Iatrogenic Cushing’s Syndrome and the Hidden Ingredient of Artri King

Posted on January 8, 2026 by MaryO

Abstract

Cushing’s syndrome is a rare disorder caused by prolonged exposure to glucocorticoids, either from endogenous overproduction or exogenous sources, with exogenous steroid use being the most common etiology. Clinical manifestations may include moon facies, abdominal striae, easy bruising, muscle weakness, and complications such as osteoporosis and fragility fractures. Many remedies and supplements marketed for inflammatory conditions are sold online or over the counter, and some may contain hidden or undisclosed steroids that can lead to hypercortisolism. We present a case of a 52-year-old man with osteoporosis who sustained fragility fractures and became wheelchair-bound due to progressive lower extremity weakness. Evaluation demonstrated suppression of the hypothalamic-pituitary-adrenal axis, with undetectable salivary and urinary cortisol levels. Further investigation revealed long-term use of Artri King, a supplement for musculoskeletal pain that contains undisclosed glucocorticoids. This case highlights the risk of unregulated supplements causing iatrogenic Cushing’s syndrome and its associated complications.

Introduction

Cushing’s syndrome represents a constellation of signs and symptoms resulting from prolonged exposure to glucocorticoids [1]. Common manifestations may include moon facies, facial plethora, abdominal striae, easy bruising, and proximal muscle weakness [1]. Etiologies may be adrenocorticotropic hormone (ACTH)-dependent, originating from pituitary or ectopic sources, or ACTH-independent, such as adrenal pathology. In everyday clinical practice, however, exogenous glucocorticoid exposure remains the most common cause [2,3].

Exogenous steroids are available in multiple formulations, including oral, parenteral, inhaled, and topical preparations, and may be prescribed by healthcare providers or found in commercial products sold online or over the counter [4]. Prolonged exposure can result in hypercortisolism and its associated complications [5]. Therefore, careful assessment for exogenous steroid use is essential when evaluating patients with suspected Cushing’s syndrome. We report a case of iatrogenic Cushing’s syndrome secondary to the use of Artri King, a “herbal” supplement containing undisclosed glucocorticoids.

Case Presentation

A 52-year-old male with a history of prediabetes presented with osteoporosis and fragility fractures. Osteoporosis was diagnosed during imaging performed for the evaluation of back pain, which revealed thoracic spine compression fractures as well as a healed rib fracture. As a result, he became wheelchair-bound due to progressive lower extremity weakness. The patient denied prior trauma and had no family history of osteoporosis or pathologic fractures. He denied the use of steroids, proton pump inhibitors, anticoagulants, or antiseizure medications. He did not smoke and reported no alcohol use. There was no history of hypogonadism, bone disease, or fractures during childhood. Biochemical evaluation revealed a normal complete blood count, with pertinent laboratory results summarized in Table 1.

Laboratory test Value Units Reference range
Total testosterone 415 ng/dL 264–916
Intact parathyroid hormone 9.4 pg/mL 8.7–77.1
Corrected serum calcium 9.6 mg/dL 8.6–10.3
24-hour urine calcium 144 mg/24 hours 100–300*
Plasma adrenocorticotropic hormone Undetectable pg/mL 7–63*
Late-night salivary cortisol Undetectable µg/dL ≤0.09*
24-hour urine free cortisol Undetectable µg/24 hours 10–50*
Table 1: Biochemical laboratory results.

*: Reference intervals may vary by assay method and laboratory.

Given the presence of fragility fractures and physical examination findings consistent with Cushing’s syndrome, including moon facies, dorsocervical and supraclavicular fat fullness, and purplish striae (Figure 1), further evaluation was pursued. Laboratory testing demonstrated an undetectable serum ACTH level, and both late-night salivary cortisol and 24-hour urinary free cortisol levels were undetectable, raising concern for exogenous glucocorticoid exposure (Table 1). Dual-energy X-ray absorptiometry demonstrated a spinal bone mineral density of 0.686 g/cm² with a T-score of −3.7.

Purplish-(violaceous)-abdominal-striae-over-the-abdomen.
Figure 1: Purplish (violaceous) abdominal striae over the abdomen.

On further questioning, the patient reported taking Artri King for two years, obtained from Mexico, for joint pain and arthritis. A review of U.S. Food and Drug Administration (FDA) reports confirmed that Artri King contains hidden ingredients, including dexamethasone, not listed on its label. The supplement was discontinued, and the patient was started on a gradual steroid taper to minimize glucocorticoid withdrawal symptoms and allow for the recovery of hypothalamic-pituitary-adrenal (HPA) axis function.

