Characteristics of SARS-CoV-2, COVID-19, and laboratory diagnosis / Características del SARS-CoV-2, COVID-19 y su diagnóstico en el laboratorio

La enfermedad COVID­19 es causada por el virus SARS-CoV-2, descrito por primera vez en diciembre del 2019 en Wuhan, China, y declarada en marzo del 2020 como una pandemia mundial. Actualmente existen diversos métodos diagnósticos para COVID-19, siendo el estándar de oro la detección del material genético mediante la reacción en cadena de la polimerasa (PCR), en su variante, la RT-PCR, que detecta el material genético de tipo ARN presente en el virus. Sin embargo, es necesario disponer de pruebas rápidas con alta sensibilidad y precisión para realizarlas a gran escala y brindar un diagnóstico oportuno. Adicionalmente, se debe disponer de otras herramientas que, si bien no van a establecer un diagnóstico, le van a permitir al profesional brindar un mejor manejo clínico y epidemiológico que ayuden a predecir el agravamiento del paciente y su posible ingreso a UCI, destacando entre estas los niveles de dímero D, linfocitos, ferritina, urea y creatinina, entre otras. En esta revisión se evalúa la utilidad y limitaciones de los diferentes métodos diagnósticos para COVID-19, al igual que las características, fisiopatología y respuesta inmune al SARS-CoV-2, así como algunos aspectos preanalíticos de importancia que ayudan a minimizar errores en el diagnóstico como consecuencia de procedimientos incorrectos en la toma, transporte y conservación de la muestra, y que permiten al profesional emitir resultados veraces y confiables. Lo anterior se realizó basado en artículos originales, revisiones y guías clínicas

COVID­19 is caused by the SARS-CoV-2 virus, first described in December 2019 in Wuhan, China, and declared a global pandemic in March 2020. Currently there are various diagnostic methods for COVID-19, the gold standard is the detection of genetic material through polymerase chain reaction (PCR) in its variant, RT-PCR, which detects RNA-type genetic material present in the virus. However, it is necessary to have rapid tests with high sensitivity and precision to be performed on a large scale and provide timely diagnosis. Furthermore, other tools must be available, and although they will not establish the diagnosis, will allow the professional to provide better clinical and epidemiological management that will help predict the worsening of the patient and possible admission to the ICU. Among these, levels of D-dimer, lymphocytes, ferritin, urea and creatinine. In this review, the usefulness and limitations of the different diagnostic methods for COVID-19 are evaluated, as well as the characteristics, pathophysiology and immune response to SARS-CoV-2, and some important preanalytical aspects that allow minimizing diagnostic errors as a consequence of incorrect procedures in the collection, transport and conservation of the sample, that allow the professional to yield accurate and reliable results. This article was completed based on original articles, reviews and clinical guidelines

COVID-19: a perspective focus on IL-17/Th17 / COVID-19: perspectivas terapéuticas en IL-17/Th17

RESUMEN Las células T helper-17 (Th17) y la interleuquina (IL) IL-17 desempeñan funciones biológicas relacionadas con la protección contra infecciones por bacterias extracelulares y hongos. En algunas enfermedades inflamatorias y autoinmunes hay una secreción persistente y estas participan en su patogénesis. Recientemente, se ha postulado la participación de las respuestas IL-17/Th17 en la patogénesis de la enfermedad por coronavirus 2019 (COVID-19). El objetivo de esta revisión es resumir la evidencia del papel de la IL-17/Th17 en la inmunopatogénesis del COVID-19, como sustento de la possible utilización de los inhibidores de IL-17 en el manejo terapéutico de esta infección.

SUMMARY Interleukin 17 (IL-17)-producing helper T cells (Th17) and IL-17 play an important role in the defense against extracellular bacteria and fungi; however, persistent secretion of IL-17 is also an important component in the pathogenesis of many inflammatory and autoimmune diseases. Recent evidence suggests that Th17 cells and IL-17 are also involved in the immunopathogenesis of COVID-19. This review summarizes the evidence related with the role of Th17/IL-17 in severe COVID-19, which support the possible use of IL-17/IL-17R inhibitors in the treatment of this infection.

