Transsphenoidal Surgery Leads to Remission in Children with Cushing’s Disease

Posted on January 19, 2026 by MaryO

Transsphenoidal surgery — a minimally invasive surgery for removing pituitary tumors in Cushing’s disease patients — is also effective in children and adolescents with the condition, leading to remission with a low rate of complications, a study reports.

The research, “Neurosurgical treatment of Cushing disease in pediatric patients: case series and review of literature,” was published in the journal Child’s Nervous System.

Transsphenoidal (through the nose) pituitary surgery is the main treatment option for children with Cushing’s disease. It allows the removal of pituitary adenomas without requiring long-term replacement therapy, but negative effects on growth and puberty have been reported.

In the study, a team from Turkey shared its findings on 10 children and adolescents (7 females) with the condition, who underwent microsurgery (TSMS) or endoscopic surgery (ETSS, which is less invasive) — the two types of transsphenoidal surgery.

At the time of surgery, the patients’ mean age was 14.8 years, and they had been experiencing symptoms for a mean average of 24.2 months. All but one had gained weight, with a mean body mass index of 29.97.

Their symptoms included excessive body hair, high blood pressure, stretch marks, headaches, acne, “moon face,” and the absence of menstruation.

The patients were diagnosed with Cushing’s after their plasma cortisol levels were measured, and there was a lack of cortical level suppression after they took a low-dose suppression treatment. Measurements of their adrenocorticotropic (ACTH) hormone levels then revealed the cause of their disease was likely pituitary tumors.

Magnetic resonance imaging (MRI) scans, however, only enabled tumor localization in seven patients: three with a microadenoma (a tumor smaller than 10 millimeters), and four showed a macroadenoma.

CD diagnosis was confirmed by surgery and the presence of characteristic pituitary changes. The three patients with no sign of adenoma on their MRIs showed evidence of ACTH-containing adenomas on tissue evaluation.

Eight patients underwent TSMS, and 2 patients had ETSS, with no surgical complications. The patients were considered in remission if they showed clinical adrenal insufficiency and serum cortisol levels under 2.5 μg/dl 48 hours after surgery, or a cortisol level lower than 1.8 μg/dl with a low-dose dexamethasone suppression test at three months post-surgery. Restoration of normal plasma cortisol variation, eased symptoms, and no sign of adenoma in MRI were also requirements for remission.

Eight patients (80%) achieved remission, 4 of them after TSMS. Two patients underwent additional TSMS for remission. Also, 1 patient had ETSS twice after TSMS to gain remission, while another met the criteria after the first endoscopic surgery.

The data further showed that clinical recovery and normalized biochemical parameters were achieved after the initial operation in 5 patients (50%). Three patients (30%) were considered cured after additional operations.

The mean cortisol level decreased to 8.71 μg/dl post-surgery from 23.435 μg/dl pre-surgery. All patients were regularly evaluated in an outpatient clinic, with a mean follow-up period of 11 years.

Two patients showed pituitary insufficiency. Also, 2 had persistent hypocortisolism — too little cortisol — one of whom also had diabetes insipidus, a disorder that causes an imbalance of water in the body. Radiotherapy was not considered in any case.

“Transsphenoidal surgery remains the mainstay therapy for CD [Cushing’s disease] in pediatric patients as well as adults,” the scientists wrote. “It is an effective treatment option with low rate of complications.”

 

From https://cushingsdiseasenews.com/2019/01/15/transsphenoidal-surgery-enables-cushings-disease-remission-pediatric-patients-study/

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Diagnostic Performance of Desmopressin Stimulation Test in Pediatric Cushing’s Disease

Posted on January 13, 2026 by MaryO

Abstract

Objective

To evaluate the diagnostic performance of the desmopressin (DDAVP) stimulation test in pediatric patients with Cushing’s disease (CD), and to compare its accuracy and safety profile to the ovine corticotropin-releasing hormone (oCRH) stimulation test.

Design

A retrospective cohort study.

Methods

Pediatric patients with CD who underwent peripheral or bilateral inferior petrosal sinus sampling (BIPSS) stimulation testing with either DDAVP or oCRH were included. Patients were matched 1:1 for age, sex, and tumor size. The performance of each test was assessed by evaluating ACTH and cortisol responses and calculating test sensitivities.

Results

In peripheral stimulation testing, DDAVP demonstrated 96.9% sensitivity for cortisol and 81.3% for ACTH, while oCRH showed 93.8% and 96.9% sensitivities respectively (p > 0.05). Percentage change of ACTH was higher in the CRH group compared to DDAVP. In BIPSS, the DDAVP stimulation showed sensitivity 73.3% for baseline and 80% for post-stimulation results, while oCRH had sensitivity 93.3% and 100% respectively. Central-to-peripheral ACTH ratios were similar across groups. No major adverse events were reported, and both tests were well tolerated.

Conclusion

Although the DDAVP stimulation test demonstrates lower diagnostic accuracy compared to the CRH test, it still provides sufficient sensitivity and given its availability and lower cost, it represents a pragmatic alternative to CRH stimulation.

Significance statement

The diagnosis of pediatric CD is challenging due to the rarity of the condition and limited access to dynamic testing agents such as ovine corticotropin-releasing hormone (oCRH). This study provides the largest pediatric evaluation of the desmopressin (DDAVP) stimulation test, demonstrating its diagnostic accuracy and safety profile comparable to oCRH stimulation. The findings support the use of DDAVP as a reliable and practical alternative for diagnosing CD in children, particularly in settings where oCRH is unavailable. This work addresses a critical gap in pediatric endocrinology and has the potential to improve diagnostic pathways and outcomes in this population.

