Citations

Abstract Osteomyelitis pubis, a rare form of osteomyelitis affecting the pubic bone and symphysis, is an often-misdiagnosed condition accounting for less than 1% of all osteomyelitis cases. We present the case of a 41-year-old-male diabetic patient on sodium-glucose-co-transporter-2 (SGLT2) inhibitors, specifically dapagliflozin, who developed osteomyelitis pubis and associated septic arthritis and pyomyositis. Despite a well-controlled diabetes profile and the absence of typical risk factors, the patient's condition progressed rapidly leading to severe pain and functional impairment. Imaging studies revealed extensive infection, and culture results identified Pseudomonas aeruginosa , necessitating a complex, multistage antibiotic regimen. The patient responded positively to treatment but experienced complications, including drug-induced agranulocytosis. This case underscores the potential link between SGLT2 inhibitors and osteomyelitis, highlighting the need for increased clinical vigilance and the careful assessment of risks when prescribing these medications to diabetic patients. Further research is warranted to better understand the association between SGLT2 inhibitors and osteomyelitis pubis.

Abstract Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease linked to repetitive traumatic brain injury, but its prevalence and risk factors in the general population remain poorly defined. We investigated CTE neuropathological changes (CTE-NC) in an admixed, population-based clinicopathological cohort. Neuropathological evaluation was conducted on brain samples from 1151 individuals in the University of São Paulo Biobank for Aging Studies collected from 2004 to 2022. CTE-NC and aging-related tau astrogliopathy (ARTAG) were assessed across 14 963 histological slides using p-tau immunostaining. Clinical, cognitive, and neuropsychiatric data were obtained via informant interviews; information on sports exposure and traumatic brain injury history was limited. Seven cases (0.6%) met criteria for CTE-NC, mean age at death 73.4 ± 12.5 years; 1 was female. Dementia was present in 43% of CTE-NC cases; 57% exhibited neuropsychiatric symptoms. Most common co-pathologies were Alzheimer disease-type changes, ARTAG, and argyrophilic grain disease. Comprehensive exposure histories were unavailable for most cases; 2 had documented soccer involvement. These findings indicate that CTE-NC is rare in this population-based Brazilian cohort and predominantly affects males with frequent coexisting neuropathologies. Findings align with reports from high-income countries and support prioritizing primary prevention by reducing exposure to repetitive head impacts in sport and other settings.

Abstract Objective To examine the influence of demographics on organ damage in a broad, multiethnic cohort of patients with Behçet’s syndrome (BS). Methods In this cross-sectional ancillary analysis of the PROBE project, the investigated demographic variables were sex, age, education level and geographic area of residence. Damage was measured by the BS Overall Damage Index (BODI). Multivariate linear (β) and logistic (adjusted odds ratio [adjOR]) regression analyses examined associations between demographics and the extent and prevalence of damage. Results A total of 970 patients were enrolled. The median (interquartile range) age was 40 (31–50) years; 56.5% were males; 21.4% had a low level of education. The median BODI score was 1 (0–3), with 65.6% of patients having a BODI ≥1. Males had higher damage (β 0.103) and a higher prevalence of total (adjOR 1.7, per 10 years), ocular (adjOR 1.6), and vascular (adjOR 2.1) damage. Age was associated with greater damage (β 0.104), and a higher prevalence of overall (adjOR 1.4), neuropsychiatric (adjOR 1.2) and miscellaneous (adjOR 2.0) damage. Low education was associated with a greater frequency of overall (adjOR 1.9) and ocular (adjOR 1.6) damage. North African patients experienced greater damage than South European (β 0.400) and Middle Eastern (β 0.314) patients, as well as a higher risk of overall damage (adjOR 13.9 and 10.7, respectively) across all organ domains, except for the reproductive and gastrointestinal systems. Conclusions This study demonstrates how the extent, prevalence and characteristics of damage in BS vary with demographic factors, underscoring their importance in research and personalized management.