COVID-19 and Dermal Fillers: Should We Really Be Concerned? / COVID y rellenos faciales ¿realmente debemos preocuparnos?

SARS-CoV-2 has caused millions of infections and deaths worldwide and case numbers continue to rise. Besides the effect of the virus on key organs - leading to respiratory illness, anosmia, diarrhea, and fever and other complications - delayed inflammatory reactions to hyaluronic acid dermal fillers, mainly in the face, have also been reported to occur after confirmed SARS-CoV-2 infections and in vaccinated individuals. While delayed inflammatory reactions tend to be self-limiting, they should be diagnosed and treated with corticosteroids, hyaluronidase, and/or antibiotics when necessary. The inflammation is generally not severe, yet these complications are classified as serious adverse events by the US Food and Drug Administration. They appear to be delayed type IV hypersensitivity reactions triggered by the immune system in the presence of SARS-CoV-2 or other viruses, such as those causing influenza, although the underlying mechanisms have not been fully elucidated. Because the longevity of dermal fillers is increasing, while the pandemic continues to evolve and new vaccines are under development, the long-term effects on hyaluronic acid fillers and other bioimplant materials should be studied. Physicians must also be encouraged to report these reactions, however mild, to ensure accurate records.

Cardiovascular vulnerability in COVID-19 elderly patients: getting into the biological mechanisms / Vulnerabilidad cardiovascular en adultos mayores con COVID-19: conociendo los mecanismos biológicos

The COVID-19 pandemic has had an important impact on older adults, conferring a worse prognosis. Older adults may have atypical presentations, which can delay the diagnosis of the disease, making its evolution more unfavorable. In addition to the cardiovascular damage mechanisms conferred by SARS-CoV-2 infection, the changes inherent in the aging cardiovascular and immune system favor the appearance of cardiovascular complications in a more relevant way in this population. The objective of this article will be to summarize the knowledge about cardiovascular involvement in older adults and explain its pathophysiological mechanisms, to alert about the early recognition and timely treatment of these complications.

La pandemia por COVID-19 ha impactado de forma importante en los adultos mayores, confiriéndoles un peor pronóstico. Los adultos mayores pueden tener presentaciones atípicas, las cuales pueden retrasar el diagnóstico de la enfermedad, haciendo su evolución más desfavorable. Además de los mecanismos de daño cardiovascular conferidos por la infección por SARS-CoV-2, los cambios inherentes al sistema cardiovascular e inmune ya envejecido, favorecen la aparición de complicaciones cardiovasculares de forma más relevante en esta población. El objetivo de este artículo será resumir los conocimientos sobre el involucro cardiovascular en adultos mayores y explicar los mecanismos fisiopatológicos de este, para alertar sobre el reconocimiento temprano y tratamiento oportuno de estas complicaciones.

Can systemic immune inflammation index at admission predict in-hospital mortality in chronic kidney disease patients with SARS-CoV-2 infection?

BACKGROUND AND AIM: Patients with chronic kidney disease (CKD) are susceptible to SARS-CoV-2 infection and more prone to develop severe disease. It is important to know predictors of poor outcomes to optimize the strategies of care. METHODS: 93 patients with CKD and 93 age-sex matched patients without CKD were included in the study. Data on demographic, clinical features, hematological indices and outcomes were noted and compared between the groups. Neutrophile to lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune inflammation index (SII) (platelet counts×neutrophil counts/lymphocyte counts) and lymphocyte-to-CRP ratio (LCR) were calculated on admission and the association of these markers with disease mortality in CKD patients was identified. RESULTS: CKD patients had higher risk of severe disease, and mortality compared to non-CKD patients (72% vs 50.5%, p=0.003, 36.6% vs 10.8%, p<0.001, respectively) and were more likely to have higher values of immuno-inflammatory indices (leukocyte count, neutrophil, NLR, SII and C-reactive protein, etc.) and lower level of lymphocyte and LCR. Also, higher levels of NLR, SII, PLR and lower level of LCR were seen in CKD patients who died compared to those recovered. In a receiver operating characteristic curve analysis, NLR, SII, PLR and LCR area under the curve for in-hospital mortality of CKD patients were 0.830, 0.811, 0.664 and 0.712, respectively. Among all parameters, NLR and SII gave us the best ability to distinguish patients with higher risk of death. Based on the cut-off value of 1180.5, the sensitivity and specificity of the SII for predicting in-hospital mortality were found to be 67.5% and 79.6%, respectively. The corresponding sensitivity and specificity of the NLR were 85.2% and 66.1%, respectively, at the cut-off value of 5.1. Forward stepwise logistic regression analysis showed that NLR (≥5.1), SII (≥1180.5) and LCR (≤9) were predictors for in-hospital mortality. CONCLUSION: We report for the first time that SII is able to distinguish COVID-19 infected CKD patients of worse survival and it is as powerful as NLR in this regard. As SII is easily quantified from blood sample data, it may assist for early identification and timely management of CKD patients with worse survival.

