Cushing’s Syndrome, Cortisol, and Cognitive Competency: A Case Report

Posted on July 2, 2017 by MaryO
Published online 2017 Apr 6. doi:  10.1159/000470833
PMCID: PMC5422746
Neil Oronsky,a Bennett Thilagar,b,* Carolyn M. Ray,c Scott Caroen,b Michelle M.C. Lybeck,b Lindsey Ferry,b Ronald A. Voves,b and Bryan Oronskyb
Author information ► Article notes ► Copyright and License information ►

Abstract

Glucocorticoids are associated with immunosuppression and neuropsychiatric complications. We describe the case of a carcinoid patient with Cushing’s syndrome (CS) and neurocognitive impairment due to ectopic ACTH production who developed sepsis and died because of his family’s decision to withdraw antibiotic treatment. This report is presented to illustrate the importance of advanced-care planning in patients with CS.

Key Words: Cushing’s syndrome, Carcinoid patient, Glucocorticoids, ACTH, Immunosuppression, Neurocognitive impairment, Advanced directives

Introduction

Cushing’s syndrome (CS) is a general term for a cluster of endocrine abnormalities characterized by chronic cortisol overproduction. Characteristic clinical comorbidities include metabolic complications (e.g., visceral obesity, diabetes mellitus, and dyslipidemia), cardiovascular complications (e.g., systemic arterial hypertension, atherosclerosis, and thromboembolism), bone complications (e.g., osteoporosis and osteoarthritis) infective complications, and neuropsychiatric disorders (e.g., major depression, mania, anxiety, and cognitive impairment) [1]. CS may be exogenous and iatrogenic due to corticosteroid administration or endogenous due to excessive ACTH secretion, most commonly from a pituitary adenoma, referred to, somewhat confusingly, as Cushing’s disease, or less commonly from a nonpituitary tumor (ectopic CS) and primary adrenal neoplasms [2]. Several studies link untreated CS to fatal infectious complications [3]. This report describes the case of a 60-year-old carcinoid patient with cognitive impairment due to hypercortisolism from CS who developed bacteremia; his condition deteriorated, and he died after a decision was made to withdraw care.

Case Presentation

A 60-year-old male with metastatic bronchopulmonary neuroendocrine tumor treated on a clinical trial for over 5 months was admitted to the hospital with complaints of fever, agitation, and weakness. His medical history was significant for newly diagnosed CS secondary to ACTH secretion; he had been hospitalized 2 weeks earlier for CS-induced hyperglycemic crisis. On admission, the patient presented with classic cushingoid habitus of facial plethora, moon facies, muscle atrophy, abdominal striae, and truncal obesity. His physical examination was significant for bilateral crackles and agitation consistent with corticosteroid psychosis. The arterial blood gas analysis on room air was pH 7.497, PaCO2 29 mm Hg, PaO2 71 mm Hg, and oxygen saturation 95%.

Laboratory data were significant for hyperglycemia, hypokalemia, and leukocytosis with bandemia. The chest CT scan showed no definite evidence of pulmonary thromboembolism.

As respiratory failure was imminent, he was transferred to the intensive care unit and mechanically ventilated. The highest positive end-expiratory pressure and FiO2 required to maintain oxygenation were 5 cm H2O and 50%, respectively. Cultures were taken from bronchial secretions directly after endotracheal intubation and from urine and blood. The patient was diagnosed with Staphylococcus aureus bacteremia, and based on susceptibility testing, he was started on vancomycin and Zosyn. In addition to antibiotics, the patient received lisinopril for CS-induced hypertension and insulin sliding scale to control hyperglycemia.

Since high circulating levels of glucocorticoids due to ectopic ACTH secretion predispose to infection and impair immune function and clearance of bacteria, the immediate plan was to start him on mifepristone (600 mg daily) as a glucocorticoid receptor antagonist to counteract the immunosuppressive and cognitive effects of the endogenous hypercortisolism. As soon as the patient’s condition improved (which would have been expected given the known reversibility of hypercortisolism), cytoreductive chemotherapy would have been restarted to reduce the paraneoplastic stimulus. However, the patient’s family with medical power of attorney refused consent and withdrew him from the ventilator. The patient died shortly thereafter.

