Steroid-induced Hyperglycemia Research Articles

IDF23-0458 Management of Steroid-Induced Hyperglycemia: A Case Report of Diabetes Mellitus Patient during COPD Acute Exacerbation

IDF23-0458 Management of Steroid-Induced Hyperglycemia: A Case Report of Diabetes Mellitus Patient during COPD Acute Exacerbation

Prevalence of Steroid-Induced Hyperglycemia in King Abdulaziz Specialist Hospital, Taif City, Saudi Arabia.

Background Hyperglycemia is a common side effect of high-dose steroid therapy in hospitalized patients. Objectives To assess the prevalence of hyperglycemia among hospitalized patients receiving steroid therapy. Methods A retrospective study was conducted among 245 patients. The inclusion criteria were patients undergoing steroid therapy and admitted to a single tertiary care hospital due to medical complications or exacerbation of the diseases they were suffering from. Data encompassing patient demographics, admission, discharge dates, comorbidities, medication histories, laboratory results (including blood glucose levels), and documented corticosteroid administrations were meticulously gathered from electronic health records (EHRs). A logistic regression model analysis was done to predict the risk factors of poor glycemic control among hospitalized patients. Results The prevalence of hyperglycemia among the patients who were on steroid therapy was 34.2%. About 70.7% of the patients who required insulin at the time of admission required >17 units, and the insulin requirement was significantly higher among patients who received dexamethasone compared to other steroids (p<0.05). Older age (>65 years) was found to be independently associated with poor glycemic control (p<0.05). Conclusion The study revealed that almost one-third of patients on steroid therapy had hyperglycemia. Monitoring of patients for hyperglycemia after beginning high-dose steroid therapy should be done.

Implementing a Standardized Workflow for Early Detection of Steroid-Induced Hyperglycemia: A Quality Improvement Project

Implementing a Standardized Workflow for Early Detection of Steroid-Induced Hyperglycemia: A Quality Improvement Project

Effect of Steroid Treatment on Tissue Damage Markers in Diabetic Patients

Steroid-induced hyperglycemia challenges primary care providers. Understanding and managing these effects are insufficient despite widespread glucocorticoid use. Our study aimed to investigate the impact of steroid treatment on tissue damage markers in diabetic patients. We determined the liver enzymes, blood biochemistry, and interleukins (IL-12, IL-17A, IL-6, and IL1B) before and after steroid treatment. The results revealed a significant increase in creatinine levels among the active patients compared to the control group. The mean concentrations of ALT and ALP in the active patients (on steroids) were 43 ± 3.1 and 112 ± 10.2 U/L, respectively, significantly higher than the active control (24 ± 5.1). Our study also found that IL-12, IL-17A, IL-6, and IL-10 were upregulated 5.2, 16.2, 2.13, and 5.11 times, respectively, compared to the control. The blood sugar levels (RBS) showed positive correlations with Neutrophils (r = 0.81, P = 0.012), IL-12 (r = 0.68, P = 0.028), and IL-6 (r = 0.51, P = 0.03). In conclusion, our research demonstrated the significance of inflammation and tissue damage in the expression patterns associated with type 2 diabetes and its effects.

Optimal initial insulin dosage for managing steroid-induced hyperglycemia in hospitalized COVID-19 patients: A retrospective single-center study.

To determine the optimal initial insulin dosage for controlling hyperglycemia in COVID-19 patients receiving steroids, an area with limited data. We retrospectively analyzed 156 COVID-19 patients with steroid-induced hyperglycemia treated with insulin. Patients were categorized by their total daily dose of subcutaneous insulin therapy when starting dexamethasone ⩾6 mg/day or equivalent dose of glucocorticoid: Group A (⩽0.29 units/kg), Group B (0.3-0.49 units/kg), Group C (0.5-0.69 units/kg), and Group B (⩾0.7 units/kg). Treatment failure was defined as mean blood glucose level > 280 mg/dL for two consecutive days after initiating insulin or any blood glucose ⩾ 400 mg/dL. The mean age was 64 ± 14 years, with 50% male, and a mean body mass index of 26.9 ± 6.9 kg/m2. Most had preexisting type 2 diabetes (62%). Mean admission blood glucose and HbA1c were 233 ± 112 mg/dL and 7.8 ± 2.3%, respectively. Group A had the lowest HbA1c (6.7 ± 1.2%), while group D had the highest (9.8 ± 2.5%). Median daily dexamethasone dosage or equivalent was 36 (IQR 16.72) mg, with no significant differences in among groups. Group A had the lowest treatment failure rate. There were no significant differences in treatment failure rate between Groups B, C, and D. Additionally, there were no statistically significant differences in mean BG across the groups: Group A 232 ± 42 mg/dL, Group B 247 ± 57 mg/dL, Group C 247 ± 61 mg/dL, and Group D 227 ± 67 mg/dL (p = 0.2). Group D had a significantly higher rate of level 1 hypoglycemia (p = 0.008), while no differences in clinically significant hypoglycemia (level 2 or 3) were observed between groups. Among patients requiring TDD ⩾ 0.3 units/kg/day, there was no significant difference in treatment failure rate between Groups B, C, and D. Group D had the highest rate of level 1 hypoglycemia. This initial insulin dosage for hospitalized COVID-19 patients on high-dose steroid therapy should be personalized.