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Introduction

ACTH-secreting pituitary adenomas (PAs) causing Cushing’s disease (CD) represent the majority (~ 70–80%) of cases of endogenous Cushing’s syndrome (CS) in children older than 5 years of age [1, 2]. The diagnosis of CS can be complex and often requires multiple dynamic tests [3]. The Pituitary and Endocrine Societies recommend a stepwise diagnostic approach for suspected CS, starting with screening tests and proceeding to localization studies if hypercortisolism is confirmed [4, 5]. However, variability in assay performance, limited test availability, and the high incidence of incidental findings (such as pituitary incidentalomas), continue to pose challenges in selecting the most appropriate diagnostic tools and interpreting their results.

For patients with ACTH-dependent hypercortisolism, the diagnostic workup focuses on localizing the source of ACTH excess, most commonly a PA, though ectopic ACTH-secreting neuroendocrine tumors are also possible [5]. This becomes particularly challenging when pituitary MRI fails to reveal a visible tumor, which may occur in up to one third of patients [6]. ACTH-secreting PAs express receptors for corticotropin-releasing hormone (CRH) and administration of ovine-CRH (oCRH) stimulates ACTH and cortisol release [7]. The oCRH stimulation test, performed either in peripheral sampling or during bilateral inferior petrosal sinus sampling (BIPSS), has long been validated as a minimally invasive method to differentiate CD from ectopic sources of ACTH [8, 9]. However, the discontinuation of manufacturing of oCRH in the United States and the lower cost of alternative stimulants such as desmopressin (DDAVP, a synthetic arginine vasopressin analogue) have led to increased use of the DDAVP stimulation test.

DDAVP stimulates ACTH release via AVPR1b receptors found in corticotroph PAs, but not typically expressed in normal pituitary tissue or ectopic ACTH-secreting tumors [10]. Therefore, a rise in ACTH and cortisol following DDAVP is suggestive of CD [11, 12]. However, the lack of pediatric specific safety and accuracy data limit its use in the pediatric population.

In this study we describe the procedure of DDAVP stimulation test performed with peripheral sampling or in the context of BIPSS, and we compare its performance with the CRH test in a pediatric cohort.

Methods

Study design and patient selection

This was a single-center, retrospective study conducted at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) in Bethesda, Maryland. All patients were enrolled under an IRB-approved protocol (Protocol ID: NCT 00001595) and they were evaluated at the National Institutes of Health (NIH) Clinical Center (CC). Written informed consent was provided by all parents and assent by pediatric patients if developmentally appropriate for all research procedures.

We identified patients with a final diagnosis of CD who have undergone peripheral DDAVP stimulation test (n = 32) or BIPSS with DDAVP stimulation (n = 15) between 2021 and 2025 (DDAVP group). We then reviewed our historic cohort and identified patients who have undergone peripheral oCRH stimulation test or BIPSS with oCRH stimulation during their diagnostic workup, matched 1:1 for age, sex and tumor size (CRH group).

The diagnosis of CS was based on clinical features and standard biochemical testing, including a 1 mg (or weight-based adjusted dose) overnight oral dexamethasone suppression test, late-night serum cortisol, and/or 24-hour (24h) urinary free cortisol (UFC), in accordance with current guidelines and adjusted for the pediatric population [3, 5]. All patients were eventually diagnosed with CD either by histologic confirmation of the diagnosis on the resected tumor, or clinical and biochemical remission after transsphenoidal surgery (TSS). Demographic, clinical, biochemical, imaging, surgical, and histopathology data were collected for analysis. Tumor size was recorded based on the MRI report, or if no adenoma was reported at the MRI, tumor size was recorded as 0.5 mm since the thinnest slice of the images we obtain are 1 mm, acknowledging that this assumption could underestimate the size of a larger tumor which lacked radiographic characteristics to be distinguished in the MR images. Cortisol was measured with solid-phase, competitive chemiluminescent enzyme immunoassay (CMIA) on Siemens Immulite 2500 analyzer (Malvern, PA) until 2020 and on Abbott Architect from 2020 until 2025. ACTH was measured with CMIA on Siemens Immulite 2500 analyzer until 2012 and on Immulite 200 XPi analyzer from 2012 until 2025. UFC was measured with chemiluminescent enzyme immunoassay until 2011 and with High Performance Liquid Chromatography/Tandem Mass Spectrometry since 2011 (LC-MS/MS). UFC is reported as both absolute values (mcg/24h) and as the fold change from the upper limit of normal (ULN), to account for variable reference range per age and assay.

Peripheral stimulation test

Patients were admitted at the inpatient pediatric floor of NIH CC at least one day prior to the procedure. An intravenous (IV) catheter was placed in the forearm at least one hour prior to the test initiation (most commonly 1–2 days prior to testing). Patients were fasting and remained lying in bed for the duration of the test. Samples were collected at times − 15 and 0 min prior to administration of stimulant at approximately 8:00am.

