [624 (497-685) vs 743 (674-781) nmol/L, p=0.011)]. The 60th-minute total cortisol levels of 8 of the 20 (40%) amyloidosis patients were <500 nmol/L, but only three of these 8 patients had stimulated FCI <12 nmol/mg suggesting an adrenal insufficiency (15%). Conclusion: ACTH stimulation test and cortisol measurements should be considered in renal amyloidosis patients with severe proteinuria to avoid false positive results if only ACTH stimulation test is used. It will be appropriate to evaluate this group of patients together with estimated measurements as FCI.


Author(s):  
Ahmet Bahadir Ergin ◽  
Amir H. Hamrahian ◽  
A. Laurence Kennedy ◽  
Manjula K. Gupta

Author(s):  
Ahmet Bahadir Ergin ◽  
Amir H. Hamrahian ◽  
A. Laurence Kennedy ◽  
Manjula K. Gupta

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Muhammad Atique Alam Khan ◽  
Iqra Iqbal ◽  
Puneet Dhillon ◽  
Waqas Ullah

Abstract Introduction: Tumor cells often express a programmed death-ligand 1 (PD-L1), which binds to the programmed death receptor-1 (PD-1) on activated T-cells to induce immune tolerance. Among the class of immune checkpoint inhibitors (ICI), Nivolumab is an anti-PD-1 antibody which blocks these tumor cell interactions. Although some endocrinopathies have been reported for other PD-1 inhibitors, the adverse event of adrenalitis with nivolumab has not been reported before. Clinical Case: A 65-year-old female presented to the hospital with complaints of nausea, vomiting, fatigue, and headache for five days. She was recently diagnosed with metastatic lung adenocarcinoma, complicated by cerebellar metastases, and the left cerebellar mass was resected. She was also started on Nivolumab. Her blood pressure was 98/65 mmHg on the presentation. Serum sodium was 122mEq/L (normal 135–145) and potassium was 5mEq/L (3.5–5). TSH, LH, and prolactin were all normal. Aldosterone was low: 23pmol/L (27.7–582.5) and renin was high: 11 ng/ml/h (0.167- 1.38). Morning cortisol levels were low: 2.2 ug/dl (5- 25) and concomitant ACTH was high: 78 pg/ml (7.2- 63.3). Upon standard high dose cosyntropin stimulation test, basal cortisol was 2.0 ug/dl (5- 25). Cortisol level 30 minutes post cosyntropin was 7.1 ug/dl, while Cortisol 60 minutes post cosyntropin was 12.2 ug/dl (normal &gt;18 -20 ug/dl). Considering the low cortisol levels with high ACTH, and an inadequate rise in cortisol after the ACTH stimulation test, adrenal insufficiency was suspected as a result of adrenalitis due to Nivolumab. Hyponatremia along with low aldosterone and high renin levels also reinforced this clinical diagnosis. A computerized tomographic scan of the chest abdomen and pelvis only showed calcified uterine fibroids. She was initially resuscitated with intravenous fluids. Hydrocortisone 100 mg every 8 hours was started and then gradually tapered down to 60mg every 12 hours. Fludrocortisone was also initiated at 0.2mg daily. Symptoms began to improve, and sodium levels normalized to136 mEq/dl. She was discharged on 30mg of hydrocortisone and 0.1 mg of fludrocortisone daily and is stable since then. Conclusion: This is a rare case of Nivolumab-induced adrenalitis. It highlights the importance of checking for adrenal insufficiency in a patient who presents with symptoms of hypotension and hyponatremia while being on ICI drugs, as unidentified adrenal insufficiency and adrenal crisis can be fatal.


2018 ◽  
Vol 31 (4) ◽  
pp. 429-433 ◽  
Author(s):  
Ryan J. McDonough ◽  
Patria Alba ◽  
Kavitha Dileepan ◽  
Joseph T. Cernich

AbstractBackground:The High Dose Adrenocorticotropic Hormone (ACTH) Stimulation Test is the gold standard to diagnose adrenal insufficiency. Normal adrenal function is defined as a peak cortisol response to pharmacologic stimulation with cosyntropin of ≥18 μg/dL. Our practice was to obtain cortisol levels at 0, 30 and 60 min after cosyntropin administration. Once a value of ≥18 μg/dL has been obtained, adrenal insufficiency is ruled out and there is little diagnostic utility in subsequent stimulated levels.Methods:We aimed to decrease laboratory utilization by developing a results-based algorithm in the electronic medical record (EMR). Cortisol levels were analyzed on the 0 and 60 min samples; then an EMR discern rule automatically generated an order to analyze the 30-min sample if the 60-min cortisol level was subnormal.Results:Exclusion of adrenal insufficiency was excluded using one stimulated cortisol level in 8% prior to algorithm development. After several plan-do-study-act cycles, 99% of normal tests were performed using only one stimulated cortisol level.Conclusions:This laboratory-based algorithm resulted in reduced laboratory utilization, and aligned our practice to recommendations of the Pediatric Endocrine Society. Similar algorithms could be created for other dynamic tests to reduce unnecessary laboratory utilization.


2016 ◽  
Vol 64 (2) ◽  
pp. S266-S267
Author(s):  
J. Profitós ◽  
L. Albert ◽  
O. Giménez-Palop ◽  
M. Vergara ◽  
B. Dalmau ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document