C-reactive protein-to-lymphocyte ratio is a reliable marker in patients with COVID-19 infection: the CLEAR COVID study.

OBJECTIVE: COVID-19 infection is characterized with elevation of inflammatory markers in bloodstream. A novel inflammatory marker, C-reactive protein (CRP)-to-lymphocyte ratio (CLR), is suggested to be associated with inflammation. We aimed to compare the CLR values of the deceased COVID-19 patients to the CLR of survived subjects. MATERIALS AND METHODS: The patients with COVID-19 whom presented to outpatient or inpatient clinics of AbantIzzet Baysal University Hospital were enrolled to the present retrospective study. Subjects were grouped as either deceased or survived. CLR values of the groups were compared. RESULTS: Study cohort was consisted of 568 subjects in deceased and 4753 patients in survived group. Median CLR of the deceased and survived groups were 90 (0.2-1679)% and 11 (0.2-1062)%, respectively (p < 0.001). The sensitivity (75%) and specificity (70%) of CLR (> 23.4% level) in detecting mortality were higher than those of CRP and ferritin (AUC 0.80, p < 0.001, 95% CI 0.78-0.82). CONCLUSION: We suggest that elevated CLR levels in COVID-19 patients on admission should alert physicians for poor outcome.

OBJETIVO: La infección por Covid-19 se caracteriza por elevación de marcadores inflamatorios en el torrente sanguíneo. Se sugiere que un nuevo marcador inflamatorio, la proporción de C-reactive protein (CRP) a linfocitos (CLR), está asociado con la inflamación. Nuestro objetivo fue comparar los valores de CLR de los pacientes fallecidos con Covid-19 con el CLR de los sujetos sobrevivientes. MATERIALES Y MÉTODOS: Los pacientes con Covid-19 que se presentaron en clínicas ambulatorias o de hospitalización del Hospital Universitario Abant Izzet Baysal se inscribieron en el presente estudio retrospectivo. Los sujetos se agruparon como fallecidos o sobrevivientes. Se compararon los valores de CLR de los grupos. RESULTADOS: La cohorte del estudio estuvo compuesta por 568 sujetos en el grupo fallecido y 4753 pacientes en el grupo sobreviviente. La mediana de CLR de los grupos fallecidos y sobrevivientes fue 90 (0.2-1679)% y 11 (0.2-1062)%, respectivamente (p < 0.001). La sensibilidad (75%) y la especificidad (70%) de CLR (nivel > 23.4%) en la detección de mortalidad fueron superiores a las de CRP y ferritina (AUC 0.80, p < 0.001, IC 95%: 0,78-0.82). CONCLUSIÓN: Sugerimos que los niveles elevados de CLR en pacientes con Covid-19 al ingreso deberían alertar a los médicos sobre un resultado deficiente.