Discussion

Advance directives are written to guarantee autonomy in the event that individual decision-making capacity is lost due to disease severity or treatment [4]. However, as a blanket statement that may contain overly broad (or overly specific) prewritten blocks of text, especially for cancer patients, the content of advance directives may or may not necessarily apply to and/or the patient’s wishes may or may not be correctly interpreted during acute, temporary and potentially reversible conditions that occur during cancer treatment such as infection due to ectopic CS.

Given the potential for cognitive impairment and other acute sequelae such as difficult-to-treat infections from the development of ectopic CS, this case illustrates the importance of revisiting the advance directive when a medical diagnosis associated with temporary cognitive impairment such as CS is made.

Statement of Ethics

The authors have no ethical conflicts to disclose.

Disclosure Statement

The authors have no conflicts of interest to declare.

References

1. Pivonello R, Simeoli C, De Martino MC, Cozzolino A, De Leo M, Iacuaniello D, Pivonello C, et al. Neuropsychiatric disorders in Cushing’s syndrome. Front Neurosci. 2015;9:129. [PMC free article][PubMed]
2. Tsigos C, Chrousos GP. Differential diagnosis and management of Cushing’s syndrome. Annu Rev Med. 1996;47:443–461. [PubMed]
3. Bakker RC, Gallas PR, Romijn JA, Wiersinga WM. Cushing’s syndrome complicated by multiple opportunistic infections. J Endocrinol Invest. 1998;21:329–333. [PubMed]
4. Halpern NA, Pastores SM, Chou JF, Chawla S, Thaler HT. Advance directives in an oncologic intensive care unit: a contemporary analysis of their frequency, type, and impact. J Palliat Med. 2011;14:483–489.[PMC free article] [PubMed]
Articles from Case Reports in Oncology are provided here courtesy of Karger Publishers

Filed under: Cancer, Cushing's, Rare Diseases, symptoms | Tagged: , , , , , , , , , | Leave a comment »

Grading system may predict recurrence, progression of pituitary neuroendocrine tumors

Posted on June 27, 2017 by MaryO

The risk for recurrence or progression of pituitary neuroendocrine tumors in adults is significantly associated with age and tumor type, according to findings published in The Journal of Clinical Endocrinology & Metabolism.

Gérald Raverot, MD, PhD, of Hospices Civils de Lyon, Federation d’Endocrinologie du Pole Est in France, and colleagues evaluated 374 adults (194 women) who underwent surgery for a pituitary neuroendocrine tumor (mean age at surgery, 51.9 years) between February 2007 and October 2012 to test the value of a new classification system on prognostic relevance.

Tumors were classified using a grading system based on invasion on MRI, immunocytochemical profile, Ki-67 mitotic index and p53 positivity. Noninvasive tumors were classified as grade 1a, noninvasive but proliferative tumors were grade 1b, invasive tumors were grade 2a, invasive and proliferative tumors were grade 2b and metastatic tumors were grade 3.

Macroadenomas were the most common type of tumor based on MRI classification (82.1%), followed by microadenoma (13.6%) and giant adenoma (4.3%).

Information on grade was available for 365 tumors; grade 1a was the most common (51.2%), followed by grades 2a (32.3%), 2b (8.8%) and 1b (7.7%).

The progression-free survival analysis included 213 participants from the original cohort during a mean follow-up of 3.5 years. A recurrent event occurred in 52 participants, and progression occurred in 37 participants. The risk for recurrence and/or progression was associated with age (P = .035), tumor type (P = .028) and grade (P < .001). The risk for recurrence and/or progression was increased with grade 2b tumors compared with grade 1a tumors (HR = 3.72; 95% CI, 1.9-7.26) regardless of tumor type. Invasion was significantly associated with recurrence in grade 2a tumors (HR = 2.98; 95% CI, 1.89-4.7), whereas proliferation was not significantly associated with prognosis for grade 1b (HR = 1.25; 95% CI, 0.73-2.13).

“This prospective study confirms the usefulness of our previously proposed classification and may now allow clinicians to adapt their therapeutic strategies according to prognosis, but may also be used to stratify patients and evaluate therapeutic efficacy in future clinical trials,” the researchers wrote. “Further progress can be expected, in particular if an improved understanding of molecular abnormalities associated with pituitary tumorigenesis generates better biomarkers.” – by Amber Cox

Disclosures: The researchers report no relevant financial disclosures.

