The development and persistence of symptoms following SARS-CoV-2 infection, known as Post-COVID-19 Condition (PCC) or "long COVID," represents a global health challenge. In this prospective cross-sectional study, we conducted a detailed assessment of the physical condition of 46 patients using handgrip dynamometry, ergoespirometry, and the 6-minute walk test (6MWT). The results revealed a loss of muscle strength and poor exercise tolerance primarily due to peripheral muscle involvement. To complement and better understand these findings, we compared the blood metabolome and lipidome of 13 patients with PCC, 13 patients with acute COVID-19 infection, and 13 healthy controls using magnetic resonance spectroscopy (1H-NMR). PCC patients showed lower levels of HDL-cholesterol, as well as medium and dense HDL particles, which could contribute to a pro-atherogenic and pro-inflammatory state. Although no significant differences were observed in glycoproteins, we found decreased glucose and increased lactate levels, supporting the hypothesis of mitochondrial dysfunction in PCC patients. Additionally, elevated glycine and reduced glutamate levels may be related to the neurological symptoms associated with the condition. We also observed increased levels of glutamine, leucine, and isoleucine, indicating protein hypercatabolism and metabolic stress. These findings suggest that alterations in the metabolome and lipidome of PCC patients may be contributing to the persistence of their symptoms.

Community-acquired pneumonia (CAP) remains a major health concern, with oxidative stress and inflammation playing key roles in its pathophysiology. This study examines the potential of paraoxonase-1 (PON1)-related variables as biomarkers for diagnosing and managing CAP. A prospective case-control study included 78 patients with community-acquired pneumonia (CAP) who were hospitalized and 80 healthy controls. Serum PON1 concentration (PON1c), PON1 arylesterase (ARE) and paraoxonase (PARX) activities, and inflammatory markers (C-reactive protein, procalcitonin, and C-C motif chemokine ligand 2 were measured and compared with lipid profiles and clinical severity scores. Receiver operating characteristic curve analysis was used to assess their diagnostic and prognostic value. CAP patients exhibited significantly lower ARE and PARX activities but higher PON1c levels than controls, with these changes correlating with increased inflammatory markers and decreased total and high-density lipoprotein cholesterol concentrations. PON1-related variables demonstrated strong diagnostic accuracies (areas under the curve >0.90), outperforming traditional inflammatory markers. However, although these variables provided insights into disease severity and pathophysiology, their prognostic value and ability to differentiate microbial etiologies were limited. These findings suggest that PON1-related variables may serve as promising diagnostic biomarkers for CAP, but their role in prognosis and guiding antimicrobial therapy requires further investigation. Future studies should validate these results in larger and more diverse populations while exploring the mechanistic involvement of PON1 in CAP progression.

This prospective observational study compared the 1H NMR blood lipidomes and metabolomes of 71 patients with community-acquired pneumonia (CAP), 75 patients with COVID-19 pneumonia, and 75 healthy controls (matched by age and sex) to identify potential biomarkers and pathways associated with respiratory infections. Both pneumonia groups had comparable severity indices, including mortality, invasive mechanical ventilation, and intensive care unit admission rates. Patients with COVID-19 pneumonia exhibited more pronounced hypolipidemia, with significantly lower levels of total cholesterol and LDL-c compared to patients with CAP. Atherogenic lipoprotein subclasses (VLDL-cholesterol, IDL-cholesterol, IDL-triglyceride, and LDL-triglyceride/LDL-cholesterol) were significantly increased in severe cases of both pneumonia types, while lower HDL-c and small, dense HDL particles were associated with more severe illness. Both infected groups showed decreased esterified cholesterol and increased triglycerides, along with reduced phosphatidylcholine, lysophosphatidylcholine, PUFA, omega-3 fatty acids, and DHA. Additionally, infected patients had elevated levels of glucose, lactate, 3-hydroxybutyrate, and acetone, which are linked to inflammation, hypoxemia, and sepsis. Increased levels of branched-chain amino acids, alanine, glycine, and creatine, which are involved in energy metabolism and protein catabolism, were also observed. Neurotransmitter synthesis metabolites like histidine and glutamate were higher in infected patients, especially those with COVID-19. Notably, severe infections showed a significant decrease in glutamine, essential for lymphocyte and macrophage energy. The severity of COVID-19 pneumonia was also associated with elevated glycoprotein levels (glycoprotein A, glycoprotein B, and glycoprotein F), indicating an inflammatory state. These findings suggest that metabolomic and lipidomic changes in pneumonia are connected to bioenergetic pathways regulating the immune response.

