ResearchPad - neuroendocrine-pituitary-pathologies Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[SUN-312 Strikingly Low Prevalence of Pituitary Incidentalomas in Our Hospital]]> Introduction: Pituitary incidentalomas (PIs) have been reported in 10.6% of autopsies, 4-20% in computed tomography scans (CT) and 10-38% in magnetic resonance imaging (MRI), most of them microincidentalomas(<1cm). They may be have autonomous hormonal activity or impair normal gland function. The frequency of PIs in Uruguay is unknown. We aimed to investigate the prevalence of pituitary incidentalomas in our Hospital. Methods: We retrospectively identified all patients who underwent brain CT and MRI at our hospital over a 1-year period for disorders other than known or suspected pituitary disease. The period covered was from January 1 to December 31, 2017. We reviewed all scans; anamnesis and biochemical evaluation was performed on patients who presented PIs. Results: During this period 3894 patients underwent imaging studies. MRI was performed in 1146 patients, and CT in 2748 of them. Mean age was 53,1 ± 19 years, with similar gender distribution (50.6% women). Most imaging studies where ordered in the emergency department (43%), followed by the outpatient clinics (29%) and inpatient wards (28%). Most common reasons that led to request the image were trauma (20.4%), headaches (11.3%) and stroke (10.9%). We detected two PIs, which accounts for a prevalence of 5 cases per 10,000 individuals per year (0.05%). Both where detected by CT, with a MRI done later to further evaluate them. Final diagnosis was of a vascular aneurysm and a sellar meningioma. Work-up showed a secondary hypothyroidism in the patient with the sellar meningioma. No cases of pituitary adenomas were found. Discussion: We observed a strikingly lower prevalence of PIs than that reported in the literature. In addition, no PIs where found in MRI. Moreover, no pituitary adenoma was discovered. The reasons for these findings are unknown. In our study scans were not focused to the pituitary fossa so small lesions may have been missed. However, Esteves et al(1) reported a prevalence of PIs 5.8% in 1232 patients who had head MRI/CT, not pituitary MRI. In addition, the majority were pituitary adenomas, almost 40% of them microadenomas. Slices of 2-mm thickness were obtained in the scans, similar to imaging techniques used in other studies. Most reports have longer study duration (3-5 years).Our hospital is a teaching hospital where fellows evaluate scans initially, which are then reevaluated by neuroradiologists. This may account for the prevalence found, as sensitivity may be lower when professionals in training evaluate scans. In addition, frequency of pituitary hipointensity areas may decrease as the number of reviewers increase. Furthermore, this low prevalence could be related to difference in population characteristics.Conclusions: We found a very low prevalence of PIs in our hospital. More studies are warranted to further investigate frequency of PIs in our country. (1)Esteves et al. Pituitary. 2015;18(6):777-81.

<![CDATA[SUN-307 Partial Secondary Adrenal Insufficiency and Growth Hormone Deficiency in Fibromyalgia]]> Introduction: Low or borderline cortisol concentrations and impaired response to dynamic testing have been reported in patients with fibromyalgia, potentially related to hypothalamus-pituitary dysfunction.1,2 Superimposed adrenal insufficiency (AI) may contribute to some fibromyalgia symptoms or delay improvement in patients enrolled in fibromyalgia treatment programs. We hypothesized that a subset of patients with fibromyalgia have: 1) partial secondary AI and concomitant growth hormone (GH) deficiency 2) a discordance in Cosyntropin stimulation test and 3) improvement in fibromyalgia symptoms with initiation of glucocorticoid and/or GH replacement.

Design: This was a retrospective study of patients with fibromyalgia diagnosed with partial secondary AI based on abnormal insulin tolerance test (peak cortisol < 18 mcg/dL) at our institution from June 2002 to August 2019. Patients were excluded if they had other reasons for adrenal insufficiency, including steroid exposure and opioid use.

