Accidental Cushing Syndrome

Posted on February 5, 2024 by MaryO

Abstract

We present a patient with Cushing syndrome secondary to accidental intake of corticosteroid tablets—a 66-year-old woman with a history of well-controlled hypertension, who over the course of a few weeks developed full-blown Cushing syndrome with uncontrolled blood pressure, typical central fat accumulation, and easy bruising. The clinical features further worsened upon increase of the dosage of her antihypertensive medication because of rising blood pressure. Biochemical analyses showed low cortisol and ACTH concentrations. Inspection of the patient’s medications revealed that she had accidentally been taking corticosteroids tablets, prescribed for her husband, instead of antihypertensives, ie, dexamethasone 4 mg and then 8 mg, instead of candesartan at the same dose.

This case highlights the necessity of a thorough review of the medications taken by patients suspected to have exogenous Cushing syndrome, including inspection of the original packaging, and not just relying on information from the patient and electronic health records. This case also highlights the need of special labeling on the packaging for the easy identification of corticosteroid-containing medications given their widespread availability.

Introduction

Cushing syndrome (CS) is a disorder caused by prolonged and excessive exposure to glucocorticoids. The most common cause of CS is exogenous or iatrogenic, ie, CS caused by administration of glucocorticoids due to inflammatory, autoimmune, or neoplastic diseases. Endogenous CS is a rare condition, caused by either hypersecretion of ACTH from the pituitary gland, ectopic ACTH production, or hypersecretion of cortisol from the adrenal glands.

It is of great importance to exclude exogenous CS in all patients who present with signs and symptoms compatible with the syndrome. The following case highlights the need to rule out exogenous CS via a face-to-face review of the medications taken by a patient with CS, rather than only relying on the patient’s history and electronic health record.

Case Presentation

A 66-year-old woman was referred to our department for investigation of suspected CS. She was diagnosed with essential hypertension a couple of years earlier and was prescribed tablet candesartan 4 mg daily. Apart from an otherwise well-controlled hypertension, the patient had a history of bilateral hip replacement, the first performed in 2020 and the second 2 years later.

During the 6 weeks prior to our evaluation, the patient had noticed an increasing fat accumulation around her abdomen, upper back, neck, and over the collar bones, despite minimal increase of her body weight. Moreover, the patient had developed a rounded face and increased growth of facial hair, especially on the chin, as well as thin and fragile skin that bruised easily. About 1.5 weeks before she was referred to our clinic, the dose of candesartan was increased by her general practitioner from 4 to 8 mg daily because of rapidly worsening hypertension, confirmed by monitoring 24-hour ambulatory blood pressure.

Diagnostic Assessment

The physical examination of the patient revealed central obesity and multiple bruises that the patient could not recall. Increased growth of fine hairs on the chin and facial plethora was present. Blood pressure was 165/88 mmHg. The patient did not have any signs of abdominal stretch marks, nor did she have any obvious muscle wasting in the arms and legs (Fig. 1). When comparing to photographs taken about 6 months prior to the examination, the differences were obvious (Fig. 2).

 

Figure 1.

The patient few weeks prior to admission for evaluation of Cushing syndrome.

 

Figure 2.

The patient many months before the onset of Cushing syndrome.

Biochemical evaluation revealed unmeasurable plasma cortisol at 12:00 PM, 4:00 PM, and 6:00 AM (<28 nmol/L, reference 102-535 nmol/L; <1.01 μg/dL, reference 3.69-19.39 μg/dL). Serum ACTH was also undetectable (<0.2 pmol/L, reference 1.6-13.9 pmol/L; <0.91 pg/mL, reference 2.27-63.18 pg/mL), which raised suspicion of exogenous CS. The patient firmly denied any intake of anything other than her candesartan tablets. She even stated that she avoided any analgesics after the hip replacement previously the same year, nor had she received any intra-articular cortisone injection. The patient gave a very trustworthy and consistent impression, which inevitably led us to proceed to further investigation of the adrenal glands and the pituitary gland to exclude rarer forms of CS, such as cyclic CS and/or pituitary apoplexy of an ACTH-producing pituitary adenoma. The magnetic resonance imaging of the pituitary and the computed tomography of the adrenal glands were normal. Except for the low cortisol and ACTH levels, endocrine workup was unremarkable (Table 1).

