Dexamethasone Suppression Test Research Articles

Establishing BMI-Related thresholds for the 1 mg dexamethasone suppression test: a retrospective analysis

Establishing BMI-Related thresholds for the 1 mg dexamethasone suppression test: a retrospective analysis

The 1-mg overnight low-dose dexamethasone suppression test cut-off in establishing the diagnosis of Cushing's syndrome

The 1-mg overnight low-dose dexamethasone suppression test cut-off in establishing the diagnosis of Cushing's syndrome

Relationship Between Dexamethasone Suppression Test Cortisol Level > 0.9 μg/dL and Depression and Quality of Life in Adrenal Incidentalomas: Single Centre Observational Case-Control Study Depression and Quality of Life in Adrenal Incidentalomas

There has been increasing evidence that patients with adrenal incidentalomas (AI) who have 1 mg dexamethasone suppression test (DST) cortisol levels >0.9 μg/dL may be exposed to the adverse consequences of hypercortisolaemia. We aim to evaluate whether there is a difference in Beck depression inventory-II (BDI-II) and quality of life (QoL) score in AI patients based on the threshold of a DST cortisol level >0.9 μg/dL. This case-control study included 42 non-functional AI (NFAI), 53 mild autonomic cortisol secretion (MACS) and 42 healthy controls (HCs). In addition, patients were categorized as ≤0.9 and >0.9 μg/dL according to their DST cortisol results. There was no difference in the QoL and BDI-II scores of MACS compared to NFAI. The BDI-II score was higher and QoL was lower in MACS and NFAI compared to HCs. The difference in QoL and BDI-II scores between MACS and NFAI remained insignificant when the DST cortisol levels threshold was graded upwards (5.0 μg/dL). The prevalence of depression was higher in the AI >0.9 μg/dL group than the AI ≤0.9 μg/dL group (respectively, 16.7% and 55.8%, p=0.003), BDI-II scores were higher in the AI >0.9 μg/dL group than in the AI ≤0.9 μg/dL group and HCs. The DST was an independent factor affecting the frequency of depression (odds ratio: 1.39, p=0.037). MACS and NFAI patients had similar QoL and depression scores according to the 1.8 μg/dL and above, whereas, had lower QoL and higher depression scores according to the 0.9 μg/dL.

The influence of cortisol co-secretion on clinical characteristics and postoperative outcomes in unilateral primary aldosteronism.

The prevalence of unilateral primary aldosteronism (UPA) with cortisol co-secretion varies geographically. To investigate the prevalence and clinical characteristics of UPA with cortisol co-secretion in a Chinese population. Retrospective cohort study. We recruited 580 patients with UPA who underwent cosyntropin stimulation test (CST) after the 1-mg dexamethasone suppression test (DST) and retrospectively analyzed the clinical characteristics and postoperative outcomes of UPA with and without cortisol co-secretion. UPA with cortisol co-secretion (1 mg DST>1.8 ug/dL) was identified in 65 of 580 (11.2%) patients. These patients were characterized by older age, longer duration of hypertension, higher concentration of plasma aldosterone and midnight cortisol, lower adrenocorticotropic hormone (ACTH) and dehydroepiandrosterone sulfate (DHEAS), larger tumor diameter, and more history of diabetes mellitus. Cortisol and aldosterone levels were higher and DHEAS level was lower in UPA with cortisol co-secretion at 0-120 min after CST. Among 342 UPA patients with KCNJ5 gene sequencing and follow-up results, the complete clinical success rate was lower in UPA with cortisol co-secretion (33.3% vs. 56.4%, P<0.05); the complete biochemical success rate and KCNJ5 mutation did not differ between the two groups. Age, tumor size, and ACTH were independent predictors of UPA with cortisol co-secretion. Sex, BMI, duration of hypertension, KCNJ5 mutation, and cortisol co-secretion were independent predictors for complete clinical success in UPA after surgery. UPA with cortisol co-secretion is not uncommon in China, but the clinical features were distinctly different from those without co-secretion. Cortisol co-secretion is an independent risk factor for incomplete clinical success after surgery in UPA.

Mild autonomous cortisol secretion: pathophysiology, comorbidities and management approaches.