Background We scrutinized variations in the proton nuclear magnetic resonance (1H-NMR) lipoprotein and glycoprotein profiles among hospitalized individuals with infectious diseases. Methods We obtained sera from 124 patients with COVID-19, 50 patients with catheter-related bacterial infections, and 50 healthy volunteers. Results were interpreted using machine learning. Results COVID-19 patients had bigger and more abundant VLDL particles than the control group and higher VLDL-cholesterol and VLDL-triglyceride concentrations. Patients with bacterial infections showed similar trends, but differences often did not reach statistical significance. Both types of patients showed lower LDL-cholesterol concentrations than the controls. LDL were larger, and the number of particles was lower than that of the healthy individuals. HDL particles had decreased cholesterol and increased triglycerides. Small particles were reduced. Glycoproteins were increased in both groups of patients. All these alterations were more pronounced in COVID-19 patients than those with bacterial infections. The diagnostic accuracy of these profiles exceeded 90% when distinguishing between healthy individuals and patients, and 85% when differentiating between the two patient groups. Conclusion Our findings highlight the potential of 1H-NMR analysis for lipoproteins and glycoproteins as infection biomarkers. Additionally, they reveal differences between viral and bacterial infections, shedding light on an area with promising clinical significance.

Background and aims: HDL particles may act to buffer host cells from excessive inflammatory mediators. The aim of this study is to investigate if the lipid profile provides a prognostic biomarker for COVID-19 outcomes.Methods: This was a prospective study of the characteristics of 125 adult COVID-19 patients with a lipid profile performed on the day of admission analyzed with regard to clinical outcomes.Results: Seventy-seven patients (61.2%) were men, with a mean age of 66.3 (15.6) years. 54.1% had bilateral pneumonia. The all-cause mortality rate during hospitalization was 20.8%. We found a direct association between more severe disease assessed by the WHO classification, admission to the ICU and death with more pronounced lymphopenia, higher levels of CRP, ferritin (p < 0.001), D-dimer and lactate dehydrogenase (LDH) all statistically significant. Lower leves of HDL-c and LDL-c were also associated with a worse WHO classification, ICU admission, and death,. HDL-c levels were inversely correlated with inflammatory markers CRP (r =-0.333; p < 0.001), ferritin (r =-0.354; p < 0.001), D-dimer (r =-0.214; p < 0.001), LDH (r =-0.209; p < 0.001. LDL-c levels were significantly associated with CRP (r =-0.320; p < 0.001) and LDH (r =-0.269; p < 0.001). ROC curves showed that HDL [AUC = 0.737(0.586-0.887), p = 0.005] and lymphocytes [AUC = 0.672(0.497-0.847], p < 0.043] had the best prognostic accuracy to predict death. In a multivariate analysis, HDL-c (b =-0.146(0.770-0.971), p = 0.014) and urea (b = 0.029(1.003-1.057), p = 0.027) predicted mortality.Conclusion: Hypolipidemia including HDL levels at admission identifies patients with a higher risk of death and worse clinical manifestations who may require more intensive care.(c) 2023 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Introducción: Para lograr niñas y niños más sanos y brillantes, el Ministerio de Salud (Minsa) promueve el uso de micronutrientes en papillas mixtas para lactantes de 6 a 35 meses. El objetivo de la investigación fue determinar los factores de adherencia al consumo de micronutrientes en madres de niños menores de 3 años Clas El Carmen Olivo, distrito San Juan Bautista Ica enero 2017. El estudio es cuantitativo, descriptivo y transversal. La población estuvo conformada por 165 madres de niños menores de 3 años, de los cuales se tomó un muestreo probabilístico. Resultados: en los datos generales de las madres donde el 57%(66) tienen entre 18-25 años; el 67%(78) tiene secundaria, 64%(74) es conviviente; 64%(74) tienen de 2 a 3 hijos; en ocupación el 66%(76) es ama de casa, el 52%(60) de los niños tiene de 6 a 13 meses de edad, el 52%(60) es de sexo masculino, el 41%(48) siempre cumple con sus controles Cred, el 28 %(32) ha sido diagnosticado de anemia y el 36%(42) de los niños ha presentado alguna enfermedad durante los últimos tres meses. Respecto a la variable factores de adherencia al consumo de micronutrientes según factor social, actitudinal, relacionado al tratamiento y factor cognoscitivo fueron desfavorables con 54%(63), 57%(66), 52%(60), 72%(84) y favorables en 46%(53), 43%(50), 48%(56), 69%(80); 28%(32) obteniendo un consolidado global al consumo de micronutrientes de desfavorables en 54%(63) y favorables en 46%(53).

