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INTRODUCTION: This study was aimed to identify risk factors associated with unfavorable outcomes (composite outcome variable: mortality and need for mechanical ventilation) in patients hospitalized in Galicia with COVID-19 pneumonia. METHODS: Retrospective, multicenter, observational study carried out in the 8 Galician tertiary hospitals. All Patients admitted with confirmed COVID-19 pneumonia from 1st of March to April 24th, 2020 were included. A multivariable logistic regression analysis was performed in order to identify the relationship between risk factors, therapeutic interventions and the composite outcome variable. RESULTS: A total of 1292 patients (56.1% male) were included. Two hundred and twenty-five (17.4%) died and 327 (25.3%) reached the main outcome variable. Age [odds ratio (OR) = 1.03 (95% confidence interval (CI): 1.01-1.04)], CRP quartiles 3 and 4 [OR = 2.24 (95% CI: 1.39-3.63)] and [OR = 3.04 (95% CI: 1.88-4.92)], respectively, Charlson index [OR = 1.16 (95%CI: 1.06-1.26)], SaO2 upon admission [OR = 0.93 (95% CI: 0.91-0.95)], hydroxychloroquine prescription [OR = 0.22 (95%CI: 0.12-0.37)], systemic corticosteroids prescription [OR = 1.99 (95%CI: 1.45-2.75)], and tocilizumab prescription [OR = 3.39 (95%CI: 2.15-5.36)], significantly impacted the outcome. Sensitivity analysis using different alternative logistic regression models identified consistently the ratio admissions/hospital beds as a predictor of the outcome [OR = 1.06 (95% CI: 1.02-1.11)]. CONCLUSION: These findings may help to identify patients at hospital admission with a higher risk of death and may urge healthcare authorities to implement policies aimed at reducing deaths by increasing the availability of hospital beds.
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Antivirais/uso terapêutico , COVID-19/mortalidade , COVID-19/terapia , Corticosteroides/uso terapêutico , Idoso , Idoso de 80 Anos ou mais , COVID-19/epidemiologia , Comorbidade , Feminino , Hospitais/estatística & dados numéricos , Humanos , Hidroxicloroquina/uso terapêutico , Masculino , Pessoa de Meia-Idade , Respiração Artificial , Estudos Retrospectivos , Fatores de Risco , Espanha/epidemiologia , Resultado do TratamentoRESUMO
No disponible
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Humanos , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Fenótipo , Suscetibilidade a Doenças/epidemiologia , Exacerbação dos SintomasRESUMO
No disponible
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Humanos , Eosinófilos , Doença Pulmonar Obstrutiva Crônica , Administração por Inalação , CorticosteroidesRESUMO
No disponible
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Humanos , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Doença Pulmonar Obstrutiva Crônica/história , Eosinofilia/epidemiologia , Eosinofilia/genética , Fenótipo , Espirometria/instrumentação , Espirometria/métodos , EspirometriaRESUMO
La enfermedad pulmonar obstructiva crónica (EPOC) supone un grave problema de salud pública en nuestro país. La EPOC es una enfermedad tratable, prevenible e infradiagnosticada. El estudio EPISCAN reveló una prevalencia en España del 10,2% entre individuos de 40-80 años, con un infradiagnóstico del 73%. En atención primaria ocupa un 8,5% de todas las consultas, con un impacto económico muy elevado. Estos pacientes presentan un cierto grado de inflamación sistémica caracterizado por un aumento de la concentración plasmática de algunos mediadores inflamatorios, como IL-1, IL-6, IL-8, PCR o TNF alfa, que también están relacionados con alteraciones endoteliales y la arteriosclerosis. En el continuo de la EPOC, las comorbilidades que con más frecuencia aparecen son: cardiopatía isquémica, insuficiencia cardíaca, ictus, hipertensión arterial, diabetes mellitus tipo 2, insuficiencia renal, osteoporosis, miopatía, ansiedad, depresión, deterioro cognitivo, desnutrición, anemia y cáncer de pulmón
Chronic obstructive pulmonary disease (COPD) is a serious public health problem in our country. COPD is a treatable and preventable disease which is underdiagnosed. The EPISCAN study revealed a prevalence of 10.2% in Spain between individuals of 40-80 years, with 73% underdiagnosis. In Primary Care occupies 8.5% of all queries with a high economic impact. These patients exhibit some degree of systemic inflammation characterized by increased plasma levels of some inflammatory mediators such as IL-1, IL-6, IL-8, CRP and TNF, which are also related to endothelial disorders and arteriosclerosis. In the continuum of COPD, comorbidities most frequently appear are: ischemic heart disease, heart failure, stroke, hypertension, type 2 diabetes mellitus, renal failure, osteoporosis, myopathy, anxiety, depression, cognitive impairment, malnutrition, anemia and lung cancer