Results: We identified 22 patients (18 women, 82%) diagnosed with partial AI at a median age of 38 years (range 19-65). The fibromyalgia symptoms included fatigue (n=22, 100%), pain (n=22, 100%), sleep disturbance (n=15, 68%), and bowel changes (n=13, 59%). The median morning cortisol concentration was 8.6 mcg/dL (range 1.1-11); 9 patients (41%) had a morning cortisol concentration below the normal range (7 mcg/dL). The median ACTH level was 15.5 pg/mL (range 7.7-54). Nineteen patients had baseline IGF1 levels, with a median z-score of -0.94 (range -1.96 to 1.70). MRI pituitary imaging was performed in 20 patients and showed no significant pituitary pathology.

All patients achieved hypoglycemia <=40 mg/dL during the insulin tolerance test. Peak median cortisol level was 11 mcg/dL (range 5.4-17). Nineteen patients (86%) also had partial GH deficiency (defined as a peak GH < 4 ng/mL) with a median GH level of 0.36 ng/mL (range 0.03-3.83). Cosyntropin stimulation test was performed in 13 patients (59%) with a 1 mcg dose in 2 patients and 250 mcg dose in 11 patients. The peak cortisol was >=18 mcg/dL in 10 (77%) patients. All patients were started on physiologic glucocorticoid replacement, and 12 patients were started on GH replacement. Endocrinology follow-up information was available for 13 patients, and 8 (62%) reported symptom improvement after starting treatment.

Conclusions: Patients with fibromyalgia can have co-existing partial secondary AI and GH deficiency as defined by insulin-induced hypoglycemia. Cosyntropin stimulation test can be used in patients with fibromyalgia, but a normal test does not rule out partial secondary AI. Replacing the underlying deficiency improved symptoms in some patients demonstrating certain fibromyalgia symptoms may overlap with AI and GH deficiency.

1Gur et al. Ann Rheum Dis. 2004. 63(11):1504-1506.

2Kirnap et al. Clin Endocrinol (Oxf). 2001. 55(4):455-459.

<![CDATA[SUN-297 Development of a Local Reference Range for Hypertonic Saline-Stimulated Copeptin]]> Differentiating between primary polydipsia and central diabetes insipidus (DI) can be challenging. The water deprivation test has traditionally been used to diagnosis DI, however has poor diagnostic accuracy (1). Direct measurement of anti-diuretic hormone (ADH) is limited clinically. Copeptin is the C-terminal glycoprotein moiety of ADH prohormone, and correlates well with plasma ADH. Unlike ADH, copeptin is easy to measure (2).

Hypertonic saline stimulated copeptin measurements have recently been described for the diagnosis of central DI. A copeptin cut-off of >4.9 pmol/L has a diagnostic accuracy of 96.5% for distinguishing primary polydipsia from central DI (3). A copeptin assay has recently been established in our laboratory. Validation of hypertonic saline-stimulated copeptin concentrations in our local population is needed before this test can be used with confidence in patients presenting to our institution with polyuria-polydipsia syndrome. The aim of this study was to develop a local reference range for hypertonic saline-stimulated copeptin in healthy volunteers.

Twenty healthy volunteers (10 male and 10 female) were recruited. Subjects underwent a hypertonic saline test, as previously described (3). Hypertonic saline (3%) was administered as an initial 250 mL bolus followed by 0.15 mL/kg/minute until a target serum sodium of ≥150 mmol/L was reached. At this time, blood was drawn for copeptin.

Twelve healthy volunteers (7 females; 5 males) have undergone the study to date. Median age was 28 years (range 26-50); median body weight 75.7 kg (range 57.9 -94.5); median baseline plasma sodium 138 mmol/L (range 136 - 140) and median serum osmolality 289.5 (range 281-297). Median peak sodium was 152 mmol/L (range 150-154) with osmolality 314.5 mmol/kg (range 306-320). Median volume of hypertonic saline infused was 1583 mL (1230-2177) and median hypertonic saline stimulated copeptin was 29.2 pmol/L (9.6-167.4). Overall symptom burden was 5/10 (range 3/10-9/10). There were no serious adverse events.

Development of a local reference range for hypertonic saline stimulated copeptin measurements will assist in interpretation of the test in our local population of patients presenting with polyuria-polydipsia syndrome.


