Treatment Efficacy of Continuous Renal Replacement on Symptoms, Inflammatory Mediators, and Coagulation Function in Patients with Sepsis-Associated Acute Kidney Injury

Introduction: The aim of this study is to compare the treatment efficacy between continuous renal replacement therapy (CRRT) and conventional intermittent hemodialysis (IHD) in patients with sepsis (SIRS) combined with acute kidney injury (AKI) and its impact on inflammatory mediators and coagulation function. Method: 122 patients (25–60 years) with SIRS combined with AKI were enrolled in the sudy. The study group (SG) comprised 62 patients who received CRRT (8–10 h/day) + routine treatment, whereas the control group (CG) comprised 60 patients who received conventional IHD (4 h/day, 3 times per week) + routine treatment. inflammatory mediators and coagulation function measures were assessed and compared in each group. Results: C-reactive protein, blood creatinine, blood urea nitrogen, blood lactic acid, oxygenation index, central venous oxygen saturation, SOFA (Sequential Organ Failure Assessment) score, interleukin 6, interleukin 8, hypersensitive C-reactive protein, tumor necrosis factor-α, prothrombin time, activated partial thromboplastin time, FIB, and platelet count were better in the SG than in the CG (p < 0.05). The 12- and 24-month survival rates were significantly higher in the SG than in the CG (p < 0.05). Conclusions: CRRT can effectively improve clinical symptoms, remove inflammatory factors, and maintain blood coagulation function in patients with SIRS combined with AKI. It is more efficient than IHD treatment and is worthy of clinical promotion (AU)

Anaphylaxis: Mediators, Biomarkers, and Microenvironments

The life-threatening nature of anaphylactic reactions has increased interest in discovering new biomarkers that could improve diagnosis and prevention. However, the diverse nature of the clinical features and the etiology and pathogenesis of anaphylaxis hinder the identification of valuable molecular indicators of disease. Most studies on anaphylaxis focus on the immune system. Anaphylactic reactions are characterized primarily by IgE-mediated activation of mast cells and basophils and release of mediators. Determination of serum tryptase levels is the main in vitro test used to confirm the reaction, although there are no biomarkers that can predict it. Nevertheless, recent research has postulated that alternative pathways, cell types, and systems are involved. Consequently, various molecular products have been explored and considered potential biomarkers, although none of them are yet used in clinical practice. The products that are altered in patients with anaphylaxis include vasoactive agents, proteases, proteoglycans, lipids, interleukins, cytokines, products of the complement-contact and coagulation systems, circulating proteins, extracellular vesicles, microRNAs, and metabolites. The recognition of biological processes and molecular pathways affecting the microenvironments involved in anaphylaxis will considerably improve clinical practice and the identification of better molecular markers. We offer a broad review of the various mediators described in anaphylaxis, consider their usefulness as potential biomarkers of this pathological event, and examine their role in the molecular basis of the reaction (AU)

Epalrestat suppresses inflammatory response in lipopolysaccharide-stimulated RAW264.7 cells

Introduction and objectives: Lipopolysaccharide (LPS) is a potent inducer of inflammatory response. Inflammation is a major risk factor for many diseases. Regulation of inflammatory mediator and pro-inflammatory cytokine levels could be a potential therapeutic approach to treat inflammatory injury. The purpose of the present study was to determine whether epalrestat (EPS), which is used for the treatment of diabetic neuropathy, suppresses inflammatory response in LPS-stimulated RAW264.7 cells. Material and methods: The effects of EPS at near-plasma concentration on the levels of pro-inflammatory cytokines and inflammatory mediators was examined using by MTS assay, quantitative RT-PCR analysis, and western blotting in LPS-stimulated RAW264.7 cells. Results: EPS suppressed mRNA and protein expression levels of pro-inflammatory cytokines, including IL-1β, IL-6, and TNFα, in RAW264.7 cells stimulated with LPS. EPS also affected inflammatory mediators such as iNOS and NF-κB in LPS-stimulated RAW264.7 cells. Conclusions: In this study, we demonstrated for the first time that EPS suppresses inflammatory response in LPS-stimulated RAW264.7 cells. From these results, we propose that targeting the regulation of pro-inflammatory cytokine levels and inflammatory mediators by EPS is a promising therapeutic approach to treat inflammatory injury. It is expected that EPS, whose safety and pharmacokinetics have been confirmed clinically, would be useful for the treatment of inflammatory diseases (AU)

Suppressive effect of tamarixetin, isolated from Inula japonica, on degranulation and eicosanoid production in bone marrow-derived mast cells