BackgroundWest Nile virus (WNV) is a mosquito-borne flavivirus that can cause Central Nervous System infection in humans. Previous autochthonous cases of WNV encephalitis have been described in Spain, but none in Catalonia.Materials and methodsWe report on the first two autochthonous cases of encephalitis in humans caused by the West Nile virus (WNV) diagnosed in Catalonia (northeastern region of Spain).ResultsAn old married couple presented with clinical and biological signs compatible with viral encephalitis. Acute and convalescent serum samples showed IgM and IgG positivity for WNV. In addition, IgM was also detected in cerebrospinal fluid in the male patient. The serological results were later confirmed by microneutralization assays.ConclusionsWNV infection must be considered in patients presenting with meningoencephalitis with viral CSF characteristics when common pathogens are excluded.

BackgroundSystemic Lupus Erythematosus (SLE) is an autoimmune disease with a high risk of atherosclerosis and cardiovascular events. It was previously reported by our group that low-density lipoprotein (LDL) particles isolated from SLE patients, during an active state of the disease (‘flare’), promoted an exaggerated inflammatory response in human aortic endothelial cells (HAECs). However, the molecular mechanisms underlying this response still remain elusive.ObjectivesThe hypothesis of this study is that these SLE-LDLs would be using receptor LOX-1, associated with inflammatory conditions and altered lipoproteins, to generate the proatherogenic response in HAECs.MethodsLOX-1 pharmacological inhibitor k-carrageenan was used before the stimulation of HAECs with LDLs isolated from healthy controls (10), non-active (13), or active-SLE patients (13). Gene expression, protein, and cell migration assays were performed to evaluate HAECs inflammatory response.ResultsLOX-1 inhibition with k-carrageenan significantly reduced the expression of vascular cell adhesion molecule 1 (VCAM-1) and restored the gene expression of endothelial nitric oxide synthase (eNOS) in HAECs incubated with non-active SLE LDLs.ConclusionWhile VCAM-1 down-regulation was expected, the immediate next step derived from the observed results will be a deeper understanding of how LOX-1 inhibition may restore the endothelial ability to synthetize NO in the presence of altered LDL. This will allow gaining insight not only on the development of atherosclerosis but also on the clue mechanisms involved in the pathogenesis of SLE.Disclosure of InterestsNone declared

Abstract Background Excessive inflammation contributes to the morbidity and mortality of severe coronavirus disease 2019 (COVID-19) pneumonia. Recombinant human plasma gelsolin (rhu-pGSN) improves disease outcomes in diverse experimental models of infectious and noninfectious inflammation. Methods In a blinded, randomized study, 61 subjects with documented COVID-19 pneumonia having a World Health Organization (WHO) Severity Score of 4 to 6 and evidence of a hyperinflammatory state were treated with standard care and either adjunctive rhu-pGSN 12 mg/kg or an equal volume of saline placebo given intravenously at entry, 12 hours, and 36 hours. The prespecified coprimary outcomes were survival without major respiratory, hemodynamic, or renal support on Day 14 and the incidence of serious adverse events (SAEs) during the 90-day study period. Results All subjects receiving ≥1 dose of study drug were analyzed. Fifty-four of 61 subjects (88.5%) were WHO severity level 4 at entry. The proportions of subjects alive without support on Day 14 were 25 of 30 rhu-pGSN recipients (83.3%) and 27 of 31 placebo recipients (87.1%). Over the duration of the study, WHO Severity Scores improved similarly in both treatment groups. No statistically significant differences were observed between treatment groups at any time point examined. Two subjects died in each group. Numerically fewer subjects in the rhu-pGSN group had SAEs (5 subjects; 16.7%) or ≥ Grade 3 adverse events (5 subjects; 16.7%) than in the placebo group (8 subjects [25.8%] and 9 subjects [29.0%], respectively), mostly involving the lungs. Three rhu-pGSN recipients (10.0%) were intubated compared to 6 placebo recipients (19.4%). Conclusions Overall, subjects in this study did well irrespective of treatment arm. When added to dexamethasone and remdesivir, no definitive benefit was demonstrated for rhu-pGSN relative to placebo. Safety signals were not identified after the administration of 3 doses of 12 mg/kg rhu-pGSN over 36 hours. The frequencies of SAEs and intubation were numerically fewer in the rhu-pGSN group compared with placebo.