1. Fenske W, Quinkler M, Lorenz D, Zopf K, Haagen U, Papassotiriou et al. Copeptin in the differential diagnosis of the polyuria-polydipsia syndrome- revisiting the direct and indirect water deprivation tests. JCEM. 2011;96:1506-1515

2. Timper K, Fenske W, Kuhn F, Frech N, Arici B, Rutishauser J et al. Diagnostic accuracy of copeptin in the differential diagnosis of the polyuria-polydipsia syndrome: a prospective multicenter study. JCEM. 2015;100:2268-2274

3. Fenske, W, Refardt J, Chifu I, Schnyder I, Winzeler B, Drummond J. A copeptin-based approach in the diagnosis of diabetes insipidus. NEJM. 2018;379:428-439

<![CDATA[SUN-313 Depression, Subjective Stress and Serum Osteocalcin Concentrations in People with Type 2 Diabetes Mellitus]]> Serum osteocalcin is emerging as a potential marker of glucose homeostasis and risk of type 2 diabetes mellitus (T2DM). In mice, osteocalcin knockouts exhibit depressive-like behaviours but knockouts of a putative osteocalcin receptor, GPR158, are resistant to chronic unpredictable mild stress. Recently, osteocalcin release from bone has been suggested to mediate some aspects of the acute stress response. Here, we assess relationships between serum osteocalcin, depression and perceived stress in people with T2DM. Participants with T2DM were assessed for whether they met the DSM-5 criteria for Major Depressive Disorder using the research version of the Structured Clinical Interview for DSM-5 depression criteria (SCID-5RV). Subjective stress was assessed using the Perceived Stress Scale (PSS) with higher scores indicating greater subjective stress. Serum carboxylated (cOCN) and uncarboxylated (unOCN) osteocalcin were assayed from fasting morning blood by commercial ELISA. Among 87 participants (mean age 62.9±9.5, 52% women), 18 (26%) were experiencing a depressive episode (7 men, 11 women). Both serum unOCN and cOCN were associated with higher PSS scores in participants with depression (unOCN, r=0.566, p=0.014; cOCN, r=0.564, p=0.015) but not in those without depression (unOCN, r=0.002, p=0.985; cOCN, r=0.090, p=0.463). A significant interaction was found between depression and PSS scores predicting serum unOCN in a linear model adjusted for age, sex, body mass index, antidepressant use and HbA1c (F=6.225, p=0.015). The results are consistent with reports that osteocalcin release from bone may be a mediator of stress perception; however, among people with T2DM, this relationship was observed only among those currently experiencing a depressive episode.

<![CDATA[SUN-294 The Effects of Traumatic Brain Injury on Pituitary Function: A Systematic Review and Meta-Analysis]]> Background: The impact of traumatic brain injury (TBI) on pituitary function remains unclear. Yet, applying appropriate diagnostic and treatment strategies for affected patients is crucial for mitigating morbidity related to hypopituitarism and improving patient outcomes. Currently, data regarding the prevalence of post-TBI hypopituitarism and its predisposing factors are inconsistent. The goals of this systematic review and meta-analysis were to evaluate the prevalence of acute and chronic post-TBI hypopituitarism and assess for predictors of pituitary dysfunction.

Methods: Ovid MEDLINE In-Process & Other Non-Indexed Citations, Ovid MEDLINE, Ovid EMBASE, Ovid Cochrane Central Register of Controlled Trials, Ovid Cochrane Database of Systematic Reviews, Scopus, Web of Science, and references of key articles were searched from inception to 2019. Studies enrolling ≥20 adult patients with TBI and reporting on pituitary dysfunction were included. A total of 992 studies were generated by the initial search. Titles and abstracts were screened in duplicate by two independent reviewers for inclusion criteria. Of these, 265 full text manuscripts were subsequently reviewed for eligibility. Predefined data were extracted from 14 representative studies for the preliminary analysis (7 cross-sectional studies, 6 prospective studies, and 1 retrospective study).