 
Table 1.

Biochemical evaluation of the patient with Cushing syndrome at baseline, ie, at admission

Hormone tested Value Normal Range
Plasma cortisol at 08:00 AM <1.01 mcg/dL (<28 nmol/L) 3.70-19.39 mcg/dL (102-535 nmol/L)
ACTH <0.91 pg/mL (<0.2 pmol/L) 7.27-63.18 pg/mL (1.6-13.9 pmol/L)
TSH 1.0 mIU/L (1.0 mIU/L) 0.4-3.7 mIU/L (0.4-3.7 mIU/L)
Free T4 1.01 ng/dL (13 pmol/L) 0.76-1.32 ng/dL (9.8-17 pmol/L)
IGF-1 142 ng/mL (18.60 nmol/L) 38-162 ng/mL (4.98-21.22 nmol/L)
Prolactin 374 mIU/L (17.58 mcg/L) 63-561 mIU/L (2.96-26.37 mcg/L)
FSH 90 mIU/mL (90 IU/L) 27-133 mIU/mL (post-menopausal) (27-133 IU/L)
LH 16 mIU/mL (16 IU/L) 5.2-62 mIU/mL (post-menopausal) (5.2-62 IU/L)
SHBG 6.07 mcg/mL (54 nmol/L) 2.25-17.42 mcg/mL (20-155 nmol/L)
Testosterone 8.65 ng/dL (0.30 nmol/L) 11.53-34.58 ng/dL (0.4-1.2 nmol/L)
Estradiol <19.07 pg/mL (<70 pmol/L) <28.06 pg/mL (<103 pmol/L) (post-menopausal with no hormone substitute)
Aldosterone 9.05 ng/dL 0.251 pmol/L <23.61 ng/dL (recumbent position) <655 nmol/L
Renin 8.25 mIU/L 2.8-40 mIU/L (recumbent position)
DHEAS 14.81 mcg/dL (0.4 µmol/L) 29.63-181.48 mcg/dL (0.8-4.9 µmol/L)
HbA1c 45 mmol/mol (6.3 %) 31-46 mmol/mol (5-6.4 %)

Abnormal values are shown in bold font. Values in parenthesis are International System of Units (SI).

Abbreviations: ACTH, adrenocorticotropic hormone; TSH, thyroid-stimulating hormone; T4, thyroxine; IGF-1, insulin-like growth factor 1; FSH, follicle-stimulating hormone; LH, luteinizing hormone; SHBG, sex hormone binding globulin; DHEAS, dehydroepiandrosterone sulfate; HbA1c, glycated hemoglobin.

On day 3 after admission, we noted that plasma cortisol at 8:00 AM was measurable, though still low, at 134 nmol/L (4.86 μg/dL), which reinforced our first suspicion of exogenous CS and prompted a more thorough review of the patient’s medication. At this time, we asked the patient to show us the tablets that she had been taking at home and that she still carried in her purse. To the patient’s frank surprise, it turned out that she was indeed carrying tablets containing 4 mg dexamethasone in the belief that they were candesartan 4 mg tablets. The dexamethasone 4 mg tablet the patient had (generic) was white, scored with a diameter of 6 mm (Fig. 3A). The candesartan 4 mg tablet the patient had been dispensed (generic) was also white, scored and with a diameter of 7 mm (Fig. 3B).

 

Figure 3.

A. Tablet Dexamethasone 4 mg. White, scored, diameter 6 × 6 mm. B. Tablet Candesartan 4 mg. White, scored, diameter 7 × 7 mm.

Treatment

The patient was discharged with the same antihypertensive medications as prior to the deterioration and referred to her general practitioner for follow-up of blood pressure. Upon clinical evaluation 5 months after discharge, she showed no signs or symptoms of CS (Fig. 4).

 

Figure 4.

The patient 5 months after the resolution of Cushing syndrome.

