Cushing’s Testing at NIH

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:

Basal Cortisol Elevated in Patients with ACTH-Staining Pituitary Macroadenoma

Preoperative identification of patients with silent adrenocorticotrophic hormone-secreting tumors could potentially change the approach to management. A new study aimed to determine whether a preoperative adrenocorticotrophic hormone stimulation test for evaluation of nonfunctional pituitary macroadenoma could aid in identifying adrenocorticotrophic hormone-staining pathology yielded large variability and did not allow clinical utility.

Thus, researchers concluded that larger, multicenter research is needed to determine whether this test can be useful.

“As ACTH stimulation tests are performed routinely when evaluating macroadenoma when there is no suspicion for a state of endogenous hypercortisolism, we sought to determine if the test could reliably identify these pathologies during the preoperative evaluation. We hypothesized that patients with subclinical Cushing’s disease or silent ACTH-secreting tumors would have a higher delta cortisol on the ACTH stimulation tests vs. other types of macroadenoma pathologies,” Kevin Pantalone, DO, ECNU, FACE, staff endocrinologist and director of clinical research in the department of endocrinology at Cleveland Clinic, told Endocrine Today.

Pantalone and colleagues performed a retrospective chart review of 148 patients with pituitary macroadenoma who underwent preoperative ACTH stimulation tests, with the goal of determining whether the test can aid in the identification of ACTH-staining pathology.

Overall, 9.5% of patients showed diffuse staining, 50.6% showed other-staining (diffuse staining for anterior pituitary hormones other than ACTH) and 39.9% showed no staining (no staining for any anterior pituitary hormones).

The researchers calculated delta total cortisol at 30 and 60 minutes from baseline and reviewed preoperative ACTH stimulation tests. Additionally, Pantalone and colleagues compared the basal and maximal delta cortisol between the ACTH-staining pituitary macroadenoma and the non-ACTH staining (n = 134), other staining (n = 75) and non-staining (n = 59) tumors.

According to data reported at the American Association of Clinical Endocrinologists Annual Scientific and Clinical Congress, the ACTH-staining group had higher mean basal cortisol levels compared with the non-ACTH-staining (P = .012), other staining (P = .018) and the non-staining (P = .012) tumors. The researchers found no significant differences in maximal delta cortisol between the groups.

“While we found basal cortisol levels were higher in patients with ACTH-staining pituitary microadenoma vs. non-ACTH-staining macroadenoma, the large variability in cortisol values did not allow for clinical utility,” Pantalone told Endocrine Today.

“Unfortunately, in the end, our study was limited by the number of cases with ACTH-staining pathology. Thus, we were unable to determine if the ACTH stimulation test could reliably assist clinicians in potentially identifying ACTH-staining pathology in the preoperative setting,” he said. “A multicenter study, affording a large number of ACTH-staining tumors, is needed. This may allow for us to determine if the ACTH-stimulation test can really be clinically useful in preoperatively identifying ACTH-staining pathology.” – by Amber Cox

Primary Adrenal Insufficiency (PAI)

 Al-Jurayyan NA
Background: Primary adrenal insufficiency (PAI) in children is an uncommon, but potentially fatal. The current symptoms include weakness, fatigue, anorexia, abdominal pain, weight loss, orthostatic hypotension, salt craving and characterized by hyperpigmentation.
Material and Methods: This is a retrospective, hospital based-study, conducted at King Khalid University Hospital (KKUH), during the period January 1989 and December 2014. Review of medical record of patient diagnosed with primary adrenal insufficiency. The diagnosis was based on medical history, physical examination and low levels of glucocorticoids and raised adrenocorticotropic hormone (ACTH). Appropriate laboratory and radiological investigations were also reviewed.
Results: During the period under review, January 1989 and December 2014, a total of 125 patients with the diagnosis of primary adrenal insufficiency were seen. Inherited disorders like congenital adrenal hyperplasia and hypoplasia were common, 85.5%. However, variable autoimmune mediated etiologic diagnosis accounted for, 13%, were also seen. The appropriate various laboratory and radiological investigations should be planned.
Conclusion: Although, congenital adrenal hyperplasia was the commonest etiology, however, congenital adrenal hypoplasia should not be over looked. The diagnosis of PAI can be challenging in some patients, and therefore appropriate serological and radiological investigations should be done.

Topical Steroid Use in Psoriasis Patient Leads to Severe Adrenal Insufficiency

This article is written live from the American Association of Clinical Endocrinologists (AACE) 2017 Annual Meeting in Austin, TX. MPR will be reporting news on the latest findings from leading experts in endocrinology. Check back for more news from AACE 2017.

 

At the AACE 2017 Annual Meeting, lead study author Kaitlyn Steffensmeier, MS III, of the Dayton Veterans Affairs (VA) Medical Center, Dayton, OH, presented a case study describing a patient “who developed secondary adrenal insufficiency secondary to long-term topical steroid use and who with decreased topical steroid use recovered.”