Characteristics and Clinical Outcomes of COVID-19 Patients with Hyperglycemia: Retrospective Cohort Study from a COVID-19 Referral Hospital, Bandung, Indonesia

Background: COVID-19 often causes severe complications in patients with metabolic disorders such as diabetes mellitus. On the other hand, inflammation caused by infection may also trigger insulin resistance resulting in hyperglycemia and related to disease severity. This study aimed to describe the characteristics and clinical outcomes of COVID-19 patients with hyperglycemia at one of the COVID-19 referral hospital in Bandung, Indonesia.Methods: This study was a retrospective cohort study using secondary data from medical records of COVID-19 patients admitted to Dr. Hasan Sadikin General Hospital from March 2020 to March 2021. This study included all patients with confirmed COVID-19, aged &gt;18 years, and had at least one blood glucose test at admission. Patients were grouped based on three possible types of hyperglycemia namely diabetes mellitus, reactive hyperglycemia, and steroid-induced hyperglycemia, and then compared their characteristics and disease outcomes.Results: This study identified 1,114 patients’ medical records and included 1,013 data in the analysis. Hyperglycemia occurred in 45.1% of COVID-19 patients. The most common hyperglycemia types were diabetes mellitus (55.7%), reactive hyperglycemia (37.4%), and steroid-induced hyperglycemia (7%). The steroid-induced hyperglycemia group had similar characteristics as the diabetes group. The reactive hyperglycemia group exhibited a metabolic syndrome pattern resembling pre-diabetic conditions. The highest rates of severe disease and mortality were seen in the steroid-induced hyperglycemia group, followed by the diabetes group.Conclusion: There is an elevated prevalence of hyperglycemia in COVID-19 patients with diabetes. The steroid-induced hyperglycemia group has the most unfavorable outcomes. These observations emphasize the importance of identifying hyperglycemic conditions to improve management and outcomes.

Steroid-Induced Hyperglycemia and Its Effect on Outcomes of R-CHOP Chemotherapy for Diffuse Large B-Cell Lymphoma.

We performed a retrospective chart review of 188 patients with DLBCL treated with R-CHOP through CancerCare Manitoba (CCMB) from 1 January 2010 to 31 December 2014. Patients diagnosed with DLBCL were identified using the Manitoba Cancer Registry. The CCMB electronic medical record was reviewed to examine the association between steroid-induced hyperglycemia and subsequent infection, including febrile neutropenic events and overall survival (OS). Patients who developed hyperglycemia with steroid exposure became hyperglycemic during their first R-CHOP cycle. No significant differences in OS or rates of infection were found between euglycemic and hyperglycemic subjects. Patients destined to develop steroid-induced hyperglycemia declare themselves early in the course of steroid exposure. No statistically significant reduction in overall survival attributable to steroid-induced hyperglycemia was found.