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Humanos , Doença Pulmonar Obstrutiva Crônica/complicações , Doenças Cardiovasculares/epidemiologia , Fatores de Risco , Mediadores da Inflamação/análise , Inflamação/fisiopatologiaRESUMO
No disponible
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Humanos , Medicina , Física , Volume Expiratório Forçado , Previsões , Probabilidade , Pneumologia , Valores de ReferênciaRESUMO
La sarcoidosis es una enfermedad pleomórfica que en ocasiones puede presentar hipertensión pulmonar (HP). Existe poca información sobre la asociación de estas 2 enfermedades, en muchos casos de pequeñas series de pacientes enviados para trasplante. Presentamos 4 casos con afectación pulmonar leve en los que se realizó cateterismo derecho y se utilizó tratamiento específico para HP. Tras consentimiento informado, se hizo un estudio genético que mostró mutaciones en genes relacionados con HP en 3 pacientes. Se trata del primer estudio que proporciona información genética en este tipo de HP
Sarcoidosis is a pleomorphic disease that can present with pulmonary hypertension (PH). What little information is available about the association of these two diseases comes mainly from small series of patients scheduled for transplant. We present 4 cases of mild pulmonary involvement in whom right catheterisation was performed and PH-specific therapy was administered. After obtaining written consent, a genetic study was performed that showed mutations in PH-related genes in 3 of the patients. This is the first study of its kind to yield genetic information for this type of PH
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Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Hipertensão Pulmonar/complicações , Hipertensão Pulmonar/genética , Sarcoidose/complicações , Sarcoidose/genética , Análise Mutacional de DNA/métodos , Mutagênese , Mutagênese/fisiologia , Consentimento Livre e Esclarecido , Cateterismo/métodosAssuntos
Medicina , Física , Volume Expiratório Forçado , Previsões , Humanos , Probabilidade , Pneumologia , Valores de ReferênciaRESUMO
Chronic obstructive pulmonary disease (COPD) is a serious public health problem in our country. COPD is a treatable and preventable disease which is underdiagnosed. The EPISCAN study revealed a prevalence of 10.2% in Spain between individuals of 40-80 years, with 73% underdiagnosis. In Primary Care occupies 8.5% of all queries with a high economic impact. These patients exhibit some degree of systemic inflammation characterized by increased plasma levels of some inflammatory mediators such as IL-1, IL-6, IL-8, CRP and TNF, which are also related to endothelial disorders and arteriosclerosis. In the continuum of COPD, comorbidities most frequently appear are: ischemic heart disease, heart failure, stroke, hypertension, type 2 diabetes mellitus, renal failure, osteoporosis, myopathy, anxiety, depression, cognitive impairment, malnutrition, anemia and lung cancer.
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Doenças Cardiovasculares/epidemiologia , Inflamação/epidemiologia , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Doenças Cardiovasculares/fisiopatologia , Humanos , Inflamação/fisiopatologia , Mediadores da Inflamação/sangue , Pessoa de Meia-Idade , Prevalência , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Fatores de Risco , Espanha/epidemiologiaRESUMO
Sarcoidosis is a pleomorphic disease that can present with pulmonary hypertension (PH). What little information is available about the association of these two diseases comes mainly from small series of patients scheduled for transplant. We present 4 cases of mild pulmonary involvement in whom right catheterisation was performed and PH-specific therapy was administered. After obtaining written consent, a genetic study was performed that showed mutations in PH-related genes in 3 of the patients. This is the first study of its kind to yield genetic information for this type of PH.