Background: Upper gastrointestinal bleeding (UGIB) is a common medical emergency associated with significant morbidity, mortality, and healthcare costs. Many patients undergo early endoscopy despite the absence of active bleeding. PillSense is a novel Food and Drug Administration (FDA)-cleared ingestible capsule that rapidly detects the presence of blood in the upper GI tract and may optimize triage decisions. Methods: We conducted a retrospective study evaluating the impact of PillSense on the management of suspected UGIB in an academic center. The primary outcome was the association between capsule results and clinical decision-making, including endoscopy deferral, prioritization, outpatient scheduling, and airway protection. Secondary outcomes included transfusion requirements, time-to-endoscopy, endoscopic intervention, and 30-day adverse events. Results: A total of 28 patients (mean age 64.4 ± 17.9 years, 82.7% male) were included. Compared with negative results, positive results were associated with higher transfusion requirements (median 3 (IQR 3–6) vs. 2 (IQR 1–3.25) units; p = 0.041) and shorter time-to-endoscopy (median 0.2 (IQR 0.01–1) vs. 2 (IQR 1–15.5) days; p = 0.017). In high-risk for sedated endoscopy patients, negative results were associated with EGD deferral in 53.8%, with no subsequent adverse events within 30 days. Endoscopic intervention was performed in 62.5% of positive-result patients versus 9.5% of negative-result patients. Conclusions: The PillSense results were associated with differences in triage and management of high-risk patients with suspected UGIB. Its rapid, accurate, and non-invasive results may reduce unnecessary urgent endoscopy procedures, improve resource utilization, and enhance patient safety, particularly in the highest-risk populations.

Background Patients with single-ventricle physiology are often palliated with the Fontan operation, which may involve the creation of a fenestration. We aimed to evaluate differences in cardiopulmonary exercise test (CPET) performance between patients with fenestrated and non-fenestrated Fontan circulation. Methods Patients with a Fontan circulation referred to CPET between 2006 and 2024 were included and were categorised based on their fenestration status at the time of CPET. Logistic regression analyses were performed to assess the impact of fenestration on peak oxygen consumption (VO 2 ), and Cox proportional hazard to evaluate the impact of fenestration on cardiovascular outcomes (death, heart transplant and Fontan-related hospitalisation). Results Of the 184 patients, 141 were classified as non-fenestrated and 43 as fenestrated. The minute ventilation-carbon dioxide production (V E /VCO 2 slope) was higher in the fenestrated (36.9±7.9) versus (33.2±6.2; p=0.009) in the non-fenestrated group. There was no significant difference in predicted VO 2 between groups (non-fenestrated 51.9%±14.4 vs 51.3%±15.6; p=0.7). Resting oxygen saturation was higher in the non-fenestrated group (93%±4.7 compared with fenestrated group 90.1%±5; p<0.001). Fontan fenestration was not significantly associated with the composite outcome; older patient age at the time of the CPET, cirrhosis and ventricular ejection fraction <40% were significantly associated with higher risk, while higher resting systolic blood pressure, left ventricular morphology and higher predicted peak VO 2 were protective. Conclusions The increased hypoxia and reduced ventilatory efficiency associated with Fontan fenestration offset any potential benefits, resulting in similar exercise performance between the groups. Fontan fenestration was not significantly associated with cardiovascular outcomes.

ABSTRACT Alzheimer's disease (AD), a leading cause of dementia in the elderly, is traditionally characterized by neurodegeneration driven by amyloid‐beta plaques and tau tangles. However, emerging evidence reveals that AD's impact extends beyond the brain, significantly affecting skeletal health. This review integrates clinical and transgenic mouse model data to elucidate the mechanistic interplay between AD pathology and bone metabolism. AD patients exhibit increased risk for hip fractures and low bone mineral density (BMD), independent of cognitive impairment severity. We found altered calcium and alkaline phosphate levels in the blood of patients with mild cognitive impairment and AD, as assessed from the Alzheimer's Disease Neuroimaging Initiative data. Convergent risk factors—age, sex, APOE4 genotype, smoking, and vitamin D deficiency—contribute to both neurodegeneration and bone fragility. Key molecular pathways, such as Wnt/β‐catenin signaling and TREM2‐mediated osteoclast regulation, underscore shared mechanisms driving disease pathology in both systems. Mouse models of AD consistently demonstrate disrupted bone remodeling, impaired osteoblast function, and heightened osteoclast activity. Therapeutic strategies targeting overlapping pathways, including lithium, anti‐FSH antibodies, and NF‐κB inhibitors, show promise in mitigating both cognitive decline and bone loss. Collectively, these insights advocate for a more integrated view of AD that includes skeletal comorbidities, potentially guiding the development of dual‐purpose interventions.