In the DDAVP group, 10mcg of DDAVP (2.5mL of 4mcg/mL solution) was administered via IV push over 30 s, followed by a 2mL normal saline flush. Samples were then collected at additional timepoints after administration of DDAVP at + 15, +30, + 45, and + 60 min. In a subset of patients, samples were collected at + 10, +20, + 30, +45, and + 60 min but results were not considered significantly different and eventually protocol was adjusted to sampling every 15 min. For this subset of patients (n = 7) the highest value of samples at + 10 and + 20 min was used as the + 15 min value. Patients were advised to follow moderate fluid restriction after DDAVP administration (max 40oz/1.2 L) for 24 h post-procedure, unless otherwise indicated by the treating physician. Intake/output monitoring was recommended for 24 h, and a repeat basic metabolic panel was obtained the following day.

In the CRH group, after baseline samples were obtained, patients received 1mcg/kg, max 100mcg, of oCRH via IV push, and samples were collected at times + 15, +30, and + 45 min after administration [3].

Samples were analyzed for cortisol and ACTH and the percentage change from baseline was calculated as: [(peak level after stimulation – baseline level)/baseline level]*100. The DDAVP test was considered consistent with CD based on previously published criteria: >18% increase in cortisol and >33% increase in ACTH [12]. The CRH test was considered consistent with CD if there was >20% increase in cortisol and >35% increase in ACTH [3].

Bilateral inferior petrosal sinus sampling (BIPSS)

BIPSS was performed based on standard protocols by an interventional radiologist under anesthesia as previously described [13]. Briefly, catheters were advanced to bilateral petrosal sinuses via radiological guidance through femoral veins. Blood samples were collected at all timepoints simultaneously from each of the petrosal sinus catheter (right, left) and peripheral samples drawn from a vascular catheter introducer sheath in a femoral vein. Baseline samples were collected at − 5 and 0 min. In the DDAVP group, after collecting samples at time 0 min, 10mcg of DDAVP (2.5mL of 4mcg/mL solution) was administered as an IV push over 30 s, followed by a 2mL normal saline flush. In the CRH group, after collecting samples at time 0 min, 1mcg/kg, max 100mcg, of oCRH was administered as an IV push over 30 s via peripheral IV catheter. Post-stimulation blood samples were collected at + 3, +5, and + 10 min. Patients who received DDAVP were advised to follow moderate fluid restriction as described above. Test results were considered consistent with CD if the baseline central:peripheral (C:P) ACTH ratio was >2 and/or the stimulated C:P ratio >3 [14,15,16].

Statistical analysis

Baseline characteristics were summarized using descriptive statistics. Non-normally distributed data are shown as median [Q1, Q3] and were compared between groups with the Wilcoxon rank-sum test. Normally distributed data are shown as mean (standard deviation, SD) and were compared between groups with student’s t-test. Categorical data are shown as counts and proportions and were compared between groups using χ2 test or Fisher’s exact test as appropriate. To assess whether hormone levels or ratios changed significantly over time and differed between the CRH and DDAVP groups, variables were log-transformed to achieve approximately normal distribution, and two-way repeated measures analysis of variance (ANOVA) was performed with time and stimulation group as fixed effects. Area under the curve (AUC) was calculated for timepoints from 0 min to 45 min for the peripheral stimulation test, and from 0 min to 10 min for BIPSS. Sensitivity was calculated using predefined criteria, and Fisher’s exact test was employed to compare sensitivity between the CRH and DDAVP groups. Missing data were considered as missing by chance and were not replaced. A p-value < 0.05 was considered statistically significant. Analyses were conducted using R/RStudio software.

Results

Cohort characteristics

In the peripheral stimulation test cohort, a total of 64 patients were included, consisting of 34 males (53%) and 30 females (47%). In accordance with the selection criteria, the two groups (DDAVP and CRH) were similar in age at time of testing, tumor size, and proportions of negative MRI at diagnosis. Markers of hypercortisolemia were also similar between the two groups, including late night serum cortisol, 24h UFC, and morning ACTH levels.

In the BIPSS analysis, a total of 30 patients were included, consisting of 18 males (60%) and 12 females (40%). The two groups were similar in age at time of testing, tumor size, and proportions of negative MRI at diagnosis. Markers of hypercortisolemia were also similar between the two groups. All corresponding results have been summarized in Table 1.

Table 1 Characteristics of patients undergoing Desmopressin (DDAVP) and oCRH stimulation test

Stimulation test results

In the peripheral stimulation test results, although screening markers of hypercortisolemia were overall similar between the two groups, baseline serum cortisol at the time of the stimulation test was lower in the DDAVP group (14.1 mcg/dL [12.4, 16.8]) compared to the CRH group (18.7 mcg/dL [15.5, 24.7], p < 0.001), while baseline ACTH levels were similar between the two groups (47.5 pg/mL [27.5, 58.0] in the DDAVP group vs. 48.5 pg/mL [33.4, 58.6] in the CRH group, p = 0.73).

