Glucocorticoid-induced adrenal insufficiency: physiological dose tapering promotes recovery

Disclosure: R. Mehta: None. K. Lazarus: None. A. Sharma: None. K. Narula: None. Z. Htut: None. S. Choudhury: None. D.A. Papadopoulou: None. T. Tan: None. K. Meeran: None.Background: Prolonged glucocorticoid (GC) therapy is associated with increased morbidity and mortality. Discontinuation is a challenge due to the risk of developing GC-induced adrenal insufficiency (GC-AI). Current guidelines recommend against weaning if a morning cortisol is less than 300 nmol/L despite being on a physiological dose of prednisolone. This threshold may be overly cautious and could limit successful weaning. Methods: We conducted a retrospective study of 65 patients with long-term GC use for inflammatory disease, who were undergoing a prednisolone wean between 2019 and 2024. Clinical outcomes and biochemical data were analysed. Serial short Synacthen tests (SSTs; n=52) in 23 patients after dose reductions at ≤5 mg were used to assess hypothalamic-pituitary-adrenal axis (HPA) recovery. Kruskal-Wallis testing compared the effect of different dose reductions on HPA axis function. Results: From the cohort of 65, 19 patients continue to wean. Of the remaining 46 patients, 37 (80%) successfully discontinued prednisolone. The median duration of prednisolone use at referral was 23 months [IQR 6.5-66.5], and the median dose was 5 mg [3.75-5]. Median time to discontinuation was 8 months [5-15.5]. Amongst those who successfully weaned, 41% (n=15) had a morning cortisol <150 nmol/L, including 5 with undetectable levels. Only 24% (n=9) exceeded 300 nmol/L, even once prednisolone had been fully weaned. In patients with a baseline HbA1c ≥42 mmol/mol, prednisolone discontinuation led to a median HbA1c reduction of 6 mmol/mol (n=6, p=0.031).Reasons for weaning failure (n=9) were: inadequate control of the primary disease (n=5), insufficient HPA axis recovery (n=3), and intolerable GC withdrawal symptoms (n=1). The 10 SSTs from the three patients unable to fully discontinue prednisolone due to inadequate HPA axis recovery all showed the following triad: adrenocorticotropic hormone ≤10.7 ng/L, morning cortisol ≤34 nmol/L, and peak cortisol ≤92 nmol/L; yet all reduced to a maintenance dose of 2 mg (n=2) or 1 mg (n=1). No adrenal crises occurred across the cohort during the weaning process.Serial SSTs demonstrated significant increases in both baseline and peak cortisol following dose reductions of 1 mg, 1.5-2 mg, and >2 mg (all p<0.01). Larger dose reductions were associated with greater increases in both morning (p=0.038) and peak (p=0.011) cortisol. Conclusion: HPA axis function in GC-AI is more dynamic than current guidelines suggest and improves with reducing prednisolone dose, even at physiological doses. Additionally, the risk of adrenal crisis appears negligible with structured weaning and appropriate safety-netting. Our findings demonstrate that strict adherence to current GC-AI guidelines prevent successful weaning, leading to unnecessary GC exposure and their associated adverse effects.Presentation: Sunday, July 13, 2025

Background:Disease-modifying anti-rheumatic drug (DMARD) use in older adults with late-onset rheumatoid arthritis (LORA) is suboptimal despite their high efficacy and tolerability in this population. In contrast, long-term glucocorticoid (GC) use...