The majority of incidentally discovered adrenal tumours are benign adrenocortical adenomas and the prevalence of adrenocortical adenomas is around 1-7% on cross-sectional abdominal imaging. These can be non-functioning adrenal tumours or they can be associated with autonomous cortisol secretion on a spectrum that ranges from rare clinically overt adrenal Cushing syndrome to the much more prevalent mild autonomous cortisol secretion (MACS) without signs of Cushing syndrome. MACS is diagnosed (based on an abnormal overnight dexamethasone suppression test) in 20-50% of patients with adrenal adenomas. MACS is associated with cardiovascular morbidity, frailty, fragility fractures, decreased quality of life and increased mortality. Management of MACS should be individualized based on patient characteristics and includes adrenalectomy or conservative follow-up with treatment of associated comorbidities. Identifying patients with MACS who are most likely to benefit from adrenalectomy is challenging, as adrenalectomy results in improvement of cardiovascular morbidity in some, but not all, patients with MACS. Of note, diagnosis and management of patients with bilateral MACS is especially challenging. Current gaps in MACS clinical practice include a lack of specific biomarkers diagnostic of MACS-related health outcomes and a paucity of clinical trials demonstrating the efficacy of adrenalectomy on comorbidities associated with MACS. In addition, little evidence exists to demonstrate the efficacy and safety of long-term medical therapy in patients with MACS.

Association between full blood count and urine steroid metabolome in patients with adrenal masses

Background: Endogenous hypercortisolism of adrenal origin is commonly associated with immune suppression. However, these patients also have signs characteristic of chronic inflammatory diseases. Better understanding of the mechanisms that alter the functioning of the immune system would allow for the development of a patient-centered approach to the treatment of corticotropin-independent endogenous Cushing's syndrome (CS).&#x0D; Aim: To assess the association between full blood count and gas chromatography-mass spectrometry-based urinary steroid excretion in patients with adrenal masses depending on malignancy grade and presence of hypercortisolism.&#x0D; Materials and methods: We retrospectively analyzed data from 42 patients with adrenal masses who had not received chemotherapy. The median age of the patients was 54 [Q25; Q75: 37; 63] years, and 76% of them were female. Preoperatively, all patients had hematology tests with differential leukocyte count. Steroid metabolome was assessed with Shimadzu GCMS-TQ8050 gas chromatography-mass spectrometer.&#x0D; Results: Twelve (12) patients had adrenocortical cancer (ACC) and CS, 9 patients had ACC without CS, 11 had adrenocortical adenomas (ACA) and CS, and 10 patients had ACA without CS. ACC patients had a higher neutrophil-to-lymphocyte ratio (NLR) than those with ACA: 3.35 [2.5; 6.3] vs 1.99 [1.41; 2.65] (р = 0.001). There was a linear correlation between NLR and serum cortisol levels after the 1 mg overnight dexamethasone suppression test (r = 0.41, p = 0.01), urinary excretion of 5β-tetrahydrocortisol (5β-THF) (r = 0.71, p 0.001) and 11β-hydroxyandrosterone (11β-OH-An) (r = 0.74, p 0.001). The ACC patients without CS had lower 5β-THF urinary excretion values, compared to ACA with CS patients: 931 [616; 1610] and 3139 [1480; 4375] mcg/24h, respectively (р = 0.007). 11β-OH-An urinary excretion in ACC patients without CS was higher than in ACA patients with CS: 1170 [806; 1266] и 602 [320; 739] mcg/24h (р = 0.007). The NLR cut-off value for adrenal mass malignancy in patients with CS exceeded 2.72 (sensitivity 90.0%, specificity 80.0%), and for the patients without hypercortisolism was above 1.92 (sensitivity 71.4%, specificity 100.0%).&#x0D; Conclusion: This is the first association identification between NLR, which is the marker of systemic inflammation, inflammation, and urinary excretion of 11β-OH-An, a metabolite of 11-hydroxyandrostenedione (a member of 11-oxygenated androgen family). This extends our understanding of the impact of hormonal activity of adrenal mass cells on the immune system.

[Clinical characteristics and prognosis of primary aldosteronism associated with subclinical Cushing syndrome].