Outcome and Follow-up

Thus, the patient had accidentally been taking her husband’s medication, with which the patient had been aiding her husband, and developed a surreptitious iatrogenic CS. In hindsight, the severity of the clinical features had been worsening and resulted in rapid deterioration alongside the increase of the dosage of the antihypertensives from 4 to 8 mg because of the rising blood pressure.

By day 5 after admission, the patient’s plasma cortisol and ACTH concentrations had normalized, as had her blood pressure.

Discussion

Exogenous hypercortisolism is the most common cause of CS, though seldomly published in the literature, and is mainly iatrogenic because of prolonged use of high doses of synthetic glucocorticoids prescribed for the treatment of nonendocrine diseases (1). A recent study has shown that as many as every seventh resident in western Sweden received a glucocorticoid prescription between 2007 and 2014 (2).

The rising use of generic medications during the past decade has resulted in corticosteroids being available in different forms, shapes, and packages that make them less easily recognizable. In many countries, corticosteroids are available over-the-counter in almost any form, whereas a variety of agents such as herbal preparations, tonics, and skin-bleaching creams may also contain corticosteroids to the unawareness of the people using them (3, 4).

There are no large studies regarding how common the unintentional use of medicines or products that contain corticosteroids. However, studies on traditional Chinese medicine have shown that illegally impure herbs and medicines containing corticosteroids are widely used, suggesting that the accidental intake of corticosteroids is more frequent than we may think (3, 5). Many cases of factitious CS have been reported as a cause of exogenous CS, which makes the diagnosis even more challenging (6-8).

The Endocrine Society Clinical Practice Guidelines for the diagnosis of CS recommend that exogenous CS be always excluded before starting the investigation of endogenous CS (9). However, a specific and definitive approach for diagnosing, respectively excluding, exogenous CS is currently lacking. In a recent review, the authors recommend that in addition to asking the patient which medicines they take, the physician should review the electronic health record and ask particularly for medications that are administered via nonoral routes, as well as over-the-counter agents as mentioned earlier (10).

If not confirmed by history, the physician is advised to proceed to the measurement of ACTH and/or dehydroepiandrosterone sulfate as well as screening for synthetic glucocorticoids (10). The results usually show low ACTH, dehydroepiandrosterone sulfate, and cortisol levels even though the clinical picture suggests CS. The cross-reactivity of hydrocortisone or cortisone, which is similar to endogenous steroids, in immunoassay-based measurements of plasma and urinary cortisol may show variable levels of cortisol. These measurements combined with low ACTH can make the diagnostic workup much more complex (7). Screening for exogenous substances with the help of high-performance liquid chromatography is usually positive and constructive (7).

It is increasingly clear that the risk of accidental ingestion of potent medicines can have deleterious effects on health. This leads us to conclude that thorough face-to-face review of the packaging of medications taken by the patient is mandatory and can spare both physicians and patients from a series of unnecessary investigations. Given the high availability, easy access, and catastrophic adverse effects of the unintentional use of corticosteroids, we therefore propose that all corticosteroid-including medications and agents be marked with a recognizable label.

Learning Points

  • Exogenous CS should be always excluded before starting investigation of endogenous CS.
  • Concerning exogenous CS, practitioners should always think broadly and ask for use of herbal preparations, skin-bleaching creams, and any over-the-counter products.
  • Unintentional use of corticosteroids can still be the case even after a thorough review of the electronic records; practitioners should always inspect the medicines the patient has taken.

Contributors

All authors (K.K., O.R., P.T.) made equal contributions to authorship. K.K., O.R., and P.T. were involved in the diagnosis and management of this patient, as well as in manuscript submission. K.K. and P.T. authored the manuscript draft. All authors (K.K., O.R., P.T.) reviewed and approved the final draft.

Funding

No public or commercial funding.

Disclosures

None declared.

Informed Patient Consent for Publication

Signed informed consent was obtained directly from the patient.

© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Evaluation of Psoriasis Patients With Long-Term Topical Corticosteroids for Their Risk of Developing Adrenal Insufficiency, Cushing’s Syndrome and Osteoporosis

Posted on January 3, 2024 by MaryO

In this study, we will investigate the possible side effects of psoriasis patients using long-term topical corticosteroids (TCS) such as adrenal insufficiency, Cushing’s Syndrome (CS) and osteoporosis and determine how these side effects develop.

