Glucocorticoids are extensively prescribed for managing immune-mediated and inflammatory diseases. While clinically effective, prolonged glucocorticoid therapy induces adverse effects that compromise physical function and may attenuate the benefits of exercise interventions. Current exercise guidelines, however, inadequately address the complexities of concurrent glucocorticoid treatment. This narrative review, which includes a systematic review, examines interactions between glucocorticoid therapy and physical exercise, evaluates existing evidence on exercise interventions in glucocorticoid-treated populations, and provides evidence-based exercise recommendations tailored to this clinical population. Glucocorticoid-induced complications-including diabetes mellitus, musculoskeletal disorders, hypertension, weight gain, cognitive impairment, and neuropsychiatric disturbances-substantially impair exercise capacity, patient engagement, and physiological adaptations to training. After searching PubMed, Scopus, and Web of Science databases from 1 January, 2000 to 10 May, 2025 for exercise interventions in glucocorticoid-treated patients, 19 studies were included (18 unique trials; n = 663, predominantly women), mainly involving rheumatoid arthritis and systemic lupus erythematosus. Overall, the methodological quality, as assessed using the Risk of Bias 2 tool, was rated as moderate to high. Exercise interventions consistently improved muscle performance and functional outcomes, whereas evidence regarding bone, cardiometabolic, cognitive, and mental health outcomes was limited or inconsistent. For optimal exercise prescription in this population, resistance training and aerobic exercise emerge as essential components, complemented by targeted strategies to enhance adherence and ensure safety. Integrating structured exercise as adjuvant therapy in long-term glucocorticoid treatment holds considerable promise for mitigating adverse effects and reducing polypharmacy burden; however, additional research is warranted to establish definitive clinical guidelines.

Frailty is a recognized prognostic factor in acute myeloid leukaemia (AML), yet its independent impact on healthcare resource utilization remains understudied. This study evaluated frailty's association with healthcare resource utilization (HRU) burden during the first year of AML treatment. We conducted a population-based retrospective cohort study using linked administrative databases in Ontario, Canada, involving 5450 AML adults (2006-2023) initiating chemotherapy. Frailty was assessed via a validated deficit-accumulation index. HRU outcomes-total-length of stay (LOS), intensive care unit (ICU)-LOS and hospital/emergency department (ED) visits-were measured as rates per person-year and their association with frailty measured as rate ratio (RR) using multivariable negative binomial regression, adjusting for age, sex and chemotherapy intensity. Frailty was independently associated with significantly higher HRU intensity. Compared to fit patients, frail patients demonstrated increased rates of total-LOS (RR 1.18), hospital/ED visits (RR 1.12) and, notably, ICU-LOS (RR 1.81). Conversely, advanced chronological age (≥65 years) correlated with lower ICU utilization (RR 0.60), suggesting critical care decisions may be more age-driven than based on physiological reserve. Frailty is a driver of HRU in AML, superiorly predicting high-acuity resource needs compared to chronological age. Routine frailty assessments are essential to inform resource allocation, guide treatment intensity, mitigate triage bias and improve value-based care.

Lacosamide is a third-generation antiseizure medication that enhances slow inactivation of voltage-gated sodium channels. Although generally well tolerated, it has been associated with cardiac conduction abnormalities, most commonly in the setting of intravenous administration, overdose, or dose escalation. We report a case of a 79-year-old woman with a history of hypertension (treated with losartan and metoprolol), restless legs syndrome (treated with ropinirole), peripheral neuropathy, and seizure disorder who presented to the emergency department with several days of intermittent confusion and generalized weakness following a recent admission for seizure-like activity, during which lacosamide had been initiated. On arrival, she was afebrile with a heart rate of 74 beats per minute, blood pressure 165/88 mmHg, and oxygen saturation 98% on room air; she was oriented to person and year but not to place, which represented a change from her baseline. Initial laboratory evaluation, including complete blood count, comprehensive metabolic panel with normal renal and hepatic function, B12, and thyroid stimulating hormone, was unremarkable, and her admission electrocardiogram showed normal sinus rhythm with a PR interval of 208 ms. While boarding in the emergency department, she received her scheduled oral lacosamide 150 mg, and approximately two hours later was found unresponsive with a heart rate in the 30s and systolic blood pressure of 50 mmHg. She responded to atropine 1 mg IV and 50μg of epinephrine IV, with improvement of her vital signs and mental status. Six hours later, she received a second scheduled dose of lacosamide 150 mg along with her home medications, including metoprolol tartrate 50 mg, and again two hours later became minimally responsive with a heart rate of 49 beats per minute, blood pressure 64/32 mmHg, and a new first-degree atrioventricular block; she again responded to atropine. The second episode was more pronounced and associated with conduction delay not previously present. No seizure activity was observed during either episode. Lacosamide was discontinued, and the patient had no further bradycardic or hypotensive events. The reproducible temporal relationship between dosing and symptoms, along with resolution after medication cessation, supports a causal association. This case highlights that clinically significant cardiac adverse effects can occur with standard oral dosing of lacosamide, particularly in older adults and in the presence of other medications that affect cardiac conduction. Emergency physicians should maintain a high index of suspicion for medication-induced bradycardia and hypotension in patients receiving lacosamide. This case also underscores how hospital boarding can increase the risk of iatrogenic harm, as patients may receive routine medications in a high-acuity environment where evolving adverse effects can be more difficult to anticipate and detect.

Iron deficiency anemia (IDA) is the most common cause of anemia worldwide and a major cause of disability, manifesting with symptoms including fatigue, weakness, exercise intolerance, worsening heart failure, impaired concentration, irritability, and depression. Women of reproductive age are disproportionately affected due to menstrual blood loss and gynecologic disorders. Iron deficiency anemia is diagnosed in patients who have both iron deficiency (ID), noted by low ferritin level and/or transferrin saturation, and anemia. Notably, iron deficiency (ID) can also occur in the absence of anemia, and overreliance on hemoglobin thresholds may risk missing the diagnosis in menstruating women due to flawed sex-specific reference ranges. Work-up for ID and IDA should focus on identifying the underlying cause of anemia, and may include a gynecologic work-up, bidirectional endoscopy, testing for Helicobacter pylori infection and celiac disease, as well as administering a trial of iron. Iron deficiency can be treated with either oral or intravenous iron. Although several guidelines address the diagnosis or management of ID and IDA, they differ in their recommendations based on the population studied, the clinical context, and the quality of the underlying evidence. Here, 2 hematologists and coauthors of the 2025 Iron Consortium Guideline published in Lancet Haematology discuss areas of guideline uncertainty relating to the diagnosis, evaluation, and treatment of patients with IDA and for Ms. B, a young woman diagnosed with ID.