Background: The aim of this study was to evaluate the inhibitory effect of tamarixetin on the production of inflammatory mediators in IgE/antigen-induced mouse bone marrow-derived mast cells (BMMCs). Materials and methods: The effects of tamarixetin on mast cell activation were investigated with regard to degranulation, eicosanoid generation, Ca2+ influx, and immunoblotting of various signaling molecules. Results: Tamarixetin effectively decreased degranulation and the eicosanoid generation such as leukotriene C4 and prostaglandin D2 in BMMCs. To elucidate the mechanism involved, we investigated the effect of tamarixetin on the phosphorylation of signal molecules. Tamarixetin inhibited the phosphorylation of Akt and its downstream signal molecules including IKK and nuclear factor κB. In addition, tamarixetin downregulated the phosphorylation of cytosolic phospholipase A2 (cPLA2) and p38 mitogen-activated protein kinase. Conclusions: Taken together, this study suggests that tamarixetin inhibits degranulation and eicosanoid generation through the PLCγ1 as well as Akt pathways in BMMCs, which would be potential for the prevention of allergic inflammatory diseases (AU)

The dilemma of chronic recurrent multifocal osteomyelitis / El dilema de la osteomielitis multifocal recurrente crónica

Chronic recurrent multifocal osteomyelitis (CRMO) is a rare idiopathic inflammatory disease that affects mainly children and young adults, resulting in significant morbidity especially if not diagnosed early. The clinical signs and symptoms are nonspecific, with a consequential delay in diagnosis. Radiological and histopathological criteria are important for its definition. Two cases of CRMO are reported, highlighting the diagnostic challenge and demonstrating the importance of timely investigations

La osteomielitis multifocal recurrente crónica (CRMO) es una enfermedad inflamatoria idiopática rara que afecta a principalmente niños y adultos jóvenes, dando por resultado morbosidad significativa sobre todo si no se diagnostica a tiempo. Los signos y síntomas clínicos son inespecíficos, entorpecer y retrasar el diagnóstico. Las pruebas radiológicas e histopatológicas son esenciales para su definición. Se divulgan dos casos de CRMO, destacando el reto diagnóstico y demostrando la importancia de las investigaciones oportunas

Relación entre marcadores hematológicos y la respuesta patológica completa al tratamiento neoadyuvante en cáncer de recto localmente avanzado / Relationship between haematological markers and patological complete response to neoadjuvant treatment in locally advanced rectal cancer

INTRODUCCIÓN: Múltiples marcadores hematológicos de inflamación pueden tener relación con un peor pronóstico en los pacientes oncológicos. PROPÓSITO: Este estudio evaluó si los cambios en marcadores hematológicos antes y después del tratamiento quimio-radioterápico (QT-RT) en cáncer de recto pueden estar asociados con la respuesta patológica completa. MATERIAL Y MÉTODO: Se revisaron retrospectivamente las historias clínicas de 140 pacientes con cáncer de recto que recibieron tratamiento radioterápico neoadyuvante seguido de resección quirúrgica fueron revisados retrospectivamente. Se realizó analítica completa antes y después del tratamiento QT-RT. Se evaluaron leucocitos, hemoglobina, neutrófilos, linfocitos, monocitos, ratio neutrófilo-linfocitos (NLR), ratio plaqueta-linfocitos (PLR) y ratio linfocitos-monocitos (LMR). RESULTADOS: La respuesta patológica completa fue de 17,5%. Los marcadores hematológicos tuvieron una disminución significativa tras el tratamiento de QT-RT (p < 0,05), sin embargo en nuestro análisis no se relacionó con la respuesta patológica completa, salvo el PLR (p = 0,027). CONCLUSIÓN: Los marcadores hematológicos antres y después del tratamiento neoadyuvante no predicen la respuesta tumoral tras QT-RT en este estudio. Sin embargo una muestra mayor puede presentar resultados estadísticamente signifiacativos, especialmente con los monocitos

INTRODUCTION: Multiple haematological markers of inflammation might be related with poor prognosis in oncological patients. PURPOSE: This study evaluated whether changes of haematological markers before and after chemo-radiotherapy treatment in rectal cancer might be associated to pathological complete response. MATERIAL AND METHODS: Medical records of 140 patients with rectal cancer who received neoadjuvant radiotherapy followed by surgical resection were retrospectively review. Complete bloods counts (CBC) was measured days before and after period of RT. We assessed white blood cells count (WBC), hemoglobin levels (Hb), neutrophils count, lymphocytes count, monocytes count, neutrophil-to-lymphocye ratio (NLR), platelet-to-lymphocyte ratio (PLR) and lymphocyte-to-monocyte ratio (LMR). RESULTS: The overall rate of pCR was 17,5%. Hematological markers had a statistically significant decrease after CRT treatment (p < 0,05), however in our analysis they do not predict complete pathological response. CONCLUSION: Haematological markers before and after neoadjuvant treatment do not predict tumor responses in this study. However, a larger sample can show statistically significant results, especially in monocytes ratio