Forty-nine patients were included in the study. The patients were divided into two groups based on the potency of the topical steroid they took and the patients’ ACTH, cortisol and bone densitometer values were evaluated.

There was no significant difference between the two groups regarding the development of surrenal insufficiency, CS and osteoporosis. One patient in group 1 and 4 patients in group 2 were evaluated as iatrogenic CS. ACTH stimulation tests of these patients in group 2 showed consistent results with adrenal insufficiency, while no adrenal insufficiency was detected in the patient in Group 1. Patients who used more than 50g of superpotent topical steroids per week compared to patients who used 50g of superpotent topical steroids per week. It was identified that patients who used more than 50g of superpotent topical steroids had significantly lower cortisol levels, with a negatively significant correlation between cortisol level and the amount of topical steroid use ( < .01).Osteoporosis was detected in 3 patients in group 1 and 8 patients in Group 2. Because of the low number of patients between two groups, statistical analysis could not be performed to determine the risk factors.

Our study is the first study that we know of that investigated these three side effects. We have shown that the development of CS, adrenal insufficiency and osteoporosis in patients who use topical steroids for a long time depends on the weekly TCS dosage and the risk increases when it exceeds the threshold of 50 grams per week. therefore, our recommendation would be to avoid long-term use of superpotent steroids and to choose from the medium-potent group if it is to be used.

ABOUT THE CONTRIBUTORS

Betul Erdem

Department of Dermatology, Van Training and Research Hospital, Van, Turkey.

Muzeyyen Gonul

Department of Dermatology, Ministry of Health, Ankara Etlik City Hospital, Ankara, Turkey.

Ilknur Ozturk Unsal

Department of Endocrine and Metabolic Disease, Ministry of Health, Ankara Etlik City Hospital, Ankara, Turkey.

Seyda Ozdemir Sahingoz

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Etomidate in the Treatment Of Cushing Syndrome

Posted on September 25, 2023 by MaryO

Cushing syndrome is a metabolic disease caused by chronic exposure to high levels of glucocorticoids. It can present as an endocrine emergency due to a rapid increase in circulating cortisol leading to increased risk of cardiovascular disease and infection. Etomidate rapidly reduces plasma cortisol levels by inhibiting the action of 11β-hidroxilase. We report the case of a patient with severe hypercortisolaemia accompanied by metabolic and psychiatric disorders in whom administration of etomidate reduced preoperative levels of cortisol.

Introduction

Cushing’s syndrome is a metabolic disease caused by chronic exposure to high levels of glucocorticoids. The main causes are ectopic ACTH secretion, adrenal tumours (adenomas or carcinomas), adrenal hyperplasia, and administration of exognous glucocorticoids—the latter being the most common aetiology.1

In most cases, Cushing’s syndrome presents an indolent course for years before diagnosis is made, although it can sometime present as an endocrine emergency due to a rapid increase in circulating cortisol levels.2 In these cases, treatment to control hypercortisolaemia must be started quickly due to the high morbidity and mortality associated with the potentially life-threatening metabolic, infectious, and neuropsychiatric alterations that occur in this syndrome.1, 2, 3, 4

The options for treating Cushing’s syndrome include surgery, radiotherapy, and pharmacological treatment. The most commonly used drugs are adrenal steroidogenesis inhibitors (ketoconazole, metyrapone),3 but this treatment is not always well tolerated and its efficacy is limited.2 Etomidate is a drug from the imidazole family that inhibits the enzyme 11β-hydroxylase, and can reduce cortisol secretion within 48−72 h.2

Section snippets

Case report

Our patient was a 27-year-old woman with no known drug allergies or personal history of interest. She was studied in April 2021 for anxious-depressive symptoms with rapidly evolving paranoid ideation and hirsutism. A Nugent test was performed, which was positive (46.1 mcg/dl), and cortisol in urine was measured (2715 mcg/24 h), leading to a diagnosis of Cushing’s syndrome.