Results: There was a total of 813 (78% male) patients with TBI. Of those with available data, 124/248 (50.0%) had mild TBI, 112/476 (23.5%) had moderate TBI, and 308/569 (54.1%) had severe TBI. Mean age at TBI diagnosis was 34.2±4.6 years, with time to evaluation of pituitary function following TBI ranging from 0 days to 120 months (mean, 27.1±35.1 months). Acute and chronic hypopituitarism was reported in 10.7% and 19.6% of patients, respectively. TBI was associated with increased risk for hypopituitarism compared to the general population (RR=765.8, 95% CI 538.8-1088.5). Secondary hypogonadism was noted in 15.7% of patients, growth hormone deficiency in 15.7%, secondary adrenal insufficiency in 11.6%, secondary hypothyroidism in 8.7%, and diabetes insipidus in 0.2%. Older age (40.4±5.5 vs 36.7±1.0 years, P<0.0001) and higher BMI (25.0±0.7 vs 23.9±0.2 kg/m2, P<0.0001) were associated with increased risk of post-TBI hypopituitarism.

Conclusion: Available moderate- to low-quality evidence suggests that post-TBI hypopituitarism is common and correlates with older age and higher BMI. Secondary hypogonadism and growth hormone deficiency are the most predominant pituitary deficiencies. Further investigations are warranted to determine the most effective strategies for identifying patients at risk for post-TBI hypopituitarism in order to implement prompt assessment and management.

<![CDATA[SUN-306 The Interaction Between Thiazide-Associated Hyponatremia and Acute Illness in Hospitalised Patients]]> Thiazide diuretics, widely used in the management of hypertension, are associated with a five times greater risk of hyponatremia (serum Na <135mmol/L) than in the general population. Hyponatremia in hospitalised patients warrants special consideration since it is associated with increased morbidity and mortality.

The aim of this study was to describe the clinical characteristics and outcomes in acutely ill medical patients with thiazide-associated hyponatremia (TAH).

We performed a retrospective, case control study examining all acute, unselected medical admissions, over a six week period, to The Royal London Hospital. Cases were defined as adults admitted to hospital with TAH (hyponatremia and a history of being prescribed thiazide diuretic pre-admission). Each case was matched by age, gender and degree of hyponatremia to a similar control - admitted with hyponatremia and no pre-admission exposure to thiazide (non-TAH). Clinical characteristics and treatment outcomes were compared between TAH and non-TAH cohorts.

A total of 1,341 consecutive acute medical admissions (49.7% men) were evaluated. Hyponatremia was detected in 240 (17.9%) admissions. Median (±SD) length of stay was longer among patients with hyponatremia compared to normonatremic patients (5.0±12.4 versus 3.0±9.2 days; p=<0.0001). In-hospital mortality was higher in the hyponatremic group (8.8% versus 4.4% p=0.005). Twenty-two cases (11 men) of TAH accounted for 9.2% of patients with hyponatremia. Median age 64±14 years was similar to other patients with hyponatremia 68±20 years. The median admission serum sodium for TAH cases was 131.5 mmol/L (IQR 126.8 - 134) with a discharge serum sodium of 136.5 mmol/L (IQR 133.8 - 139.3). When compared to matched controls, patients with TAH had similar presenting symptoms - most commonly confusion, headache and dizziness. Length of stay among TAH cases was similar to controls; 5.5±5.1 versus 4.0±3.7 days; p=0.24. Mortality (10%) was the same in both groups. Thiazide was withdrawn during admission in 14 (64%) cases.

In conclusion, acute, clinical outcomes for hospitalised patients with TAH are similar to those with comparable degrees of hyponatremia due to other causes.

<![CDATA[SUN-298 Spectrum of Imaging in Immune Checkpoint Inhibitor Induced Hypophysitis]]>


Hypophysitis (HP) is a known immune related adverse event of immune checkpoint inhibitors (CPIs), commonly associated with CTLA-4 inhibitors and rarely with PD-1/PD-L1 inhibitors. Prior studies of MRIs at HP diagnosis noted pituitary enlargement with resolution within a few weeks. In this study, we examine MRI changes in patients with CPI-induced HP.

Subjects with biochemical evidence of central hypothyroidism or central adrenal insufficiency and MRIs were reviewed by endocrinology and neuroradiology. MRIs were classified relative to HP diagnosis: baseline (at least 21 days prior), diagnosis (within 21 days), and follow up (over 21 days). Patient characteristics included age at CPI initiation, sex, race/ethnicity, personal and family history of autoimmunity, type of cancer and CPI.