Objective: To analyze the clinical characteristics and prognosis of patients with primary aldosteronism (PA) associated with subclinical Cushing syndrome (SCS). Methods: This retrospective cohort study was conducted at the First Affiliated Hospital of Chongqing Medical University in China. Patients with PA were included between January 2014 and December 2022. According to the results of 1-mg overnight dexamethasone suppression test, the patients were divided into the PA group and PA associated with SCS (PA/SCS) group. The demographic information, hormone levels, and follow-up results were analyzed. Independent sample t-test, chi-square test and Mann-Whitney U test were used for data comparison. Results: A total of 489 PA patients were enrolled in this study, of which 109 had PA/SCS (22.3%). Patients with SCS were on average older (54.4±10.7 vs. 47.4±11.0, P<0.001); had a larger proportion of women (69.7%, 76/109 vs. 57.4%, 218/380; P=0.020); and a longer duration of hypertension [96 (36, 180) vs. 60 (12, 120) months, P=0.001] than patients without SCS. There were 215 and 51 patients in the PA group and PA/SCS group, who completed adrenalectomy and follow-up, respectively. The remission rate of autonomous cortisol secretion in the PA/SCS group was 85.3% (29/34). There was no significant difference in the remission rate of autonomous aldosterone secretion among patients between the PA/SCS and PA group (94.1%, 48/51 vs. 94.4%, 203/215; P=1.000), while the clinical remission rate in the PA/SCS group was lower than that in the PA group (39.2%, 20/51 vs. 61.9%, 133/215; P=0.003). Conclusions: SCS is common in PA patients (22.3%), and the clinical remission rate is low. Screening using the 1-mg overnight dexamethasone suppression test is recommended for all patients with PA.

Development of diagnostic algorithm for Cushing's syndrome: a tertiary centre experience.

No consensus exists as the gold standard for Cushing's Syndrome (CS) screening. This study aimed to evaluate the diagnostic accuracy and utility of late-night salivary cortisol (LNSC) and cortisone (LNSE), overnight dexamethasone suppression test (ODST), and urinary free cortisol (UFC) in developing a screening algorithm for CS. A retrospective, single-centre analysis on 93 adult patients referred to the Oxford Centre for Diabetes, Endocrinology, and Metabolism for CS evaluation (2017-2022). Data were analysed using binomial logistic regression and area under the receiver-operating curve (AUROC). Fifty-three patients were diagnosed with CS. LNSC (sensitivity 87.5%, specificity 64.9%, AUC 0.76), LNSE (sensitivity 72.4%, specificity 85.7%, AUC 0.79), and ODST (sensitivity 94.7%, specificity 52.1%; AUC 0.74) demonstrated comparable effectiveness for CS diagnosis. Their combined application increased diagnostic accuracy (AUC 0.91). UFC was not statistically significant. Pre-test clinical symptom inclusion improved screening test performance (AUC LNSC: 0.83; LNSE: 0.84; ODST: 0.82). For CD diagnosis, LNSE + LNSC (AUC 0.95) outperformed ODST. Combining these with ACTH levels < 12.6pmol/L perfectly distinguished MACS (AUC 1.00). ODST (AUC 0.76) exhibited superior performance (sensitivity 100.0%, specificity 52.2%) in MACS detection. LNSC, LNSE, and ODST are robust tools for CS screening, with their combined use offering the highest diagnostic precision. LNSE, especially when used with LNSC, is highly effective for CD diagnosis, exceeding ODST accuracy. ODST is preferable for MACS identification. Integrating ACTH levels markedly improves differentiation between CD and MACS. Conversely, UFC shows limited diagnostic utility.

Machine Learning May Be An Alternative To BIPSS In The Differential Diagnosis Of ACTH-Dependent Cushing's Syndrome.

This study aimed to develop machine learning (ML) algorithms for the differential diagnosis of adrenocorticotropic hormone (ACTH)-dependent Cushing's syndrome (CS) based on biochemical and radiological features. Logistic regression algorithms were used for ML, and the area under the receiver operating characteristics curve (AUROC) was used to measure performance. We used Shapley Contributed Comments (SHAP) values, which help explain the results of the ML models to identify the meaning of each feature and facilitate interpretation. A total of 106 patients, 80 with Cushing's disease (CD) and 26 with ectopic ACTH syndrome (EAS), were enrolled in the study. The ML task was created to classify patients with ACTH-dependent CS into CD and EAS. The average AUROC value obtained in the cross-validation of the logistic regression model created for the classification task was 0.850. The diagnostic accuracy of the algorithm was 86%. The SHAP values indicated that the most important determinants for the model were the 2-day 2-mg dexamethasone suppression test, the > 50% suppression in the 8-mg high-dose dexamethasone test, late-night salivary cortisol, and the diameter of the pituitary adenoma. We have also made our algorithm available to all clinicians via a user-friendly interface. ML algorithms have the potential to serve as an alternative decision support tool to invasive procedures in the differential diagnosis of ACTH-dependent CS.