In the repeated measures analysis of cortisol during the stimulation test, significant main effect of time (p < 0.001) and group (p < 0.001) were noted, suggesting that cortisol values were significantly different over time and between the two groups. The time-by-group interaction was also significant (p = 0.031), suggesting that the pattern of change over time also differed. Furthermore, AUCs were also different between the two groups, with the CRH group having a higher AUC compared to the DDAVP group (p < 0.001). In the analysis of ACTH between the two groups, there was significant effect of time (p < 0.001), but group (p = 0.05), and the time-by-group (p = 0.11) interaction did not reach statistical significance suggesting that ACTH levels changed overtime but retained a similar overall pattern between the groups. When analyzing AUCs for the ACTH secretion, the CRH group had higher AUC compared to the DDAVP group (p < 0.001). Peak cortisol levels occurred more frequently at 30 min in the DDAVP group and at 45 min in the CRH group, while peak ACTH levels occurred more frequently at 15 min post-stimulation in both groups (Fig. 1)

Fig. 1

figure 1

Hormonal responses to desmopressin (DDAVP) and ovine corticotropin-releasing hormone (oCRH) stimulation in pediatric Cushing’s disease. (A) Serum cortisol concentrations over time following peripheral stimulation, (B) Plasma ACTH levels over time following peripheral stimulation, (C) Central: Peripheral, (C:P) ACTH ratios over time during bilateral inferior petrosal sinus sampling, (BIPSS). Lines follow median values at each timepoint for CRH (red) or DDAVP (blue) group

When looking into the percentage change from baseline, the median percentage change in cortisol was 58.2% [40.6, 85.7] after DDAVP and 82.3% [44.1, 110.0] after oCRH stimulation (p = 0.21), while the median percentage change in ACTH was 122% [53.5, 206.0] and 188.0% [117.0, 342.0] after DDAVP and oCRH stimulation respectively (p = 0.037, Fig. 2).

Fig. 2

figure 2

Group comparison of cortisol and ACTH levels in response to desmopressin (DDAVP) and ovine corticotropin-releasing hormone (oCRH) stimulation in pediatric Cushing’s disease. Percentage change from baseline in cortisol (A) and ACTH (B) levels following peripheral stimulation. Central:Peripheral (C:P) ACTH ratios at baseline (C) and post-stimulation (D) during bilateral inferior petrosal sinus sampling (BIPSS). Box plots display medians, interquartile ranges, and 1.5× IQR whiskers. Dashed lines represent diagnostic thresholds

In the BIPSS stimulation test, the repeated measures analysis noted that in both groups there was significant effect of time (p < 0.001), but group and time-by-group interaction did not differ (p > 0.05), suggesting that overall, there was a similar change of the C:P ACTH ratios between the two groups post-stimulation (Fig. 1). AUCs for C:P ratios did not reach statistical significance between the two groups (p = 0.21). Peak ratios occurred more frequently at 3 min post-stimulation in both groups. Baseline C:P ACTH ratios were similar between the two groups (5.6 [2.1, 10.6] in the DDAVP group vs. 7.5 [4.2, 20.2] in the CRH group, p = 0.20) and the maximum C:P ratios post-stimulation remained similar (17.1 [8.9, 22.1] in the DDAVP group vs. 18.5 [12.3, 65.4] in the CRH group, p = 0.37, Fig. 2).

Sensitivity analysis

Using the diagnostic thresholds specified above for the peripheral stimulation test, sensitivity in the DDAVP group was 96.9% for cortisol and 81.3% for ACTH. In comparison, the CRH group showed 93.8% sensitivity for cortisol and higher sensitivity for ACTH (96.9%, Fig. 3), which however did not differ statistically between the two groups (p > 0.05).

Fig. 3

figure 3

Sensitivity of desmopressin (DDAVP) and ovine corticotropin-releasing hormone (oCRH) stimulation tests in pediatric Cushing’s disease. Sensitivity for cortisol and ACTH results in the peripheral stimulation test (A); and the Central:Peripheral (C:P) ACTH ratio in bilateral inferior petrosal sinus sampling (B)

Eight patients (12.5%) had a false negative response in either cortisol (range of percentage change of cortisol from baseline: 1–13%) or ACTH (range of percentage change of ACTH from baseline: −31-30%). Of these, six patients underwent DDAVP and two patients had oCRH stimulation test. Only two patients had inadequate response in both cortisol and ACTH and would have been misclassified (one in each of the DDAVP and CRH groups). Of the seven patients with false negative stimulation tests, only one was documented to have a hemolyzed blood sample. All patients who underwent DDAVP stimulation had an ACTH response of > 19%.

In the BIPSS analysis, using the thresholds above, sensitivity was 73.3% and 93.3% in the DDAVP and CRH group respectively (p = 0.33) for the baseline ratios, and 80% and 100% in for the stimulated ratios (p = 0.22, Fig. 3). Five (5) patients showed an inadequate response at baseline and three of them also had a false low response post-stimulation. All three of the patients who failed both the baseline and the post-stimulation cutoffs, and who would have been misclassified as possible ectopic CS, were in the DDAVP group and were previously described in a study of negative BIPSS results [13]. Two of these three patients were noted on venograms to have poorly developed inferior petrosal veins that suggested BIPSS might not yield reliable results.

Side effects

Overall patients tolerated the procedures without significant adverse events or complications. One patient in the CRH group reported mild headache, which resolved spontaneously within a few hours. No episodes of hyponatremia or venous thrombosis were recorded.

Discussion

The diagnostic workup of CS can be challenging and complex involving many baseline and dynamic tests. Especially in the pediatric population, the rarity of the disease makes the diagnostic process more difficult. We herein present the DDAVP stimulation test in pediatric patients with CD. We report the performance of the test which although lower than oCRH, still yields sufficient sensitivity overall without significant side effects.