Background/Aims Glucocorticoids are widely prescribed by rheumatology clinicians for various conditions. These patients are at risk of glucocorticoid-induced adrenal insufficiency (GI-AI) which can lead to significant morbidity and mortality. GI-AI requires high clinical suspicion, prompt recognition and appropriate management. The aim of our study was to check knowledge and current clinical practices in management of GI-AI amongst rheumatology clinicians within the Essex region. Methods All consultants, SAS doctors, trainees and specialist-nurses working in rheumatology departments within NHS hospitals in the Essex region of the UK and part of the Essex Rheumatology Association (ERA) were invited to participate in an online survey. An online questionnaire was created with help of Google Forms and distributed by email using a weblink or QR-code. The questionnaire had 11 questions spread over 4 sections: clinician background; knowledge; current clinical practice; suggestions. The survey was revised before final distribution to verify comprehensibility and validity by two rheumatology consultants and one endocrinology consultant. Participant anonymity was maintained. Data were analysed using Excel. The Cronbach coefficient of our questionnaire was 0.77, indicating good internal consistency of survey questions (range 0-1). Results We had a total of 32 responses from ERA members, including 17 (53%) rheumatology consultants, 7 (22%) nurse specialists, 4 (12.5%) rheumatology trainees and 2 (6.3%) SAS doctors. Of the respondents, 21 (65%) had &amp;gt;10 years in rheumatology practice and 16 (50%) respondents see an average of 5-10 patients on long-term glucocorticoids on a weekly basis. Normal daily cortisol production in healthy individuals was not known to 9 (29%) respondents. The correct dose of prednisolone at which to investigate patients for GI-AI was correctly pointed out by 20 (62.5%) clinicians. In response to a knowledge question on clinical features of GI-AI, 30 (93.8%) respondents chose postural hypotension, 24 (75%) weight loss, and 28 (87.5%) myalgias/arthralgias correctly. Hydrocortisone as the most commonly used replacement therapy for GI-AI was marked correctly by 25 (78%) clinicians. GI-AI was not diagnosed by 19 (59.4%) clinicians in the last 2 years nor any referral made to endocrinology suspecting GI-AI. GI-AI is not routinely investigated by 9 (28%). Steroid cards are issued to patients by 18 (56.3%), and 19 (59.4%) educate patients about sick-day rules in clinic. Patient education on GI-AI symptoms is done by 17 (53%), and 7 (22%) do none of the above. Conclusion Our survey highlights gaps in knowledge and clinical practice of GI-AI among rheumatology clinicians within the Essex region. There are limited studies on awareness and clinical practices regarding GI-AI. We presented survey findings in an ERA meeting and educated the rheumatologists. A GI-AI pathway was developed and circulated as per best clinical practice. Steroid cards were printed for clinic rooms along with patient education material. If a similar survey may be carried out across the UK as part of a British Society for Rheumatology initiative, that data might support the need for additional structured training on GI-AI at a national level. Disclosure K.K. Garg: None. A. Nandagudi: None. A. Bharadwaj: None.

ImportanceAdrenal insufficiency is a syndrome of cortisol deficiency and is categorized as primary, secondary, or glucocorticoid induced. Although primary and secondary adrenal insufficiency are rare, affecting less than 279 per 1 million individuals, glucocorticoid-induced adrenal insufficiency is common.ObservationsPrimary adrenal insufficiency, which involves deficiency of all adrenocortical hormones, is caused by autoimmune destruction, congenital adrenal hyperplasia, pharmacological inhibition (eg, high doses of azole antifungal therapy), infection (eg, tuberculosis, fungal infections), or surgical removal of adrenal cortical tissue. Secondary adrenal insufficiency is caused by disorders affecting the pituitary gland, such as tumors, hemorrhage, inflammatory or infiltrative conditions (eg, hypophysitis, sarcoidosis, hemochromatosis), surgery, radiation therapy, or medications that suppress corticotropin production, such as opioids. Glucocorticoid-induced adrenal insufficiency is caused by administration of supraphysiological doses of glucocorticoids. Patients with adrenal insufficiency typically present with nonspecific symptoms, including fatigue (50%-95%), nausea and vomiting (20%-62%), and anorexia and weight loss (43%-73%). Glucocorticoid-induced adrenal insufficiency should be suspected in patients who have recently tapered or discontinued a supraphysiological dose of glucocorticoids. Early-morning (approximately 8 am) measurements of serum cortisol, corticotropin, and dehydroepiandrosterone sulfate (DHEAS) are used to diagnose adrenal insufficiency. Primary adrenal insufficiency is typically characterized by low morning cortisol levels (<5 µg/dL), high corticotropin levels, and low DHEAS levels. Patients with secondary and glucocorticoid-induced adrenal insufficiency typically have low or intermediate morning cortisol levels (5-10 µg/dL) and low or low-normal corticotropin and DHEAS levels. Patients with intermediate early-morning cortisol levels should undergo repeat early-morning cortisol testing or corticotropin stimulation testing (measurement of cortisol before and 60 minutes after administration of cosyntropin, 250 µg). Treatment of adrenal insufficiency involves supplemental glucocorticoids (eg, hydrocortisone, 15-25 mg daily, or prednisone, 3-5 mg daily). Mineralocorticoids (eg, fludrocortisone, 0.05-0.3 mg daily) should be added for patients with primary adrenal insufficiency. Adrenal crisis, a syndrome that can cause hypotension and shock, hyponatremia, altered mental status, and death if untreated, can occur in patients with adrenal insufficiency who have inadequate glucocorticoid therapy, acute illness, and physical stress. Therefore, all patients with adrenal insufficiency should be instructed how to increase glucocorticoids during acute illness and prescribed injectable glucocorticoids (eg, hydrocortisone, 100 mg intramuscular injection) to prevent or treat adrenal crisis.Conclusions and RelevanceAlthough primary and secondary adrenal insufficiency are rare, glucocorticoid-induced adrenal insufficiency is a common condition. Diagnosis of adrenal insufficiency involves early-morning measurement of cortisol, corticotropin, and DHEAS. All patients with adrenal insufficiency should be treated with glucocorticoids and instructed how to prevent and treat adrenal crisis.