THU353 Late Onset Of Immune Checkpoint Inhibitor-Related Diabetes After 3 Years

Abstract Disclosure: S. Avula: None. A. Ahmed: None. M. Salim: None. Z.J. Anderson: None. A. Kumar: None. A. Estrada: None. Background: Immune checkpoint inhibitor-induced diabetes mellitus (ICI-DM) is characterized by acute onset of dramatic hyperglycaemia with severe insulin deficiency following exposure to PD-1/PD-L1 inhibitors. The frequency of type 1 diabetes related to ICIs is estimated to be ∼3.5%. Endogenous insulin secretion is depleted within a few weeks of the clinical onset of diabetes. Moreover, the positive rate for islet-related autoantibodies varies from 5% to 50%. Case: 51-year-old male with a PMH of stage 4 adenocarcinoma of the lung with metastasis to brain, bone, and kidneys was sent to the ED for a POC BG above 700 mg/dl. He was diagnosed with stage 4 lung adenocarcinoma three years prior to the current presentation. He received stereotactic radiotherapy for the brain metastases, Carboplatin/pemetrexed/pembrolizumab x4 cycles, then continued maintenance therapy of pemetrexed/pembrolizumab with the last dose given 3 weeks prior. He had recent evidence of progression, so chemotherapy adjustment was planned, and he started dexamethasone 4mg on the day prior to presentation. Upon ED presentation, he reported new onset polyuria and polydipsia for 1 week accompanied by 10% weight loss over the last 3 months. His vitals were stable. Physical examination was unremarkable. Serum glucose level was found to be 726 mg/dl, Bicarbonate level 28 mEq/L (22-30), creatinine 1.99 mg/dl (baseline 1.2), venous blood PH was 7.29, Bicarbonate 24 mEq/L (24-28), anion gap 15 mEq/L (8-16), B-hydroxybutyrate 2.91 mmol/L (0.02-0.27), sodium 127 mEq/L(135-148) and HbA1c 6.3%. He received normal saline boluses and NPH insulin 15 units SQ, after which his repeat BG level was 426 mg/dl. Given prediabetic Hba1c with recent dexamethasone therapy he was thought to have steroid-induced hyperglycaemia. He was discharged on NPH 15 units daily with Novolog sliding scale. Upon clinic follow-up 1 week later, his BGs did not improve significantly despite stopping steroids. His C-peptide level was low at 0.22 ng/ml (1.10-4.40) with BG 443mg/dl, and GAD -65 antibodies were negative. He continued to have hyperglycaemia while on NPH /Novolog regimen, thus he was switched to Lantus and Novolog regimen with better glycaemic control. He continues to have significant insulin requirements 3 months later. Conclusion: Although the mean interval between the first ICI administration and T1DM development was found to be 201 ± 187 days, the development of type 1 DM may occur with longer intervals from initiating the ICI therapy. In our case, the patient developed new-onset diabetes with low C-peptide after 1,095 days from receiving the first dose of pembrolizumab. On the previous case reports, the presence of GAD-65 antibodies is typically associated with shortened intervals between receiving the ICI therapy and the development of DM. Presentation: Thursday, June 15, 2023

THU289 Hemichorea-Hemiballismus Syndrome Secondary To Steroid Induced Hyperglycemia In A Nondiabetic

Abstract Disclosure: E. Krishnaraju: None. K.N. Patolia: None. U.A. Ogar: None. S. Karki: None. A.G. Olafimihan: None. Introduction: Hemichorea-Hemiballismus syndrome (HCHB) associated with nonketotic hyperglycemia is a rare cause of acute to subacute acquired chorea. The syndrome is usually characterized by unilateral choreiform movements, poorly controlled diabetes mellitus, and striatal abnormalities on an MRI of the brain. Clinical Case: This is a case of a 70-year-old man with a history of congestive heart failure, hypertension, remote ischemic stroke, asymptomatic Paget's disease of the bone, chronic kidney disease, and statin-induced necrotizing myositis. Five months before his presentation, the patient was initiated on prednisone for myositis. On presenting to the ED, he had near resolution of his limb weakness from myositis but complained of one month of right-sided continuous involuntary tremors involving the right upper limb, lower limb, and face that resolved during his sleep. There was no family history of neurologic disorders or any history to suggest medication or illicit drug-induced movement disorders. On examination, the patient had normal cognitive functions and vital signs. Neurologic examination was remarkable for quick interspersed moderate amplitude choreiform movements of the right hand, forearm, proximal arm muscles, and right leg. Laboratory results revealed hyperglycemia and a newly elevated Hemoglobin A1c of 8.5, which was normal the year before. Infectious, hematologic, thyroid disease, and Wilson's disease workups were negative. Cerebrospinal fluid (CSF) analysis was remarkable for elevated glucose and identical oligoclonal bands in the serum and CSF, possibly suggestive of a nonspecific chronic systemic inflammatory state. Autoantibodies for paraneoplastic syndromes and autoimmune diseases, including autoimmune encephalitis were negative. There was also no evidence of occult malignancy on CT imaging of the chest, abdomen, and pelvis. MRI/MRA was significant for new small foci of susceptibility artifact in the bilateral basal ganglia, left cerebellar hemisphere, and cerebellar vermis, likely from chronic microvascular changes. The constellation of hemichorea and new onset hyperglycemia in the setting of a largely nondiagnostic workup raises suspicion for HBHC syndrome. Previous studies have found classic T1-weighted MRI hyperintensities in the basal ganglia, but normal imaging does not rule out a diagnosis of diabetic striatopathy. The patient was eventually discharged with mild improvement of his chorea after starting insulin and risperidone. Unfortunately, he was lost to follow-up and unexpectedly died of an unclear cause soon after. Conclusion: Metabolic complications of diabetes can manifest in complex ways. Non-ketotic hyperglycemic HCHB due to diabetic striatopathy is a rarely reported entity that is commonly misdiagnosed. This case is a unique presentation in a non-diabetic patient with steroid-induced hyperglycemia. Presentation: Thursday, June 15, 2023