DDAVP stimulation test is used for the differential diagnosis of pituitary versus ectopic sources of hypercortisolemia in ACTH-dependent CS. Although rare in children, infrequent cases of ectopic pediatric CS have been reported, some of which have led to devastating results, even death [2, 17, 18]. In a recent study on a non-invasive approach to differential diagnosis of ACTH-dependent CS, Frete et al. incorporated the CRH or DDAVP stimulation test in their diagnostic algorithm [12]. We have also recently described that in our cohort, pediatric patients with positive high dose dexamethasone suppression test and peripheral CRH or DDAVP stimulation test consistent with pituitary source ended up having CD irrespective of the MRI findings [2]. This could suggest that in this population, especially when IPSS would delay evaluation or is not available, DDAVP stimulation test can assist in important decisions for the management of the patient. The sensitivity of DDAVP test was lower than that of CRH for the diagnosis of CD. Similar findings were noted in a metanalysis by Ceccato et al., where CRH showed higher sensitivity than DDAVP [19]. In the absence of oCRH in some countries, DDAVP remains a safe and effective alternative for this patient population.

The utility of DDAVP stimulation test expands beyond the differential diagnosis of ACTH-dependent CS. Studies have shown that it can be used for the differential diagnosis of non-malignant hypercortisolism as well as a marker of post-operative remission, which have not been explored in this study [20, 21].

False negative and recently false positive results to DDAVP stimulation test have been reported in the literature. Although initially thought that AVPR1b receptors are located only on corticotroph tumors, some ectopic tumors show response [22]. Our false negative results are contingent to the cutoff values we used in this study. For the peripheral stimulation test, we used the latest cutoff values suggested by Frete et al. Initial descriptions of the test suggested the use of >50% change for ACTH and >20% change for cortisol, which would lead to 8 patients in our group being misclassified (instead of 6 with the current criteria). However, if we use a combination of either cortisol or ACTH response, then one patient would still be misclassified due to inadequate response to both cortisol (13%) and ACTH (26.6%). A threshold for ACTH of >20% would have identified all patients with CD in our cohort, but would potentially yield false positive results in patients with ectopic CS. In the BIPSS interpretation, we used the cutoff criteria of >2 for baseline and >3 for stimulated values. Recently a study suggested that cutoffs of C:P ACTH ratio >1.4 for baseline and >2.8 for post-stimulation results would yield better accuracy [23]. If we used those cutoffs, then one patient at baseline and two patients at post-stimulation would have been misclassified. Only one patient would have both ratios below the cutoff criteria (baseline: 1.1, post-stimulation: 1.5) and eventually be considered as ectopic CS. In the pediatric population, one major factor to consider is that technical limitations may pose difficulties in reaching the petrosal sinuses; in these cases, results are not dependent on the stimulant used.

Additional possible explanations for negative results in patients with CD may be a cyclical pattern of cortisol secretion. We have ruled out this possibility in our patients since all of them had midnight serum cortisol the night(s) prior to the test and all were elevated suggesting they had active hypercortisolemia. Technical difficulties could explain some cases where administration of the medication may not have been complete or appropriately delivered. However, most patients had decreased urine output as evidence of an effective dose of DDAVP in their circulation. Finally, as tumors may have pulsatility on ACTH secretion, it is possible that the test coincided with an endogenous pulse of the tumor ACTH secretion that further masked the effect of DDAVP administration.

Certain limitations exist for this study. We had limited patients with ectopic CS and thus we could not compare the performance of the test between patients with CD and patients with ECS. However, we did not aim to define the diagnostic cutoffs of each test but rather to assess the safety and concordance to the CRH stimulation test. Furthermore, ectopic CS is quite rare in the pediatric population that it would be very difficult to recruit enough patients. Although this is the largest to our knowledge cohort of pediatric patients with DDAVP stimulation test, the number of patients may still have been too low to detect significant differences between the tests. Finally, the historic CRH group were evaluated with variable cortisol and ACTH assays which may affect the comparison of absolute values between the two groups. Thus, we present our results also as percentage changes to compare the performance of the tests.

In conclusion, we show the performance of DDAVP stimulation test performed either peripherally or during BIPSS. The test is well tolerated, and no significant side effects were noted. The test shows comparable sensitivity and a valid alternative to the oCRH stimulation test, in the absence of this agent.

Data availability

All raw data used in this study will be deposited in data repository listed in References [24].

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Acknowledgements

This research was supported by the Intramural Research Program of the National Institutes of Health (NIH). The contributions of the NIH authors are considered Works of the United States Government. The findings and conclusions presented in this paper are those of the authors and do not necessarily reflect the views of the NIH or the U.S. Department of Health and Human Services.

Funding

Open access funding provided by the National Institutes of Health. The work was supported by the Intramural Research Program of the National Institutes of Health, Grant ZIA HD009017.

Author information

Authors and Affiliations

  1. Unit on Hypothalamic and Pituitary Disorders, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 10 Center Drive, Building 10, Rom 1-3330, MSC1103, Bethesda, MD, 20892, USA

    Yetunde B. Omotosho & Christina Tatsi

  2. Endocrine and Venous Services Section, Interventional Radiology Section, Clinical Center, National Institutes of Health, Bethesda, MD, 20892, USA

    Richard Chang & Michael Kassin

  3. Department of Pharmacy, Clinical Center, National Institutes of Health, Bethesda, MD, 20892, USA

    Erna Groat

  4. Department of Pediatrics, Clinical Center, National Institutes of Health, Bethesda, MD, 20892, USA

    Alan Quillian, Ruth Parker & Christina Tatsi

Contributions

YOB collected data, analyzed data and wrote the manuscript, RC and MK performed clinical procedures, EG reviewed clinical procedures regarding medication safety and administration, AQ and RP provided clinical care to participants, CT designed the study, procedures, data collection, data analysis, and interpretation of results. All authors reviewed the manuscript.