BACKGROUND: Remission of Cushing’s syndrome (CS) is generally defined as morning serum cortisol values <5mcg/dL (<138 nmol/L) or Urine Free Cortisol <10-20ug/dL (< 28 – 56 nmol/d) after tumor resection, which reflects suppression of the hypothalamic-pituitary-adrenal (HPA) axis by sustained hypercortisolism. Endocrine Society guidelines recommend glucocorticoid replacement until the HPA axis is normal as assessed by a morning (AM) or post-ACTH stimulation test cortisol level of approximately 18 ug/dL (500 nmol/L) or greater (1). Patients with subnormal cortisol levels remain on glucocorticoid until retested in 3-6 months. The goal of this study was to determine whether a baseline cortisol value predicts a normal response to the ACTH stimulation test.Methods: We reviewed 235 ACTH stimulation (stim) tests conducted on 76 patients with secondary adrenal insufficiency following remission of CS. Patients had resection of a single adrenal gland (n=7), pituitary adenoma [with (n=3) or without (n = 47) subsequent radiation], 70% of pituitary tissue (n=5), or ACTH secreting intrathoracic tumor (n=13). One had an ectopic ACTH secreting tumor in spontaneous remission (n=1). ACTH stim tests were conducted between 0800h and 0900h, 24 hours after the last dose of glucocorticoid, using 250 mcg of cosyntropin intravenously. Cortisol levels were measured just before administration of cosyntropin, and 30 and 60 minutes afterwards. Patients were considered to have passed the test if baseline or peak cortisol values reached > 18mcg/dL. Baseline cortisol values were compared to the ‘pass’ rate.Results: Baseline F values (ug/dL) and passing rates (# pass/total) were:<4: 1/91;4-4.9: 2/27;5-5.9: 8/31;6-6.9: 2/21;7-7.9: 7/25;8-8.9: 4/12;9-9.9: 8/12;>10 - < 15: 6/1115 – 19.5: 5/5Thus, Am cortisol values >9 ug/dl were significantly more likely to predict a normal response to ACTH stim than lower values (p<0.0001). ACTH values (n=184) did not predict peak F levels. However, no patient with ACTH value <5 pg/ml passed the test; all had peak F values of 0-10.5.Conclusion: Baseline cortisol can be a guide as to whether the more costly stimulation test is needed. In the small cohort with baseline 0800h – 0900h cortisol >15 ug/dL, all passed the test, suggesting that it is not needed in such patients. We recommend use of an ACTH stimulation test to assess recovery of the HPA axis when a morning cortisol reaches 9 mcg/dL, with an expected pass rate of about 66%.Reference: 1. Nieman LK, Biller BM, Findling JW, Murad MH, Newell-Price J, Savage MO et al. Treatment of Cushing’s Syndrome: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 100:2807, 2015.