La inflamación, la desnutrición y la infección por SARS-CoV-2: una combinación nefasta / Inflammation, malnutrition, and SARS-CoV-2 infection: a disastrous combination

La infección por SARS-CoV-2 se relaciona con un riesgo alto de malnutrición, principalmente por el aumento de los requerimientos nutricionales y la presencia de un estado inflamatorio severo y universal. Los síntomas asociados contribuyen a la hiporexia, que perpetúa el balance nutricional negativo. Además, la disfagia, especialmente posintubación, empeora y hace poco segura la ingesta. Este riesgo es mayor en pacientes ancianos y multimórbidos. La inflamación en distinto grado es el nexo común entre la COVID-19 y la aparición de desnutrición, siendo más correcto hablar de desnutrición relacionada con la enfermedad (DRE). La DRE empeora el mal pronóstico de la infección por SARS-CoV-2, sobre todo en los casos más severos. Por ello es necesario identificar y tratar precozmente a las personas en riesgo, evitando la sobreexposición y el contacto directo con el paciente. No podemos olvidarnos del papel que juega la dieta saludable tanto en la prevención como en la recuperación tras el alta

SARS-CoV-2 infection is associated with a high risk of malnutrition, mainly due to increased nutritional requirements and the presence of a severe and universal inflammatory state. Associated symptoms contribute to hyporexia, which perpetuates the negative nutritional balance. Furthermore, dysphagia, especially post-intubation, worsens and makes intake unsafe. This risk is greater in elderly and multimorbid patients. Inflammation to varying degrees is the common link between COVID-19 and the onset of malnutrition, and it is more correct to refer to disease-related malnutrition (DRM). DRM worsens the poor prognosis of SARS-CoV-2 infection, especially in the most severe cases. Therefore, it is necessary to identify and treat people at risk early, avoiding overexposure and direct contact with the patient. We cannot forget the role that a healthy diet plays in both prevention and recovery after discharge

Tratamiento y evolución del síndrome de tormenta de citoquinas asociados a infección por SARS-CoV-2 en pacientes octogenarios / Evolution and treatment of storm cytoquine syndrome associated to SARS-CoV-2 infection among octogenarians

INTRODUCCIÓN: El síndrome de tormenta de citoquinas (STC) es una complicación muy grave de los pacientes con infección por SARS-CoV-2. El tratamiento y la evolución no están bien definidos. Nuestro objetivo es describir sus características clínicas, los tratamientos empleados y su evolución clínica. PACIENTES Y MÉTODO: Estudio retrospectivo observacional de pacientes consecutivos ingresados en el período comprendido entre el 23 de marzo y el 12 de abril de 2020 con infección por SARS-CoV-2 confirmada, con neumonía por estudio radiológico o tomografía de tórax, que cumplían criterios de STC y que recibieron tratamiento. Clasificamos a los pacientes en los que recibieron solo pulsos de glucocorticoides (GC), o pulsos de GC y tocilizumab. Determinamos niveles séricos de ferritina, PCR y dímeros-D. La variable final fue la supervivencia. RESULTADOS: Veintiún pacientes con una edad de 83 años (80-88 años). La ferritina media fue de 1.056 microg/L (317-3.553), la PCR de 115,8mg/dL (22-306) y los dímeros-D de 2,9mg/L (0,45-17,5). Todos los pacientes recibieron pulsos de GC y en 2 casos simultáneamente tocilizumab. El tiempo medio de seguimiento fue de 13,7 días (8-21). La mortalidad global fue del 38,1% (8/21pacientes). Los 2 pacientes que recibieron tocilizumab fallecieron. Los fallecidos presentaron niveles significativamente más elevados de ferritina (1.254 vs. 925microg/L; p = 0,045) y PCR (197,6 vs. 76mg/dL; p = 0,007). Al final del seguimiento se observó una disminución en los parámetros bioquímicos con ferritina de 727microg/L, PCR de 27mg/dl y dímeros-D de 1,18mg/L. En 13/21 pacientes (61,9%) el STC se controló sin necesidad de añadir otros tratamientos. CONCLUSIONES: La mortalidad del STC por SARS-CoV-2 es alta a pesar del tratamiento. Una mayor respuesta inflamatoria se asoció con una mayor mortalidad. Aunque parece que el uso precoz de pulsos de GC puede controlarlo, pudiendo disminuir la necesidad de uso de otros tratamientos, con el diseño del estudio y sus limitaciones, no se puede establecer esta conclusión