Corresponding author

Correspondence to Christina Tatsi.

Ethics declarations

Disclosures

CT received research funding by Pfizer and Recordati for unrelated studies.

Competing interests

The authors declare no competing interests.

ClinicalTrials.gov ID

NCT00001595.

Additional information

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Skeletal Maturation in Children With Cushing’s Syndrome is Not Consistently Delayed

Posted on January 13, 2026 by MaryO

Skeletal maturation in children with cushing syndrome is not consistently delayed: The role of corticotropin, obesity, and steroid hormones, and the effect of surgical cure.

J Pediatr. 2014 Jan 9. pii: S0022-3476(13)01500-X. doi: 10.1016/j.jpeds.2013.11.065. [Epub ahead of print]

The Journal of Pediatrics, 01/22/2014 Clinical Article

Lodish MB, et al. – The aim of this study is to assess skeletal maturity by measuring bone age (BA) in children with Cushing syndrome (CS) before and 1–year after transsphenoidal surgery or adrenalectomy, and to correlate BA with hormone levels and other measurements. Contrary to common belief, endogenous CS in children appears to be associated with normal or even advanced skeletal maturation. When present, BA advancement in CS is related to obesity, insulin resistance, and elevated adrenal androgen levels and aromatization. This finding may have significant implications for treatment decisions and final height predictions in these children.

Methods

  • This case series conducted at the National Institutes of Health Clinical Center included 93 children with Cushing disease (CD) (43 females; mean age, 12.3 ± 2.9 years) and 31 children with adrenocorticotropic hormone–independent CS (AICS) (22 females, mean age 10.3 ± 4.5 years).
  • BA was obtained before surgery and at follow-up.
  • Outcome measures were comparison of BA in CD vs AICS and analysis of the effects of hypercortisolism, insulin excess, body mass index, and androgen excess on BA.

Results

  • Twenty-six of the 124 children (21.0%) had advanced BA, compared with the expected general population prevalence of 2.5% (P < .0001). Only 4 of 124 (3.2%) had delayed BA.
  • The majority of children (76%) had normal BA.
  • The average BA z-score was similar in the children with CD and those with AICS (0.6 ± 1.4 vs 0.5 ± 1.8; P = .8865).
  • Body mass index SDS and normalized values of dehydroepiandrosterone, dehydroepiandrosterone sulfate, androsteonedione, estradiol, and testosterone were all significantly higher in the children with advanced BA vs those with normal or delayed BA.
  • Fifty-nine children who remained in remission from CD had follow-up BA 1.2 ± 0.3 years after transsphenoidal surgery, demonstrating decreased BA z-score (1.0 ± 1.6 vs 0.3 ± 1.4; P < .0001).

From http://www.ncbi.nlm.nih.gov/pubmed/24412141

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Think Like a Doctor: Red Herrings Solved!

Posted on January 11, 2026 by MaryO

By LISA SANDERS, M.D.

On Thursday we challenged Well readers to take the case of a 29-year-old woman with an injured groin, a swollen foot and other abnormalities. Many of you found it as challenging as the doctors who saw her. I asked for the right test as well as the right diagnosis. More than 200 answers were posted.

The right test was…

The dexamethasone suppression test,though I counted those of you who suggested measuring the cortisol in the urine.

The right diagnosis was…

Cushing’s disease

More than a dozen of you got the right answer or the right test, but Dr. Davin Quinn, a consultant psychiatrist at the University of New Mexico Hospital, was the first to be right on both counts. As soon as he saw that the patient’s cortisol level was increased, he thought of Cushing’s. And he had treated a young patient like this one some years ago as a second year resident.

The Diagnosis:

Cushing’s disease is caused by having too much of the stress hormone cortisol in the body. Cortisol is made in the adrenal glands, little pyramid shaped organs that sit atop the kidneys. It is normally a very tightly regulated hormone that helps the body respond to physical stress.

Sometimes the excess comes from a tumor in the adrenal gland itself that causes the little organ to go into overdrive, making too much cortisol. More often the excess occurs when a tumor in the pituitary gland in the brain results in too much ACTH, the hormone that controls the adrenal gland.

In the body, cortisol’s most fundamental job is to make sure we have enough glucose around to get the body’s work done. To that end, the hormone drives appetite, so that enough fuel is taken in through the food we eat. When needed, it can break muscle down into glucose. This essential function accounts for the most common symptoms of cortisol excess: hyperglycemia, weight gain and muscle wasting. However, cortisol has many functions in the body, and so an excess of the hormone can manifest itself in many different ways.

Cushing’s was first described by Dr. Harvey Cushing, a surgeon often considered the father of modern neurosurgery. In a case report in 1912, he described a 23-year-old woman with sudden weight gain, mostly in the abdomen; stretch marks from skin too thin and delicate to accommodate the excess girth; easy bruising; high blood pressure and diabetes.