We evaluated changes in long-term glucocorticoid (GC) use and factors associated with persistent GC use in older adults with late-onset rheumatoid arthritis (LORA). Using 20% Medicare data from 2008 to 2017, we identified adults ≥66 years with a new diagnosis of LORA, disease-modifying antirheumatic drug (DMARD) use or at least two rheumatologist visits, and at least 12 months of follow-up data. Older adults were categorized as DMARD-exposed or DMARD-unexposed based on treatment during the 12 months after LORA diagnosis (index date). For each quarter after the index date, long-term GC use was defined as having oral GC prescriptions for at least 30 days with a dose >5 mg/day prednisone equivalent. We compared long-term GC use between quarter (Q)1 and Q4 and performed stratified mixed-effects logistic regression for factors associated with persistent GC use, defined as long-term GC use in Q2 to Q4. The cohort included 15,425 individuals with two-thirds (62.5%) being DMARD-exposed. Between Q1 and Q4, the proportion of older adults on long-term GC declined from 44.1 to 24.9% (∆19.2%) among the DMARD-exposed and from 25.8 to 17.9% (∆7.9%) among the DMARD-unexposed. One year after the index date, 13.5% of the DMARD-exposed and 9.8% of the DMARD-unexposed were persistent GC users. In stratified mixed-effects logistic models, persistent GC use was associated with low-income subsidy status among the DMARD-exposed and with greater comorbidity burden among DMARD-unexposed. Long-term GC use declined more among DMARD-exposed than DMARD-unexposed patients. One in seven DMARD-exposed and one in ten DMARD-unexposed have persistent GC use which is associated with financial barriers and multimorbidity that may limit the use of steroid-sparing DMARDs.

PurposeGlucocorticoids (GCs) are commonly used for several acute and chronic pediatric diseases. However, chronic treatment may result in hypothalamic-pituitary-adrenal axis (HPA) dysfunction. Glucocorticoid-induced adrenal insufficiency (GI-AI) is indeed the most frequent cause of adrenal insufficiency (AI) in children, possibly resulting in a life-threatening event such as adrenal crisis (AC). It is generally underestimated, especially when using non-systemic glucocorticoid formulations. This review aims at summarizing current evidence on the effects of long-term GC treatment on the HPA axis, management of GC tapering and assessment of the HPA recovery.MethodsWe conducted a narrative review of the relevant literature focusing on pathogenic mechanisms, predictive factors, diagnosis and treatment of GI-AI.ResultsAll types of GCs, whatever the route of administration, may have suppressive effects on the HPA axis, especially when compounds with higher potency and long half-life are used. Moreover, chronic GC administration is the most common cause of Cushing syndrome in children. In order to overcome the risk of GI-AI, slow withdrawal of GCs is necessary. When approaching the replacement dose, it is recommended to switch to shorter half-life formulations such as hydrocortisone. Assessment of HPA axis recovery with basal and stimulated cortisol levels may help detecting children at risk of AC that may require hydrocortisone supplementation.ConclusionThe management of GI-AI in children is challenging and many areas of uncertainty remain. Improving the knowledge on long-term GC effects on HPA in children, the management of steroid discontinuation and emergency dosing may help preventing GI-AI symptoms and acute hospital admission for AC.