The pandemic caused by the SARS-CoV-2 infection affects many aspects of public health knowledge, science, and practice around the world. Several studies have shown that SARS-CoV-2 RNA in plasma seems to be associated with a worse prognosis of COVID-19. In the present study, we investigated plasma and buffy RNA in patients with COVID-19 to determine its prognostic value. A prospective study was carried out in patients hospitalized for COVID-19, in which RNA was analyzed in plasma and the buffy coat. Morphological and immunohistochemical studies were used to detect the presence of SARS-CoV-2 in the buffy coat. In COVID-19 patients, the obtained RNA concentration in plasma was 448.3 ± 31.30 ng/mL. Of all the patients with positive plasma tests for SARS-CoV-2, 46.15% died from COVID-19. In four cases, tests revealed that SARS-CoV-2 was present in the buffy coat. Abnormal morphology of monocytes, lymphocytes and neutrophils was found. An immunohistochemical study showed positivity in mononuclear cells and platelets. Our results suggest that SARS-CoV-2 is present in the plasma. This facilitates viral dissemination and migration to specific organs, where SARS-CoV-2 infects target cells by binding to their receptors. In our study, the presence of plasma SARS-CoV-2 RNA was correlated with worse prognoses.

Many countries have seen a two-wave pattern in reported cases of coronavirus disease-19 during the 2020 pandemic, with a first wave during spring followed by the current second wave in late summer and autumn. Empirical data show that the characteristics of the effects of the virus do vary between the two periods. Differences in age range and severity of the disease have been reported, although the comparative characteristics of the two waves still remain largely unknown. Those characteristics are compared in this study using data from two equal periods of 3 and a half months. The first period, between 15th March and 30th June, corresponding to the entire first wave, and the second, between 1st July and 15th October, corresponding to part of the second wave, still present at the time of writing this article. Two hundred and four patients were hospitalized during the first period, and 264 during the second period. Patients in the second wave were younger and the duration of hospitalization and case fatality rate were lower than those in the first wave. In the second wave, there were more children, and pregnant and post-partum women. The most frequent signs and symptoms in both waves were fever, dyspnea, pneumonia, and cough, and the most relevant comorbidities were cardiovascular diseases, type 2 diabetes mellitus, and chronic neurological diseases. Patients from the second wave more frequently presented renal and gastrointestinal symptoms, were more often treated with non-invasive mechanical ventilation and corticoids, and less often with invasive mechanical ventilation, conventional oxygen therapy and anticoagulants. Several differences in mortality risk factors were also observed. These results might help to understand the characteristics of the second wave and the behaviour and danger of SARS-CoV-2 in the Mediterranean area and in Western Europe. Further studies are needed to confirm our findings.

Objectives SLE patients have an enhanced risk of atherosclerosis and cardiovascular disease. However, the increased prevalence of cardiovascular disease is not fully explained by traditional Framingham cardiovascular risk factors. Specific features of low-density lipoprotein (LDL) particles, other than plasma concentration, may induce accelerated atherosclerosis at early stages in these patients. Thus, we aimed to explore the impact of LDL from both active and inactive SLE patients on human aortic endothelial cells. Methods Human aortic endothelial cells were stimulated with the same concentration of LDL particles isolated from pooled serum that was collected from 13 SLE patients during both active and inactive states. Gene expression and cell migration assays were performed. Results Circulating LDL particles obtained from healthy volunteers and SLE patients in both remission and flare states were comparable in terms of number, cholesterol and triglyceride content, and net electric charge. Stimulation of cells with LDL from active SLE patients induced the expression of vascular cell adhesion molecule 1 (similar to 2.0-fold, P < 0.05), monocyte chemoattractant protein 1 (similar to 2.0-fold, P < 0.05) and matrix metallopeptidase 2 (similar to 1.6-fold, P < 0.01) compared with cells stimulated with LDL from inactive SLE patients. Additionally, LDL extracted from active patients increased cell migration in a wound-healing assay (1.4-fold, P < 0.05). Conclusion Our data show that, at the same LDL concentration, LDL from active SLE patients had increased proatherogenic effects on endothelial cells compared with LDL from the same patients when in an inactive or remission state.