Dr. Cushing’s case was, it turns out, a classic presentation of the illness. It wasn’t until 20 years later that he recognized that the disease had two forms. When it is a primary problem of an adrenal gland gone wild and producing too much cortisol on its own, the disease is known as Cushing’s syndrome. When the problem results from an overgrown part of the pituitary making too much ACTH and causing the completely normal adrenal glands to overproduce the hormone, the illness is called Cushing’s disease.

It was an important distinction, since the treatment often requires a surgical resection of the body part where the problem originates. Cushing’s syndrome can also be caused by steroid-containing medications, which are frequently used to treat certain pulmonary and autoimmune diseases.

How the Diagnosis Was Made:

After the young woman got her lab results from Dr. Becky Miller, the hematologist she had been referred to after seeing several other specialists, the patient started reading up on the abnormalities that had been found. And based on what she found on the Internet, she had an idea of what was going on with her body.

“I think I have Cushing’s disease,” the patient told her endocrinologist when she saw him again a few weeks later.

The patient laid out her argument. In Cushing’s, the body puts out too much cortisol, one of the fight-or-flight stress hormones. That would explain her high blood pressure. Just about everyone with Cushing’s disease has high blood pressure.

She had other symptoms of Cushing’s, too. She bruised easily. And she’d been waking up crazy early in the morning for the past year or so – around 4:30 – and couldn’t get back to sleep. She’d heard that too much cortisol could cause that as well. She was losing muscle mass – she used to have well-defined muscles in her thighs and calves. Not any more. Her belly – it wasn’t huge, but it was a lot bigger than it had been. Cushing’s seemed the obvious diagnosis.

The doctor was skeptical. He had seen Cushing’s before, and this patient didn’t match the typical pattern. She was the right age for Cushing’s and she had high blood pressure, but nothing else seemed to fit. She wasn’t obese. Indeed, she was tall (5- foot-10) and slim (150 pounds) and athletic looking. She didn’t have stretch marks; she didn’t have diabetes. She said she bruised easily, but the endocrinologist saw no bruises on exam. Her ankle was still swollen, and Cushing’s can do that, but so can lots of other diseases.

The blood tests that Dr. Miller ordered measuring the patient’s ACTH and cortisol levels were suggestive of the disease, but many common problems — depression, alcohol use, eating disorders — can cause the same result. Still, it was worth taking the next step: a dexamethasone suppression test.

Testing, Then Treatment:

The dexamethasone suppression test depends on a natural negative feedback loop whereby high levels of cortisol suppress further secretion of the hormone. Dexamethasone is an artificial form of cortisol. Given in high doses, it will cause the level of naturally-occurring cortisol to drop dramatically.

The patient was told to take the dexamethasone pills the night before having her blood tested. The doctor called her the next day.

“Are you sure you took the pills I gave you last night?” the endocrinologist asked her over the phone. The doctor’s voice sounded a little sharp to the young woman, tinged with a hint of accusation.

“Of course I took them,” she responded, trying to keep her voice clear of any irritation.

“Well, the results are crazy,” he told her and proposed she take another test: a 24-hour urine test.

Because cortisol is eliminated through the kidneys, collecting a full day’s urine would show how much cortisol her body was making. So the patient carefully collected a day’s worth of urine.

A few days later, the endocrinologist called again: her cortisol level was shockingly high. She was right, the doctor conceded, she really did have Cushing’s.

An M.R.I. scan revealed a tiny tumor on her pituitary. A couple of months later, she had surgery to remove the affected part of the gland.

After recovering from the surgery, the patient’s blood pressure returned to normal, as did her red blood cell count and her persistently swollen ankle. And she was able to once again sleep through the night.

Red Herrings Everywhere:

As many readers noted, there were lots of findings that didn’t really add up in this case. Was this woman’s groin sprain part of the Cushing’s? What about the lower extremity swelling, and the excess red blood cell count?

In the medical literature, there is a single case report of high red blood cell counts as the presenting symptom in a patient with Cushing’s. And with this patient, the problem resolved after her surgery – so maybe they were linked.

And what about the weird bone marrow biopsy? The gastritis? The enlarged spleen? It’s hard to say for certain if any of these problems was a result of the excess cortisol or if she just happened to have other medical problems.

Why the patient didn’t have the typical symptoms of Cushing’s is easier to explain. She was very early in the course of the disease when she got her diagnosis. Most patients are diagnosed once symptoms have become more prominent

By the time this patient had her surgery, a couple of months later, the round face and belly characteristic of cortisol excess were present. Now, two years after her surgery, none of the symptoms remain.

From http://well.blogs.nytimes.com/2014/01/17/think-like-a-doctor-red-herrings-solved/?_php=true&_type=blogs&_r=0

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Cushing’s Disease: When Symptoms Are Mistaken for Menopause

Posted on January 11, 2026 by MaryO

After 8 years of menopause-like symptoms, a 62 year old patient discovered she actually had Cushing’s disease. Read about her long journey to get a diagnosis and her success in finding her dream-come-true neurosurgeon.

A Mysterious Decline in Health

When Elisabeth N., 62, started developing symptoms that included obesity, osteoporosis, insomnia, kidney stones and hair loss, she attributed it to what most women her age would: menopause. Back in 2000 she never would have thought those seemingly normal symptoms for a woman her age would lead her to Santa Monica to be treated eight years later by Daniel Kelly, MD., neurosurgeon and director of the Pacific Pituitary Disorders Center at Pacific Neuroscience Institute and Saint John’s Health Center. In fact, it wasn’t till February of 2008 that she learned it could all be caused by something completely different.