BackgroundLimited information exists on postoperative hypocortisolism and hypothalamus–pituitary–adrenal axis recovery in patients with adrenal incidentaloma following unilateral adrenalectomy. We evaluated frequency of postoperative hypocortisolism and predictors for recovery in non-aldosterone-producing adrenocortical adenoma patients after unilateral adrenalectomy.MethodsA retrospective analysis of 32 adrenal incidentaloma patients originally included in the ITACA trial (NCT04127552) with confirmed non-aldosterone-producing adrenocortical adenoma undergoing unilateral adrenalectomy from September 2019 to April 2023 was conducted. Preoperative assessments included adrenal MRI, anthropometrics, evaluation of comorbidities, adrenal function assessed via ACTH, urinary free cortisol, and 1 mg dexamethasone suppression test. ACTH and serum cortisol or Short Synacthen test were performed within 6 days, 6 weeks, 6 months, and a year after surgery.ResultsSix days postoperative, 18.8% of patients had normal adrenal function. Among those with postoperative hypocortisolism, 53.8% recovered by 6 weeks. Patients with earlier adrenal recovery (6 weeks) had lower preoperative 1 mg dexamethasone suppression test (median 1 mg dexamethasone suppression test 76.2 [61.8–111.0] nmol/L vs 260.0 [113.0–288.5] nmol/L, p < 0.001). Univariate analysis showed preoperative 1 mg dexamethasone suppression test negatively related with baseline ACTH levels (r = − 0.376; p = 0.041) and negatively associated with the 6-week baseline (r = − 0.395, p = 0.034) and 30-min cortisol levels during Short Synacthen test (r = − 0.534, p = 0.023). Logistic regression analysis demonstrated preoperative 1 mg dexamethasone suppression test as the only biochemical predictor for 6-week adrenal recovery: ROC curve identified a 1 mg dexamethasone suppression test threshold of 131 nmol/L predicting 6-week recovery with 89.5% sensitivity and 72.7% specificity (AUC 0.87; 95% CI 66.9–98.7, p < 0.001). Other preoperative assessments (tumor size, ACTH levels and anthropometrics) were not associated with postoperative hypothalamus–pituitary–adrenal axis function, but the presence of diabetes was associated with a lower probability of recovery (OR = 24.55, p = 0.036). ACTH levels increased postoperatively in all patients but did not predict hypothalamus–pituitary–adrenal axis recovery.ConclusionsThe preoperative 1 mg dexamethasone suppression test cortisol value and presence of diabetes are the only relevant predictor of hypothalamus–pituitary–adrenal axis recovery in patients with non-aldosterone- producing adrenocortical adenoma undergoing surgery, regardless other clinical and biochemical variables. Notably, pre- and postoperative ACTH levels did not predict hypothalamus–pituitary–adrenal axis recovery. These findings point towards the potential for saving resources by optimizing their allocation during follow-up assessments for patients with non-aldosterone-producing adrenocortical adenoma undergoing unilateral adrenalectomy.

Glucocorticoid-induced adrenal insufficiency (GIAI) is a hypothalamic-pituitary-adrenal (HPA) axis dysfunction caused by long-term use of exogenous steroids. Adrenal crisis (AC) is an acute complication of GIAI and one of the reasons for the increased risk of death. This study aims to analyze the clinical characteristics of GIAI patients with AC and explore the related risk factors. Clinical data of adult GIAI patients treated at our hospital between January 1, 2014, and December 31, 2023 were included. The demographic characteristics, clinical characteristics, laboratory tests and comorbidities of the patients were collected. Univariate and multivariate regression analyses were used to explore the variables related to the occurrence of AC, and prediction models were constructed. 51 patients (13.75%) developed AC during hospitalization. Mortality was significantly higher in patients with AC than in those without AC. Multivariate logistic regression analysis showed that infection, psychiatric symptoms, serum sodium, albumin, neutrophil-lymphocyte ratio (NLR) and eosinophil-lymphocyte ratio (ELR) were independent risk factors for AC. Among the prediction models constructed by machine learning algorithms, logistic regression model had the best prediction effect. This study investigated the clinical characteristics of AC in GIAI patients. NLR and ELR may be effective predictors of AC in GIAI patients, and combined with other clinically significant indicators, an effective prediction model was constructed. Logistic regression model had the best performance in predicting AC in GIAI patients.