Objectives. To identify potential biomarkers of disease activity analysing the proteome of high-density lipoprotein (HDL) particles from SLE patients in clinical remission and when they develop a flare compared with a healthy control group. Methods. Quantitative proteomic analyses of purified HDL were performed using Tandem Mass Tag isobaric tag-labelling and nanoLC-Orbitrap (nLC-MS/MS) from nine SLE patients in clinical remission when they developed a flare and from nine healthy controls (9-9-9). We verified the identified proteins by Western blot and ELISA in a cohort of 104 SLE women patients, 46 healthy women and 14 SLE patients when a flare developed. Results. We found 17 proteins with a significant fold-change (>1.1) compared with the control group. In lupus patients experiencing a flare compared with those in remission, we identified four proteins with a significant fold-change (C4, Indian Hedgehog protein, S100A8 and gelsolin). Plasma gelsolin (pGSN) levels were decreased in the 104 SLE patients (176.02(74.9) mcg/l) compared with the control group (217.13(86.7) mcg/l); P=0.005 and when they developed a clinical flare (104.84(41.7) mcg/l); P=0.002). pGSN levels were associated with HDL cholesterol levels (r = 0.316, P<0.001). Antimalarial treated patients showed significant higher levels of pGSN (214.56(88.94) mcg/l regarding 170.35(66.36) mcg/l); P = 0.017. Conclusion. Decreased pGSN are associated with clinical disease activity in SLE patients. Antimalarial treatment and HDL cholesterol are associated with higher levels of pGSN.

AIMS:Patients with systemic lupus erythematosus (SLE) suffer from accelerated atherosclerosis. Their most common cause of death is a cardiovascular disease (CVD), in spite of the presence of moderate lipid alterations and normal cardiovascular risk scores. However, cholesterol still accumulates in the arteries of SLE patients, so we aim to identify additional factors that may help explain the residual risk that exists in these patients. We focus on investigating whether the net charge contributes significantly to both the development and the progression of atherosclerosis in patients with SLE.METHODS:The lipoproteins from 78 patients with SLE and 32 controls were isolated via sequential ultracentrifugation. Lipoprotein subclasses distributions were analyzed via nuclear magnetic resonance spectroscopy and the net charges of very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) were measured using a Zetasizer Nano-ZS. The degree of atherosclerosis (carotid intima-media thickness [cIMT]) was determined in all the participants.RESULTS:Each lipoprotein class exhibited a negative net charge. IDL and LDL net charge correlated negatively with cIMT (r = -0.274, P = 0.034; r = -0.288; P = 0.033, respectively) in patients with SLE. This effect was independent of age, body mass index (BMI), gender, tobacco consumption, high-sensitivity C-reactive protein (hsCRP), lipid concentration and lipoprotein particle number. LDL net charge explained 4% of the cIMT variability among these patients; this contribution was also independent of age, BMI, gender, tobacco consumption, lipids levels, apolipoproteins and hsCRP.CONCLUSIONS:Low-density lipoprotein net charge may be considered a new independent contributor to subclinical atherosclerosis in SLE patients. The observed relationship was independent of lipid concentrations and extends the prominent role that IDL and LDL play in cardiovascular risk.