From https://www.healio.com/endocrinology/neuroendocrinology/news/in-the-journals/%7B4dbd524c-4534-42e3-a1dc-4e3a0d82a0f1%7D/grading-system-may-predict-recurrence-progression-of-pituitary-neuroendocrine-tumors

Filed under: Cushing's, pituitary, Rare Diseases | Tagged: , , , , | Leave a comment »

Cushing’s Syndrome: A Tale of Frequent Misdiagnosis

Posted on June 24, 2017 by MaryO
by Jessica Rotham, National Center for Health Research

What is it?

Cushing’s syndrome is a condition you probably have never heard of, but for those who have it, the symptoms can be quite scary.  Worse still, getting it diagnosed can take a while.  Cushing’s syndrome occurs when the tissues of the body are exposed to high levels of cortisol for an extended amount of time. Cortisol is the hormone the body produces to help you in times of stress. It is good to have cortisol at normal levels, but when those levels get too high it causes health problems.  Although cortisol is related to stress, there is no evidence that Cushing’s syndrome is directly or indirectly caused by stress.

Cushing’s syndrome is considered rare, but that may be because it is under-reported. As a result, we don’t have good estimates for how many people have it, which is why the estimates for the actual number of cases vary so much–from 5 to 28 million people.[1] The most common age group that Cushing’s affects are those 20 to 50 years old.  It is thought that obesity, type 2 diabetes, and high blood pressure may increase your risk of developing this syndrome.[2]

What causes Cushing’s Syndrome?

Cushing’s syndrome is caused by high cortisol levels. Cushing’s disease is a specific form of Cushing’s syndrome. People with Cushing’s disease have high levels of cortisol because they have a non-cancerous (benign) tumor in the pituitary gland.  The tumor releases adrenocorticotropin hormone (ACTH), which causes the adrenal glands to produce excessive cortisol.

Cushing’s syndrome that is not Cushing’s disease can be also caused by high cortisol levels that result from tumors in other parts of the body.  One of the causes is “ectopic ACTH syndrome.” This means that the hormone-releasing tumor is growing in an abnormal place, such as the lungs or elsewhere.  The tumors can be benign, but most frequently they are cancerous. Other causes of Cushing’s syndrome are benign tumors on the adrenal gland (adrenal adenomas) and less commonly, cancerous adrenal tumors (adrenocortical carcinomas). Both secrete cortisol, causing cortisol levels to get too high.

In some cases, a person can develop Cushing’s syndrome from taking steroid medications, such as prednisone. These drugs, known as corticosteroids, mimic the cortisol produced by the body. People who have Cushing’s syndrome from steroid medications do not develop a tumor.[3]

What are the signs and symptoms of Cushing’s Syndrome?

The appearance of people with Cushing’s syndrome starts to change as cortisol levels build up. Regardless of what kind of tumor they have or where the tumor is located, people tend to put on weight in the upper body and abdomen, with their arms and legs remaining thin; their face grows rounder (“moon face”); they develop fat around the neck; and purple or pink stretch marks appear on the abdomen, thighs, buttocks or arms. Individuals with the syndrome usually experience one or more of the following symptoms: fatigue, muscle weakness, high glucose levels, anxiety, depression, and high blood pressure. Women are more likely than men to develop Cushing’s syndrome, and when they do they may have excess hair growth, irregular or absent periods, and decreased fertility.[4]

Why is Cushing’s Syndrome so frequently misdiagnosed?

These symptoms seem distinctive, yet it is often difficult for those with Cushing’s syndrome to get an accurate diagnosis.  Why?  While Cushing’s is relatively rare, the signs and symptoms are common to many other diseases. For instance, females with excess hair growth, irregular or absent periods, decreased fertility, and high glucose levels could have polycystic ovarian syndrome, a disease that affects many more women than Cushing’s.   Also, people with metabolism problems (metabolic syndrome), who are at higher than average risk for diabetes and heart disease, also tend to have abdominal fat, high glucose levels and high blood pressure.[5]