Discussion

Cushing’s syndrome is a rare disorder characterized by a constellation of signs and symptoms affecting multiple organ systems as a result of prolonged exposure to excess cortisol. Hypercortisolism may result from endogenous overproduction of cortisol or from exposure to exogenous glucocorticoids [1]. Regardless of etiology, clinical manifestations commonly include moon facies, abdominal striae, truncal obesity, and easy bruising [1]. Patients with Cushing’s syndrome may also develop complications such as hyperglycemia, uncontrolled hypertension, proximal muscle weakness, and reduced BMD, which can lead to fragility fractures [2]. These complications significantly impair quality of life and may be fatal if the condition is not diagnosed and treated promptly [3].

Endogenous hypercortisolism is less common, with an estimated incidence of 2-3 cases per million per year [4]. However, recent studies suggest a higher prevalence among individuals with diabetes mellitus, osteoporosis, particularly those with fragility fractures, and hypertension [5]. Cushing’s syndrome can be classified as ACTH-dependent, in which ACTH originates from the pituitary gland or an ectopic source, or ACTH-independent, typically due to adrenal adenoma, adrenal hyperplasia, or adrenal carcinoma [5]. Although exogenous glucocorticoid exposure is the most common cause of Cushing’s syndrome, the true incidence of iatrogenic Cushing’s syndrome remains unknown [6]. Rarely, Cushing’s syndrome may result from concurrent exogenous steroid use and endogenous cortisol overproduction, which presents diagnostic challenges [6].

Glucocorticoid-containing medications are widely used in the management of inflammatory diseases, malignancies, and post-transplant care [7,8]. All forms of exogenous glucocorticoids, including oral, inhaled, injectable, and topical preparations, can cause features of hypercortisolism when used at high doses or for prolonged periods [9-12]. Extended exposure, particularly at higher doses, may also result in secondary adrenal insufficiency, even with topical formulations [13]. In addition to conventional glucocorticoids, other medications may induce iatrogenic hypercortisolism; for example, high-dose megestrol exhibits glucocorticoid-like activity and can produce Cushing’s syndrome-like features [14]. Furthermore, drugs that inhibit cytochrome P450 metabolism, such as itraconazole, can impair steroid clearance and increase systemic glucocorticoid exposure [15].

Of increasing concern is the availability of steroid-containing supplements sold over the counter or online without prescription [16]. These products are commonly marketed for conditions such as arthritis and other inflammatory disorders [16]. Prolonged use may cause Cushing’s syndrome with complications such as skin atrophy, obesity, myopathy, and fractures. The U.S. FDA has issued multiple warnings regarding dietary supplements and conventional foods found to contain undisclosed pharmaceutical ingredients [17]. A 2016 study evaluating 12 over-the-counter “adrenal support” supplements in the United States found that most contained at least one steroid hormone [18]. Another analysis of FDA warnings on unapproved pharmaceutical ingredients reported that 37.5% of products marketed for inflammatory conditions, including joint and muscle pain, contained dexamethasone [19]. Among these products, Artri King, marketed for joint pain and arthritis, has been associated with multiple FDA reports of adverse events due to undisclosed dexamethasone and methylprednisolone. These supplements remain widely available online, in select retail stores, and internationally [20].

Conclusions

This case highlights the importance of considering unregulated supplements as a potential source of exogenous glucocorticoids in patients presenting with osteoporosis and unexplained fragility fractures. Although the patient initially denied steroid use, detailed history revealed prolonged exposure to Artri King, resulting in iatrogenic Cushing’s syndrome with HPA axis suppression. Before discontinuation of steroid-containing supplements, evaluation for adrenal insufficiency is essential. Gradual tapering of glucocorticoids remains the standard approach to prevent withdrawal symptoms and support recovery of adrenal function.