INTRODUCTION: Cytokine storm syndrome (CTS) is a serious complication of patients with SARS-CoV-2 infection. Treatment and evolution in octogenarians are not well defiREVned. Our objective is to describe its clinical characteristics, the treatments and its clinical evolution. PATIENTS AND METHOD: Retrospective observational study of consecutive patients admitted in the period between March 23 and April 12, 2020 with confirmed SARS-CoV-2 infection, with pneumonia by radiological study or chest tomography, whith STC criteria and who received treatment. We classified patients as those who received only glucocorticoid (GC) pulses, or GC and tocilizumab pulses. We determined serum levels of ferritin, CRP and D-dimers. The final variable was survival. RESULTS: 21 patients, (80-88 years). The mean ferritin was 1056 microg/L (317-3,553), CRP 115.8mg/dL (22-306) and D-dimers 2.9m/L (0.45-17.5). All patients received GC pulses and in 2 cases simultaneously tocilizumab. The mean follow-up time was 13.7 days (8-21). The overall mortality was 38.1% (8/21 patients). The 2 patients who received tocilizumab died. The deceased had significantly higher levels of ferritin (1,254 vs. 925microg/L; P=.045) and CRP (197.6 vs. 76mg / dL; P=.007). At the end of the follow-up, a decrease in the biochemical parameters was observed with ferritin of 727microg/L, CRP of 27mg/dl and D-dimers of 1.18mg/L. In 13/21 patients (61.9%), the CTS was controlled without the need to add other treatments. CONCLUSIONS: STC mortality from SARS-CoV-2 is high despite treatment. A greater inflammatory response was associated with a higher mortality. Although it seems that the early use of GC pulses could control it, and the use of other treatments such as tocilizumab shouldo be, with the study design and its limitations, this conclusion cannot be stablished

Effects of exercise training on smoking-induced cardiopulmonary diseases. A review of the physiological mechanisms / Efectos del entrenamiento físico en la enfermedad cardiopulmonar inducida por el tabaquismo: revisión de los mecanismos fisiológicos

OBJECTIVE: Cigarette smoking triggers a plethora of biological mechanisms that promote the development of cardiovascular and respiratory diseases. Some preclinical studies have shown that exercise training could be effective in blunting oxidative stress and inflammatory response induced by cigarette smoking. Therefore, we aim to analyze the effect of exercise training on pulmonary and cardiovascular system in experimental models of cigarette smoking. METHODS: A systematic search was performed in order to identify studies addressed to evaluate the effects of exercise training on pulmonary and/or cardiovascular damage induced by cigarette smoking in animal models. RESULTS: fourteen articles were identified, all of them performed in rats or mice. Running and swimming were the only training methods and whole-body smoke exposition was the most prevalent smoking protocol used in the studies. CONCLUSION: The studies support the hypothesis that exercise training performed before, concurrently or after smoking can blunt or even revert the oxidative stress and inflammatory response in animals exposed to cigarette smoke, which could contribute to recovering its cardiovascular and respiratory function

OBJETIVO: El tabaquismo desencadena diversos mecanismos biológicos que producen el desarrollo de enfermedades cardiovasculares y pulmonares. Algunos estudios preclínicos han demostrado que el entrenamiento físico puede ser eficaz en la reducción del estrés oxidativo y de la respuesta inflamatoria inducida por el tabaquismo. Por tanto, nuestro objetivo ha sido analizar el efecto del entrenamiento físico en los sistemas pulmonar y cardiovascular en modelos experimentales de tabaquismo. MÉTODO: Se realizo una búsqueda sistemática para localizar estudios orientados al análisis de los efectos del entrenamiento físico sobre los daños pulmonares y/o cardiovasculares inducidos por el tabaquismo en modelos animales. RESULTADOS: Se identificaron catorce estudios, todos realizados en ratas o ratones. Correr o nadar fueron los únicos métodos de entrenamiento y la exposición de cuerpo entero al humo del tabaco fue el protocolo de tabaquismo mas frecuentemente usado en los estudios. CONCLUSIÓN: Los estudios sustentan la hipótesis de que el entrenamiento físico realizado antes, durante o después del tabaquismo, puede reducir o incluso revertir, el estrés oxidativo y la respuesta inflamatoria en animales expuestos al humo del tabaco, lo que podría contribuir en la recuperación de la función cardiovascular y respiratoria

Arteriosclerosis e inflamación. Nuevos enfoques terapéuticos / Atherosclerosis and inflammation. New therapeutic approaches