Problems in testing for Cushing’s

When Cushing’s syndrome is suspected, a test is given to measure cortisol in the urine. This test measures the amount of free or unbound cortisol filtered by the kidneys and then released over a 24 hour period through the urine. Since the amount of urinary free cortisol (UFC) can vary a lot from one test to another—even in people who don’t have Cushing’s—experts recommend that the test be repeated 3 times. A diagnosis of Cushing’s is given when a person’s UFC level is 4 times the upper limit of normal.  One study found this test to be highly accurate, with a sensitivity of 95% (meaning that 95% of people who have the disease will be correctly diagnosed by this test) and a specificity of 98% (meaning that 98% of  people who do not have the disease will have a test score confirming that).[6] However, a more recent study estimated the sensitivity as only between 45%-71%, but with 100% specificity.[7]  This means that the test is very accurate at telling people who don’t have Cushing’s that they don’t have it, but not so good at identifying the people who really do have Cushing’s.  The authors that have analyzed these studies advise that patients use the UFC test together with other tests to confirm the diagnosis, but not as the initial screening test.[8]  

Other common tests that may be used to diagnose Cushing’s syndrome are: 1) the midnight plasma cortisol and late-night salivary cortisol measurements, and 2) the low-dose dexamethasone suppression test (LDDST).  The first test measures the amount of cortisol levels in the blood and saliva at night.  For most people, their cortisol levels drop at night, but people with Cushing’s syndrome have cortisol levels that remain high all night. In the LDDST, dexamethasone is given to stop the production of ACTH.  Since ACTH produces cortisol, people who don’t have Cushing’s syndrome will get lower cortisol levels in the blood and urine. If after giving dexamethasone, the person’s cortisol levels remain high, then they are diagnosed with Cushing’s.[9]

Even when these tests, alone or in combination, are used to diagnose Cushing’s, they don’t explain the cause. They also don’t distinguish between Cushing’s syndrome, and something called pseudo-Cushing state.

Pseudo-Cushing state

Some people have an abnormal amount of cortisol that is caused by something unrelated to Cushing’s syndrome such as polycystic ovarian syndrome, depression, pregnancy, and obesity. This is called pseudo-Cushing state.  Their high levels of cortisol and resulting Cushing-like symptoms can be reversed by treating whatever disease is causing the abnormal cortisol levels. In their study, Dr. Giacomo Tirabassi and colleagues recommend using the desmopressin (DDAVP) test to differentiate between pseudo-Cushing state and Cushing’s.  The DDAVP test is especially helpful in people who, after being given dexamethasone to stop cortisol production, continue to have moderate levels of urinary free cortisol (UFC) and midnight serum cortisol.[10]

An additional test that is often used to determine if one has pseudo-Cushing state or Cushing’s syndrome is the dexamethasone-corticotropin-releasing hormone (CRH) test. Patients are injected with a hormone that causes cortisol to be produced while also being given another hormone to stop cortisol from being produced. This combination of hormones should make the patient have low cortisol levels, and this is what happens in people with pseudo-Cushing state.  People with Cushing’s syndrome, however, will still have high levels of cortisol after being given this combination of hormones.[11]

How can Cushing’s be treated?

Perhaps because Cushing’s is rare or under-diagnosed, few treatments are available. There are several medications that are typically the first line of treatment.  None of the medications can cure  Cushing’s, so they are usually taken until other treatments are given to cure Cushing’s, and only after that if the other treatment fails.

The most common treatment for Cushing’s disease is transsphenoidal surgery, which requires the surgeon to reach the pituitary gland through the nostril or upper lip and remove the tumor.  Radiation may also be used instead of surgery to shrink the tumor.  In patients whose Cushing’s is caused by ectopic ACTH syndrome, all cancerous cells need to be wiped out through surgery, chemotherapy, radiation or a variety of other methods, depending on the location of the tumor. Surgery is also recommended for adrenal tumors.  If Cushing’s syndrome is being caused by corticosteroid (steroid medications) usage, the treatment is to stop or lower your dosage.[12]

Medications to control Cushing’s (before treatment or if treatment fails)

According to a 2014 study in the Journal of Clinical Endocrinology and Metabolism, almost no new treatment options have been introduced in the last decade. Researchers and doctors have focused most of their efforts on improving existing treatments aimed at curing Cushing’s. Unfortunately, medications used to control Cushing’s prior to treatment and when treatment fails are not very effective.