The patient was a 63-year-old white male with a 23-year history of psoriasis. For 18 years, the patient had been applying Clobetasol Propionate 0.05% topically on several areas of his body every day. Upon presentation to the endocrine clinic for evaluation of his low serum cortisol, the patient complained of a 24-pound weight gain over a 2-year period, feeling fatigued, as well as facial puffiness.

Laboratory analysis found that the patient’s random serum cortisol and ACTH levels were low (0.2µg/dL and <1.1pg/mL, respectively). According to the study authors, “the labs were indicative of secondary adrenal insufficiency.” Additionally, a pituitary MRI “showed a 2mm hypoenhancing lesion within the midline of the pituitary gland consistent with Rathke’s cleft cyst versus pituitary microadenoma.”

The patient was initiated on 10mg of hydrocortisone in the morning and 5mg in the evening and was instructed to decrease the use of his topical steroid to one time per month. For the treatment of his psoriasis, the patient was started on apremilast, a phosphodiesterase-4 enzyme (PDE4) inhibitor, and phototherapy.

After 2.5 years, the patient had a subnormal response to the cosyntropin stimulation test. However, after 3 years, a normal response with an increase in serum cortisol to 18.7µg/dL at 60 minutes was obtained; the patient was then discontinued on hydrocortisone. Additionally, a stable pituitary tumor was shown via a repeat pituitary MRI.

The study authors explained that, although secondary adrenal insufficiency is not commonly reported, “one study showed 40% of patients with abnormal cortisol response to exogenous ACTH after two weeks of topical glucocorticoids usage.” Another meta-analysis of 15 studies (n=320) revealed 4.7% of patients developing adrenal insufficiency after using topical steroids. Because of this, “clinicians need to be aware of potential side effects of prolong topical steroid use,” added the study authors.

For continuous endocrine news coverage from the AACE 2017 Annual Meeting, check back to MPR’s AACE page for the latest updates.

From http://www.empr.com/aace-2017/topical-steroid-psoriasis-clobestasol-propionate/article/654335/

Reasons You Have Flab Around Your Abdomen

Some diseases and conditions could be responsible for your abdominal fat.
Mita Majumdar | Updated: April 24, 2017 6:15 pm

Visceral fat or unhealthy belly fat that surrounds the liver and other organs in the abdomen puts you at risk for serious health problems, such as, metabolic syndrome, heart disease, and type 2 diabetes. But, what causes your pot belly or beer fat in the first place? The most obvious answers you will get is – ‘You are not exercising enough’, or, ‘you are eating too much of fatty foods or sugary foods’, or ‘you are not eating the right foods’, or ultimately, ‘It’s genetics! You got it from your parents’. All of these reasons are true, of course. However, some diseases/ disorders and conditions, too, could be responsible for your abdominal fat and these have nothing to do with not exercising or not eating right. Following are some of these disorders.

Cushing’s Syndrome

Cushing’s syndrome, also called hypercortisolism, is an endocrine disorder that occurs when your body is exposed to high cortisol levels over a long period of time. It is a treatable disorder, however, if it is chronic, the symptoms can last lifelong.

Symptoms: Symptoms vary according to the severity of the disorder. The characteristic symptoms include –

  • Fatty tissue deposits in the midsection
  • Fatty deposits in the upper back, especially between the shoulders, so that it resembles a hump
  • Puffy face
  • Violaceous stretch marks (pink or purple) on the arms, breast, stomach, and thighs that are more than 1 cm wide. [1]
  • Easy bruising
  • Fatigue
  • Hirsutism and irregularity in menstruation in women
  • Loss of libido and erectile dysfunction in men
  • Cognitive dysfunction, depression, unpredictable emotional outbursts, irritability is present in 70-85 percent of people with Cushing’s syndrome.[1]

Causes:

  • Overuse of corticosteroids
  • Overproduction of cortisol by the adrenal glands

Management:

  • Surgery is the first line of treatment for Cushing’s syndrome.
  • Medication include: [2]

a.Pituitary gland directed therapy

b.Adrenal-blocking drugs

c.Glucocorticoid receptor-antagonizing drugs

  • Pituitary radiotherapy

Addison’s disease

Addison’s disease, also called adrenal insufficiency, is a disorder where your adrenal glands produce insufficient hormones, especially, glucocorticoids including cortisol and aldosterone. It is a life-threatening disease that can affect anyone irrespective of their gender or age.

How do glucocorticoids influence abdominal fats? Glucocorticoids including cortisol convert the fats into energy in the liver. They also help your body respond to stress. When sufficient amount of glucocorticoids are not produced by the adrenal glands, the fats accumulate in the abdominal area, and you see it as flab around your middle.