El reconocimiento de la aterogénesis como un proceso dinámico en vez de un depósito pasivo de colesterol ha subrayado la existencia de mecanismos inflamatorios claves. Así, la respuesta inmune, tanto innata como adaptativa, desempeña un papel importante en el inicio y la progresión de la aterosclerosis. Más recientemente, algunos estudios clínicos han sido diseñados para abordar el impacto de las estrategias de intervención antiinflamatoria en la reducción del riesgo de enfermedad cardiovascular más allá del control de los factores clásicos de riesgo. Por todo ello, revisamos en primer lugar la contribución fisiopatológica de la inflamación en la aterosclerosis y el efecto del tratamiento farmacológico hipolipidemiante en los marcadores de inflamación. A continuación, abordamos el efecto de los fármacos antiinflamatorios clásicos, de los tratamientos farmacológicos dirigidos a mediadores inflamatorios específicos y de las vacunas en la prevención cardiovascular

The recognition of atherogenesis as an active process rather than a passive cholesterol storage disease has underlined key inflammatory mechanisms. Hence, innate and adaptive immune responses play an important role in the onset and progression of atherosclerosis. More recently, some clinical studies were designed to address the impact of anti-inflammatory intervention strategies in reducing risk of cardiovascular disease beyond the management of classic risk factors. Therefore, we review first the pathophysiological contribution of inflammation to atherosclerosis and the effect of lipid-lowering drugs on inflammatory biomarkers. Next, we address the effect of classic anti-inflammatory drugs, pharmacological therapies targeting specific inflammatory mediators and vaccines in cardiovascular prevention

Cuando el silicio transmuta en oro / When silicon transmutes in gold

Este trabajo describe las virtudes de una investigación centrada en el silicio, uno de los ingredientes más importantes pero menos conocidos de la cerveza, y su acción protectora a nivel neurodegenerativo. Entre los varios factores que contribuyen a la inducción y desarrollo de la enfermedad de Alzheimer, se encuentra el aluminio el cual tiende a concentrarse en el cerebro e inducir, entre otros mecanismos, alteraciones prooxidantes e inflamatorias. El silicio al bloquear esos efectos negativos, se convierte en un ingrediente estrella, que en términos alquimistas sugiere que puede transmutar en oro

This article describes the virtues of a research focused on silicon, one of the most important but least known ingredients in beer, and its protective action at the neurodegenerative level. Among the various factors contributing to the Alzheimer's disease induction and development, aluminum, by concentrating in brain induces, among other mechanisms, pro-oxidant and inflammatory disorders. Silicon, by blocking these negative effects, becomes a star ingredient, which in alchemist terms suggests that has the property to transmute into gold

Respuesta inflamatoria en relación con COVID-19 y otros fenotipos protrombóticos / Inflammatory response in relation to COVID-19 and other prothrombotic phenotypes

El sistema hemostático actúa en concierto con la inflamación, de forma que tras la respuesta inflamatoria diversos mediadores activan el sistema hemostático a través de disfunción endotelial, activación plaquetar y de coagulación, promoviendo la trombosis, lo que se ha denominado tromboinflamación. En este proceso adquiere especial relevancia el inflamasoma, cuya estimulación promueve respuestas inmunes innata y adaptativa. La activación del inflamasoma juega un papel fisiopatológico importante en diversas patologías que cursan con fenómenos inflamatorios y trombóticos. El papel de la tromboinflamación se ha puesto de relevancia en la pandemia por COVID-19, en la que se ha descrito una tormenta de citocinas como uno de los mecanismos responsables

The haemostatic system acts in concert with inflammation, so that after inflammatory response various mediators activate the haemostatic system through endothelial dysfunction, platelet activation and coagulation promoting thrombosis, which is termed thromboinflammation. In this process, the inflammasome acquires special relevance; its stimulation promotes innate and adaptive immune responses. Inflammasome activation plays an important physiopathological role in several disorders with inflammatory and thrombotic phenomena. The role of thromboinflammation has become relevant in the COVID-19 pandemic, in which a cytokine storm has been described as one of the responsible mechanisms

Opciones terapéuticas en el manejo de Covid-19 grave: una perspectiva de reumatología / Therapeutic options for the management of severe Covid-19: a rheumatology perspective

El inicio del nuevo coronavirus humano del síndrome respiratorio agudo grave (SARS-Cov-2) en Wuhan, China, ha desencadenado un brote respiratorio mundial (COVID-19). El síndrome de insuficiencia respiratoria agua (SIRA), el fallo multiorgánico y eventos trombóticos están entre las causas que llevan a la muerte en pacientes críticamente enfermos con COVID-19. Las citocinas inflamatorias elevadas sugieren que una "tormenta de citocinas", también conocida como síndrome de liberación de citocinas (SLC), puede jugar un papel principal en la patología de COVID-19. Adicionalmente al tratamiento anti-viral y la terapia de apoyo respiratorio en pacientes críticamente enfermos, están en investigación medicamentos únicos para esta condición. En esta revisión sintetizamos la evidencia más actual de opciones terapéuticas, incluyendo anticuerpos anti-citocinas como una estrategia intermedia para la terapia de SARS-Cov-2

