Background Chronic corticosteroid use is prevalent among surgical patients, yet its association with postoperative venous thromboembolism (VTE) has not been systematically quantified. We conducted a systematic review and meta-analysis to assess this risk. Methods We searched MEDLINE, Embase, and Cochrane Central through January 2026 (PROSPERO: CRD420261298063). Eligible studies were observational studies or RCTs examining chronic preoperative corticosteroid use and postoperative VTE in adult surgical patients. We used random-effects meta-analysis to calculate pooled risk ratios (RR)with 95% confidence intervals. Evidence certainty was assessed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach and methodological quality using the Newcastle-Ottawa Scale. Results Nine retrospective cohort studies (2,678,513 patients; 97,201 corticosteroid users) were included. Chronic corticosteroid use was associated with increased composite VTE risk (RR 1.51, 95% CI: 1.31-1.73; I2 = 71%). Pulmonary embolism (PE) did not reach statistical significance (RR 1.31, 95% CI: 0.95-1.80), while deep vein thrombosis (DVT) risk was significantly increased (RR 1.48, 95% CI: 1.19-1.84; I2 = 64%). GRADE yielded low-quality evidence for composite VTE and DVT and very low-quality evidence for PE. Conclusions Chronic preoperative corticosteroid use is associated with a 51% increased postoperative VTE risk across 2.6 million surgical patients, suggesting potential value in considering chronic corticosteroid use within perioperative VTE risk assessment, pending higher-quality prospective data. Current evidence is insufficient to support specific protocol changes; studies are needed to define
Background Circulating amyloid beta 1-40 (A beta 40), a pro-inflammatory and pro-atherogenic peptide, is an emerging biomarker in atherosclerotic cardiovascular disease (ASCVD), but evidence on its modulation by cardiovascular therapies is limited and conflicting. We explored associations between statin therapy and A beta 40 plasma levels. Methods In this prospective study, patients with dyslipidemia (n = 146) were consecutively recruited. Alpha beta 40 was measured in plasma by enzyme-linked immunosorbent assay at baseline, after a mean follow-up of 5.2 (visit 2 [V2]) and 15 months (visit 3 [V3]). Patients in whom statin treatment was initiated or intensified (n = 68, intensification group) were compared with patients who were untreated or on stable statin intensity (n = 78, control group). Results After multivariable adjustment for biologically plausible confounders, increased A beta 40 at baseline associated with ASCVD, heart failure, decreased estimated glomerular filtration rate (eGFR), and diabetes mellitus (DM). A beta 40 increased from baseline to V2 in the intensification group (p = 0.05 and adjusted p for interaction= 0.031 vs. the control group) and then stabilized. In the control group, AR40 increased at V3 compared with V2 (p = 0.043). Excluding ezetimibe-treated patients did not alter these findings. In patients with low-density lipoprotein cholesterol (LDL-C) reduction > 50% at V3, AR40 levels remained unchanged, whereas they increased in the rest of the population (adjusted p for group interaction = 0.030). Conclusion In high-risk patients, statin initiation or intensification is associated with a short-term increase, followed by a longterm return to initial AR40 circulating levels, whereas patients achieving LDL-C reduction show long-term stabilization of AR40 levels. Further research is warranted to clarify the mechanistic insights of these observations.
