The study compares the ability of the PSI (pneumonia severity index), CURB-65 (confusion, urea >7 mol·L(-1), respiratory rate ≥ 30 breaths·min(-1), blood pressure <90 mmHg systolic or ≤ 60 mmHg diastolic, and age ≥ 65 yrs), CURB and CRB-65 scales and the Severe Community-Acquired Pneumonia (SCAP) score to predict 30-day mortality in healthcare-associated pneumonia (HCAP) patients, and analyses differences in the demographics, aetiology and outcomes of community-acquired pneumonia (CAP), HCAP and pneumonia in immunocompromised patients. 629 consecutive patients admitted to a tertiary care university hospital were prospectively categorised as having CAP (n=322) or HCAP (n=307), and the HCAP patients were further sub-divided into those who were immunocompromised (n=219) or immunocompetent (n=88). The 30-day mortality rate was 9.0% in the CAP group and 24.1% in the HCAP group. In the HCAP group, the PSI and SCAP scores had similar prognostic power (area under the curve (AUC) of 0.68 and 0.67, respectively) and performed better than the CURB-65 score (AUC ≤0.62). Among the immunocompetent HCAP patients, the PSI and CURB-65 scores were more sensitive than the others at every threshold, whereas SCAP was more specific than both of these. In the immunocompromised group, the PSI was highly sensitive but poorly specific at all thresholds. Our results suggest that prognostic tools should be designed for subsets of HCAP patients.

Anemia is a common finding in elderly individuals. Several studies have shown a strong relationship between anemia, morbidity and mortality, suggesting anemia as a significant independent predictor of adverse outcome in elderly hospitalized patients. The pathophisiology of anemia in the elderly is not yet completely understood. Several mechanisms are involved. We investigated the prevalence of anemia in a cohort of 193 elderly patients admitted to the Internal Medicine Ward of Ca'Granda Policlinico Hospital along 6 months, and its relationship to comorbidities and to the length of hospitalization. Anemia was classified according to the WHO criteria. The majority of patients (48 %) had a mildmoderate, normocytic anemia; severe anemia was found in 8 out of 92 anemic patients. In a subgroup of patients erythropoietin was tested and resulted statistically higher if compared to non-anemic controls (p = 0.003). Considering the most common cause of anemia, nutritional deficiency, chronic renal disease and anemia of chronic disease were found respectively in 36, 15 and 25 % of cases. Unexplained anemia was diagnosed in 24 % of patients, according to the literature. Anemia was independently associated with increased length of hospital stay. Our study confirmed a high prevalence of anemia in elderly patients, and its association with a higher number of comorbidities and a longer stay. A correct clinical approach to anemia in elderly hospitalized patients is essential, considering its negative impact on patients' quality of life, and its social burden in term of healthcare needs and costs.

Given the highly variable clinical phenotype of Coronavirus disease 2019 (COVID-19), a deeper analysis of the host genetic contribution to severe COVID-19 is important to improve our understanding of underlying disease mechanisms. Here, we describe an extended GWAS meta-analysis of a well-characterized cohort of 3255 COVID-19 patients with respiratory failure and 12 488 population controls from Italy, Spain, Norway and Germany/Austria, including stratified analyses based on age, sex and disease severity, as well as targeted analyses of chromosome Y haplotypes, the human leukocyte antigen (HLA) region and the SARS-CoV-2 peptidome. By inversion imputation, we traced a reported association at 17q21.31 to a ~ 0.9-Mb inversion polymorphism that creates two highly differentiated haplotypes and characterized the potential effects of the inversion in detail. Our data, together with the 5th release of summary statistics from the COVID-19 Host Genetics Initiative including non-Caucasian individuals, also identified a new locus at 19q13.33, including NAPSA, a gene which is expressed primarily in alveolar cells responsible for gas exchange in the lung.

Due to the highly variable clinical phenotype of Coronavirus disease 2019 (COVID-19), deepening the host genetic contribution to severe COVID-19 may further improve our understanding about underlying disease mechanisms. Here, we describe an extended GWAS meta-analysis of 3,260 COVID-19 patients with respiratory failure and 12,483 population controls from Italy, Spain, Norway and Germany, as well as hypothesis-driven targeted analysis of the human leukocyte antigen (HLA) region and chromosome Y haplotypes. We include detailed stratified analyses based on age, sex and disease severity. In addition to already established risk loci, our data identify and replicate two genome-wide significant loci at 17q21.31 and 19q13.33 associated with severe COVID-19 with respiratory failure. These associations implicate a highly pleiotropic ~0.9-Mb 17q21.31 inversion polymorphism, which affects lung function and immune and blood cell counts, and the NAPSA gene, involved in lung surfactant protein production, in COVID-19 pathogenesis.