THU328 Appropriate Initial Insulin Dosage For Management Of Steroid-induced Hyperglycemia In Hospitalized COVID-19 Patients

Abstract Disclosure: N. Ketaroonrut: None. S. Kiertiburanakul: None. C. Sriphrapradang: None. Introduction: Steroid was recommended for the treatment of severe COVID-19 infection. There are limited studies on the management of steroid-associated hyperglycemia in hospitalized COVID-19 patients. We aimed to determine the appropriate initial insulin dosage to control hyperglycemia in hospitalized COVID-19 patients who received steroid therapy. Methods: We conducted a retrospective single-center analysis of electronic medical records of COVID-19 patients with steroid-induced hyperglycemia who had been treated with insulin. We divided the patients into 4 groups according to the total daily dose (TDD) of subcutaneous insulin therapy at the initiation of dexamethasone ≥6 mg/day or an equivalent dose of glucocorticoid. Glycemic outcomes were compared between groups. Results: A total of 156 patients [age 64±14 years; 50% men; body mass index 26.9±6.9 kg/m2; initial TDD of insulin (units/kg/day): group A, &amp;lt;0.29 (n=79); group B, 0.3-0.49 (n=33); group C, 0.5-0.69 (n=27); group D, &amp;gt;0.7 (n=17)] were included. Most patients (62%) had pre-existing type 2 diabetes. Mean admission blood glucose (BG) and HbA1c were 233±112 mg/dL and 7.8±2.3%, respectively. HbA1c was lowest in group A (6.7±1.2%) and highest in group D (9.8±2.5%). The average daily dexamethasone dosage or equivalent was 49.49±45.4 mg and there were no significant differences between the groups in the dexamethasone dose. The proportion of treatment failure (mean BG &amp;gt;280 mg/dL after the first day of insulin therapy or BG &amp;gt;400 mg/dL for at least 1 time/day) was lowest in group A. Among patients who received TDD &amp;gt;0.3 units/kg/day, group D had the lowest in both the percentage of treatment failure (B (52%) vs C (37%) vs D (29.4%), p=0.006) and mean BG during the 3 days of insulin therapy (B (246.0± 56.7 mg/dL) vs C (246.9±59.0 mg/dL) vs D (228.5±64.4 mg/dL), p=0.21). Three patients had severe hypoglycemia (BG &amp;lt;54 mg/dL) in this study (A: n=1 vs B: n=1 vs C: n=0 vs D: n=1, p=0.51). Conclusions: In the patients who require TDD &amp;gt;0.3 units/kg/day, the treatment failure of hyperglycemia was lowest in the patients who received TDD &amp;gt;0.7 units/kg/day without increasing severe hypoglycemia. This initial insulin dosage may guide physicians to achieve better glycemic control among hospitalized COVID-19 patients who received steroid therapy. Presentation: Thursday, June 15, 2023

SAT142 Utilization Of Continuous Glucose Monitoring In Diagnosis And Management Of Insulinoma