The novel SARS-CoV-2 human coronavirus in Wuhan, China, has triggered a worldwide respiratory disease outbreak (COVID-19). Acute respiratory distress syndrome (ARDS), multiorgan dysfunction and thrombotic events are among the leading causes of death in critically ill patients with COVID-19. The elevated inflammatory cytokines suggest that a "cytokine storm", also known as cytokine release syndrome (CRS), may play a major role in the pathology of COVID-19. In addition to anti-viral therapy and supportive treatment in critically ill patients, unique medications for this condition are also under investigation. Here we reviewed therapeutic options, including the antibody therapy that might be an immediate strategy for SARS-CoV-2 therapy

Anakinra, una alternativa potencial en el tratamiento de la infección respiratoria grave por SARS-CoV-2 refractaria a tocilizumab / Anakinra as a potential alternative in the treatment of severe acute respiratory infection associated with SARS-CoV-2 refractory to tocilizumab

El virus SARS-CoV-2 es un nuevo virus RNA causante de la enfermedad COVID-19, declarada como pandemia por la Organización Mundial de la Salud (OMS). Produce un cuadro de neumonía atípica que puede desembocar en un fallo multiorgánico. La desregulación del sistema inmune secundaria a la infección produce un cuadro similar al síndrome de linfohistiocitosis hemofagocítica (SLHH). Varios estudios han definido la importancia que los inhibidores de la IL-6 (tocilizumab) tienen en el tratamiento de la infección por SARS-CoV-2, sin embargo, la indicación de tratamiento con inhibidores de IL-1 (anakinra) no se encuentra establecida de forma clara. Presentamos el caso de un paciente de 51 años con neumonía bilateral secundaria a infección por SARS-CoV-2 refractaria al tratamiento antiviral y anti-IL-6 que presentó mejoría clínica y analítica tras el tratamiento con anti-IL-1 (anakinra)

SARS-CoV-2 is a new RNA virus which causes coronavirus disease 2019 (COVID-19), declared a pandemic by the World Health Organization (WHO). It triggers an atypical pneumonia that can progress to multiorgan failure. COVID-19 can cause dysregulation of the immune system, triggering an inflammatory response, and simulate haemophagocytic lymphohistiocytosis. Several studies have proposed that anti-IL-6 receptor antibodies, such as tocilizumab, play an important role in the treatment of severe acute respiratory infection associated with SARS-CoV-2. However, the role of anti-IL-1 receptor antibodies, such as anakinra, in the treatment of COVID-19 has not been established. We present a case report of a 51-year-old man diagnosed with severe respiratory infection associated with SARS-CoV-2 that was refractory to antiviral and anti-IL-6 treatment, with a favourable clinical outcome and analytical improvement after treatment with anti-IL-1 (anakinra)

Elevated serum levels of interleukin-37 correlate with poor prognosis in gastric cancer

Background: interleukin-37 (IL-37) is as a natural suppressor of the innate inflammatory and immune responses. It has also been reported to be involved in carcinogenesis and metastasis. The present case-control study was designed to investigate the role of serum levels of IL-37 in patients with gastric cancer. Methods: serum IL-37 levels were determined using the enzyme-linked immunosorbent assay in 180 patients diagnosed with gastric cancer and 100 healthy controls. The association between IL-37 levels and clinical factors was assessed. Univariate and multivariate analyses were performed to investigate the prognostic significance of these parameters in gastric cancer. Results: serum IL-37 levels in gastric cancer patients (5.606 +/- 0.837 pg/ml) were significantly higher than those in healthy controls (2.364 +/- 0.210 pg/ml, p < 0.001). High serum IL-37 levels were related to a poorly differentiated histologic type (p = 0.046) and advanced T stage (p = 0.003). The Kaplan-Meier survival analysis indicated that the high-IL-37 group had a poorer overall survival and progression-free survival (overall survival [OS]: 39.0 months vs 13.0 months, p < 0.001, progression-free survival [PFS]: 25.0 months vs 10.0 months, p < 0.001). Multivariate analyses showed serum IL-37 to be an independent prognostic factor for gastric cancer patients (OS: hazard ratios [HR] = 1.842, 95% CI: 1.190-2.854, p = 0.006; PFS: HR = 1.547, 95% CI: 1.014-2.359, p = 0.043). Conclusions: in conclusion, serum IL-37 levels were associated with poor overall survival and progression-free survival in gastric cancer patients. IL-37 may be a potential predictor of prognosis in gastric cancer