The Spectrum of Dysregulated Aldosterone Production: An International Human Physiology Study.

Primary aldosteronism is a form of low-renin hypertension characterized by dysregulated aldosterone production. To investigate the contributions of renin-independent aldosteronism, and ACTH-mediated aldosteronism, in individuals with a low-renin phenotype representing the entire continuum of blood pressure.‏. Human physiology study of 348 participants with a low-renin phenotype with severe and/or resistant hypertension, hypertension with hypokalemia, elevated blood pressure and stage I/II hypertension, and normal blood pressure. 4 international centers.‏. Saline suppression test (SST) to quantify the magnitude of renin-independent aldosteronism; dexamethasone suppression and ACTH-stimulation tests to quantify the magnitude of ACTH-mediated aldosteronism; adrenal venous sampling to determine lateralization. There was a continuum of non-suppressible and renin-independent aldosterone production following SST that paralleled the magnitude of the blood pressure continuum and transcended conventional diagnostic thresholds. In parallel, there was a full continuum of ACTH-mediated aldosteronism wherein post-SST aldosterone levels were strongly correlated with ACTH-stimulated aldosterone production (r = 0.75, P < 0.0001) and non-suppressible aldosterone production post-dexamethasone (r = 0.40, P < 0.0001). Beyond participants who met criteria for primary aldosteronism (post-SST aldosterone of ≥10 ng/dL or ≥277 pmol/L), the continuum of non-suppressible and renin-independent aldosterone production persisted below this diagnostic threshold, wherein 15% still had lateralizing aldosteronism amenable to surgical adrenalectomy, and the remainder were treated with mineralocorticoid receptor antagonists. In the context of a low-renin phenotype, there is a continuum of dysregulated aldosterone production that is prominently influenced by ACTH. A large proportion of individuals with low-renin have dysregulated aldosterone production and may benefit from aldosterone-directed therapy.

Hypothalamic-pituitary-adrenal axis hyperactivity is normalized after successful intermittent theta-burst stimulation in resistant depressed patients

The present pilot study assessed the effects of multi-session intermittent theta-burst stimulation (iTBS) applied to the left dorsolateral prefrontal cortex in 17 treatment resistant depressed inpatients (TRDs) showing cortisol non-suppression to the overnight dexamethasone suppression test (DST) at baseline (i.e., maximum post-DST cortisol [CORmax] level > 130 nmol/L). After 20 iTBS sessions, the DST was repeated in all TRDs. At baseline, post-DST CORmax levels were higher in TRDs compared to healthy control subjects (HCs; n = 17) (p < 0.0001). After 20 iTBS sessions, post-DST CORmax levels decreased from baseline (p < 0.03) and were comparable to HCs. Decreases in post-DST CORmax levels were related to decreases in 17-item Hamilton Depression Rating Scale (HAMD-17) scores (ρ = 0.53; p < 0.03). At endpoint, 10 TRDs showed DST normalization (among them 7 were responders [i.e., HAMD-17 total score > 50% decrease from baseline]), and 7 did not normalize their DST (among them 6 were non-responders) (p < 0.05). Our results suggest that successful iTBS treatment may restore normal glucocorticoid receptor feedback inhibition at the pituitary level.

Retrospective Study on Trilostane Titration Dose Treatment in Dogs with Terminal Stage of Hyperadrenocorticism