References

  1. Nieman LK: Recent updates on the diagnosis and management of Cushing’s syndrome. Endocrinol Metab (Seoul). 2018, 33:139-46. 10.3803/EnM.2018.33.2.139
  2. Dunn C, Amaya J, Green P: A case of iatrogenic Cushing’s syndrome following use of an over-the-counter arthritis supplement. Case Rep Endocrinol. 2023, 2023:4769258. 10.1155/2023/4769258
  3. Castinetti F, Morange I, Conte-Devolx B, Brue T: Cushing’s disease. Orphanet J Rare Dis. 2012, 7:41. 10.1186/1750-1172-7-41
  4. Nieman LK, Biller BM, Findling JW, Newell-Price J, Savage MO, Stewart PM, Montori VM: The diagnosis of Cushing’s syndrome: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2008, 93:1526-40. 10.1210/jc.2008-0125
  5. Manubolu S, Nwosu O: Exogenous Cushing’s syndrome secondary to intermittent high dose oral prednisone for presumed asthma exacerbations in the setting of multiple emergency department visits. J Clin Transl Endocrinol Case Rep. 2017, 6:4-8. 10.1016/j.jecr.2017.07.001
  6. Tong CV, Rajoo S: Co-occurrence of exogenous and endogenous Cushing’s syndromes-dilemma in diagnosis. Case Rep Endocrinol. 2019, 2019:2986312. 10.1155/2019/2986312
  7. Broersen LH, Pereira AM, Jørgensen JO, Dekkers OM: Adrenal insufficiency in corticosteroids use: systematic review and meta-analysis. J Clin Endocrinol Metab. 2015, 100:2171-80. 10.1210/jc.2015-1218
  8. Yasir M, Goyal A, Sonthalia S: Corticosteroid Adverse Effects. StatPearls Publishing, Treasure Island, FL; 2025.
  9. Dow A, Yu R, Carmichael J: Too little or too much corticosteroid? Coexisting adrenal insufficiency and Cushing’s syndrome from chronic, intermittent use of intranasal betamethasone. Endocrinol Diabetes Metab Case Rep. 2013, 2013:130036. 10.1530/EDM-13-0036
  10. Hopkins RL, Leinung MC: Exogenous Cushing’s syndrome and glucocorticoid withdrawal. Endocrinol Metab Clin North Am. 2005, 34:371-84, ix. 10.1016/j.ecl.2005.01.013
  11. Hughes JM, Hichens M, Booze GW, Thorner MO: Cushing’s syndrome from the therapeutic use of intramuscular dexamethasone acetate. Arch Intern Med. 1986, 146:1848-9.
  12. Weber SL: Cushing’S syndrome attributable to topical use of lotrisone. Endocr Pract. 1997, 3:140-4. 10.4158/EP.3.3.140
  13. Pektas SD, Dogan G, Cinar N: Iatrogenic Cushing’s syndrome with subsequent adrenal insufficiency in a patient with psoriasis vulgaris using topical steroids. Case Rep Endocrinol. 2017, 2017:8320254. 10.1155/2017/8320254
  14. Steer KA, Kurtz AB, Honour JW: Megestrol-induced Cushing’s syndrome. Clin Endocrinol (Oxf). 1995, 42:91-3. 10.1111/j.1365-2265.1995.tb02603.x
  15. Bolland MJ, Bagg W, Thomas MG, Lucas JA, Ticehurst R, Black PN: Cushing’s syndrome due to interaction between inhaled corticosteroids and itraconazole. Ann Pharmacother. 2004, 38:46-9. 10.1345/aph.1D222
  16. Saad-Omer SM, Kinaan M, Matos M, Yau H: Exogenous Cushing syndrome and hip fracture due to over-the-counter supplement (Artri King). Cureus. 2023, 15:e41278. 10.7759/cureus.41278
  17. Patel R, Sherf S, Lai NB, Yu R: Exogenous Cushing syndrome caused by a “herbal” supplement. AACE Clin Case Rep. 2022, 8:239-42. 10.1016/j.aace.2022.08.001
  18. Akturk HK, Chindris AM, Hines JM, Singh RJ, Bernet VJ: Over-the-counter “adrenal support” supplements contain thyroid and steroid-based adrenal hormones. Mayo Clin Proc. 2018, 93:284-90. 10.1016/j.mayocp.2017.10.019
  19. Tucker J, Fischer T, Upjohn L, Mazzera D, Kumar M: Unapproved pharmaceutical ingredients included in dietary supplements associated with US Food and Drug Administration warnings. JAMA Netw Open. 2018, 1:e183337. 10.1001/jamanetworkopen.2018.3337
  20. U.S. Food and Drug Administration. Public Notification: Artri King contains hidden drug ingredients. (2022). Accessed: December 18, 2025: https://www.fda.gov/drugs/medication-health-fraud/public-notification-artri-king-contains-hidden-drug-ingredients.

https://www.cureus.com/articles/451949-iatrogenic-cushings-syndrome-and-the-hidden-ingredient-of-artri-king#!/

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Participating in Life

Posted on January 7, 2026 by MaryO

I think that this is so important, especially with our health.  Had I not been an active participant and followed several doctors’ advice 25 years ago, I’d most likely not been here to write this.

