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Background: Large-scale multicentric studies reported that, despite advances in diagnosis, antibiotics, and surgical treatment, infective endocarditis (IE) in-hospital mortality remains high. Most data have been obtained from patients treated in infective disease wards, internal medicine, cardiology, or cardiac surgery departments and are therefore heterogeneous. The few studies focused on complicated IE patients leading to intensive care unit (ICU) admission have reported different methodologies and results. The aim of our study was to describe the epidemiological, clinical, and microbial features of critically ill patients admitted to the ICU with a definite IE diagnosis. Methods: We conducted a prospective case-series population study from January 1, 1998, to December 31, 2020. Patients were divided into 2 groups: "Ward" (group 1) and "ICU" patients (group 2), and a 1-year follow-up was performed. Results: After performing a univariate and multivariate logistic regression analysis, we found that the independent predictors of ICU admission were vegetation diameter >10 mm, abnormal PaO2/FiO2 ratio, and acute heart failure. Five independent mortality risk factors were identified: SOFA score >14, not performing surgery, age >70 years, acute heart failure, and embolic complications. Conclusions: Infective endocarditis in-hospital mortality remains high. ICU admission and mortality can be predicted by independent risk factors. [ABSTRACT FROM AUTHOR]

Abstract Background Epidemiological data indicate that obesity is a risk factor for asthma, but scientific literature is still debating the association between changes in body mass index (BMI) and airway hyperresponsiveness (AHR). Methods This study aimed at evaluating the influence of BMI on AHR, in outpatients with symptoms suggestive of asthma. 4,217 consecutive adult subjects (2,439 M; mean age: 38.2±14.9 yrs; median FEV1 % predicted: 100 [IQR:91.88-107.97] and FEV1/FVC % predicted: 85.77% [IQR:81.1-90.05]), performed a methacholine challenge test for suspected asthma. Subjects with PD20 < 200 or 200 < PD20 < 800 or PD20 > 800 were considered affected by severe, moderate or mild AHR, respectively. Results A total of 2,520 subjects (60% of all cases) had a PD20 < 3,200 μg, with a median PD20 of 366 μg [IQR:168–1010.5]; 759, 997 and 764 patients were affected by mild, moderate and severe AHR, respectively. BMI was not associated with increasing AHR in males. On the contrary, obese females were at risk for AHR only when those with moderate AHR were considered (OR: 1.772 [1.250-2.512], p = 0.001). A significant reduction of FEV1/FVC for unit of BMI increase was found in moderate AHR, both in males (β = −0.255; p =0.023) and in females (β = −0.451; p =0.017). Conclusions Our findings indicate that obesity influences AHR only in females with a moderate AHR level. This influence may be mediated by obesity-associated changes in baseline lung function.

Background: It is not clear whether mepolizumab is differently effective in allergic and nonallergic severe eosinophilic asthmatics (SEA) in real life. Objective: We tested mepolizumab effectiveness in allergic/nonallergic SEA in real life. A strict criterion to identify the 2 phenotypes was used. Method: We retrospectively considered 134 consecutive patients divided into allergic, with a positivity to at least 1 allergen to prick tests and/or IgE values ≥100 UI/mL (severe allergic eosinophilic asthma [SAEA]; n: 97–72.4%), and nonallergic, with no prick test results and normal IgE levels <100 UI/mL (severe nonallergic eosinophilic asthma [SNAEA]; n: 37–27.6%). They had taken mepolizumab for at least 6 months. Results: After 10.9 ± 3.7 months, improvements in FEV1%, FEF25–75%, exacerbation numbers, blood eosinophil (BE) counts, fractional exhaled nitric oxide (FENO) (ppb), percentages of patients that stopped/reduced short-acting β2-agonists (SABAs) or oral corticosteroid (OC), observed after treatment, were similar in both groups. Only Asthma Control Test (ACT) increases were higher in SNAEA (8 [5–9]) than in SAEA (5 [2.5–8.5]; p = 0.016). However, no differences were found after treatment in percentages of subjects with ACT ≥20, as well as with FEV1 >80%, FEF25–75 >65%, exacerbations ≤2, BE <300 cells/µL, and FENO <25 ppb between SAEA and SNAEA. Besides, no significant relationships were found, comparing SNAEA with SAEA, for FEV1% (β = −0.110; p = 0.266), FEF25–75% (β = −0.228; p = 0.06), BE counts (β = −0.012; p = 0.918), FENO (β = 0.234; p = 0.085), ACT (β = 0.046; p = 0.660), and exacerbations (β = −0.070; p = 0.437). No different associations between lung function and SNAEA occurrence when compared to SAEA condition (FEV1 >80%: OR = 1.04 [95% CI: 0.43–2.55], p = 0.923; FEF25–75 >65%: OR = 0.41 [95% CI: 0.08–2.03], p = 0.272) were detected. Neither all other parameters, such as ACT >20 (OR = 0.73 [95% CI: 0.32–1.63], p = 0.440), presence of exacerbations (OR = 1.35 [95% CI: 0.55–3.27], p = 0.512), SABA discontinuation (OR = 1.16 [95% CI: 0.40–3.39], p = 0.790), and OC cessation/reduction (OR = 3.44 [95% CI: 0.40–29.27], p = 0.258), were differently associated with 1 or the other phenotype. Conclusion: Mepolizumab can be considered as a valid therapeutic choice for either allergic or nonallergic SEA in real life. [ABSTRACT FROM AUTHOR]