Many of the medications approved by the FDA for Cushing’s syndrome and Cushing’s disease, such as pasireotide, metyrapone, and mitotane, have not been extensively studied.  The research presented to the FDA by the makers of these three drugs did not even make clear what an optimal dose was.[13] In another 2014 study, published in Clinical Epidemiology, researchers examined these three same drugs, along with ten others, and found that only pasireotide had moderate evidence to support its approval.  The other drugs, many of which are not FDA approved for Cushing’s patients, had little or no available evidence to show that they work.[14] They can be sold, however, because the FDA has approved them for other diseases.  Unfortunately, that means that neither the FDA nor anyone else has proven the drugs are safe or effective for Cushing patients.

Pasireotide, the one medication with moderate evidence supporting its approval, caused hyperglycemia (high blood sugar) in 75% of patients who participated in the main study for the medication’s approval for Cushing’s.  As a result of developing hyperglycemia, almost half (46%) of the participants had to go on blood-sugar lowering medications. The drug was approved by the FDA for Cushing’s anyway because of the lack of other effective treatments.

Other treatments used for Cushing’s have other risks.  Ketoconazole, believed to be the most commonly prescribed medications for Cushing’s syndrome, has a black box warning due to its effect on the liver that can lead to a liver transplant or death.  Other side effects include: headache, nausea, irregular periods, impotence, and decreased libido. Metyrapone can cause acne, hirsutism, and hypertension. Mitotane can cause neurological and gastrointestinal symptoms such as dizziness, nausea, and diarrhea and can cause an abortion in pregnant women.[15]

So, what should you do if you suspect you have Cushing’s Syndrome?

Cushing’s syndrome is a serious disease that needs to be treated, but there are treatment options available for you if you are diagnosed with the disease. If the symptoms in this article sound familiar, it’s time for you to go see your doctor. Make an appointment with your general practitioner, and explain your symptoms to him or her.  You will most likely be referred to an endocrinologist, who will be able to better understand your symptoms and recommend an appropriate course of action.

 

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

  1. Nieman, Lynette K. Epidemiology and clinical manifestations of Cushing’s syndrome, 2014. UpToDate: Wolters Kluwer Health
  2. Cushing’s syndrome/ disease, 2013. American Association of Neurological Surgeons. http://www.aans.org/Patient%20Information/Conditions%20and%20Treatments/Cushings%20Disease.aspx
  3. Cushing’s syndrome, 2012. National Endocrine and Metabolic Diseases: National Institutes of Health. http://endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx#treatment
  4. Cushing’s syndrome, 2012. National Endocrine and Metabolic Diseases: National Institutes of Health. http://endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx#treatment
  5. Cushing’s syndrome, 2012. National Endocrine and Metabolic Diseases: National Institutes of Health. http://endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx#treatment
  6. Newell-Price, John, Peter Trainer, Michael Besser and Ashley Grossman. The diagnosis and differential diagnosis of Cushing’s syndrome and pseudo-Cushing’s states, 1998. Endocrine Reviews: Endocrine Society
  7. Carroll, TB and JW Findling. The diagnosis of Cushing’s syndrome, 2010. Reviews in Endocrinology and Metabolic Disorders: Springer
  8. Ifedayo, AO and AF Olufemi. Urinary free cortisol in the diagnosis of Cushing’s syndrome: How useful?, 2013. Nigerian Journal of Clinical Practice: Medknow.
  9. Cushing’s syndrome, 2012. National Endocrine and Metabolic Diseases: National Institutes of Health. http://endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx#treatment
  10. Tirabassi, Giacomo, Emanuela Faloia, Roberta Papa, Giorgio Furlani, Marco Boscaro, and Giorgio Arnaldi. Use of the Desmopressin test in the differential diagnosis of pseudo-Cushing state from Cushing’s disease, 2013. The Journal of Clinical Endocrinology & Metabolism: Endocrine Society.
  11. Cushing’s syndrome, 2012. National Endocrine and Metabolic Diseases: National Institutes of Health. http://endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx#treatment
  12. Cushing’s syndrome, 2012. National Endocrine and Metabolic Diseases: National Institutes of Health. http://endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx#treatment
  13. Tirabassi, Giacomo, Emanuela Faloia, Roberta Papa, Giorgio Furlani, Marco Boscaro, and Giorgio Arnaldi. Use of the Desmopressin test in the differential diagnosis of pseudo-Cushing state from Cushing’s disease, 2013. The Journal of Clinical Endocrinology & Metabolism: Endocrine Society.
  14. Galdelha, Monica R. and Leonardo Vieira Neto. Efficacy of medical treatment in Cushing’s disease: a systematic review, 2014. Clinical Endocrinology: John Wiley & Sons.
  15. Adler, Gail. Cushing syndrome treatment & management, 2014. MedScape: WebMD.