BackgroundLong-term glucocorticoid (GC) therapy is commonly used to treat rheumatological conditions. This may result in tertiary adrenal insufficiency, as a result of suppression of the HPA axis, when GC doses are weaned/withdrawn. There is little published data about tertiary adrenal insufficiency in this group. This study aims to further evaluate prevalence, characteristics and recovery of adrenal insufficiency in these patients at a large UK teaching hospital.MethodsWe retrospectively identified patients seen in outpatient clinics between January 2014 and September 2019 who had received tapering doses of long-term GC to treat their underlying condition (largely patients with polymyalgia rheumatica, giant cell arteritis or other vasculitis) and had either had a 9am cortisol or short synacthen test (SST). Data were collected using a standardised proforma.ResultsThere was a total of 238 patients, median age of 71 years with a female preponderance (75%). Mean duration of glucocorticoid use was 63.3 months. Mean peak dose of glucocorticoid was 29.2mg.142 patients had 9am cortisol as the first line test to assess adrenal function. 65% of these were considered sub-optimal based on local protocol (cortisol <350nmol/L). 38% of these patients went on to have SST, of which 56% continued to show evidence of sub-optimal cortisol production. All patients where baseline 9am cortisol was <100nmol/L failed to reach stimulated cortisol of >500nmol/L on SST, whereas 31% failed SST if 9am cortisol was 250-350 nmol/L.In total 138 SSTs were performed of which 51% (n=70) were abnormal (cortisol <500nmol/L post synacthen). When baseline cortisol was <100nmol/L on SST, all patients had a suboptimal peak response. However, where baseline cortisol on SST was >350 nmol/L only 3% had a sub-optimal peak cortisol.32 of these patients with an abnormal baseline SST went on to have a repeat SST within 2 years. 50% (n=16) continued to be suboptimal. Of the 32 patients, 38% (n=12) were switched to hydrocortisone with 33% showing complete adrenal recovery, average time to recovery of 25 months. 62% (n=20) patients did not switch, with 60% demonstrating recovery within the same time period (p=0.05). Mean ACTH levels in patients who had sub-optimal SST were 23.1 ng/L (n=19). ACTH levels were not different between those who recovered and those who did not (p=0.23).ConclusionOur study suggests that tertiary adrenal insufficiency is highly prevalent in this cohort of patients with rheumatological conditions requiring long-term glucocorticoid therapy. A 9am cortisol threshold of greater than 350nmol/L excludes most patients with adrenal insufficiency. These data also suggest no significant difference in adrenal recovery if switched to hydrocortisone versus continuing on prednisolone. ACTH levels were not fully suppressed in patients with adrenal insufficiency and did not predict recovery.

Glucocorticoid-induced adrenal insufficiency (GC-AI) is a potentially life-threatening side effect of glucocorticoid therapy. Currently, there is no consensus on monitoring and treating GC-AI in inflammatory bowel disease (IBD) patients. This systematic review and meta-analysis aimed to determine the prevalence of GC-AI in IBD patients following glucocorticoid use. Additionally, a Delphi panel was conducted to develop evidence-based expert opinions on evaluating and managing GC-AI in IBD patients. Thirty-four articles were included in this study. Of these, 26 articles reported the prevalence of GC-AI in IBD patients. Statements were generated and rated by a panel of adult and pediatric gastroenterologists using a 1-9 scale. Statements were classified as inappropriate, uncertain, or appropriate based on the median panel rating and the degree of disagreement. The prevalence of GC-AI across all studies was 26.9% (95% CI: 18.9-36.8, I2: 96%). The panel emphasized the importance of maintaining a high suspicion for GC-AI in IBD patients treated with systemic glucocorticoids and considering risk factors such as exogenous glucocorticoid use ≥4 weeks at doses ≥5mg of prednisone-equivalent. Recommendations for initial screening and management of GC-AI are provided. The management of GC-AI in special populations, such as those in the perioperative setting is also addressed. The panel underscored the need to consider GC-AI assessment in clinical trial design. GC-AI is a serious, often underrecognized side effect of glucocorticoid use. This study presents expert opinions on the evaluation and management of GC-AI in IBD patients, emphasizing the need for vigilance and appropriate management strategies.