Objective: This study analysed whether the persistence of both reversible airway obstruction (RAO) and elevated BE counts was associated to reduced asthma control and accelerated lung function decline in treated severe asthmatics. Methods: About 202 severe asthmatics were studied after 12–120 months of step‐5 treatment associated to anti‐IgE therapy. Following treatments, reversibility tests, after inhaling 400 mcg of Salbutamol, were performed. FEV1 > 12% or ≤12% changes differentiated RAO+ from RAO− subjects. Blood eosinophil (BE) counts after treatment were considered. Results: Pre‐/post‐treatment bronchodilator FEV1% and ACT were lower (61% [50–71], 74.4% [62.5–83.7] and 20[18–22]), whereas BE were higher (380 cells/µl [170–590]) in RAO+ compared to RAO− subjects (77% [64–88], p = 0.0001, 81.8% [66.1–94.3], p = 0.0001, 21[18–23], p = 0.045 and 230 cells/µl [80–360], p = 0.003). A negative relationship between SABA‐induced FEV1% changes and pre‐bronchodilator FEV1% (β = −0.551%; p = 0.0001) and ACT (β = −0.059; p = 0.038) was found. Conversely, post‐treatment BE levels were positively related (β = 145.565 cells/µl; p = 0.003) to FEV1 > 12% increases. A rising trend of pre‐/post‐bronchodilator FEV1% in time was observed in RAO− subjects with BE < 300 cells/µl. Conversely, we highlighted significant declining tendencies of pre/post‐bronchodilator FEV1% in RAO+ patients with BE > 300 cells/µl reaching lower values after more than 36 months of step‐5 treatment (59.6% [39.9–72.1] vs 74[66.5–89.2] of RAO+ individuals with BE < 300 cells/µl [p = 0.026] and 81.6% [66.1–91.8] of RAO‐subjects with BE > 300 cells/µl [p = 0.009]). Conclusion: Persistent SABA‐induced FEV1 > 12%, especially when associated to BE > 300 cells/ml, may be a marker of accelerated lung function decline in severe asthmatics despite maximal step‐5 treatment. The highest bronchodilation associated to the lowest BE levels should be the main goal of asthma treatment to prevent such decline. [ABSTRACT FROM AUTHOR]

Byline: Bruno. Sposato, Marco. Scalese, Andrea. Pammolli, Raffaele. Scala, Mario. Naldi Objective: This study tried to evaluate whether a methacholine test may be influenced by the seasons. Methods: We considered [...]

Objective:The aim of this review was to understand whether FEV1 decline measured during the follow-up of asthmatic subjects (FEV1 variation between two different measurements at a distance of at least 5 years) may have a role in their management. Methods:Articles, commentaries and reviews relating to the topic were searched in PubMed. Results:Patients with an accelerated FEV1 decline (430 ml/year) may be either steroid-resistant/difficult-to-treat asthmatics or not adequately treated because they are either under-perceivers or poorly adherent to their therapy. Sometimes they may be unable to use devices correctly. Untreated rhinitis and incorrect lifestyle (obesity status, a high-fat diet and lack of exercise) must be considered when facing a pulmonary function decline. Identifying asthmatics with an accelerated FEV1 decline, even with well controlled symptoms, may allow us to make possible treatment adjustments or to remove potentially harmful environmental exposure and suggest a correct lifestyle. Depending on FEV1 decline severity, we may detect different asthma phenotypes. One type is characterized by no/low lung function reduction. Among moderate/severe 'declining' subjects, there may be a group that might be responsive to treatment and a second one with a quicker loss in lung function that may be unresponsive to therapy. Conclusion:FEV1 decline calculation should be assessed early in clinical practice over the course of time in order to make all possible variations in treatment, environmental exposure and lifestyle more efficacious overall for declining subjects responsive to anti-inflammatory therapy. Further studies are necessary to validate this approach to asthma. [ABSTRACT FROM AUTHOR]