Adapted from https://www.center4research.org/cushings-syndrome-frequent-misdiagnosis/

Filed under: adrenal, Cushing's, Diagnostic Testing, pituitary, Rare Diseases | Tagged: , , , , , , , , , , , , | Leave a comment »

Pediatric Endocrine Society Provides Guidance for Growth Hormone Use in Pediatric Patients

Posted on June 3, 2017 by MaryO

HealthDay News—Use of growth hormone in children and adolescents should be considered carefully, with assessment of the risks and benefits necessary for each patient, according to guidelines published in the January issue of Hormone Research in Paediatrics.

Adda Grimberg, MD, from the Perelman School of Medicine at the University of Pennsylvania in Philadelphia, and colleagues updated guidelines on the use of growth hormone, focusing on idiopathic short stature (ISS), GH deficiency (GHD), and primary insulin-like growth factor-I (IGF-I) deficiency (PIGFD). The guidelines were written on behalf of the Pediatric Endocrine Society.

The researchers recommend use of growth hormone for children and adolescents with GHD. Prospective recipients of growth hormone treatment should receive guidance regarding potential adverse effects and should be monitored for these effects. Parents and clinicians should take a shared decision-making approach to treating patients with ISS, and assess the physical and physiological burdens for the child, while considering the risks and benefits of treatment.Follow-up assessment of benefit and psychosocial impact should be conducted at 12 months after initiation and dose optimization of GH. IGF-I therapy is recommended for patients with severe PIGFD. Diagnosis of PIGFD/GH insensitivity syndrome should be based on a combination of factors that fall into four stages.

Physicians with expertise in managing endocrine disorders in children should provide consultation for evaluation of GHD-ISS-PIGFD and manage treatment.

“The taskforce suggests that the recommendations be applied in clinical practice with consideration of the evolving literature and the risks and benefits to each individual patient,” the authors write. “In many instances, careful review highlights areas that need further research.”

Several authors disclosed financial ties to the pharmaceutical industry.

RELATED ARTICLES

Reference

Grimberg A, DiVall SA, Polychronakos C, et al; on behalf of the Drug and Therapeutics Committee of the Pediatric Endocrine Society. Guidelines for growth hormone and insulin-like growth factor-I treatment in children and adolescents: growth hormone deficiency, idiopathic short stature, and primary insulin-like growth factor-I deficiency. Horm Res Paediatr. 2016;86(6):361-397. doi: 10.1159/000452150

 From http://www.endocrinologyadvisor.com/adrenal/growth-hormone-use-in-pediatric-patients/article/634909/

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Cushing’s Testing at NIH

Posted on May 21, 2017 by MaryO
Rank Status Study
1 Recruiting Study to Evaluate CORT125134 in Patients With Cushing’s Syndrome

Condition: Cushing’s Syndrome
Intervention: Drug: CORT125134
2 Recruiting Cushing’s Disease Complications

Condition: Cushing’s Disease
Intervention: Other: Exams and questionnaires
3 Recruiting The Accuracy of Late Night Urinary Free Cortisol/Creatinine and Hair Cortisol in Cushing’s Syndrome Diagnosis

Condition: Cushing Syndrome
Intervention:
4 Recruiting Treatment for Endogenous Cushing’s Syndrome

Condition: Endogenous Cushing’s Syndrome
Intervention: Drug: COR-003
5 Recruiting Saliva Cortisol Measurement as a Screening Test for Suspicious Cushings Syndrome in Children.