Assuntos
Hipertensão Pulmonar/etiologia , Sarcoidose/complicações , Receptores de Proteínas Morfogenéticas Ósseas Tipo II/deficiência , Receptores de Proteínas Morfogenéticas Ósseas Tipo II/genética , Bosentana , Progressão da Doença , Epoprostenol/análogos & derivados , Epoprostenol/uso terapêutico , Evolução Fatal , Feminino , Humanos , Hipertensão Pulmonar/tratamento farmacológico , Hipertensão Pulmonar/fisiopatologia , Canal de Potássio Kv1.5/deficiência , Canal de Potássio Kv1.5/genética , Masculino , Pessoa de Meia-Idade , Mutação , Fenilpropionatos/uso terapêutico , Mutação Puntual , Piridazinas/uso terapêutico , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Testes de Função Respiratória , Sarcoidose/genética , Citrato de Sildenafila/uso terapêutico , Sulfonamidas/uso terapêutico , Tadalafila/uso terapêutico , Resultado do TratamentoRESUMO
Introducción: La hipertensión arterial pulmonar (HAP) es una enfermedad en la que se implican, entre otras, la vía del óxido nítrico (NO). Se ha descrito un polimorfismo en el gen de la sintasa inducible del NO (NOS2) que consiste en la repetición del pentanucleótido CCTTT dando lugar a menor producción de NO. El objetivo del estudio fue conocer si este polimorfismo incrementa la susceptibilidad para desarrollar HAP. Métodos: Se compararon 64 pacientes diagnosticados de HAP grupos I y IV y 50 controles sanos. Mediante PCR se genotiparon las muestras de ADN para este polimorfismo. Se comparó la distribución en ambos grupos y se correlacionó con parámetros clínicos, hemodinámicos y respuesta terapéutica. Resultados: Se observó una distribución significativamente diferente en el número de repeticiones entre pacientes y controles (p < 0,0001). Agrupando las muestras en formas cortas (ambos alelos con menos de 12 repeticiones) y largas (≥ 12 repeticiones) se observó que los primeros tenían un riesgo casi 4 veces superior de desarrollar HAP (odds ratio: 3,83; IC 95%: 1,19-12,32; p = 0,024). No hubo diferencias entre los tipos más frecuentes de HAP ni en la respuesta terapéutica o supervivencia. No existió correlación entre parámetros hemodinámicos y el número de repeticiones en los pacientes, solo débil correlación con la presión arterial pulmonar sistólica. Conclusiones: Existen diferencias significativas en la distribución del polimorfismo CCTTT del gen NOS2 entre pacientes con HAP y población sana. Una menor repetición del pentanucleótido CCTTT en el gen de la NOS2 podría incrementar el riesgo de desarrollar HAP
Introduction: One of the pathways involved in pulmonary arterial hypertension (PAH) is the nitric oxide (NO) pathway. A polymorphism in the inducible NO synthase (NOS2) gene has been described, consisting of the CCTTT pentanucleotide repeat, which causes a reduction in NO production. The aim of this study was to determine if this polymorphism increases susceptibility to developing PAH. Methods: Sixty-four patients with a diagnosis of PAH groups I and IV and 50 healthy controls were compared. DNA genotyping of the samples for this polymorphism was performed using PCR. The distribution between both groups was compared and correlated with clinical and hemodynamic parameters and therapeutic response. Results: A significantly different distribution was observed in the number of repeats between patients and controls (P < 0.0001). When the samples were categorized by short forms (both alleles with less than 12 repeats) and long forms (≥12 repeats), it was observed that the former had an almost 4-fold risk of developing PAH (odds ratio: 3.83; 95% CI: 1.19-12.32, P = 0.024). There were no differences between the most common types of PAH, either in therapeutic response or survival. There was no correlation between hemodynamic parameters and the number of repeats in the patients, and only a weak correlation with systolic PAH. Conclusions: There are significant differences in the distribution of the NOS2 promotor CCTTT polymorphism between patients with PAH and the healthy population. A minor CCTTT pentanucleotide repeat in the NOS2 gene may increase the risk of developing PAH
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Humanos , Hipertensão Pulmonar/fisiopatologia , Óxido Nítrico Sintase/farmacocinética , Biomarcadores/análise , Fatores de Risco , Polimorfismo Genético , Marcadores Genéticos , Predisposição Genética para Doença , Estudos de Casos e ControlesRESUMO
INTRODUCTION: One of the pathways involved in pulmonary arterial hypertension (PAH) is the nitric oxide (NO) pathway. A polymorphism in the inducible NO synthase (NOS2) gene has been described, consisting of the CCTTT pentanucleotide repeat, which causes a reduction in NO production. The aim of this study was to determine if this polymorphism increases susceptibility to developing PAH. METHODS: Sixty four patients with a diagnosis of PAH groupsi and iv and 50 healthy controls were compared. DNA genotyping of the samples for this polymorphism was performed using PCR. The distribution between both groups was compared and correlated with clinical and haemodynamic parameters and therapeutic response. RESULTS: A significantly different distribution was observed in the number of repeats between patients and controls (P<.0001). When the samples were categorised by short forms (both alleles with less than 12repeats) and long forms (≥12 repeats), it was observed that the former had an almost 4-fold risk of developing PAH (odds ratio: 3.83; 95%CI: 1.19-12.32, P=.024). There were no differences between the most common types of PAH, either in therapeutic response or survival. There was no correlation between haemodynamic parameters and the number of repeats in the patients, and only a weak correlation with systolic PAH. CONCLUSIONS: There are significant differences in the distribution of the NOS2 promotor CCTTT polymorphism between patients with PAH and the healthy population. A minor CCTTT pentanucleotide repeat in the NOS2 gene may increase the risk of developing PAH.