Twenty-six subjects met the inclusion criteria. The mean age was 59 years; 62% were male and 86% were non-Hispanic white. Nineteen percent had a personal history and 31% a family history of autoimmunity. Fifty percent had melanoma. At HP diagnosis, 46% were on PD-1/PD-L1 inhibitors, 42% were on combination PD-1/CTLA-4 inhibitors and 12% were on CTLA-4 inhibitors.

Median time from CPI initiation to HP diagnosis was 95 days. Time to HP was shorter on a CTLA-4 inhibitor combination or monotherapy (median 82 days) compared to a PD-1/PD-L1 inhibitor monotherapy (median 220 days; Wilcoxon rank sum, p <0.01). Central adrenal insufficiency was present in all patients not yet on steroids. Central hypothyroidism was common (10/19) in those without primary thyroid disease and was not associated with type of CPI (Fisher’s exact, p=0.18).

Thirteen subjects had baseline MRIs, 18 had MRIs at HP diagnosis and 13 had MRIs in the follow up period. Baseline MRIs were normal in 12/13; one subject had an enlarged pituitary. At diagnosis, 10 had an enlarged pituitary, 7 a normal pituitary and 1 a partially empty sella. CTLA-4 inhibitor exposure was associated with pituitary enlargement at diagnosis: 9/11 compared to 1/7 on PD-1/PD-L1 inhibitor (Fisher’s exact, p <0.04). Of the subjects who had follow-up MRIs, 3 had an enlarged pituitary, 7 a normal pituitary and 3 a partially empty sella. Follow up imaging did not differ between treatment types (Fisher’s exact, p >0.05). Timing of MRI was significantly associated with pituitary appearance (Fisher’s exact, p <0.01).

The MRI appearance of HP presents as a spectrum, from a partially empty sella, normal pituitary to an enlarged pituitary. HP diagnosed in the setting of CTLA-4 inhibitor treatment occurs earlier and is more likely to induce an enlarged pituitary gland compared to PD-1/PD-L1 monotherapy, which occurs later and is associated with a normal appearing MRI at diagnosis. This suggests that the pathogenesis of HP following CPI exposure may vary depending on the type of CPI.

<![CDATA[SUN-301 Importance of Sexual Function Assessment in Multidimensional Evaluation of AGHD Patients: Results from the MAGHD Study]]> <![CDATA[SUN-303 Effects of Open-Label, Adjunctive Ganaxalone Treatment on Resistant Depression in Postmenopausal Women: A Pilot Study]]>


Resistance to selective serotonin reuptake inhibitor and serotonin norepinephrine reuptake inhibitor treatment occurs in about 50% to 70% of patients with major depressive disorder (MDD), a condition associated with significant morbidity that affects women at higher rates than men. Few well-tolerated, effective augmentation therapies are available for such patients, and new therapeutic strategies for resistant depression are needed. The neuroactive steroid metabolite of progesterone, allopregnanolone, is a positive allosteric modulator of GABA

receptors and a putative treatment for mood disorders. We performed a pilot study to determine whether an oral allopregnanolone analog (ganaxolone) may be effective adjunctive therapy for resistant depression in postmenopausal women. Ten postmenopausal women (age 62.8±6.3 years, range 53–69) with resistant depression [current DSM-IV major depressive episode per the Structured Clinical Interview for DSM-IV, Montgomery-Asberg Depression Rating Scale (MADRS) ≥16 despite treatment with an adequately dosed antidepressant for ≥6 weeks] were studied. Open-label ganaxolone (225 mg BID, increased to 450 mg BID if tolerated) was administered for 8 weeks, followed by a 2-week taper. Mean total MADRS depression score (primary endpoint) decreased by 8 weeks [24.4±1.6 (SEM) to 12.8±2.9,

=0.015] and persisted over the two-week taper (

=0.019); 44% of subjects experienced response (score decrease ≥50%) and remission (final score <10), which persisted in 100% and 50% of subjects at 10 weeks, respectively. Secondary endpoints showed significant improvement, including the Inventory of Depressive Symptomatology-Self-Report (IDS-SR;