ObjectiveTo investigate the metabolic and immunologic factors associated with the presence of central arterial stiffness as measured by the augmentation index (AIx).MethodsWe conducted a cross‐sectional study of 69 female patients with systemic lupus erythematosus (SLE) compared with a control group of 34 healthy women. The anthropometrical variables, the vascular studies, and the analytic data were obtained the same day. The AIx was assessed by peripheral arterial tonometry. The analysis of lipoprotein populations was performed using nuclear magnetic resonance (NMR) spectroscopy.ResultsArterial stiffness was increased in patients with SLE compared with control subjects (mean ± SD 20.30 ± 21.54% versus 10.84 ± 11.51%; P = 0.0021). Values for the AIx were correlated with the Framingham risk score (r = 0.481, P < 0.001), carotid intima‐media thickness (r = 0.503, P < 0.001), systolic blood pressure (r = 0.270, P < 0.001), and age (r = 0.365, P < 0.001). Patients receiving antimalarial drugs had a lower AIx (mean ± SD 11.74 ± 11.28% versus 24.97 ± 20.63%; P = 0.024). The AIx was correlated with the atherogenic lipoproteins analyzed by NMR. The immunologic variables associated with the AIx were C4 (r = 0.259, P = 0.046) and IgM anti–β2‐glycoprotein I (IgM anti‐β2GPI) (r = 0.284, P = 0.284). In the multivariate analysis, age (β = 0.347, 95% confidence interval [95% CI] 0.020–0.669, P = 0.035), IgM β2GPI (β = 0.321, 95% CI 0.024–0.618, P = 0.035) and small dense high‐density lipoprotein (HDL) particles (β = 1.288, 95% CI 0.246–2.329, P = 0.017) predicted the AIx.ConclusionSLE patients had increased arterial stiffness compared with healthy control subjects. Arterial stiffness was decreased in patients treated with antimalarial drugs. Age, IgM β2GPI, and the number of small dense HDL particles predicted the AIx.

Background Patients affected by Systemic Lupus Erythematosus (SLE) show an increase in cardiovascular mortality and morbidity. The accelerated atherosclerosis observed in patients with SLE cannot be entirely explained by the traditional cardiovascular risk factors. Patients with SLE show increased subclinical atherosclerosis determined by an increased carotid arterial thickness, endothelial dysfunction and central arterial stiffness. Analysis of lipoproteins by magnetic nuclear resonance (MNR) provide information of those lipoproteins associated with sublcinial atherosclerosis in SLE. Objectives To investigate the metabolic and immunological factors associated with the presence of central arterial stiffness determined by the Augmentation Index (AIx) as well as the detailed analysis of the lipid profile performed by magnetic nuclear resonance (MNR) Methods Descriptive cross-sectional study of 69 women with SLE compared with a control group of 34 age matched healthy women. On the same day of the study, blood extraction, physical examination and augmentation index (AIx) obtained by Peripheral Arterial Tonometry were performed. The carotid intima-media thickness (IMTc) was also performed on the same day of the study to correlate the arterial stiffness with another subclinical atherosclerosis marker. Analysis of lipoprotein populations by NMR (Liposcale,Biosfer Teslab) were performed. Results Patients with SLE showed significant increased arterial stiffness respect the control group (20.30 (21.54)% vs 10.84 (11.51)%, P=0.0021)The values of AIx were well correlated with Framingham risk score (r=0.486, P <0.001) as well as the IMTc (r=0.456, P<0.001). The classic cardiovascular risk factors associated with the AIx were the SBP levels (r=0.456, P<0.001) and age (r=0.456, P <0.001). Patients under antimalarial drugs showed significant decreased AIx (11.74 (11.28) vs 24.97 (20.63); P=0.024. Immunological variables associated with AIx were levels of C4 (r=0.259; P=0.046) and the IgM-β2-glycoprotein levels (r=0.284, P=0.284).As for the lipoprotein populations, AI values correlated with ApoB plasma levels, remnant particles, the number of large, medium and small VLDL particles, the number of small LDL particles and the number of small-dense HDL particles. In the multivariate analysis we found that age (β=0.377 (0.117–0.636), P=0.005) IgM-B2-GLP levels (β=0.303 (0.026–0.580),P=0.033) and the small-dense HDL particles (β=1,463 (0.605–2.322), P=0.001). Conclusions SLE patients show increased central arterial stiffness respect healthy population. Patients treated with antamalarial drugs show lower arterial stifness. In multivariate analyses variables that predicted levels of AIx were age, levels of IgM-β2-glycoprotein and the number of small-dense HDL particles. Disclosure of Interest None declared

To investigate if HDL cholesterol (HDL-c) could be a biomarker of the degree of severity according to prognostic prediction scores in community-acquired pneumonia (CAP) or the development of clinical complications such as pleural effusion.