Abstract Disclosure: V. Phan: None. P. kretschmer: None. A.G. Pittas: None. Background: Insulinoma is a rare condition that can cause life-threatening hypoglycemia. Its diagnosis and management are challenging due to the requirement of a prolonged fasting test and frequent blood glucose testing. Continuous glucose monitoring (CGM) is widely available in diabetes management; however, its usage in people without diabetes is limited due to lack of evidence. Here, we report an acutely ill patient where we used professional CGM to streamline and expedite the diagnosis of insulinoma, and personal CGM to titrate medical management with diazoxide. Clinical Case: An 81-year-old woman with complex past medical history was admitted for chest pain and shortness of breath, found to have non-ST-elevation myocardial infarction. During inpatient work up, she experienced several hypoglycemia episodes that resolved with oral glucose intake. She had a history of recurrent hypoglycemia and prior MRI showing pancreatic tumor; however, outside records did not reveal biochemical work-up for insulinoma. Her symptoms were unpredictable, so a professional CGM (Freestyle Libre) was placed. CGM data revealed persistent nocturnal hypoglycemia, and occasional postprandial hypoglycemia. Patient-recorded symptoms were present in less than half of the hypoglycemic periods detected by CGM, indicating hypoglycemia unawareness. Given her acute cardiac condition and knowing her nocturnal hypoglycemia pattern from CGM, we performed a modified 72-hour fasting test that started at midnight and was able to capture a hypoglycemia episode within only 2.5 hours of initiation. Her plasma glucose was 57 mg/dL, insulin was 13 uIU/mL, C-peptide was 1.33 uIU/mL, and proinsulin was 9.5 pmol/L. She had a negative screen for sulfonylurea and there was no evidence of antibodies to insulin, suggesting a diagnosis of insulinoma. While awaiting localization studies, the patient was started on diazoxide. We used the personal CGM connected to our clinic portal to monitor glycemia at home and titrate diazoxide dose and frequency. CGM data showed nocturnal hypoglycemia and minimal daytime hypoglycemia, therefore, we recommended diazoxide only at bedtime to minimize daytime side effects and hyperglycemia. On one occasion, the patient was on as short course of prednisone which typically causes hyperglycemia during the day and hypoglycemia in early morning. CGM allowed us to monitor patterns of steroid-induced hyperglycemia, and we moved the prednisone dose to bedtime which resulted in euglycemia overnight. Conclusion: CGM can be a valuable tool in diagnosing and managing people with insulinomas. The CGM provides information about hypoglycemia frequency and pattern. It also helps detect hypoglycemia unawareness. With CGM, we can choose the right timing for 72-hour fasting test to minimize the length of the procedure. As outpatient, CGM also makes monitoring response to diazoxide a seamless process. Presentation: Saturday, June 17, 2023

Chronic Glucocorticoid Exposure Induced an S1PR2-RORγ Axis to Enhance Hepatic Gluconeogenesis in Male Mice.

It is well-established that chronic glucocorticoid exposure causes hyperglycemia. While glucocorticoid receptor (GR) stimulates hepatic gluconeogenic gene transcription, additional mechanisms are activated by chronic glucocorticoid exposure to enhance gluconeogenesis. We found that chronic glucocorticoid treatment activated sphingosine-1-phosphate (S1P)-mediated signaling. Hepatic knockdown of hepatic S1P receptor 1 (S1PR1) had no effect on chronic glucocorticoid-induced glucose intolerance but elevated fasting plasma insulin levels. In contrast, hepatic S1PR3 knockdown exacerbated chronic glucocorticoid-induced glucose intolerance without affecting fasting plasma insulin levels. Finally, hepatic S1PR2 knockdown attenuated chronic glucocorticoid-induced glucose intolerance and reduced fasting plasma insulin levels. Here we focused on dissecting the role of S1PR2 signaling in chronic glucocorticoid response on glucose homeostasis. We found that chronic glucocorticoid-induced hepatic gluconeogenesis, gluconeogenic gene expression, and GR recruitment to the glucocorticoid response elements (GREs) of gluconeogenic genes were all reduced in hepatic S1PR2 knockdown male mice. Hepatic S1PR2 knockdown also enhanced glucocorticoid suppression of RAR-related orphan receptor gamma (RORγ) expression. Hepatic RORγ overexpression in hepatic S1PR2 knockdown mice restored glucocorticoid-induced glucose intolerance, gluconeogenic gene expression, and GR recruitment to their GREs. Conversely, RORγ antagonist and the reduction of hepatic RORγ expression attenuated such glucocorticoid effects. Thus, chronic glucocorticoid exposure induces a S1PR2-RORγ axis to cooperate with GR to enhance hepatic gluconeogenesis. Overall, this work provides novel mechanisms of and pharmaceutical targets against steroid-induced hyperglycemia.