To explore the diagnostic yield of bronchoscopic rapid on-site evaluation (B-ROSE) in patients with severe invasive bronchopulmonary aspergillosis (IBPA) and provide evidence for starting antifungal treatment before microbiological results were available. A prospective cohort study was conducted to select patients with severe pneumonia suspected of IBPA admitted to the respiratory intensive care unit (RICU) in the First Affiliated Hospital of Xinjiang Medical University from June 2014 to June 2022, and those who were primarily infected with other pathogens (such as bacteria, Mycobacterium tuberculosis) at admission were excluded. Whether the antifungal treatment was initiated or not on the basis of the bedside B-ROSE, the B-ROSE was administered as soon as possible within 24 hours after admission to RICU. The current international definition of invasive aspergillosis was used as the gold diagnostic standard, the diagnostic accordance rate, the sensitivity and specificity of B-ROSE were calculated respectively, and the receiver operator characteristic curve (ROC curve) was also plotted, to evaluate the predictive value in diagnosing IBPA. A total of 176 patients with severe pneumonia suspected of IBPA were included in the study. According to international diagnostic standards, there were 81 cases of IBPA and 95 cases of non-IBPA. According to the early diagnosis of B-ROSE, there were 89 cases of IBPA and 87 cases of non-IBPA. The diagnostic accordance rate of B-ROSE was 84.09% (148/176), the area under the ROC curve for B-ROSE in diagnosing severe IBPA was 0.844, the 95% confidence interval (95%CI) was 0.782-0.905, the sensitivity was 87.65%, the specificity was 81.05%, the positive predictive value was 79.78%, the negative predictive value was 88.51%, the rate of underdiagnosis was 12.35% (10/81), and the rate of misdiagnosis was 18.95% (18/95). Compared with the true negative group, the proportion of long-term (≥ 14 days) use of glucocorticoid [70.0% (7/10) vs. 9.1% (7/77), P < 0.01] and the proportion of cases with diabetes [40.0% (4/10) vs. 10.4% (8/77), P < 0.05] were significantly higher in the false negative group (underdiagnosis group). However, B-ROSE of both groups showed mucosal bleeding, congestion and edema [100.0% (10/10) vs. 94.8% (73/77), P > 0.05], indicating that acute mucosal inflammation was non-characteristic. Compared with the true positive group, the proportion of long-term (≥ 14 days) use of glucocorticoid in the false positive group (misdiagnosis group) was significantly reduced [33.3% (6/18) vs. 60.6% (43/71), P < 0.05]. The B-ROSE results showed the proportion of cases with mucosal white spots, black plaques and pseudomembrane was significantly reduced [16.7% (3/18) vs. 52.1% (37/71), P < 0.01] in the misdiagnosed group, which suggest that cases of long-term use of glucocorticoid and cases with B-ROSE showing mucosal white spots, black plaques and pseudomembrane were less likely to be misdiagnosed. The main diseases that were easily misdiagnosed as IBPA included pulmonary tuberculosis (38.9%, 7/18), inflammatory lung adenocarcinoma (27.8%, 5/18) and pulmonary vasculitis (16.7%, 3/18). Before obtaining microbiological evidence, B-ROSE can assist in decision-making of early anti-aspergillus treatment for severe IBPA. This method is prompt, simple, and has high accuracy and reliability. If B-ROSE lacks characteristic manifestations, especially for severe pneumonia in patients with long-term use of glucocorticoid or diabetes, attention should be paid to the underdiagnosis of IBPA. Diseases such as lung tuberculosis, inflammatory lung adenocarcinoma and lung vasculitis should be vigilant against misdiagnosis as IBPA.

BackgroundThe number of older adults living with rheumatoid arthritis (RA) is growing as the world population is aging. Older adults with RA are less likely to receive disease modifying anti-rheumatic...

Older adults with rheumatoid arthritis (RA) account for up to one-third of the RA population and are less likely to receive optimal treatment. For the subgroup of older adults with late-onset RA (LORA), who experience more symptomatic and progressive disease, suboptimal treatment could be more consequential than the general population who age with RA. We evaluated use of disease-modifying antirheumatic drugs (DMARDs) in older adults with a new diagnosis of LORA. In this retrospective observational study, we identified adults 66 years of age or older with a new diagnosis of LORA using Medicare data from 2008 to 2017. Information on baseline patient characteristics and DMARD initiation during the first 12 months after LORA diagnosis were collected. We also assessed concomitant use of glucocorticoids (GCs). We identified 33,373 older adults with new diagnosis of LORA. Average age at LORA diagnosis was 76.7 (SD 7.6); 75.4% were female, 76.9% were White, and 35.6% had low-income subsidy (LIS). Less than one-third were initiated on a DMARD (28.9%). In multivariable analyses, DMARD initiation was associated with younger age, fewer comorbidities, and absence of LIS status. Concomitant long-term (>3 months) GC use was higher among those on any DMARD (44.3%) compared with those without (15.2%). DMARD initiation after new diagnosis of LORA is low despite current clinical practice guidelines recommending early aggressive initiation of treatment. Long-term GC use is common among those on any DMARDs, raising concern for suboptimal DMARD use. Further studies are needed to understand drivers of DMARD use in older adults.

Glucocorticoid-Induced Adrenal Insufficiency: A Study of the Incidence in Hospital Patients and A Review of Peri-Operative Management