A CT scan showed a large mass on the right adrenal gland, compatible with a primary adrenal gland tumour (Fig. 1).

Discussion

Endogenous Cushing’s syndrome is characterized by over-production of cortisol. In patients such as ours, the syndrome presents in its most serious form, with very high hypercortisolaemia and metabolic, cardiovascular, and neuropsychiatric disorders. Cushing’s syndrome is a medical emergency due to its association with several comorbidities and its high rate of mortality.5 The first therapeutic option is surgical resection of the underlying tumour; however, the accompanying hypercortisolaemia

Conclusion

In its severe form, Cushing’s syndrome is a medical emergency that must be rapidly controlled.

Etomidate is both safe and effective, and has shown promising results in the treatment of severe hypercortisolaemia.

We believe that these patients should be admitted to the Anaesthesia Intensive Care Unit during etomidate therapy in order to monitor their level of consciousness, lung function, and haemodynamics, and to closely monitor cortisol and electrolyte levels.

Ethical considerations

Informed consent was obtained for the use of patient information for teaching and research purposes in accordance with our hospital protocol.

Conflict of interests

None.

Funding

The authors have not received any funding for this manuscript.

References (8)

  • A. Ferriere et al.

    Cushing’s syndrome: Treatment and new therapeutic approaches

    Best Pract Res Clin Endocrinol Metab

    (2020)
  • Juszczak A, Morris D, Grossman A. Cushing’s Syndrome [Internet]. South Dartmouth (MA): MDText.com, Inc; 2000 [revised…
  • T.B. Carroll et al.

    Continuous Etomidate Infusion for the Management of Severe Cushing Syndrome: Validation of a Standard Protocol

    J Endocr Soc

    (2018)
  • V.A. Preda et al.

    Etomidate in the management of hypercortisolaemia in Cushing’s syndrome: a review

    Eur J Endocrinol

    (2012)
There are more references available in the full text version of this article.

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Short-Term Oral Corticosteroid Use Tied to Higher Risks of GI Bleeds, Sepsis, Heart Failure

Posted on August 8, 2020 by MaryO

Study Authors: Tsung-Chieh Yao, Ya-Wen Huang, et al.; Beth I. Wallace, Akbar K. Waljee

Target Audience and Goal Statement: Primary care physicians, rheumatologists, pulmonologists, dermatologists, gastroenterologists, cardiologists

The goal of this study was to examine the associations between oral corticosteroid bursts and severe adverse events among adults in Taiwan.

Question Addressed:

  • What were the associations between steroid bursts and severe adverse events, specifically gastrointestinal (GI) bleeding, sepsis, and heart failure?

Study Synopsis and Perspective:

It has long been known that long-term use of corticosteroids can be both effective and toxic. Long-term use is associated with adverse effects such as infections, GI bleeding/ulcers, cardiovascular disease (CVD), Cushing syndrome, diabetes and metabolic syndromes, cataracts, glaucoma, and osteoporosis. Most clinical practice guidelines caution against long-term steroid use unless medically necessary.

Action Points

  • In a retrospective cohort study and self-controlled case series, prescriptions for oral steroid bursts were found to be associated with increased risks for gastrointestinal bleeding, sepsis, and heart failure within the first month after initiation, despite a median exposure of just 3 days.
  • Note that the risks were highest 5 to 30 days after exposure, and attenuated during the subsequent 31 to 90 days.

Instead, clinical practice guidelines recommend steroid bursts for inflammatory ailments such as asthma, inflammatory bowel disease, and rheumatoid arthritis. Waljee and colleagues noted in 2017 that they are most commonly used for upper respiratory infections, suggesting that many people are receiving steroids in the real world.

In a retrospective cohort study and self-controlled case series, prescriptions for oral steroid bursts — defined as short courses of oral corticosteroids for 14 or fewer days — were found to be associated with increased risks for GI bleeding, sepsis, and heart failure within the first month after initiation, despite a median exposure of just 3 days, according to Tsung-Chieh Yao, MD, PhD, of Chang Gung Memorial Hospital in Taoyuan, and colleagues.

