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Adults hospitalized for community-acquired pneumonia (CAP) have an increased risk of myocardial infarction. Corticosteroid treatment lowers CAP morbidity and mortality, but it is not known whether it influences in-hospital myocardial infarction.The aim of the present study was to investigate the potential interplay between corticosteroid treatment and in-hospital myocardial infarction in adults with CAP.We retrospectively analyzed adults with CAP referred to the University Hospital Policlinico Umberto I (Rome, Italy), consecutively recruited, and prospectively followed until discharge. The primary outcome was the occurrence of myocardial infarction during hospitalization. We used propensity score-adjusted Cox models to examine the association between corticosteroid use and myocardial infarction.Seven hundred fifty-eight patients (493 males, 265 females; mean ± standard deviation age, 71.7 ± 14.4 yr) were included in the study. Of these, 241 (32%) were treated with systemic corticosteroids (methylprednisolone, betamethasone, or prednisone). During follow-up, 62 (8.2%) had a myocardial infarction during their hospitalization (incidence, 0.72 per 100 person-days; 95% confidence interval [CI], 0.55 to 0.92). Those treated with corticosteroids had a lower incidence of myocardial infarction (0.42 per 100 person-days) than those not treated with corticosteroids (0.89 per 100 person-days; absolute rate difference, -0.48 per 100 person-days; 95% CI, -0.85 to -0.10). In a propensity score-adjusted Cox model, corticosteroid use was associated with a lower incidence of myocardial infarction (hazard ratio, 0.46; 95% CI, 0.24 to 0.88; P = 0.02).We found that in-hospital corticosteroid treatment was associated with a lower incidence of myocardial infarction in adults hospitalized with CAP.

Background Urinary 8‐iso‐ PGF 2α, a marker of oxidative stress, is influenced by the activation of NOX 2. It is unclear if platelets 8‐iso‐ PGF 2α contribute to urinary 8‐iso‐ PGF 2α. Methods and Results In a cross‐sectional study, platelet, urinary, and serum 8‐iso‐ PGF 2α were determined in subjects with downregulation (X‐linked chronic granulomatous disease [ X‐CGD ], n=25) and upregulation (type II diabetic patients [T2D], n=121) of NOX 2 and 153 controls matched for sex and age. In diabetic patients (n=18), the above variables were repeated before and after 7 days treatment with 100 mg/day aspirin or 100 mg/day aspirin plus 40 mg/day atorvastatin. In vitro study was performed to see the contribution of blood cells to serum 8‐iso‐ PGF 2α. Compared with controls, X‐CGD patients had lower platelet, serum, and urinary 8‐iso‐ PGF 2α values; conversely, diabetic patients had higher values of 8‐iso‐ PGF 2α compared with controls. Urinary 8‐iso‐ PGF 2α significantly correlated with both platelet and serum 8‐iso‐ PGF 2α in the 2 cohorts. A parallel increase of platelet, serum, and urinary 8‐iso‐ PGF 2α by aspirin and a parallel decrease by aspirin plus atorvastatin were detected in the interventional study. In vitro study demonstrated that platelets contribute to 37% of serum 8‐iso‐ PGF 2α and that only 13% of it is of extravascular origin. Conclusions The study suggests that NOX 2 contributes to the formation of 8‐iso‐ PGF 2α in both platelets and urine. The direct correlation between platelet and urinary 8‐iso‐ PGF 2α suggests that, at least partly, urinary 8‐iso‐ PGF 2α reflects platelet 8‐iso‐ PGF 2α production. Analysis of serum 8‐iso‐ PGF 2α may represent a novel tool to investigate the production of 8‐iso‐ PGF 2α by blood cells including platelets. Clinical Trial Registration URL: ClinicalTrials.gov. Unique Identifier: NCT01250340 .