Condition: Cushings Syndrome
Intervention: Other: Children refered to the obesity clinic
6 Recruiting Safety and Efficacy of LCI699 for the Treatment of Patients With Cushing’s Disease

Condition: Cushing’s Disease
Intervention: Drug: LCI699
7 Recruiting Treatment of Cushing’s Disease With R-roscovitine

Condition: Cushings Disease
Intervention: Drug: R-roscovitine
8 Recruiting A Study of ATR-101 for the Treatment of Endogenous Cushing’s Syndrome

Condition: Cushing Syndrome
Interventions: Drug: ATR-101;   Drug: Placebos
9 Recruiting Evaluation of 68Ga-DOTATATE PET/CT, Octreotide and F-DOPA PET Imaging in Patients With Ectopic Cushing Syndrome

Condition: Cushing Syndrome
Interventions: Drug: F-DOPA PET Scan;   Drug: Mifepristone;   Drug: Ga-DOTATATE;   Drug: Octreoscan;   Other: CT, MRI
10 Not yet recruiting Endocrine Cardiomyopathy in Cushing Syndrome: Response to Cyclic GMP PDE5 inhibitOrs

Condition: Cushing’s Syndrome Cardiomyopathy
Intervention: Drug: Tadalafil
11 Recruiting Long-term Beneficial Metabolic Effects of Adrenalectomy in Subclinical Cushing’s Syndrome of Adrenal Incidentaloma

Condition: Cushing Syndrome
Intervention: Procedure: surgery
12 Recruiting Long Term Safety and Efficacy of Pasireotide s.c. in Patients With Cushing’s Disease

Condition: Cushings Disease
Intervention: Drug: SOM230
13 Recruiting New Imaging Techniques in the Evaluation of Patients With Ectopic Cushing Syndrome

Condition: Cushing Syndrome
Interventions: Drug: Pentetreotide;   Drug: 18-F-fluorodeoxyglucose;   Drug: (18F)-L-3,4-dihydroxyophenylalanine (18F-DOPA)
14 Not yet recruiting Targeting Iatrogenic Cushing’s Syndrome With 11β-hydroxysteroid Dehydrogenase Type 1 Inhibition

Condition: Iatrogenic Cushing’s Disease
Interventions: Drug: AZD4017 and prednisolone;   Drug: Placebo Oral Tablet and prednisolone
15 Not yet recruiting Assessment of Persistent Cognitive Impairment After Cure of Cushing’s Disease

Condition: Cushing’s Disease
Intervention: Device: Virtual radial task in 3D
16 Recruiting Biomarker Expression in Patients With ACTH-Dependent Cushing’s Syndrome Before and After Surgery

Condition: Cushing’s Syndrome
Intervention:
17 Recruiting Efficacy and Safety Evaluation of Osilodrostat in Cushing’s Disease

Condition: Cushing’s Disease
Interventions: Drug: osilodrostat;   Drug: osilodrostat Placebo
18 Recruiting Effects of Metyrapone in Patients With Endogenous Cushing’s Syndrome

Condition: Cushing’s Syndrome
Intervention: Drug: metyrapone
19 Recruiting Adrenal Venous Sampling in Patients With Overt or Subclinical Cushings Syndrome, and Bilateral Adrenal Tumors

Condition: Cushing Syndrome
Intervention: Radiation: Adrenal venous sampling
20 Recruiting Glycemic Fluctuations in Newly Diagnosed Growth Hormone-Secreting Pituitary Adenoma and Cushing Syndrome Subjects

Condition: Pituitary Adenoma
Intervention: Device: continuous glucose monitoring
Rank Status Study
21 Recruiting Targeted Therapy With Gefitinib in Patients With USP8-mutated Cushing’s Disease

Conditions: Cushing’s Disease;   Corticotrophin Adenoma
Intervention: Drug: Gefitinib
22 Recruiting Cardiac Steatosis in Cushing’s Syndrome

Conditions: Endocrine System Disease;   Cardiovascular Imaging
Intervention: Other: 1H magnetic resonance spectroscopy and CMRI
23 Recruiting Study of Management of Pasireotide-induced Hyperglycemia in Adult Patients With Cushing’s Disease or Acromegaly

Conditions: Cushing’s Disease;   Acromegaly
Interventions: Drug: Pasireotide s.c.;   Drug: Sitagliptin;   Drug: Liraglutide;   Drug: Insulin;   Drug: Pasireotide LAR;   Drug: Metformin
24 Recruiting Study of Efficacy and Safety of Osilodrostat in Cushing’s Syndrome