Symptoms:

  • Hyperpigmentation
  • Extreme fatigue
  • Low blood sugar and low blood pressure
  • Salt craving as one of the functions of adrenal glands is to maintain the sodium-potassium balance in the body
  • Nausea, vomiting, abdominal pain
  • Weight loss but gain in abdominal fat

Causes:

  • Insufficient production of adrenal cortex hormones
  • Stopping of prescribed corticosteroids
  • Tuberculosis and other infections of adrenal glands
  • Spread of cancer to the adrenal glands

Management:

  • Oral corticosteroids or corticosteroid injections
  • Intravenous injections of hydrocortisone, saline solution, and dextrose in case of Addisonian crisis

Stress

Chronic stress is a very big cause of belly fat. When you are exposed to stress, a chain reaction starts in the body because of the dysregulation of HPA axis of the neuroendocrine system. HPA axis is a complex interaction between the hypothalamus, pituitary gland, and adrenal glands. The hypothalamus produces a corticotropin releasing hormone (CRH) and vasopressin. These together stimulate the secretion of adrenocorticotropic hormone (ACTH). ACTH is transported by the blood to the adrenal glands, which then produces corticosteroids, mainly, cortisol from cholesterol. One of the functions of cortisol is to signal the body to store fat, and specifically, the fat storage occurs in the abdominal area, where the cortisol receptors are greater. Researchers have found that stress causes hyperactivation of HPA axis, leading to accumulation of fat tissue, especially in the abdomen region.

So, the more and longer you are stressed (or if you are chronically stressed), chances are that you will be carrying more belly fat!

Ascites

Ascites is the buildup of fluid in the abdominal space. Ascites usually occurs in people with cancer, and it is then called malignant ascites. Onset of ascites is generally the terminal phase in cancer. Ascites also occurs in patients with liver cirrhosis, kidney failure, or heart disease.

Symptoms:

The first sign of ascites is an increase in abdominal girth accompanied by weight gain. [4] Although it looks like it is belly fat, it is actually the fluid that causes the bulging.

Other symptoms include:

  • Shortness of breath
  • Nausea and vomiting
  • Swelling in the feet and ankle
  • Decreased appetite, sense of fullness, bloating
  • Fatigue
  • Haemorrhoids

Management:

If the ascites is not causing any discomfort, it may not require any treatment. Treatment of ascites can have many side effects. Talk to your doctor before you go in for management/ treatment.

Abdominal hernia

Abdominal hernia is a swelling or a bulge in the abdominal area where an organ or fatty tissue pushes through a weak spot in the abdominal wall. The abdominal wall is made up of tough connective tissue and tendons that stretch from the ribs to the groin. Depending on the position of the weakness in your abdominal wall, the hernia can be inguinal (groin), femoral (upper thigh), umbilical (belly button), hiatal (upper stomach), or even incisional. Incisional hernia can occur when the intestine pushes through a weak spot at the site of abdominal surgery.

Symptoms:

  • Visible bulge that may or may not cause discomfort
  • Feeling of heaviness in the abdomen
  • Sharp pain when you strain or lift objects

Causes:

  • Constipation and diarrhoea
  • Persistent coughing and sneezing
  • Straining or suddenly lifting a heavy object

Management:

  • Umbilical hernia, common in young children, mostly resolves by itself as the abdominal muscles get stronger.
  • Other abdominal hernia normally do not resolve by themselves. Doctors suggest waiting and watching.
  • If treatment is required, surgery is the only option. Surgery involves pushing the hernia back into the abdomen and repairing the abdominal wall.

Menopause

Menopause is certainly not a disease or a disorder. It is the time in a woman’s life when she stops menstruating and cannot become pregnant because her ovaries stop producing the required amounts of hormones oestrogen and progesterone. A woman reaches menopause when she has not had her periods for 12 months.

Symptoms:

  • Hot flashes and/ or night sweats
  • Vaginal dryness
  • Mood swings
  • Sleep disturbances

It is very common to gain belly fat during menopause. This is because of the low oestrogen levels. Oestrogen seems to influence the distribution of fat in the body, in a way that the fat is redistributed from the hips, buttocks, and thighs to the belly. However, a study published in the journal Metabolism reported that though women did significantly gain belly fat, especially deep inside the belly, relative fat distribution is not significantly different after menopause. [5] But the fact remains that women do gain flab in the abdomen after menopause.

Belly fat can be seriously harmful. If your belly fat is not because of the above-mentioned conditions, you can lose it by adopting a healthy lifestyle that includes sleeping enough, exercising regularly, eating right, and reducing stress.

Reference

  1. Sharma ST, Nieman LK, Feelders RA. Cushing’s syndrome: epidemiology and developments in disease management. Clinical Epidemiology. 2015;7:281-293. doi:10.2147/CLEP.S44336.
  1. Feelders RA, Hofland LJ. Medical treatment of Cushing’s disease. J Clin Endocrinol Metab. 2013;98:425–438.
  1. Kyrou I, Chrousos GP, Tsigos C. Stress, visceral obesity, and metabolic complications. Ann N Y Acad Sci. 2006 Nov;1083:77-110.
  1. Sinicrope FA. Ascites. In: Kufe DW, Pollock RE, Weichselbaum RR, et al., editors. Holland-Frei Cancer Medicine. 6th edition. Hamilton (ON): BC Decker; 2003.
  2. Franklin RM, Ploutz-Snyder L, Kanaley JA. Longitudinal changes in abdominal fat distribution with menopause. Metabolism. 2009 Mar;58(3):311-5. doi: 10.1016/j.metabol.2008.09.030.

Adapted from http://www.thehealthsite.com/diseases-conditions/reasons-you-have-flab-around-your-abdomen-f0417/

 

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