Objective The systemic immune-inflammation index (SII) is an established prognostic marker in coronary artery disease. This study investigated the association between SII and 1-year prognosis in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI), and explored its potential utility in informing P2Y(12) inhibitor selection. Methods A total of 15,123 consecutive ACS patients undergoing PCI between January 2021 and December 2022 were enrolled. Patients were stratified into high-and low-inflammation groups based on the optimal SII cut-off derived from receiver operating characteristic analysis. The primary endpoint was 12-month ischemic events, defined as a composite of cardiac death, myocardial infarction, and stroke. Propensity-score matching was performed to compare ticagrelor-based versus clopidogrel-based dual antiplatelet therapy within each group. Results The optimal SII cut-off was 651 & times; 10(9)/L. Elevated SII was associated with increased ischemic events (HR 1.86; 95% CI: 1.52-2.28; p < 0.0001) and all-cause mortality (HR 2.44; 95% CI: 1.90-3.13; p < 0.0001). In the low-SII group (1,422 matched pairs), ticagrelor was associated with increased bleeding risk (HR 2.15; 95% CI: 1.60-2.88; p < 0.0001) without association with ischemic benefit. In the high-SII group (1,299 matched pairs), ticagrelor was associated with reduced ischemic events (HR 0.52; 95% CI: 0.33-0.83; p = 0.006), cardiac death (HR 0.45; 95% CI: 0.23-0.86; p = 0.015), and all-cause mortality (HR 0.40; 95% CI: 0.23-0.70; p = 0.001) without association with increased major bleeding. Conclusion The SII is associated with 12-month post-PCI ischemic and mortality risk and demonstrates potential as a candidate biomarker for risk stratification, with exploratory observations of ticagrelor benefit in high-SII and clopidogrel adequacy in low-SII patients.
Most patients treated for chronic lymphocytic leukaemia (CLL) fail to achieve measurable residual disease (MRD) negativity. The role of maintenance with the immunomodulatory drug lenalidomide in these patients is unclear. A randomised multicentre phase III trial (ACTRN12610000060044) was conducted in Australia and France to assess the effect of 2 years of daily lenalidomide maintenance versus observation in patients with CLL and residual disease after initial immunochemotherapy. The primary end-point was time to disease progression or death from randomisation. Between May 2011 and January 2018, 143 patients were randomised to receive lenalidomide (n = 71) or observation (n = 72). Median progression-free survival (PFS) was longer with lenalidomide at 64.6 months (95% confidence interval [CI] 47.7 to not reached) versus 42.4 months (95% CI 32.3-61.6) in the observation arm (p = 0.039). Lenalidomide benefit persisted for 3 years after maintenance cessation. There was no difference in overall survival. More patients taking lenalidomide achieved MRD negativity, especially those who received at least 20 maintenance cycles. Lenalidomide led to more cytopenias, infections and gastrointestinal effects. There were no cases of acute lymphoblastic leukaemia. In patients with CLL selected by the presence of residual disease at the end of initial chemoimmunotherapy, lenalidomide maintenance increased the chance of achieving MRD negativity and prolonged PFS.
More than 400 million people have chronic obstructive pulmonary disease (COPD), with exacerbations representing a major health burden. Although the overall incidence of invasive pulmonary aspergillosis (IPA) in patients with COPD with hospitalized exacerbation is only 1% to 4%, certain factors substantially increase this frequency. Risk factors compromising defenses against Aspergillus spp. in COPD patients include systemic or high-dose inhaled corticosteroids; comorbidities including bronchiectasis, diabetes, and cardiovascular disease; and prolonged courses of antibiotics. An international group of experts met to develop criteria for diagnosing IPA based on existing literature and consensus in nonventilated COPD patients. The preliminary diagnostic recommendations were further evaluated by additional experts using the Delphi methodology. A hospitalized exacerbation of COPD with 2 or more of the above clinical risk factors should prompt (1) a computed tomography scan of the chest; (2) sending a respiratory sample (sputum, induced sputum or bronchoscopy sample) for direct microscopy for fungi, high-volume fungal culture, and preferably Aspergillus PCR and, if a bronchoscopy sample is obtained, then also Aspergillus antigen (galactomannan); and (3) a serum sample for galactomannan and Aspergillus IgG. The combination of a high-risk COPD patient, with compatible imaging abnormalities and any 2 positive tests (2 samples or different tests on the same respiratory sample) for Aspergillus is sufficient to establish the diagnosis of IPA with enough confidence to initiate antifungal therapy and/or enroll the patient in a clinical or epidemiological study of IPA in COPD. Additional studies are required to augment performance data for most assays in COPD and validate the proposed diagnostic criteria.