Melatonina : bases científicas para su uso en el COVID 19

La Melatonina es una hormona que actúa facilitando la aparición del sueño fisiológico. Además presenta potentes acciónes antiinflamatoria y antioxidante, con lo que ha demostrado ya ser capaz de ejercer efectos muy beneficioso sobre las alteraciones ligadas al envejecimiento que aparecen en el sistema cardiovascular y especialmente en pulmón, donde nuestro grupo ha podido constatar un efecto protector frente a procesos de estrés oxidativo , inflamatorios y de muerte celular programada ( apoptosis).. Aunque no es una sustancia antivírica, sin embargo ha demostrado tener efectos muy positivos en algunos modelos experimentales de infección por vírus disminuyendo la carga viral y también reduciendo la oxidación y la inflamación con lo que atenúa la gravedad de la enfermedad. En el COVID 19 es capaz también de interferir en el proceso infectivo que ocurre a través de los receptores de ACE2 y de EGF pues es capaz de bloquear dichas interacciones con lo que disminuye la viremia. Concretamente reduce la actividad del inflamasoma NLRP3 con lo que bloquea la liberación masiva de citoquinas disminuyendo el proceso inflamatorio lo que supone una mejoría de la evolución de la enfermedad. Por todo ello la melatonina puede desempeñar un importante papel en el tratamiento del COVID 19.Alternate : Melatonin is a hormone that acts facilitating the appearance of physiological sleep It has also a very evident antinflammatory and antioxidant capacities that result in beneficial actions on the aging processes in the cardiovascular system and in the lungs where our group has detected a protective action against oxidative stress , inflammation and apoptosis . Although melatonin is not viricidal by itself in some models of viral infections it has demonstrated its ability to reduce viral load and also inflammation and oxidation, reducing the severity of the disease. In COVID 19 melatonin has been shown to be able to interfere with the infectious process that takes place through ACE2 and EGF receptors being able to block these interactions thus reducing viremia .It is able to block the activation of the NLRP3 inflammasome thus dramatically reducing the massive secretion of cytokines and markedly reducing hyperinflammation and apoptosis leading to a better evolution of the disease .For all these reasons melatonin could play an important role in the treatment of COVID 19.

COVID-19 and diabetes mellitus in cognitive impairment: an undrawn relationship

Cognitive impairment is a potential short- and long-term disease consequence of COVID-19 virus, the exact mechanism is still in debate. One of their potential linking is with diabetes. Diabetes and COVID-19 infection have possible multiple common mechanisms that could ensue cognitive impairment as pulmonary microthrombi (silent hypoxia);endothelial dysfunction;cerebral vascular injury oxidative stress;renin-angiotensin-aldosterone system;and galectine and interferon responses. In addition, histological markers as amyloid AB plaques and neurofibrillary tangle of Tau protein are common in both pathologies. Despite of this evidence, diabetes mellitus and COVID-19 in cognitive impairment are establishing a bright light in terms of neurological progress. This article describes the relationship between diabetes mellitus and COVID-19 as potential cause of cognitive impairment. (English) [ FROM AUTHOR]

Neutrophil-to-lymphocyte ratio is not associated with risk of sarcopenia in elderly COVID-19 patients.

BACKGROUND: To assess the existence of association between neutrophil to lymphocyte ratio (NLR) and the risk of sarcopenia in COVID-19 patients. METHODS: A retrospective cross-sectional study was conducted in a university hospital with patients with an active COVID-19 infection admitted to the nursing ward or intensive care unit (ICU) between September to December 2020. Sarcopenia risk was assessed using the Strength, Assistance for walking, Rise from a chair, Climb stairs and Falls (SARC-F). Biochemical analyses were assessed by circulating of C-reactive protein, D-dimer, neutrophils, lymphocytes count and NLR. Sixty-eight patients were evaluated and divided into tertiles of NLR values and the association between NLR and sarcopenia risk were tested using the linear regression analyses and p<0.05 were considered as significant. RESULTS: Sixty-eight patients were evaluated and divided in NLR tertiles being the 1st (men=52.2%; 71.1±9.0 y; NLR: 1.1-3.85), 2nd (women=78.3%; 73.2±9.1 y; NLR: 3.9-6.0) and 3rd (men=72.7%; 71.7±10.4 y; NLR: 6.5-20.0). There was a difference between the tertiles in relation to the first to the biochemical parameters of total neutrophils count (p=0.001), C-reactive protein (p=0.012), and D-dimer (p=0.012). However, no difference was found in linear regression analysis between tertiles of NLR and SARC-F, if in total sample (p=0.054) or divided by sex, if men (p=0.369) or women (p=0.064). CONCLUSION: In elderly patients hospitalized with COVID-19, we do not find an association between the risk of sarcopenia and NLR.