Steroid Toxicity in Immune Thrombocytopenia – A Series of Unfortunate Events: A Case Report

Immune thrombocytopenia (ITP) is a common bleeding disorder characterised by isolated thrombocytopenia, due to immune-mediated accelerated platelet destruction, usually without any specific or identifiable precipitating factor. ITP most commonly presents with bleeding associated with a low platelet count &lt;100×109/L. Corticosteroids are the first line of treatment in adults. However, steroid-induced complications are widespread in patients with ITP, and sometimes are more atrocious than the risk of bleeding associated with thrombocytopenia. The authors report the case of a 29-year-old male with ITP with recurrent episodes of epistaxis, who was treated with prednisolone for 8 weeks and developed acne, steroid-induced hyperglycaemia, and urinary tract infection with epididymitis and pyocele. A few weeks later, the patient developed blurring of vision, and was found to have central serous chorioretinopathy. They were treated adequately for each of these complications, and had complete resolution of symptoms following cessation of steroids. While acne and hyperglycaemia are common, urinary tract infections with epididymitis and central serous chorioretinopathy are infrequent complications following steroid administration. The complexity of adverse events and the challenges in diagnosing and treating these unique complications prompted the authors to report this case.

152-LB: Implementing a Pilot Clinic for Steroid-Induced Hyperglycemia in Graft vs. Host Disease

Introduction: Malignant hematologic disorders are often treated with hematopoietic stem cell transplantation. This can be complicated by graft versus host disease (GVHD). Treatment is high dose corticosteroids, which often leads to steroid induced hyperglycemia (SIH). Uncontrolled hyperglycemia is associated with increased morbidity and mortality. Despite evidence favoring glycemic control in this population, there are no formal protocols or clinics in place to achieve this. Methods: The University of Kansas Blood and Marrow Transplant Program collaborated with the Department of Endocrinology to establish a pilot clinic for patients with GVHD who have SIH. Over 12 months, patients were referred to a physician assistant specializing in diabetes. They were seen at 1-4 week intervals based on acuity and glycemic control. Data was collected on blood glucose, hemoglobin A1c, fructosamine, steroid doses, insulin doses, hospitalizations, infections, and death. Results: 64 patients were referred to this clinic. 24 were excluded due to lack of hyperglycemia or declined being seen. Median time to index visit from referral was 20.5 days (IQR 8.25-29). Median A1c at index visit was 5.9 (IQR 5.4-7.2) and at 3 months was 5.3 (IQR 4.6-6.3). Median highest glucose within the first 3 months was 230 mg/dL (IQR 183-362) and at 3-6 months was 161 mg/dL (IQR 119.8-247, p-value = 0.0025). Median lowest glucose at 3 months was 86 mg/dL (IQR 78.5-103) and at 6 months was 87 mg/dL (IQR 75-115.8). There were 20 patients who were hospitalized and 9 patient deaths. Conclusions: Managing SIH is complex and requires a multidisciplinary approach. Patients who were seen had reduced episodes of hyperglycemia without increased episodes of hypoglycemia. A1c is an unreliable measurement in this patient population due to high cell turnover and frequent transfusions. Future studies using continuous glucose monitors could be investigated to assess the efficacy and feasibility of this pilot clinic. Disclosure D. Pham: None. K. Grdinovac: None. J. Leal: None. L. Rodriguez: None. A. Salva: None. W. Wesson: None. J. McGuirk: None.

Steroids Induced Hyperglycemia: Its Effects and Management

Steroids are medications that have been widely utilized for a number of ailments, both acute and chronic. The action of endogenous steroids, nuclear hormones that penetrate cell membranes to bind to certain glucocorticoid receptors in the cytoplasm of target cells to form glucocorticoid-receptor (GR) complexes, is mimicked by synthetic glucocorticoids. The translocated activated GR complex regulates DNA transcription in the cell nucleus. The main factor for drug-induced hyperglycemia is steroids. They not only worsen hyperglycemia in those who already have diabetes mellitus (DM), but they can also lead to DM in people who've not previously experienced it. Their incidence can reach up to 46% of patients, and their glucose levels can rise by up to 68% over baseline. Steroid effects are often narrow and reversible. Drug-induced diabetes is supposed to go away as steroid doses are decreased because their impact on endocrine metabolism returns to normal; however, this is often not the case. The synthesis of lipolysis, proteolysis, and hepatic glucose is increased by glucocorticoids (GCs) because they act as a substrate for oxidative stress metabolism. A wide range of medical conditions has been treated with GCs. Although steroid-induced hyperglycemia has been proven to be medically effective, it is still a widespread and potentially dangerous issue that must be taken into consideration when administering any GC dose. The most common scenario requires the use of insulin, particularly when the serum glucose level is greater than 200 mg/dL.&#x0D; Keywords: Steroids, Glucocorticoids, Hyperglycemia, Resistance, Insulin