The risks were highest 5 to 30 days after exposure, and attenuated during the subsequent 31 to 90 days, they reported in Annals of Internal Medicine.

The self-controlled case series was based on national medical claims records. Included were adults, ages 20-64, covered by Taiwan’s National Health Insurance in 2013-2015.

Out of a population of more than 15.8 million, study authors identified 2,623,327 people who received a steroid burst during the study period. These individuals were age 38 on average, and 55.3% were women. About 85% had no baseline comorbid conditions.

The most common indications for the steroid burst were skin disorders and respiratory tract infections.

The incidence rates among patients prescribed steroid bursts were 27.1 per 1,000 person-years for GI bleeding (incidence rate ratio [IRR] 1.80, 95% CI 1.75-1.84), 1.5 per 1,000 person-years for sepsis (IRR 1.99, 95% CI 1.70-2.32), and 1.3 per 1,000 person-years for heart failure (IRR 2.37, 95% CI 2.13-2.63).

Absolute risk elevations were similar in patients with and without comorbid conditions, meaning that the potential for harm was not limited to those at high risk for these adverse events.

The study authors acknowledged that they could not adjust for disease severity and major lifestyle factors such as alcohol use, smoking, and body mass index; because these factors were static, the effect could be eliminated using the self-controlled case series design. Their reliance on prescription data also meant they could not tell if patients actually complied with oral corticosteroid therapy. Furthermore, the exclusion of the elderly and younger populations also left room for underestimation of the risks of steroid bursts, they said.

Source References: Annals of Internal Medicine 2020; DOI: 10.7326/M20-0432

Editorial: Annals of Internal Medicine 2020; DOI: 10.7326/M20-4234

Study Highlights and Explanation of Findings:

Over the 3-year study period, steroid bursts were commonly prescribed to adults. Such prescriptions were written for common conditions, including skin disorders and upper respiratory tract infections. The highest risks for GI bleeding, sepsis, and heart failure occurred within the first month after receipt of the steroid burst, and this risk was attenuated during the subsequent 31 to 90 days.

“Our findings are important for physicians and guideline developers because short-term use of oral corticosteroids is common and the real-world safety of this approach remains unclear,” the researchers wrote. Notably, one corticosteroid that fits the bill is dexamethasone — a medication that holds promise for the treatment of critically ill COVID-19 patients, although it is not generally prescribed orally for these patients.

Based on preliminary results, the NIH’s COVID-19 treatment guidelines panel recommended the use of “dexamethasone (at a dose of 6 mg per day for up to 10 days) in patients with COVID-19 who are mechanically ventilated and in patients with COVID-19 who require supplemental oxygen but who are not mechanically ventilated.” In addition, they recommend “against using dexamethasone in patients with COVID-19 who do not require supplemental oxygen.”

“We are now learning that bursts as short as 3 days may increase risk for serious AEs [adverse events], even in young and healthy people. As providers, we must reflect on how and why we prescribe corticosteroids to develop strategies that prevent avoidable harms,” wrote Beth Wallace, MD, and Akbar Waljee, MD, both of the VA Ann Arbor Healthcare System and Michigan Medicine.

On the basis of the reported risk differences in the study, Wallace and Waljee calculated that one million patients exposed to corticosteroid bursts experienced 41,200 GI bleeding events, 400 cases of sepsis, and 4,000 cases of new heart failure per year that were directly attributed to this brief treatment.

“Although many providers already avoid corticosteroids in elderly patients and those with comorbid conditions, prescribing short bursts to ‘low-risk’ patients has generally been viewed as innocuous, even in cases where the benefit is unclear. However, Yao and colleagues provide evidence that this practice may risk serious harm, making it difficult to justify in cases where corticosteroid use lacks evidence of meaningful benefit,” they wrote in an accompanying editorial.

“Medication-related risks for AEs can, of course, be outweighed by major treatment benefit. However, this study and prior work show that corticosteroid bursts are frequently prescribed for self-limited conditions, where evidence of benefit is lacking,” Wallace and Waljee noted.