18F-FDG-PET/CT in SARS-CoV-2 infection and its sequelae.

In recent months, much of the scientific efforts have focused on research on SARSCoV-2 infection and its consequences in humans. Still, many aspects remain unknown. It is known that the damage caused by SARS-CoV-2 is multifactorial and that its extension goes beyond lung inflammation and the acute phase, with the appearance of numerous complications and sequelae. To date, knowledge about the usefulness of 18F-FDG-PET/CT in the acute phase has been limited to the incidental detection of SARS-CoV-2 unsuspected pneumonia. Recent studies have been appearing collecting the findings of 18F-FDG-PET/CT in long COVID-19 or persistent COVID-19 state as well as the alterations caused after mass vaccination of the population in the metabolic studies. This work aims to review the existing literature focusing on these three issues and to briefly present our own preliminary experience.

Hipótesis sobre las conexiones entre COVID-19 severo en niños y nutrición: una revisión narrativa.

INTRODUCTION: Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). Compared with adults, children with SARS-CoV-2 infection may have fewer and less severe symptoms. Gastrointestinal symptoms are commonly reported in children, sometimes as the only manifestation of the disease, and most often manifest as anorexia, diarrhea, nausea and vomiting, or abdominal pain. Although most children have asymptomatic or mild disease, 10 % of those infected may experience serious or critical disease, or even death. Multisystem inflammatory syndrome is a rare but serious condition recently reported in children with COVID-19. Studies indicate that children with obesity are at higher risk of developing severe COVID-19, and inflammation associated with obesity could be one of the factors that worsens COVID-19 symptoms due to an increased inflammatory response involving molecules such as interleukin 6, tumor necrosis factor alpha, and monocyte chemoattractant protein. On the other hand, evidence has been reported of a higher protein expression of ACE2 in the visceral adipose tissue of obese and malnourished humans, and this could be associated with complications and severity of COVID-19. Therefore, regulation of the intake of macronutrients or micronutrients could be used as a strategy to reduce the consequences of COVID-19. Diet in general and bioactive compounds could play an important role in the prevention of the inflammatory cascade. The micronutrients with the most evidence suggesting a role in immune support are vitamins C and D, zinc, and polyphenols.

INTRODUCCIÓN: La enfermedad por coronavirus 2019 (COVID-19) está causada por el virus "síndrome respiratorio agudo severo-coronavirus 2" (SARS-CoV-2). En comparación con los adultos, los niños con infección por SARS-CoV-2 pueden tener menos síntomas y estos pueden ser menos graves. Los síntomas gastrointestinales se informan comúnmente en los niños, a veces como única manifestación de la enfermedad. Los más comunes son anorexia, diarrea, náuseas y vómitos, y dolor abdominal. Aunque la mayoría de los niños tienen un cuadro leve o asintomático, el 10 % de los infectados pueden experimentar un cuadro grave o crítico, e incluso la muerte. El síndrome inflamatorio multisistémico es una afección poco común, pero grave, que se documentó recientemente en niños con COVID-19. Los estudios indican que los niños con obesidad tienen mayor riesgo de desarrollar COVID-19 grave, y la inflamación asociada con la obesidad podría ser uno de los factores que empeoran los síntomas de la COVID-19 debido a una respuesta inflamatoria aumentada en donde se ven involucradas moléculas como la interleucina 6, el factor de necrosis tumoral alfa y la proteína quimioatrayente de monocitos. Por otro lado, se ha encontrado evidencia de una mayor expresión proteica de ACE2 en el tejido adiposo visceral de los seres humanos obesos y desnutridos, y esto podría estar asociado a las complicaciones y la severidad de la COVID-19. Por tanto, la regulación de la ingesta de macronutrientes o micronutrientes podría utilizarse como estrategia para reducir las consecuencias de la enfermedad. La dieta en general y los compuestos bioactivos podrían desempeñar un papel importante en la prevención de la cascada inflamatoria. Los micronutrientes con mayor evidencia indicativa de que desempeñan un papel en el apoyo inmunológico son las vitaminas C y D, el zinc y los polifenoles.

Neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio and systemic immune-inflammation index in patients with COVID-19-associated pneumonia.

INTRODUCTION: There are hematological parameters that correlate severity and predict mortality mainly in septic and inflammatory states. OBJECTIVE: To correlate the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and systemic immune-inflammation index (SIII) with COVID-19 severity. METHOD: Descriptive, analytical, retrospective study of patients with COVID-19 pneumonia, in whom NLR, PLR and SIII were analyzed. RESULTS: One-hundred patients were included, 54 men and 46 women, with a mean age of 49.4 ± 19.3 years. NLR, PLR and SIII means were 10.7 ± 10.9, 290.1 ± 229.2, and 2.6 ± 3.4 x 109, respectively. In 54 %, pneumonia was mild, and in 46 %, severe. Regarding hospital outcomes, 75 % were discharged due to improvement and 25 % died. NLR, PLR and SIII means of the patients who died versus the patients who improved were 20.4 ± 16.9 versus 7.5 ± 4.9 (p = 0.001), 417.1 ± 379.7 versus 247.7 ± 127.4 (p = 0.038) and 4.8 ± 6.1 versus 1.9 ± 1.2 × 109 (p = 0.030), respectively. CONCLUSION: Hematological parameters can be used in patients with COVID-19-associated pneumonia as predictors of severity and prognosis. INTRODUCCIÓN: Existen índices hematológicos que correlacionan la severidad y predicen la mortalidad, principalmente en ­estados sépticos y de inflamación. OBJETIVO: Correlacionar los índices neutrófilo/linfocito (INL), plaqueta/linfocito (IPL) e inmunidad/inflamación sistémica (IIIS) con la severidad de COVID-19. MÉTODO: Estudio descriptivo, analítico y retrospectivo de pacientes con neumonía por COVID-19, en quienes se analizaron INL, IPL e IIIS. RESULTADOS: Se incluyeron 100 pacientes, 54 hombres y 46 mujeres, con una media de 49.4 ± 19.3 años. Las medias de INL, IPL e IIIS fueron 10.7 ± 10.9, 290.1 ± 229.2 y 2.6 ± 3.4 × 109, respectivamente. En 54 %, la neumonía fue leve y en 46 %, grave. En cuanto a los desenlaces hospitalarios, 75 % egresó por mejoría y 25 % falleció. Las medias de INL, IPL e IIIS de los pacientes que fallecieron versus las de los pacientes que mejoraron fueron 20.4 ± 16.9 versus 7.5 ± 4.9 (p = 0.001), 417.1 ± 379.7 versus 247.7 ± 127.4 (p = 0.038) y 4.8 ± 6.1 versus 1.9 ± 1.2 × 109 (p = 0.030), respectivamente. CONCLUSIÓN: Los índices hematológicos en pacientes con neumonía por COVID-19 pueden ser empleados como predictores de severidad y pronóstico.

Neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio and systemic immune-inflammation index in patients with COVID-19-associated pneumonia / Índices neutrófilo/linfocito, plaqueta/linfocito e inmunidad/inflamación sistémica en pacientes con neumonía por COVID-19