Part II: Interactive case: Drug‐induced endocrine disorders

Part <scp>II</scp>: Interactive case: <scp>Drug‐induced</scp> endocrine disorders

Cross-sectional study to describe the severity, bio-chemical associations, and final outcomes of COVID-19-associated rhino-orbital-cerebral mucormycosis in a tertiary hospital of East India

The second wave of coronavirus disease 2019 (COVID-19) pandemic triggered a mucormycosis epidemic in India. Diabetes mellitus and dysregulated immune response were contributors, and rhino-orbital-cerebral mucormycosis (ROCM) was the most common presentation. It is however not known whether bio-chemical parameters at presentation correlate with stage of ROCM or final outcome in terms of vision or mortality.This retrospective, hospital-based study included all in-patients of mucormycosis with ophthalmic manifestations at presentation admitted during June 1, 2021 to August 31, 2021. It aimed to evaluate the association between severity of infection, serum levels of HbA1c, ferritin, interleukin-6 (IL-6), C-reactive protein (CRP), and D-dimer levels at presentation and outcome.There were altogether 47 eligible cases having a mean age of 48.8 ± 10.9 years with a male:female ratio of 2.6:1; forty-two (89.4%) had pre-existing diabetes, and five (10.6%) had steroid-induced hyperglycemia. The mean HbA1c among diabetics was 9.7 ± 2.1. HbA1c and serum CRP showed an increase over subsequent stages, which was not statistically significant (P = 0.31). IL-6 values for all stages were similar (P = 0.97). Only serum ferritin levels showed a statistically significant increase over stages (P = 0.04). IL-6 was significantly lower (P = 0.03) in patients who survived, whereas CRP levels were significantly lower in patients who had final visual acuity (VA) better than only perception of light (P = 0.03).Uncontrolled diabetes mellitus is a significant association of ROCM. Serum ferritin levels at presentation best correlate with extent of the disease. CRP levels are best to prognosticate cases that will have sufficient VA to carry on activities of daily living, whereas IL-6 levels are best associated with survival.

E013 Co-production of a quality improvement project to address glucocorticoid toxicity