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Utilidad de la calprotectina sérica como biomarcador de actividad inflamatoria en la enfermedad inflamatoria intestinal / The use of serum calprotectin as a biomarker for inflammatory activity in inflammatory bowel disease

Introducción: para el correcto manejo de la enfermedad inflamatoria intestinal (EII) precisamos de marcadores no invasivos, fiables y sencillos que permitan detectar la actividad inflamatoria de forma precoz. Uno de estos marcadores biológicos podría ser la calprotectina sérica (CS). Material y métodos: inclusión prospectiva de pacientes con EII que iban a realizarse una colonoscopia por práctica clínica habitual. Se determinaron: CS, calprotectina fecal (CF) y parámetros analíticos convencionales. Se realizaron los índices clínicos (Harvey y Walmsley) así como los endoscópicos correspondientes en cada escenario (Simple Endoscopic Score Crohn Disease [SES-CD] y Mayo). Resultados: se incluyeron 53 pacientes; el 51% (27 pacientes) con colitis ulcerosa (CU) y el 49% (26 pacientes) con enfermedad de Crohn (EC). En CU los valores de CS fueron significativamente superiores con actividad endoscópica Mayo 2/3 (mediana 10,39 mg/ml [IQR: 7,4-12,2]) frente aquellos con Mayo 0/1 (mediana 4,07mg/ml [IQR: 2,9-7,2]) (p = 0,01). El área bajo la curva ROC (AUCROC) fue 0,85, obteniendo para un punto de corte de CS de 4,4 mg/dl una sensibilidad y especificidad del 83,3% y 81,25%, respectivamente. Además, al comparar con otros marcadores serológicos de actividad (proteína C reactiva [PCR], velocidad de sedimentación globular [VSG], hemoglobina [Hb] y plaquetas) se obtuvo un AUCROC superior. Cuando comparamos la CS con los hallazgos endoscópicos en EC, no hubo diferencias estadísticamente significativas (SES CD > 3: 20,1 [IQR: 16,8-23,4] vs. SESC ≤ 3:6,25 [IQR: 5,4-7,1]) (p = 0,8). Conclusiones: la CS es un buen marcador indirecto de la actividad inflamatoria y existe correlación con los hallazgos endoscópicos en CU, aunque sin diferencias estadísticamente significativas en EC

Introduction: simple, reliable and non-invasive biomarkers are needed to enable the early detection of inflammatory activity for the correct management of inflammatory bowel disease (IBD). One of these biomarkers may be serum calprotectin (SC). Material and methods: a prospective study was performed of patients with IBD due to undergo a colonoscopy as part of the common clinical practice. The study parameters included SC, fecal calprotectin (FC) and conventional blood test parameters. Clinical indices (Harvey and Walmsley) and relevant endoscopic scores were completed for each scenario (Simple Endoscopic Score Crohn Disease [SES-CD] and Mayo). Results: fifty-three patients were included in the study, 51% (27 patients) with ulcerative colitis (UC) and 49% (26 patients) with Crohn's disease (CD). The CS values in UC were significantly higher with an endoscopic Mayo score 2/3 (median score 10.39 mg/ml [IQR: 7.4-12.2]) compared to those with a Mayo score of 0/1 (median 4.07 mg/ml [IQR: 2.9-7.2]) (p = 0.01). The area under the ROC curve (AUCROC) was 0.85 and the sensitivity and specificity were 83.3% and 81.25%, respectively, for a SC cut-off point of 4.4 mg/dl. Furthermore, a higher AUCROC was obtained in comparison with other serological markers for activity (C-reactive protein [CRP], erythrocyte sedimentation rate [ESR], hemoglobin [Hb] and platelets). There were no statistically significant differences in the comparison between SC and endoscopic findings in CD (SES CD > 3: 20.1 [IQR: 16.8-23.4] vs SESC ≤ 3:6.25 [IQR: 5.4-7.1]) (p = 0.8). Conclusions: SC is a good indirect marker of inflammatory activity and there was a correlation with endoscopic findings in UC. However, there were no statistically significant differences in the case of CD

Estrogen and estrogen receptor signaling promotes allergic immune responses: Effects on immune cells, cytokines, and inflammatory factors involved in allergy

Hypersensitivity occurs when the body is stimulated by an antigen, resulting in an immune response, and leads to a physiological disorder or abnormal tissue trauma. Various immune cells, cytokines, and inflammatory mediators are involved in the immune responses related to allergic diseases, which are the core of anaphylaxis. Estrogen receptors are widely distributed in immune cells, which combine with estrogen and participate in allergic responses by affecting immune cells, cytokines, and inflammatory factors. We aimed to summarize the association between estrogen and allergic reactions to provide a scientific basis for understanding and studying the mechanisms of allergic diseases