A Sister’s Observation Leads to a Breakthrough

“I wouldn’t have known about Cushing’s disease if it weren’t for my youngest sister; I’m 25 years older and so fortunate she has her medical degree,” explained Elisabeth, a kitchen and bath designer in Mesa, Arizona. “We hadn’t seen one another for five years when we visited in February of 2008. My appearance had drastically changed by then. She told me, ‘Don’t be scared, Bethie, but I think you should be tested for Cushing’s.’”

Learning About Cushing’s Disease

cushing's disease symptoms infographic

Elisabeth started researching Cushing’s disease right away and was relieved to learn that a cure was possible. Cushing’s is a hormonal disorder caused by high levels of the hormone cortisol. Symptoms include upper-body obesity, fragile skin that bruises easily, weakened bones, severe fatigue, weak muscles, high blood pressure, high blood glucose, increased thirst and urination, depression and a fatty hump between the shoulders. Women can also experience irregular menstrual periods and excess hair growth on their bodies. It can be caused by taking glucocorticoids such as prednisone or if there is a problem with a person’s pituitary gland or hypothalamus.

A Long and Uncertain Testing Journey

Elisabeth immediately set up a doctor’s appointment to get her cortisol and adrenocorticotropic hormone (ACTH – the pituitary hormone that stimulates the adrenal glands to make cortisol) levels tested. Over the next nine months Elisabeth went through several blood, urine, saliva and plasma tests for her cortisol and ACTH production and had an MRI. The tests showed elevated cortisol and ACTH levels but the initial impression was that her levels were not high enough to indicate Cushing’s disease and her pituitary MRI showed no apparent tumor. Elisabeth met with both a pituitary neurosurgeon and an endocrinologist, but both determined her condition not to be Cushing’s.

“My cortisol was not high enough; I wasn’t obese enough; I wasn’t disabled enough; I wasn’t depressed enough,” Elisabeth said.

Finding the Missing Clue

She felt frustrated by the diagnosis and continued to research possibilities online. It was during this research that she stumbled upon an article comparing MRI Tesla strengths. It recommended getting a Tesla 3.0 with contrast to pick up small abnormalities. Elisabeth scheduled a new MRI at the beginning of November. This time the scan detected a 6 mm tumor on the right side of her pituitary gland. Additional hormonal testing also confirmed that she did indeed have high ACTH and cortisol levels consistent with Cushing’s, “I was thrilled to finally have proof I had Cushing’s, but terrified because I knew I’d have to have brain surgery to remove it,” Elisabeth said. “I knew I wanted transsphenoidal surgery – the safest, most successful procedure with the least complications if done by an experienced surgeon.”

Understanding the Endonasal Transsphenoidal Approach

endonasal procedure illustration

Endonasal transsphenoidal tumor removal, aka endoscopic endonasal approach, such as what Elisabeth needed, is a surgery that uses the nostril as the entry point with visualization from the operating microscope and endoscope. The approach passes through the back of the nasal cavity and into the sphenoid sinus to the skull base without facial incisions, brain retraction or post-operative nasal packing.

“This type of surgery is ideal for removing over 99% of pituitary adenomas, like what Elisabeth had and is considered first-line therapy for patients with Cushing’s disease,” Dr. Kelly explained. “Untreated or incompletely treated, Cushing’s disease is a very serious condition leading to uncontrolled hypertension, diabetes, weight gain and increased mortality.”

Choosing the Right Surgeon

With all the months she had to prepare for a diagnosis, Elisabeth knew exactly what needed to be done.

“I’d known I wanted Dr. Kelly to perform surgery but never imagined it could happen,” Elisabeth said. “I found him online. He’s ranked as one of the world’s top neurosurgeons specializing in this type of surgery. While watching his YouTube videos, I was awed by his kindness, patience, sense of humor, approachability, professionalism and complete lack of arrogance in spite of his fame. I’m still pinching myself that I had the fortune and honor to become one of his patients.”

A Life-Changing Call

Dr. Daniel Kelly and Dr. Chester Griffiths perform surgery

Figuring she didn’t have anything to lose, Elisabeth called Dr. Kelly’s office and asked if he was accepting new patients (he was) and how long was his waiting list (she could see him next week). Elisabeth was astounded. She immediately mailed Dr. Kelly all the test results, films and reports she could gather.

“Two days later, Dr. Kelly personally called and left a message, indicating it appeared there was indeed an ACTH secreting adenoma on my pituitary gland and to call him back,” Elisabeth said. “I was blown away. I’d have expected to win the lottery first.”

Successful Surgery and a New Beginning

Dr. Kelly arranged to perform Elisabeth’s surgery two weeks later on November 26 – the day before Thanksgiving. Her cortisol levels fell dramatically within 24 hours of surgery. She has remained in remission since then. Years after surgery, she continues to feel like a new person and regularly stays in contact with Dr. Kelly and his office staff.

About Dr. Daniel Kelly

Dr. Daniel Kelly, a board-certified neurosurgeon, is the director and one of the founders of the Pacific Neuroscience Institute, director of the Pacific Brain Tumor Center and Pacific Pituitary Disorders Center, and is Professor of Neurosurgery at Saint John’s Cancer Institute at Providence Saint John’s Health Center. Considered to be one of the top neurosurgeons in the US, he is a multiple recipient of the Patients’ Choice Award and Southern California Super Doctors distinction.

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