=0.003), MADRS Reduced Sleep subscale (

<0.001), Symptoms of Depression Questionnaire (SDQ) total score (

=0.012), and SDQ subscales for disruptions in sleep quality (

=0.003) and changes in appetite and weight (

=0.009) over 8 weeks. No significant effects were observed on quality of life or sexual function. All subjects experienced sleepiness and fatigue; 60% experienced dizziness. In conclusion, adjunctive ganaxolone in this open label pilot study appeared to exert antidepressant effects in postmenopausal women with resistant depression but produces sedation with twice-daily dosing. The observed positive effects on sleep and the potential for sustained treatment effects merit further study, as ganaxolone may be particularly beneficial to patients with depression and insomnia. Randomized, placebo-controlled studies are necessary to rule out placebo effects. Given the sedation experienced by most participants, nighttime dosing only should be considered for future studies. Finally, should rigorous studies confirm an antidepressant effect, it will be important to identify subsets of women who respond (e.g. women with neuroactive steroid dysregulation) and mechanisms of action.

<![CDATA[SUN-308 Central Adrenal Insufficiency Is Rare in Adults with Prader-Willi Syndrome]]> 230 nmol/L (7.6 g/dL) was considered sufficient. For Dutch, French and Swedish patients who underwent ITT, cortisol >500 nmol/L (18.1 μg/dL) was considered sufficient. For British patients cortisol >450 nmol/L (16.3 μg/dL) was considered sufficient, as this center used a different assay. Additionally, we reviewed medical files of 645 adults with PWS from Italy (240), France (110), the Netherlands (110), Australia (60), Spain (45), Sweden (38) and the United Kingdom (42) for symptoms of hypocortisolism/adrenal crisis during surgery. Results: Data on 81 adult subjects (46 males and 35 females), median age (range) 25.2 yr (18.0 – 55.5), median BMI (range) 29.1 kg/m2 (20.0 – 62.0), with genetically confirmed PWS were collected. 33 subjects (41%) were using GH treatment since childhood. Multiple-dose MTP was performed in 45 subjects and ITT in 36 subjects. Both tests were well tolerated by all individuals. CAI was excluded in 80 of 81 patients. One patient with a peak cortisol level of 494 nmol/L (just below cut-off level of 500 nmol/L) was prescribed hydrocortisone for use during physical stress. There was no relation between baseline cortisol and ITT/multiple-dose MTP results. Even patients with a low baseline cortisol level (lowest: 102.0 nmol/L) had normal responses. Among the 645 patients whose medical files were reviewed, 200 had undergone surgery without perioperative corticosteroids treatment. None of them displayed any features of hypocortisolism/adrenal crisis. Conclusions: CAI is rare (1.2%) in adults with PWS. Based on these results, we recommend against routinely prescribing corticosteroids stress-doses in adults with PWS. Funding: CZ foundation. ]]> <![CDATA[SUN-293 Acute and Long Term Evaluation of Pituitary Functions in Patients with Advanced Heart Block Requiring Pacemaker Implantation: A Pilot Study]]> <![CDATA[SUN-299 Flash Glucose Sensor Monitoring for Patients with Endogenous Hyperinsulinaemic Hypoglycaemia]]> <![CDATA[SUN-304 Hypophisitis in Patients with and Without Autoimmune Rheumatological Disease]]> <![CDATA[SUN-300 Improvement in Cardiovascular Risk Factors in Long Term Follow up of Hypopituitary Septagenarian and Octagenarian Patients]]> <![CDATA[SUN-302 Incidence Trends in Lung and Gastroenteropancreatic Neuroendocrine Neoplasms]]> <![CDATA[SUN-311 Adrenal Reserve Testing with the Glucagon Stimulation Test (GST) and Cosyntropin Stimulation Test (CST) in Deployed Veterans with Mild Traumatic Brain Injury]]> <![CDATA[SUN-310 Growth Hormone Deficiency and Replacement Therapy: Association with Health-Related Physical Fitness]]> <![CDATA[SUN-305 Hair Cortisol Measurement: An Innovative Method for Diagnosis and Follow-Up in Patients with Cushing’s Disease]]> o ≤ 1 UNL) and HCM (> o ≤ 128 pg/mg), determinations were associated (Chi2, p= 0.18), however, the concordance was acceptable (Kappa index = 0.276).After dividing CD patients according to HCM, 35% (n=8) had normal HCM: mHCM 113.5 (62-126) and mUFC 0.45 (0.1- 4.4). Among them, 63% (n=5) had controlled CD (mHCM 110, 62-121; mUFC 0.39, 0.1-0.85); 25% (n=2) had active CD (mUFC 2.7, 1.1-4.4; mHCM 121, 75-126). 