Abstract Hyperadrenocorticism (HAC) in dogs is routinely treated with trilostane single-dose (CTG) which is reported to cause adverse reactions. The current retrospective study of several dogs with terminal stage of HAC aimed to compare the clinical, hematological, and biochemical effects of trilostane titration-dose treatment (TTG) with the single-dose treatment (CTG). All clinical cases (n=7) were confirmed on HAC by anamnestic, clinical, hematology, biochemistry, and low-dose dexamethasone suppression test findings, indicative for Cushing’s disease. Two cases were treated with CTG (2.2-6.7 mg/kg, single dose daily) and their treatment was discontinued on the second week due to adverse reactions. The TTG cases were treated for up to 12 weeks (0.5 mg/kg once daily for 7 days, and then with 0.5 mg/kg twice daily for 7 days). Blood samples and clinical checks were performed on 0., 4., and 12. weeks of the treatment. Hemoglobin was non-significantly higher in TTG at 12 weeks. Alanine transaminase was significantly lower in the TTG cases on the 12. week of the treatment (78.04±15.37 U/L) compared to the 0-week (137.81±24.03 U/L), and 4-week samples (131.92±23.36 U/L). No significant differences were observed with the CTG cases. Alkaline phosphatase was significantly lower on 12-week samples in TTG (251.02±93.06) compared to the 4-week (567.94±283.93 U/L), and 0-week samples (1,341.84 U/L). In conclusion, TTG has indicated to have significantly higher tendency to decrease alanine transaminase and alkaline phosphatase, alleviating the negative effects on the liver. The clinical findings were more adverse for the CTG.

Predicting postoperative hypocortisolism in patients with non-aldosterone-producing adrenocortical adenoma: a retrospective single-centre study.

Limited information exists on postoperative hypocortisolism and hypothalamus-pituitary-adrenal axis recovery in patients with adrenal incidentaloma following unilateral adrenalectomy. We evaluated frequency of postoperative hypocortisolism and predictors for recovery in non-aldosterone-producing adrenocortical adenoma patients after unilateral adrenalectomy. A retrospective analysis of 32 adrenal incidentaloma patients originally included in the ITACA trial (NCT04127552) with confirmed non-aldosterone-producing adrenocortical adenoma undergoing unilateral adrenalectomy from September 2019 to April 2023 was conducted. Preoperative assessments included adrenal MRI, anthropometrics, evaluation of comorbidities, adrenal function assessed via ACTH, urinary free cortisol, and 1mg dexamethasone suppression test. ACTH and serum cortisol or Short Synacthen test were performed within 6days, 6 weeks, 6 months, and a year after surgery. Six days postoperative, 18.8% of patients had normal adrenal function. Among those with postoperative hypocortisolism, 53.8% recovered by 6 weeks. Patients with earlier adrenal recovery (6 weeks) had lower preoperative 1mg dexamethasone suppression test (median 1mg dexamethasone suppression test 76.2 [61.8-111.0] nmol/L vs 260.0 [113.0-288.5] nmol/L, p < 0.001). Univariate analysis showed preoperative 1mg dexamethasone suppression test negatively related with baseline ACTH levels (r = -0.376; p = 0.041) and negatively associated with the 6-week baseline (r = -0.395, p = 0.034) and 30-min cortisol levels during Short Synacthen test (r = -0.534, p = 0.023). Logistic regression analysis demonstrated preoperative 1mg dexamethasone suppression test as the only biochemical predictor for 6-week adrenal recovery: ROC curve identified a 1mg dexamethasone suppression test threshold of 131nmol/L predicting 6-week recovery with 89.5% sensitivity and 72.7% specificity (AUC 0.87; 95% CI 66.9-98.7, p < 0.001). Other preoperative assessments (tumor size, ACTH levels and anthropometrics) were not associated with postoperative hypothalamus-pituitary-adrenal axis function, but the presence of diabetes was associated with a lower probability of recovery (OR = 24.55, p = 0.036). ACTH levels increased postoperatively in all patients but did not predict hypothalamus-pituitary-adrenal axis recovery. The preoperative 1mg dexamethasone suppression test cortisol value and presence of diabetes are the only relevant predictor of hypothalamus-pituitary-adrenal axis recovery in patients with non-aldosterone- producing adrenocortical adenoma undergoing surgery, regardless other clinical and biochemical variables. Notably, pre- and postoperative ACTH levels did not predict hypothalamus-pituitary-adrenal axis recovery. These findings point towards the potential for saving resources by optimizing their allocation during follow-up assessments for patients with non-aldosterone-producing adrenocortical adenoma undergoing unilateral adrenalectomy.

Autoimmune Disorders Associated With Surgical Remission of Cushing's Disease : A Cohort Study.