I see this all the time, though.  Whatever the doctor says is true.  People will say that the doctor gave me this or that med but they don’t know what it is for.

I just don’t get how people can take meds and not have a clue what they are, how they work, how they might interact with other drugs they may be taking.  But it happens because people blindly follow whatever a doctor may give them.

Participation is so important – you have to know how YOU’RE feeling, what YOUR symptom are.  Do your own research.  Your doctor doesn’t know what it feels like to live in your body no matter how much you try to tell him/her.

Ultimately, you are the one who cares most about yourself and the only one who can make a difference through your research, thoughts and actions.

Just because a doctor gives you something, you don’t have to take it.  24 years ago a locally well-known neurologist “gave me” Xanax. Since he couldn’t see my tumor with his Magnetic Resonance Imaging (MRI) machine there was “no possibility” that it existed.  Had I followed his advice, taken the Xanax and stopped pursuing a Cushing’s diagnosis I would most have likely died by now.

The doctor was going by the odds.  The odds were that I really didn’t have a pituitary tumor.  But I’m not a statistic and neither are you.  Follow your instincts and take care of YOU.  This is the only life you’ll ever have.

The most healing thing we can do for ourselves is to participate in the process of our lives as fully as we can-even when the unexpected and the fearful happen.

~Today’s Page-a-Day calendar

What do YOU do to keep participating in your health care and daily life?

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Cushing’s Syndrome Treatments

Posted on January 7, 2026 by MaryO
Medications, Surgery, and Other Treatments for Cushing’s Syndrome

Written by | Reviewed by Daniel J. Toft MD, PhD

Treatment for Cushing’s syndrome depends on what symptoms you’re experiencing as well as the cause of Cushing’s syndrome.

Cushing’s syndrome is caused by an over-exposure to the hormone cortisol. This excessive hormone exposure can come from a tumor that’s over-producing either cortisol or adrenocorticotropic hormone (ACTH—which stimulates the body to make cortisol). It can also come from taking too many corticosteroid medications over a long period of time; corticosteroids mimic the effect of cortisol in the body.

The goal of treatment is to address the over-exposure. This article walks you through the most common treatments for Cushing’s syndrome.

Gradually decreasing corticosteroid medications: If your doctor has identified that the cause of your Cushing’s syndrome is corticosteroid medications, you may be able to manage your Cushing’s syndrome symptoms by reducing the overall amount of corticosteroids you take.

It’s common for some people with certain health conditions—such as arthritis and asthma—to take corticosteroids to help them manage their symptoms. In these cases, your doctor can prescribe non-corticosteroid medications, which will allow you to reduce—or eliminate—your use of corticosteroids.

It’s important to note that you shouldn’t stop taking corticosteroid medications on your own—suddenly stopping these medications could lead to a drop in cortisol levels—and you need a healthy amount of cortisol. When cortisol levels get too low, it can cause a variety of symptoms, such as muscle weakness, fatigue, weight loss, and low blood pressure, which may be life-threatening.

Instead, your doctor will gradually reduce your dose of corticosteroids to allow your body to resume normal production of cortisol.

If for some reason you cannot stop taking corticosteroids, your doctor will monitor your condition very carefully, frequently checking to make sure your blood glucose levels as well as your bone mass levels are normal. Elevated blood glucose levels and low bone density are signs of Cushing’s syndrome.

Surgery to remove a tumor: If it’s a tumor causing Cushing’s syndrome, your doctor may recommend surgery to remove the tumor. The 2 types of tumors that can cause Cushing’s are pituitary tumors (also called pituitary adenomas) and adrenal tumors. However, other tumors in the body (eg, in the lungs or pancreas) can cause Cushing’s syndrome, too.

Pituitary adenomas are benign (non-cancerous), and most adrenal tumors are as well. However, in rare cases, adrenal tumors can be malignant (cancerous). These tumors are called adrenocortical carcinomas, and it’s important to treat them right away.

Surgery for removing a pituitary tumor is a delicate process. It’s typically performed through the nostril, and your surgeon will use tiny specialized tools. The success, or cure, rate of this procedure is more than 80% when performed by a surgeon with extensive experience. If surgery fails or only produces a temporary cure, surgery can be repeated, often with good results.

