Background. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-COV-2) infection elicits inflammatory manifestations that relate with a cytokine storm. Objective. The aim of this research was to assess the role of circulating interleukin 6 (IL-6) levels and other inflammatory markers in patients with coronavirus disease 2019 (COVID-19) on metabolic functions and accompanying clinical complications. Patients and Methods. A total of 165 patients diagnosed with COVID-19 pneumonia were examined for medical features and inflammatory markers such as blood IL-6, CRP, ferritin, LDH, neutrophil/lymphocyte index (NLI), D-Dimer, and Red Cell Distribution Width (RDW). Regression analyses concerning electronically collected medical data were adjusted by appropriate factors and confounding variables. Results. Plasma IL-6 determinations evidenced a consistent association with hospital stay days, Intensive Care Unit (ICU) admission, and mortality rates. Similar trends were found for other proinflammatory variables, where ferritin and NLI showed a remarkable value as surrogates. Hyperglycaemia and the Charlson Comorbidity Index Score were positively associated with the inflammatory response induced by the SARS-COV-2 infection. An unhealthy lifestyle such as smoking and alcoholic drinks consumption as well as excessive body adiposity influenced inflammatory-related outcomes in the screened patients. Conclusion. IL-6 together with other inflammatory biomarkers accompanied poor clinical and metabolic outcomes in COVID-19-infected patients. IL-6 may result in a suitable proxy to individually categorise patients in order to manage this infectious pandemic.

Background. Coronavirus disease 2019 (COVID-19) has a high mortality in certain group of patients. We analysed the impact of baseline immunosuppression in COVID-19 mortality and the role of severe lymphopenia in immunocompromised subjects. Methods. We analysed all patients admitted with COVID-19 in a tertiary hospital in Madrid between March 1st and April 30th 2020. Epidemiological and clinical data, including severe lymphopenia (<500 lymphocytes/mm³) during admission, were analysed and compared based on their baseline immunosuppression condition. Results. A total of 1594 patients with COVID-19 pneumonia were hospitalised during the study period. 166 (10.4%) were immunosuppressed. Immunocompromised patients were younger (64 vs. 67 years, p = 0.02) but presented higher rates of hypertension, diabetes, heart, neurological, lung, kidney and liver disease (p < 0.05). They showed more severe lymphopenia (53% vs 24.1%, p < 0.001), lower SapO₂/FiO₂ ratios (251 vs 276, p = 0.02) during admission and higher mortality rates (27.1% vs 13.5%, p < 0.001). After adjustment, immunosuppression remained as an independent factor related to mortality (Odds Ratio (OR): 2.24, p < 0.001). In the immunosuppressed group, age (OR = 1.06, p = 0.01), acute respiratory distress syndrome (ARDS) (OR = 12.27, p = 0.017) and severe lymphopenia (OR = 3.48, p = 0.04) were the factors related to high mortality rate. Conclusion. Immunosuppression is an independent mortality risk factor in COVID-19. Severe lymphopenia should be promptly identified in these patients.

Introduction: coronavirus disease 2019 (COVID-19) encompasses a wide spectrum of symptoms, including respiratory, gastrointestinal, hematological, and dermatological manifestations. The virus interaction with cells located in the respiratory tract causes the release of inflammatory mediators, whose involvement could be exacerbated by co-existing obesity, diabetes, and cardiovascular events. Objectives: the objective of this research was to analyze the clinically metabolic status in patients who have suffered COVID-19 disease in order to predict the outcome. Methods: this research is a retrospective study based on a cohort of 165 consecutively admitted patients with criteria for COVID-19 pneumonia according to WHO guidelines at the Hospital Universitario Puerta de Hierro between March and April 2020. Recorded variables included demographic and epidemiological data plus diagnoses as well as morbid complications during hospitalization. The Biochemistry Unit Laboratory carried out laboratory analyses according to validated operational procedures. The statistical tests included univariate and multivariate models adjusted for baseline characteristics and clinically relevant features. Results: the most frequent comorbidity in our cohort was arterial hypertension (44.0 %), followed by dyslipidemia (32.1 %), obesity (30.9 %), and diabetes mellitus (20.0 %). The association between admission to the intensive care unit (ICU) with body mass index (BMI) in a multivariate model was statistically significant, evidencing that obese subjects (BMI = 30 kg/m(2)) have a 19 % higher risk of requiring ICU care. The univariate model revealed a statistically significant association between obesity and ICU admission and length of hospital stay (p < 0.05). The relationship between baseline blood glucose and in-hospital mortality was also statistically significant (p = 0.03), as well as with total cholesterol and ICU admission (p = 0.007). Conclusions: obesity is related to a longer time of hospitalization and a higher rate of admissions to the ICU. Low total cholesterol levels and abnormal baseline blood glucose were risk factors for ICU requirement and in-hospital mortality. Patient categorization based on obesity could be valuable in the development of a precision medicine model within the COVID-19 pandemic.

Viral infections activate the innate immune response and the secretion of inflammatory cytokines. They also alter oxidative stress markers, which potentially can have an involvement in the pathogenesis of the disease. The aim of this research was to study the role of the oxidative stress process assessed through lactate dehydrogenase (LDH) on the severity of COVID-19 measured by oxygen saturation (SaO₂) and the putative interaction with inflammation. The investigation enrolled 1808 patients (mean age of 68 and 60% male) with COVID-19 from the HM Hospitals database. To explore interactions, a regression model and mediation analyses were performed. The patients with lower SaO₂ presented lymphopenia and higher values of neutrophils-to-lymphocytes ratio and on the anisocytosis coefficient. The regression model showed an interaction between LDH and anisocytosis, suggesting that high levels of LDH (>544 U/L) and an anisocytosis coefficient higher than 10% can impact SaO₂ in COVID-19 patients. Moreover, analysis revealed that LDH mediated 41% (p value = 0.001) of the effect of anisocytosis on SaO₂ in this cohort. This investigation revealed that the oxidative stress marker LDH and the interaction with anisocytosis have an important role in the severity of COVID-19 infection and should be considered for the management and treatment of the oxidative phenomena concerning this within a precision medicine strategy.