“As we reflect on how to respond to these findings, it is useful to note the many parallels between use of corticosteroid bursts and that of other short-term medications, such as antibiotics and opiates. All of these treatments have well-defined indications but can cause net harm when used — as they frequently are — when evidence of benefit is low,” they emphasized.

Last Updated August 07, 2020
Reviewed by Dori F. Zaleznik, MD Associate Clinical Professor of Medicine (Retired), Harvard Medical School, Boston

Primary Source

Annals of Internal Medicine

Source Reference: Yao TC, et al “Association between oral corticosteroid bursts and severe adverse events: a nationwide population-based cohort study” Ann Intern Med 2020; DOI: 10.7326/M20-0432.

Secondary Source

Annals of Internal Medicine

Source Reference: Wallace BI, Waljee AK “Burst case scenario: why shorter may not be any better when it comes to corticosteroids” Ann Intern Med 2020; DOI: 10.7326/M20-4234.

Additional Source

MedPage Today

Source Reference: Lou N “Sobering Data on Risks of Short-Term Oral Corticosteroids” 2020.

From https://www.medpagetoday.org/primarycare/generalprimarycare/87959?xid=nl_mpt_DHE_2020-08-08&eun=g1406328d0r&utm_term=NL_Daily_DHE_dual-gmail-definition&vpass=1

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Steroid Medication for Nasal Obstruction in Infants May Cause Cushing’s Syndrome

Posted on March 10, 2018 by MaryO

Intranasal steroid drops used to treat nasal obstruction may cause Cushing’s syndrome and adrenal insufficiency in infants, a case study of two patients suggests.

The study, “Iatrogenic Cushing’s syndrome and adrenal insufficiency in infants on intranasal dexamethasone drops for nasal obstruction – Case series and literature review,” was published in the International Journal of Pediatric Otorhinolaryngology.

Children with nasal obstruction may have severe delays in development and can face life-threatening complications later in life such as obstructive sleep apnea and cardiopulmonary problems.

While intranasal steroid drops have become increasingly popular as a substitute for surgery, they can have adverse effects. In addition to suppressing the immune system and changing metabolism, high levels of corticosteroids in the blood may cause Cushing’s syndrome.

Researchers at Weill Cornell Medical College presented two cases of adrenal gland insufficiency and Cushing’s syndrome caused by intranasal dexamethasone drops. Dexamethasone is a type of corticosteroid medication.

First, they described the case of a 3-month-old boy who was taken to the hospital following a life-threatening episode at home after feeding. A physical evaluation revealed nasal congestion with no additional anatomic abnormalities.

Treatment with nasal dexamethasone drops three times a day improved his breathing. While the dosage was later decreased to three drops once daily, a congestion episode led the mother to increase the dose back to the initial recommendation.

After seven weeks of treatment, the boy was noted to have facial puffiness, leading to an endocrine evaluation that revealed low cortisol levels. The dose was eventually reduced, and the boy’s cortisol levels returned to normal after several months.

The second case was a 6-week-old boy with a history of chronic congestion and difficulty feeding. He had severe nasal obstruction and required intubation due to respiratory distress. A nasal exam revealed damaged mucosa with severe nasal cavity narrowing, and he began treatment with three ciprofloxacin-dexamethasone drops three times a day.

After two and a half weeks of treatment, the boy’s cortisol levels were considerably low, and adrenal insufficiency was diagnosed. The treatment dose was reduced in an attempt to improve cortisol levels, but nasal obstruction symptoms continued.

The child then underwent surgery to resolve his nasal obstruction, and the treatment with steroid drops was discontinued. While his cortisol levels subsequently improved, they continued to be low, suggesting that he may have a hormone-related disease.

Despite the benefits of steroid-based nasal drops, small infants are more sensitive to steroid compounds. In addition, nasal drops are more easily absorbed than nasal sprays, suggesting that infants taking these medications should be better controlled for side effects.

“Patients started on this therapy must be closely monitored in a multi-disciplinary fashion to ensure patient safety and optimal symptom resolution,” the researchers suggested.

From https://cushingsdiseasenews.com/2018/03/09/cushing-syndrome-infants-can-be-caused-by-steroid-based-nasal-drops-study-suggests/

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