If you have surgery to remove an adrenal tumor or tumor in your lungs or pancreas, your surgeon will typically remove it through a standard open surgery (through an incision in your stomach or back) or minimally invasive surgery in which small incisions are made and tiny tools are used.

In some cases of adrenal tumors, surgical removal of the adrenal glands may be necessary.

Radiation therapy for tumors: Sometimes your surgeon can’t remove the entire tumor. If that happens, he or she may recommend radiation therapy—a type of treatment that uses high-energy radiation to shrink tumors and/or destroy cancer cells.

Radiation therapy may also be prescribed if you’re not a candidate for surgery due to various reasons, such as location or size of the tumor. Radiation therapy for Cushing’s syndrome is typically given in small doses over a period of 6 weeks or by a technique called stereotactic radiosurgery or gamma-knife radiation.

Stereotactic radiosurgery is a more precise form of radiation. It targets the tumor without damaging healthy tissue.

With gamma-knife radiation, a large dose of radiation is sent to the tumor, and radiation exposure to the healthy surrounding tissues is minimized. Usually one treatment is needed with this type of radiation.

Medications for Cushing’s syndrome: If surgery and/or radiation aren’t effective, medications can be used to regulate cortisol production in the body. However, for people who have severe Cushing’s syndrome symptoms, sometimes medications are used before surgery and radiation treatment. This can help control excessive cortisol production and reduce risks during surgery.

Examples of medications your doctor may prescribe for Cushing’s syndrome are: aminoglutethimide (eg, Cytadren), ketoconazole (eg, Nizoral), metyrapone (eg, Metopirone), and mitotane (eg, Lysodren). Your doctor will let you know what medication—or combination of medications—is right for you.

You may also need to take medication after surgery to remove a pituitary tumor or adrenal tumor. Your doctor will most likely prescribe a cortisol replacement medication. This medication helps provide the proper amount of cortisol in your body. An example of this type of medication is hydrocortisone (a synthetic form of cortisol).

Experiencing the full effects of the medication can take up to a year or longer. But in most cases and under your doctor’s careful supervision, you can slowly reduce your use of cortisol replacement medications because your body will be able to produce normal cortisol levels again on its own. However, in some cases, people who have surgery to remove a tumor that causes Cushing’s syndrome won’t regain normal adrenal function, and they’ll typically need lifelong replacement therapy.2

Treating Cushing’s Syndrome Conclusion
You may need one treatment or a combination of these treatments to effectively treat your Cushing’s syndrome. Your doctor will let you know what treatments for Cushing’s syndrome you’ll need.

From https://www.endocrineweb.com/conditions/cushings-syndrome/cushings-syndrome-treatments

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FDA Declines to Approve Relacorilant for Hypertension Linked to Hypercortisolism

Posted on January 6, 2026 by MaryO

Key takeaways:

  • The FDA issued a complete response letter for relacorilant to treat hypertension tied to hypercortisolism.
  • The investigational drug induced BP reductions for adults with hypertension in the phase 3 GRACE trial.

The FDA has issued a complete response letter for an oral selective glucocorticoid receptor antagonist under investigation for the treatment of hypertension secondary to hypercortisolism, according to an industry press release.

Corcept Therapeutics announced the FDA issued a complete response letter for relacorilant (Corcept Therapeutics). The drug is under investigation for the treatment of endogenous hypercortisolism, ovarian cancer and other disorders, according to the company.

As Healio previously reported, the phase 3 GRACE trial enrolled 152 adults with Cushing’s syndrome plus hypertension, hyperglycemia or both conditions. Participants received relacorilant for 22 weeks during an open-label phase. At 22 weeks, adults who met criteria for hypertension or hyperglycemia control entered a withdrawal phase where they were randomly assigned, 1:1, to continue relacorilant or switch to placebo for 12 weeks.

In the GRACE trial, adults with hypertension had a 7.9 mm Hg decrease in systolic blood pressure and a 5.1 mm Hg decline in diastolic BP at 22 weeks. During the randomized withdrawal phase, adults who remained on relacorilant had no change in systolic and diastolic BP, whereas those receiving placebo had a BP increase from the start of the phase to week 12.