65% had high HCM (n=15): mHCM 167 (132-459) and mUFC 1.36 (0.1-6). Most of them had active CD (n=11, 73%): mHCM 160 (132-459) and mUFC 2.2 (1.1-6). Four patients with elevated HCM (m 248, 148-334) had normal UFC (m 0.61, 0.12-0.92): 2 were in remission, 1 had normal postsurgical UFC with active disease in the follow-up and 1 had normal UFC under medical treatment.Controls (n=50) had mHCM 62.5 (40-126), significantly different from CD.CONCLUSIONSWe evaluated HCM in CD, proposing this method as an additional diagnostic test for hypercortisolism. The acceptable concordance between UFC and HCM is possibly due to the different duration of the evaluated periods.The difference in the HCM values observed between controlled or active CD patients and controls permits the consideration of the method as an alternative in the diagnosis and/or follow-up of CD. ]]> <![CDATA[SUN-309 Interleukin-2 Administration in Healthy Men Activates Cortisol Secretion in an Age-, Dose-, and Body Composition-Dependent Way]]> <![CDATA[SUN-296 Acromegaly Significantly Impacts Employees’ Health Benefit Costs and Increases Work Absenteeism]]> 30 days apart, or 1 ACRO Dx plus either a pituitary adenoma Dx or a pituitary surgery or radiosurgery claim during the study period. Controls were matched to each ACRO employee on demographic, job-related variables, region, and Charlson comorbidity index (CCI) score. Costs were adjusted using the general Consumer Price Index (CPI), medical CPI, and Rx cost CPI. Outcomes included direct costs (medical and Rx), indirect costs (absence payments by benefit type), and lost time (absences by benefit type). Outcomes were analyzed using two-part regression models (logistic followed by generalized linear) for each outcome, controlling for demographic and job-related variables, region, and CCI scores. Data are shown as likelihood or mean ± standard error. Findings are significant at P < 0.05. Results: Participants were 18–65 yr old with continuous eligibility for medical and Rx benefits for the study period. Forty seven ACRO patients and 940 controls were identified. ACRO employees were similar to the controls in most demographic (age, gender, race) and job-related variables (tenure, full-/part-time status, exempt status, salary), but had a higher CCI (0.60 ± 0.15 vs 0.30 ± 0.03; P = 0.029) and a higher incidence of chronic lung disease (31.9 vs 17.4%; P = 0.012), hyperlipidemia (27.7 vs 16.0%, P = 0.035), arthritis (19.1 vs 3.7%), diabetes (31.9 vs 8.3%), hypertension (40.4 vs 13.6%), and thyroid disease (31.9 vs 8.9%) (P < 0.0001). Patients with ACRO were 64.3% more likely to have undergone an MRI (P < 0.0001).Total indirect costs (including sick leave and disability) were higher for ACRO patients ($10,530 vs $1,157; P < 0.05) with both short-term and long-term disability comprising 96% of the difference. Compared with employees without ACRO, employees with ACRO used more short-term disability (10.9 vs 0.9 days; P = 0.0076) and had more total days absent from work (12.7 vs 3.3 days; P < 0.05). Conclusions: Our findings indicate that ACRO has far-reaching implications on direct and indirect employee health benefit costs and increased work absenteeism. Awareness by employers of ACRO-induced increased absenteeism is important to tailor working conditions and to prevent unrealistic work expectations. ]]>