Abstract Background/Aims Glucocorticoid toxicities are well-known, but patient involvement work (PMR Voices 2021) had highlighted a need for better patient education/counselling about side-effects, including early neuropsychiatric toxicity, and support for self-management. In our audit of steroid-induced hyperglycaemia, our attempts to improve counselling had proved challenging to implement. Therefore, we sought patient involvement in designing a quality improvement (QI) project informed by their lived experience. Methods Using insight gathered from previous patient involvement and the clinical team, we held a workshop with ten patient partners living with polymyalgia rheumatica (PMR) to share stories and define relevant themes. We then collected narratives using a distributed ethnographic and mixed-methods tool, Sensemaker®, designed to enable multi-perspective narrative methods at scale. The SenseMaker site was disseminated via patient organisations including PMRGCAuk, PMR GCA Scotland and VasculitisUK, along with a parallel survey for professionals. The survey centred around gathering a narrative from the perspective of the patient, healthcare professional (HCP), or carer; and self-signification of that narrative against a conceptual framework based on theory (Leventhal’s Common-sense Model) and themes identified by the patient partners. The group of ten patients discussed the emerging patterns, after which further analysis of the narratives was conducted to link them to feasible actions. Results The clinical team identified access and communication, echoed by the patient team with particular focus on trustworthy information sources, visibility of side-effects, and future health significance. We piloted and improved the survey with patient partners. In 4 weeks we received 198 patient responses, mostly from the UK, and those of 28 HCPs. HCPs informally fed back that the survey was interesting to complete because it prompted thought and reflection. The patient narratives conveyed multi-layered messages; physical and mental health were intertwined. The two groups described the same spectrum of steroid side-effects (mood disturbance commonest). Compared to HCPs, patients chose to share narratives focused less on prevention and more on managing/mitigating, and often spoke of “trustworthy information” coming from the lived experience of themselves or others, rather than medical sources. Many of the narratives suggested simple actions that might improve clinical services, yet might not have been visible in the context of clinical encounters or quantitative survey measures alone. Conclusion We used co-production to inform healthcare improvement. The method can reveal biases of perspective and entrained patterns of thinking amongst both experts and patients that can affect decision-making relevant to health outcomes. Limitations include lack of a defined sampling frame (dissemination via informal networks), and limitations related to digital exclusion; with more time/resources it would be possible to access a wider patient audience. This method helped us prioritise feasible actions to take forward in QI work to evaluate their effectiveness as we incorporate them into our service. Disclosure F. Morgan: None. H. Al-Hilali: None. M. Grover: None. L. Neill: Other; LN is a trustee of PMR GCA Scotland. E. Snowden: Other; The Sensemaker tool is used both in non-profit and commercial contexts. J. Scopes: None. G. Crowther: None. A. Rebane: None. H. Ismail: None. S.L. Mackie: Consultancies; SLM has provided consultancy on behalf of her institution for Roche/Chugai, Sanofi, AbbVie and AstraZeneca. In all cases fees were paid to her institution and no personal fees were received. Member of speakers’ bureau; SLM has given talks on behalf of her institution for Pfizer, Vifor and UCB. In all cases fees were paid to her institution and no personal fees were received. Grants/research support; As a research grant co-applicant, SLM has received research funding (partial salary support) from Vifor, paid to her institution. Other; SLM was supported by Roche to attend EULAR2019 and by Pfizer to attend ACR2021 virtually. SLM has been an investigator on clinical trials for Sanofi and GSK.

Modifying Type of Insulin to Manage Steroid-Induced Hyperglycemia: A Case Report.

Steroid-induced hyperglycemia was diagnosed in an older hospitalized patient after he was treated with the intermediate-acting glucocorticoid methylprednisolone. Before hospital admission, the patient did not have a diagnosis of diabetes. His elevated admission glucose level of 167 mg/dL along with his significant hyperglycemia after glucocorticoid initiation prompted the medical team to obtain a hemoglobin A1c result, 8.4%, which confirmed the diagnosis of type 2 diabetes. The capillary blood glucose level was elevated into the 200 to 399 mg/dL range for most of the patient's hospital stay while he was receiving subcutaneous insulin therapy of glargine and aspart correction and prandial bolus dosing. When the patient's subcutaneous insulin therapy was changed from glargine to neutral protamine Hagedorn insulin, the target glucose level range of 140 to 180 mg/dL was attained. From this case report, we determined that it is important to consider modifying subcutaneous insulin therapy by using another type of insulin when target glucose values are not achieved during the treatment of steroid-induced hyperglycemia.

Hyperglycemia and Glycemic Variability Associated with Glucocorticoids in Women without Pre-Existing Diabetes Undergoing Neoadjuvant or Adjuvant Taxane Chemotherapy for Early-Stage Breast Cancer

Glucocorticoids, which are administered with chemotherapy, cause hyperglycemia. Glycemic variability among breast cancer patients without diabetes is not well known. A retrospective cohort study was conducted involving early-stage breast cancer patients without diabetes who received dexamethasone prior to neoadjuvant or adjuvant taxane chemotherapy between August 2017-December 2019. Random blood glucose levels were analyzed, and steroid-induced hyperglycemia (SIH) was defined as a random glucose level of >140 mg/dL. A multivariate proportional hazards model was used to identify the risk factors of SIH. Out of 100 patients, the median age was 53 years (IQR: 45-63.5). A total of 45% of patients were non-Hispanic White, 28% Hispanic, 19% Asian, and 5% African American. The incidence of SIH was 67%, and glycemic fluctuations were highest in those with glucose levels of >200 mg/dL. Non-Hispanic White patients represented a significant predictor for time to SIH, with a hazard ratio of 2.5 (95% CI: 1.04, 5.95, p = 0.039). SIH was transient in over 90% of the patients, and only seven patients remained hyperglycemic after glucocorticoid and chemotherapy completion. Pretaxane dexamethasone-induced hyperglycemia was observed in 67% of the patients, with the greatest glycemic lability in those patients with blood glucose levels of >200 mg/dL. The non-Hispanic White patients had a higher risk of developing SIH.