In a press release from Corcept Therapeutics from 2024, the company announced results from the phase 3 GRADIENT trial, a randomized, double-blind, placebo-controlled trial where adults with Cushing’s syndrome caused by an adrenal adenoma or adrenal hyperplasia were randomly assigned, 1:1, to relacorilant or placebo for 22 weeks. According to the press release, the relacorilant group had a 6.6 mm Hg decline in mean systolic BP compared with baseline at 22 weeks. However, there was no significant difference in mean systolic BP change between the relacorilant and placebo groups.

As Healio previously reported, relacorilant was also assessed in a long-term extension study that enrolled adults who completed the GRACE and GRADIENT trials as well as a phase 2 hypercortisolism study. In that trial, relacorilant conferred a 10 mm Hg drop in 24-hour ambulatory systolic BP and a 7.3 mm Hg reduction in 24-hour ambulatory diastolic BP at 24 months.

In the company’s press release announcing receipt of the complete response letter, Corcept Therapeutics said the FDA acknowledged that the GRACE trial met its primary endpoint and that the GRADIENT trial provided “confirmatory evidence.” However, the FDA said it did not view relacorilant offered “a favorable benefit-risk assessment” without more data of its effectiveness, according to the press release.

“We are surprised and disappointed by this outcome,” Joseph K. Belanoff, MD, CEO of Corcept Therapeutics, said in a press release. “Our commitment to patients suffering from the effects of hypercortisolism is unwavering. I am confident we will find a way to get relacorilant to the patients it could help. We will meet with the FDA as soon as possible to discuss the best path forward.”

https://www.healio.com/news/endocrinology/20251231/fda-declines-to-approve-relacorilant-for-hypertension-linked-to-hypercortisolism?utm_source=selligent&utm_medium=email&utm_campaign=20251231ENDO&utm_content=20251231ENDO

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Genetic mutation lowers obesity in Cushing’s syndrome

Posted on January 5, 2026 by MaryO

London E. J Clin Endocrinol Metab. 2013; doi:10.1210/jc.2013-1956.

Among adult patients with Cushing’s syndrome, those with mutations in PRKAR1A, the gene that controls cAMP-dependent protein kinase, are less obese than their counterparts without these mutations, according to a recent study.

The retrospective study evaluated adrenalectomy samples from 51 patients with Cushing’s syndrome, 13 with PRKAR1A mutations and 32 without. Of the 51 patients, 40 were female and 11 were male, and patients ranged in age from 4 to 74 years.

A non-Cushing’s syndrome comparison group consisting of 6 adrenalectomy patients with aldosterone producing adenomas (APAs) was included. Additional comparison groups comprising clinical data from 89 patients with Cushing’s disease and 26 with hyperaldosteronism were also studied.

Researchers recorded the weight, height and BMI of all patients, and measured abdominal subcutaneous adipose tissue (ScAT) and periadrenal adipose tissue (PAT) using computed tomography. PAT was collected and frozen for evaluation; the extracts were assessed for levels of cAMP and protein kinase (PKA) activity, as well as for protein and mRNA expression of subunits of PKA. Diurnal cortisol levels and urine-free cortisol were also measured preoperatively.

The study found that in adults with Cushing’s syndrome, the mean BMI of those with PRKAR1A mutations was lower than that of patients with noPRKAR1A mutations (P<.05), and was not inconsistent with the hyperaldosteronism comparison group.

In pediatric patients with adrenal Cushing’s syndrome, the presence of PRKAR1A mutation did not have an impact on mean BMI z-scores. However, in comparison with pediatric patients with pituitary Cushing’s disease, the BMI z-scores were significantly lower in pediatric Cushing’s disease patients with PRKAR1Amutations (P<.05). Patients with Cushing’s syndrome without PRKAR1A mutations had significantly more PAT and ScAT than non-Cushing’s syndrome patients. Additionally, the ratio of basal-to-total (cAMP-triggered) PKA activity was significantly lower in patients with PRKAR1A mutations, suggesting greater proportions of active PKA (P<.005).

“These findings have obvious implications in the establishment of the diagnosis of CS in patients with PRKAR1A mutations: These patients may be leaner than other patients with [Cushing’s syndrome],” the study authors wrote. “Perhaps more importantly, our findings point to the importance of cAMP and or PKA signaling in the regulation of adiposity.”

Disclosures: The researchers report no relevant financial disclosures.

From http://www.healio.com/endocrinology/adrenal/news/online/%7B693f94cd-359d-4c52-8e0d-bfd0e4a51d03%7D/genetic-mutation-lowers-obesity-in-cushings-syndrome

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