Resumen Introducción: Existen índices hematológicos que correlacionan la severidad y predicen la mortalidad, principalmente en estados sépticos y de inflamación. Objetivo: Correlacionar los índices neutrófilo/linfocito (INL), plaqueta/linfocito (IPL) e inmunidad/inflamación sistémica (IIIS) con la severidad de COVID-19. Método: Estudio descriptivo, analítico y retrospectivo de pacientes con neumonía por COVID-19, en quienes se analizaron INL, IPL e IIIS. Resultados: Se incluyeron 100 pacientes, 54 hombres y 46 mujeres, con una media de 49.4 ± 19.3 años. Las medias de INL, IPL e IIIS fueron 10.7 ± 10.9, 290.1 ± 229.2 y 2.6 ± 3.4 × 109, respectivamente. En 54 %, la neumonía fue leve y en 46 %, grave. En cuanto a los desenlaces hospitalarios, 75 % egresó por mejoría y 25 % falleció. Las medias de INL, IPL e IIIS de los pacientes que fallecieron versus las de los pacientes que mejoraron fueron 20.4 ± 16.9 versus 7.5 ± 4.9 (p = 0.001), 417.1 ± 379.7 versus 247.7 ± 127.4 (p = 0.038) y 4.8 ± 6.1 versus 1.9 ± 1.2 × 109 (p = 0.030), respectivamente. Conclusión: Los índices hematológicos en pacientes con neumonía por COVID-19 pueden ser empleados como predictores de severidad y pronóstico.

Abstract Introduction: There are hematological parameters that correlate severity and predict mortality mainly in septic and inflammatory states. Objective: To correlate the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and systemic immune-inflammation index (SII) with COVID-19 severity. Method: Descriptive, analytical, retrospective study of patients with COVID-19 pneumonia, in which NLR, PLR and SII were analyzed. Results: One-hundred patients were included, 54 men and 46 women, with a mean age of 49.4 ± 19.3 years. NLR, PLR and SII means were 10.7 ± 10.9, 290.1 ± 229.2, and 2.6 ± 3.4 × 109, respectively. In 54 %, pneumonia was mild, and in 46 %, severe. Regarding hospital outcomes, 75 % were discharged due to improvement and 25 % died. NLR, PLR and SII means of the patients who died versus the patients who improved were 20.4 ± 16.9 versus 7.5 ± 4.9 (p = 0.001), 417.1 ± 379.7 versus 247.7 ± 127.4 (p = 0.038) and 4.8 ± 6.1 versus 1.9 ± 1.2 × 109 (p = 0.030), respectively. Conclusion: Hematological parameters can be used in patients with COVID-19-associated pneumonia as predictors of severity and prognosis.

[Glucocorticoids alone versus tocilizumab alone or glucocorticoids plus tocilizumab in patients with severe SARS-CoV-2 pneumonia and mild inflammation]. / Glucocorticoides solos versus tocilizumab solo o glucocorticoides más tocilizumab en pacientes con neumonía grave por SARS-CoV-2 e inflamación moderada.

AIM: To assess clinical outcomes according to the immunosuppressive treatment administered to patients with severe SARS-CoV-2 pneumonia and moderate inflammation. METHODS: A retrospective observational cohort study involving 142 patients with severe COVID-19 pneumonia and moderate inflammation divided into three treatment groups (pulses of methylprednisolone alone [groupI], tocilizumab alone [groupII] and methylprednisolone plus tocilizumab [groupIII]). The aim was to assess intergroups differences in the clinical course with a 60-day follow-up and related analytical factors. RESULTS: 14 patients (9,8%) died: 8 (10%) in groupI and 6 (9,5%) in groupsII andIII. 15 (10,6%) were admitted to ICU: 2 (2,5%) from groupI, 4 (28,5%) from groupII and 9 (18,4%) from groupIII. The mean hospital stay was longer in groupII and clinical outcome was not associated with treatment. CONCLUSIONS: Tocilizumab seems to be not associated with better clinical outcomes and should be reserved for clinical trial scenario, since its widespread use may result in higher rate of ICU admission and longer mean hospital stay without differences in mortality rate and potentially adverse events.

Statins in COVID-19: is there any foundation? / Estatinas en COVID-19: ¿existe algún fundamento?

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19). Acute respiratory distress syndrome is the main cause of death from COVID-19 and occurs due to an exaggerated inflammatory response that causes the release of pro-inflammatory cytokines such as interleukins and tumor necrosis factor-alpha (TNF-α). Statins are lipid lowering drugs with pleiotropic effects. They have shown benefit in the management of inflammatory and autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis. Furthermore, due to their immunomodulatory properties, they have been used in the treatment of various infectious diseases such as community-acquired pneumonia and influenza. In this review we analyze the pathophysiological foundations that support the use of statins as an adjunctive treatment in patients with COVID-19.