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Terapias antiinflamatorias para la enfermedad cardiovascular: vías de señalización y mecanismos / Anti-inflammatory therapies for cardiovascular disease: signaling pathways and mechanisms

Las enfermedades cardiovasculares (ECV) son una manifestación clínica de la ateroesclerosis, una enfermedad inflamatoria que se agrava en presencia de diferentes factores de riesgo como la dislipemia o la diabetes mellitus tipo 2. Los eventos cardiovasculares agudos son resultado de un proceso inflamatorio crónico no resuelto que facilita la rotura de placas inestables. Los tratamientos existentes reducen los factores de riesgo, pero no previenen los eventos isquémicos recurrentes en pacientes con riesgo residual inflamatorio caracterizado por altas concentraciones de proteína C reactiva. Una mejor comprensión del papel de la inmunidad innata y adaptativa en la ateroesclerosis ha llevado a la investigación de tratamientos antiinflamatorios para la ECV. Algunos ensayos clínicos consisten en la evaluación de dosis bajas de fármacos diseñados para otras enfermedades inflamatorias sistémicas con alto riesgo de ECV, como la artritis reumatoide y la soriasis. Otras investigaciones son estudios restrospectivos y metanálisis de la incidencia de ECV en ensayos clínicos que han evaluado diferentes fármacos en las enfermedades. Otras terapia, sin embargo, se basan en ensayos preclínicos, como las vacunas. En este manuscrito se resumen las principales estrategias antiinflamatorias y los mecanismos moleculares asociados que se están evaluando en ensayos clínicos o preclínicos

Cardiovascular diseases (CVD) are the clinical manifestation of atherosclerosis, a chronic inflammatory disease promoted by several risk factors such as dyslipidemia, type 2 diabetes mellitus, hypertension, and smoking. Acute CVD events are the result of an unresolved inflammatory chronic state that promotes the rupture of unstable plaque lesions. Of note, the existing intensive therapies modify risk factors but do not prevent life-threatening recurrent ischemic events in high-risk patients, who have a residual inflammatory risk displayed by increased C-reactive protein (CRP) levels. Better understanding of the role of innate and adaptive immunity in plaque development and rupture has led to intensive investigation of anti-inflammatory strategies for CVD. Some of them are being tested in specific clinical trials and use lower doses of existing medications originally developed for other inflammatory diseases such as rheumatoid arthritis and psoriasis, which have high CVD risk. Other investigations are retrospective and meta-analyses of existing clinical trials that evaluate the incidence of CVD in these inflammatory diseases. Others are based on preclinical testing such as vaccines. In this article, we summarize the main anti-inflammatory strategies and associated molecular mechanisms that are being evaluated in preclinical or clinical CVD studies

La relación bidireccional entre el cáncer y la ateroesclerosis / The two-way relationship between cancer and atherosclerosis

En los últimos años ha emergido un interés creciente sobre la relación entre el cáncer y las enfermedades cardiovasculares. El aumento de la esperanza de vida de ambas enfermedades ha condicionado su coexistencia cada vez más frecuente en un mismo paciente, con lo cual se ponen de relieve reacciones adversas farmacológicas que suponen un mayor riesgo para los pacientes. Esto es especialmente relevante en el caso de la ateroesclerosis, que parece compartir un sustrato fisiopatológico común con el cáncer. En esta revisión se analizan estos factores de riesgo comunes y de forma específica la relación entre los diferentes tratamientos del cáncer y el riesgo de enfermedad coronaria o cerebrovascular, así como la evidencia científica actual sobre la posible relación entre la terapia antiagregante y el riesgo de cáncer. Se repasan también de manera bidireccional la incidencia y el pronóstico del cáncer en pacientes con ateroesclerosis y viceversa, documentado en la información de los últimos estudios publicados en el campo de la cardiooncología

In the last few years, there has been growing interest in the relationship between cancer and cardiovascular disease. The increase in life expectancy in both diseases has led to their frequent coexistence in the same patient, which can lead to adverse drug reactions that increase patient risk. This is especially relevant in the case of atherosclerosis, which seems to share a common pathophysiological substrate with cancer. In this review, we analyze these common risk factors, and specifically analyze the relationship between different cancer treatments with the risk of coronary or cerebrovascular disease, as well as the current scientific evidence on the possible relationship between antiplatelet therapy and cancer risk. We also review the incidence and prognosis of cancer in patients with atherosclerosis and vice versa, based on the information reported in the most recently published studies in the field of cardio-oncology

Mediterranean diet and asthma: time for clinical trials in children

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