Glucocorticoids suppress inflammation. Autoimmune disease may occur after remission of Cushing's disease (CD). However, the development of autoimmune disease in this context is not well described. To determine 1) the incidence of autoimmune disease in patients with CD after surgical remission compared with patients with nonfunctioning pituitary adenomas (NFPAs) and 2) the clinical presentation of and risk factors for development of autoimmune disease in CD after remission. Retrospective matched cohort analysis. Academic medical center/pituitary center. Patients with CD with surgical remission and surgically treated NFPA. Cumulative incidence of new-onset autoimmune disease at 3 years after surgery. Assessment for hypercortisolemia included late-night salivary cortisol levels, 24-hour urine free cortisol (UFC) ratio (UFC value divided by the upper limit of the normal range for the assay), and dexamethasone suppression tests. Cumulative incidence of new-onset autoimmune disease at 3 years after surgery was higher in patients with CD (10.4% [95% CI, 5.7% to 15.1%]) than in those with NFPAs (1.6% [CI, 0% to 4.6%]) (hazard ratio, 7.80 [CI, 2.88 to 21.10]). Patients with CD showed higher prevalence of postoperative adrenal insufficiency (93.8% vs. 16.5%) and lower postoperative nadir serum cortisol levels (63.8 vs. 282.3 nmol/L) than patients with NFPAs. Compared with patients with CD without autoimmune disease, those who developed autoimmune disease had a lower preoperative 24-hour UFC ratio (2.7 vs. 6.3) and a higher prevalence of family history of autoimmune disease (41.2% vs. 20.9%). The small sample of patients with autoimmune disease limited identification of independent risk factors. Patients achieving surgical remission of CD have higher incidence of autoimmune disease than age- and sex-matched patients with NFPAs. Family history of autoimmune disease is a potential risk factor. Adrenal insufficiency may be a trigger. Recordati Rare Diseases Inc.

An Overlooked Disease: Minimal Autonomous Cortisol Secretion (MACS). A Narrative Review.

A far more common disease than Cushing's syndrome is subclinical hypercortisolism or mild autonomous cortisol secretion (MACS), with an overall prevalence of 0.2-2%. This review aims to shed light on the prevalence, screening and diagnostic criteria, comorbidities, and management of Mild Autonomous Cortisol Secretion (MACS). Studies eligible targeted MACS regarding prevalence, screening, comorbidities, management, and clinical outcome. This is a mini-review. IRB approval was not needed. The 1 mg Dexamethasone suppression test (DST) remains the first screening test. MACS is associated with adverse cardiometabolic and renal outcomes, osteoporosis and osteopenia, immunodeficiency, depression, coagulopathy, and sarcopenia. Surgery is the gold standard treatment. Medical therapy is recommended when surgery is contraindicated or not feasible. Clinically silent hypercortisolism is a frequent entity that necessitates early detection and treatment. The production of cortisol should be looked at as a spectrum where subtle, undetectable levels can still be produced. They know its association with adverse health outcomes. MACS is no longer considered an asymptomatic disorder; repeated hormonal and functional tests are crucial to prevent multiorgan damage.

Cortisol dynamics, quality of life and fatigue following traumatic brain injury in childhood.

Traumatic brain injury (TBI) is a leading cause of acquired neurological morbidity. The prevalence of post-traumatic hypopituitarism (PTHP) and associated morbidity after childhood TBI is unclear. Our study investigated long term HPA (hypothalamus-pituitary-adrenal) axis function, in a prospective childhood TBI and control cohort, using measures of cortisol/cortisone secretion (physiological, stimulated), HPA axis feedback and exploring associations with fatigue, depression and Quality of Life (QoL) outcomes. All TBI participants had data concerning severity and mechanism of TBI. All groups had clinical assessment, pituitary/brain MRI, questionnaire measures of QoL, fatigue, depression and salivary cortisone profiles including dexamethasone suppression test. In addition participants with Moderate/Severe TBI had ethical approval for baseline endocrine blood tests, overnight 12-hour venous sampling of cortisol and growth hormone, and stimulated HPA axis evaluation with an insulin tolerance test (ITT). Seventy-two participants with moderate/severe (n=31, age 19.8±4.2 years) or mild TBI (n=24, age 17.8±5.1 years) and matched controls (n=17, age 18.5±5.5 years) took part. Time post TBI was 6.8-10.8 years. Baseline endocrine tests confirmed normal thyroid and posterior pituitary function. One female with moderate/severe TBI had hypogonadism. Pituitary neuroimaging was normal in all participants. In 2/25 ITT and 9/22 overnight serum profiles peak cortisol was <500nmol/l. The two participants with suboptimal ITT cortisol response (392 and 483nmol/L) also had low peak spontaneous serum levels (227 and 447nmol/L respectively). Salivary cortisone profiles showed preservation of HPA axis circadian rhythm and suppression with dexamethasone in all but one TBI participant. TBI participants had higher morning salivary cortisone levels compared to controls. Fatigue was reported by 20/46 TBI participants but only 1/14 controls. Fatigue was not associated with stimulated (ITT) or spontaneous (overnight profile) cortisol, however one TBI participant with severe fatigue had a suboptimal ITT cortisol response. Specific QoL attributes of health state (cognition, memory) were impaired in TBI participants compared to controls. Although not as prevalent as previously reported, HPA axis dysfunction does occur in survivors of childhood TBI confirming the need for endocrine surveillance. However, in most of our paediatric TBI survivors assessed 7-11 years post-TBI, HPA function and circadian rhythmicity was preserved or had recovered. Chronic fatigue is a common concern post TBI but in the majority not associated with frank HPA axis dysfunction. Morning salivary cortisone levels were higher in TBI survivors, (who have a high prevalence of fatigue) compared to healthy controls, despite the recognised association of chronic fatigue with cortisol hyposecretion.