Conditions: Cushing’s Syndrome;   Ectopic Corticotropin Syndrome;   Adrenal Adenoma;   Adrenal Carcinoma;   AIMAH;   PPNAD
Intervention: Drug: Osilodrostat
25 Recruiting Effects of Hormone Stimulation on Brain Scans for Cushing s Disease

Condition: Pituitary Neoplasm
Intervention: Drug: Acthrel
26 Recruiting Does Serum-DXM Increase Diagnostic Accuracy of the Overnight DXM Suppression Test in the Work-up of Cushing’s Syndrome?

Conditions: Cushing’s Syndrome;   Adrenal Incidentalomas;   Alcoholism;   Obesity
Intervention:
27 Recruiting Adrenalectomy Versus Follow-up in Patients With Subclinical Cushings Syndrome

Condition: Adrenal Tumour With Mild Hypercortisolism
Intervention: Procedure: Adrenalectomy
28 Recruiting Study of Adrenalectomy Versus Observation for Subclinical Hypercortisolism

Conditions: Hypercortisolism;   Cushing Syndrome
Interventions: Procedure: Adrenalectomy;   Other: Observation
29 Not yet recruiting Dynamic Hormone Diagnostics in Endocrine Disease

Conditions: Adrenal Insufficiency;   Congenital Adrenal Hyperplasia;   Cushing Syndrome;   Growth Hormone Deficiency;   Acromegaly;   Primary Hyperaldosteronism
Intervention: Other: 27 hour subcutaneous fluid sampling
30 Recruiting An Investigation of Pituitary Tumors and Related Hypothalmic Disorders

Conditions: Abnormalities;   Craniopharyngioma;   Cushing’s Syndrome;   Endocrine Disease;   Pituitary Neoplasm
Intervention:
31 Recruiting Ga-68-DOTATOC -PET in the Management of Pituitary Tumours

Condition: Pituitary Tumours
Intervention: Procedure: Gallium-68 DOTATOC PET
32 Recruiting Efficacy of Mifepristone in Males With Type 2 Diabetes Mellitus

Conditions: Type 2 Diabetes Mellitus;   Insulin Resistance
Interventions: Drug: Mifepristone 600 mg daily;   Drug: Placebo
33 Recruiting Targeted Therapy With Lapatinib in Patients With Recurrent Pituitary Tumors Resistant to Standard Therapy

Conditions: Pituitary Adenomas;   Prolactinomas
Intervention: Drug: Lapatinib
34 Recruiting Mutations of Glucocorticoid Receptor in Bilateral Adrenal Hyperplasia

Condition: General Glucocorticoid Resistance
Intervention: Genetic: blood collection for mutation characterization
35 Recruiting Defining the Genetic Basis for the Development of Primary Pigmented Nodular Adrenocortical Disease (PPNAD) and the Carney Complex

Conditions: Cushing’s Syndrome;   Hereditary Neoplastic Syndrome;   Lentigo;   Neoplasm;   Testicular Neoplasm
Intervention:
36 Not yet recruiting Reduction by Pasireotide of the Effluent Volume in High-output Enterostomy in Patients Refractory to Usual Medical Treatment

Condition: Enterostomy
Interventions: Drug: Pasireotide;   Drug: Placebo
37 Recruiting Mifepristone for Breast Cancer Patients With Higher Levels of Progesterone Receptor Isoform A Than Isoform B.

Condition: Breast Cancer
Intervention: Drug: Mifepristone
38 Recruiting SOM230 Ectopic ACTH-producing Tumors

Condition: Ectopic ACTH Syndrome
Intervention: Drug: Pasireotide
39 Recruiting Decreasing Rates of Intraurethral Catheterization Postoperatively in Spine Surgery

Condition: Post-operative Urinary Retention
Interventions: Drug: Tamsulosin;   Drug: Placebo
40 Recruiting Adrenal Tumors – Pathogenesis and Therapy

Conditions: Adrenal Tumors;   Adrenocortical Carcinoma;   Cushing Syndrome;   Conn Syndrome;   Pheochromocytoma
Intervention:

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