Assessment of plasma dexamethasone levels after 1-mg dexamethasone suppression test in adults with obesity.

The 1-mg overnight dexamethasone suppression test is the most frequently used screening test for Cushing's syndrome. It has been proposed that people with obesity may have insufficient plasma dexamethasone levels for the test which may result in false positives. We sought to compare the plasma dexamethasone levels after 1-mg dexamethasone suppression test in healthy obese participants and in optimal-weight participants. A total of 30 optimal-weight participants (BMI ≤ 25 kg/m2 ) and 62 obese participants (BMI > 25 kg/m2 ) were enroled in the study. Obese participants were further divided into class 1 (25-29.9 kg/m2 ) and class 2 (>30 kg/m2 ). After a standard overnight 1-mg dexamethasone suppression test, blood samples were obtained for serum cortisol and plasma dexamethasone levels. Plasma dexamethasone levels were quantified using liquid chromatography - mass spectrometry (LC-MS/MS). No significant difference in plasma dexamethasone levels were found between obese and optimal-weight participants (3.31 ± 1.35 vs. 2.82 ± 1.11 nmol/L, mean ± SD; p = .09 respectively). There were also no correlations found between sex, BMI, body surface area and plasma dexamethasone levels. There was also no significant difference in the proportion of participants who achieved a plasma dexamethasone level >3.3 nmol/L in comparison between obesity class 1, obesity class 2, and optimal-weight groups. Our results suggest that obesity does not affect plasma dexamethasone levels. However, dexamethasone measurement may still be helpful in patients who are being investigated for Cushing's syndrome and suspected to have a false-positive DST.

The Overnight Low-Dose Dexamethasone Suppression Test Can Be Used to Evaluate Patients With Chronic Kidney Disease.

The Overnight Low-Dose Dexamethasone Suppression Test Can Be Used to Evaluate Patients With Chronic Kidney Disease.

Retroperitoneal synovial sarcoma

Synovial sarcoma of the retroperitoneum is a rare and aggressive tumor. In some cases, differential diagnosis between retroperitoneal sarcoma and adrenocortical cancer is difficult due to the similar clinical and intrascopic manifestations of these neoplasms. The final diagnosis is established based on the results of histological, immunohistochemical and genetic studies. The most important step in the treatment of synovial sarcoma is complete removal of the tumor. However, despite the radical nature of the intervention, the incidence of local relapse and metastasis remains high.&#x0D; AIM: to conduct a retrospective analysis of the parameters of operated patients with synovial sarcoma of the retroperitoneum.&#x0D; This study is aimed at studying the results of examination and surgical treatment of patients with synovial sarcoma of the retroperitoneal space who were hospitalized in the E.E. Eichwald Clinic surgical department of the North-Western State Medical University named after. I.I. Mechnikov.&#x0D; The patients were assessed for hormonal status using an immunoassay to determine the levels of adrenocorticotropic hormone, cortisol, aldosterone, renin, normetanephrine and metanephrine in the blood, and a dexamethasone suppression test has been performed at a dose of 1 mg. High-performance liquid chromatography has determined 6 glucocorticoids in the blood serum: cortisol, cortisone, corticosterone, 11-deoxycorticosterone, 11-dehydrocorticosterone, 11-deoxycortisol. The urine steroid profile was studied in all the patients using gas chromatography-mass spectrometry. All the patients underwent computed tomography of the abdominal organs and retroperitoneal space with contrast, morphological and immunohistochemical examination of the removed material. The material was fixed in 10% neutral buffered formalin. The pieces were then subjected to standard wiring followed by embedding in paraffin. Sections 2–3 microns thick were prepared from the resulting blocks and stained with hematoxylin and eosin. Immunohistochemical studies were performed on paraffin sections. A panel of monoclonal antibodies was used: protein S-100 (poly), pancytokeratin (AE1/AE3), EMA, cytokeratin-8, -18, chromogranin A, synaptophysin, α-inhibin, SOX-10, CD99, TLE-1, bcl- 2, GATA-3. Postoperative outcomes and follow-up were assessed according to the information in the medical records and data obtained from a telephone conversation with each patient. Statistical processing of the results has not been out due to rare cases of the disease.

P-62 Silent Corticotroph Adenoma or Cyclic Cushing's Syndrome?

Abstract Introduction Silent corticotroph adenomas (pituitary neuroendocrine tumours (PitNET)) are a rare subset of nonfunctioning adenomas. The higher aggressiveness in terms of invasion and recurrence make these tumors dangerous and close follow-up in experienced centers is recommended. Clinical Case A 21-year-old obeseo (Body Mass Index:31.71) male patient unable to lose weight and complaining of headaches was referred to the Department of Neurosurgery for a pituitary macroadenoma. He had previously used liraglutide treatment Many purple striae were also seen on the body of the patient, who stated that his wounds did not heal easily. Visual acuity and visual field were normal. There was no neurodeficiency. Endocrinological evaluation revealed that the tumor was nonfunctioning (Table 1). Magnetic resonance imaging of the pituitary gland showed a mass lesion in the right side of the pituitary gland extending to the suprasellar and parasellar area (Knosp grade II) (Fig.1). The tumor with soft consistency was totally removed by endoscopic binostril transsphenoidal approach. The postoperative cortisol was 11.53 µg/dl (6.02-18.4) and free T4 was 1.32 ng/dL (0.93-1.7). The patient had a transient diabetes insipidus in the postoperative course, and he was discharged on the 4th day after surgery. Pathological examination revealed a pituitary adenoma immunostaining diffusely with ACTH, other hormones were unexpressed. Ki-67 was %2. Histological invasion of the dura was noted. Although the patient was clinically overweight and had purple striae suggestive of Cushing's syndrome (CS), his cortisol and ACTH levels were normal and suppressible with 1 mg dexamethasone suppression test. However, his tumour tissue showed diffuse ACTH expression, which led to the diagnosis of a silent ACTH adenoma. Since the clinical findings were not completely silent, could we assume that he suffered from cyclic CS? Cyclic (intermittent or periodic) CS is a condition characterised by alternating periods of transiently elevated cortisol levels followed by normal to reduced levels. The diagnosis of cyclic CS requires the presence of at least three confirmed episodes of elevated cortisol levels interspersed with two periods of normal cortisol levels. As we know, the cortisol secretion cycle is unpredictable and laboratory tests during the normal cortisol secretion period of the cyclic CS often show negative results as in our patient. Conclusion Postoperative follow-up of a silent corticotroph PitNET and cyclic CS patient, both of whom require close and life-long monitoring.Figure 1.Magnetic resonance imaging of the pituitary gland; coronal sections T1- weighted (a), T2-weighted (b), sagittal (c), and coronal (d) sections with T1 contrast enhancement. The mass lesion on the right side of the pituitary gland extending superiorly to the right internal carotid artery contains a hemorrhagic fluid component with heterogeneous contrast enhancement, is 16*12*9 mm in size, and corresponds to a hemorrhagic pituitary macroadenoma.  Table 1.Hormonal values at presentationACTH, adrenocorticotropic hormone; DST, dexamethasone suppression test; fT4, free thyroxine; IGF-1, insulin-like growth factor 1; PRL, prolactin; TSH, thyroid-stimulating hormone.