Is the long-term mortality similar in COVID-19 and community-acquired pneumonia?

Introduction: There are no data on the association of type of pneumonia and long-term mortality by the type of pneumonia (COVID-19 or community-acquired pneumonia [CAP]) on long-term mortality after an adjustment for potential confounding variables. We aimed to assess the type of pneumonia and risk factors for long-term mortality in patients who were hospitalized in conventional ward and later discharged. Methods: Retrospective analysis of two prospective and multicentre cohorts of hospitalized patients with COVID-19 and CAP. The main outcome under study was 1-year mortality in hospitalized patients in conventional ward and later discharged. We adjusted a Bayesian logistic regression model to assess associations between the type of pneumonia and 1-year mortality controlling for confounders. Results: The study included a total of 1,693 and 2,374 discharged patients in the COVID-19 and CAP cohorts, respectively. Of these, 1,525 (90.1%) and 2,249 (95%) patients underwent analysis. Until 1-year follow-up, 69 (4.5%) and 148 (6.6%) patients from the COVID-19 and CAP cohorts, respectively, died (p = 0.008). However, the Bayesian model showed a low probability of effect (PE) of finding relevant differences in long-term mortality between CAP and COVID-19 (odds ratio 1.127, 95% credibility interval 0.862-1.591; PE = 0.774). Conclusion: COVID-19 and CAP have similar long-term mortality after adjusting for potential confounders.

Cyclooxygenase-2 is up-regulated in lung parenchyma of chronic obstructive pulmonary disease and down-regulated in idiopathic pulmonary fibrosis.

BACKGROUND AND AIM OF THE WORK: In vitro studies have suggested that fibroblasts from idiopathic pulmonary fibrosis (IPF) may have an impaired induction of cyclooxygenase (Cox)-2. We have investigated Cox-1 and Cox-2 expression in lung tissue from IPF. METHODS: Cox-1 and Cox-2 expression were determined using RT-competitive PCR and immunohistochemistry in pulmonary biopsies from IPF (n = 22), chronic obstructive pulmonary disease (COPD) (n = 13), and lung tissue from subjects undergoing pleurodesis for spontaneous pneumothorax (control group, n = 17). RESULTS: Immunohistochemical analysis showed that the score of Cox-2 positive cells was higher in COPD (1 +/- 0) with respect to fibrosis (0.37 +/- 0.1, p < 0.05) and controls (0.57 +/- 0.2). There were no differences between fibrosis and controls in Cox-2 positive cells. The expression of Cox-2 mRNA was significantly higher in COPD (3.26 +/- 0.72 x 10(6) molecules cDNA/microg total RNA) in comparison to IPF (0.57 +/- 0.17) and controls (0.54 +/- 0.16) (p < 0.001). After IL-1beta stimulation (1-10 ng/ml) Cox-2 mRNA basal expression increased significantly in controls (from 35 +/- 12 to 94 +/- 4 x10(6) molecules cDNA/microg total RNA, p < 0.01) and in COPD (from 38 +/- 8 to 92 +/- 3, p < 0.01). In contrast, no significant changes in Cox-2 mRNA expression were found in IPF (from 30 +/- 12 to 43 +/- 16). CONCLUSIONS: Our results suggest that differences in Cox-2 expression may play a role in the regulation of inflammatory responses in lung diseases. Excessive activity is associated with the development of chronic obstructive lung disease, while a limited activation following pro-inflammatory stimulation might contribute to fibrogenic responses.

[Outcomes and clinical characteristics of patients with pulmonary fibrosis and respiratory failure admitted to an intensive care unit. A study of 20 cases]. / Características clínicas y pronóstico de los pacientes con fibrosis pulmonar que ingresan en cuidados intensivos por insuficiencia respiratoria. Análisis de 20 casos.

BACKGROUND AND OBJECTIVE: Previous reports on the outcome of patients with pulmonary fibrosis admitted to the intensive care unit (ICU) suggest a bad prognosis. The aim of our study was to evaluate the course and prognosis of patients with pulmonary fibrosis admitted to the ICU of our hospital because of acute respiratory failure. PATIENTS AND METHOD: Retrospective, case-series, observational study. We evaluated the clinical records of patients with pulmonary fibrosis referred to the intensive care unit in a tertiary university teaching hospital between January 1986 and June 2002. Complete information on the diagnosis and clinical course of the pulmonary disease, pulmonary function tests, current clinical status, ventilatory support and adjunctive therapies applied in the ICU, length of stay and mortality was collected. RESULTS: Twenty patients were included, 14 with idiopathic pulmonary fibrosis and 6 with pulmonary fibrosis and associated collagen vascular diseases. The mean (SD) interval between the diagnosis of fibrosis and the admission to ICU was 14 (20) months. All patients presented with severe acute respiratory failure (PaO2/FiO2 < 200). The cause of clinical worsening was identified in 8 (40%) cases (5 bacterial and 3 fungal infections). In the ICU, 17 patients required mecanical ventilation. All patients worsened progressively, with refractory hypoxemic respiratory failure (100%) and hemodynamic instability after endotraqueal intubation (70%). Mechanical ventilation was associated with a 100% mortality. CONCLUSION: An identifiable cause of acute respiratory failure could not be found in a significant proportion of patients despite a systematic work-up. Mechanical ventilation and aggressive life support measures do not seem to provide any further benefit in patients with pulmonary fibrosis and severe respiratory failure.

Características clínicas y pronóstico de los pacientescon fibrosis pulmonar que ingresan en cuidadosintensivos por insuficiencia respiratoria.Análisis de 20 casos / Outcomes and clinical characteristics of patients with pulmonary fibrosis and respiratory failure admitted to an intensive care unit. A study of 20 cases

FUNDAMENTO Y OBJETIVO: Diversos estudios indican que el pronóstico global de los pacientes con fibrosis pulmonar que ingresan en unidades de cuidados intensivos (UCI) es muy malo. El objetivo de este trabajo fue investigar la evolución y el pronóstico de los pacientes con fibrosis pulmonar que requieren ingreso en cuidados intensivos por insuficiencia respiratoria aguda. PACIENTES Y MÉTODO: Estudio observacional retrospectivo de serie de casos. Se evaluó a los pacientes con fibrosis pulmonar ingresados en la UCI de un hospital terciario entre enero de 1986 y junio de 2002. Se recogieron datos sobre el diagnóstico de base, evolución clínica y tratamiento, estudio funcional respiratorio, ingreso actual, abordaje clínico, ventilación mecánica, comportamiento mecánico y gasométrico, días de estancia y mortalidad. RESULTADOS: Se incluyó a 20 pacientes, 14 con fibrosis pulmonar idiopática y 6 con fibrosis asociada a colagenosis. El tiempo medio (DE) transcurrido desde el diagnóstico de fibrosis hasta el ingreso en la UCI fue de 14 (20) meses. Todos presentaban insuficiencia respiratoria grave (PaO2/FiO2 < 200). La causa de la insuficiencia respiratoria se identificó en 8 casos (en 5 era una infección bacteriana y en 3 una infección fúngica). En los 12 casos restantes (60 por ciento) no se identificó ningún agente causal. Durante el ingreso en la UCI 17 pacientes precisaron ventilación mecánica; en los tres casos restantes se limitó el esfuerzo terapéutico. Todos, sin excepción, presentaron una mala evolución, destacando la alta incidencia de hipoxemia refractaria (100 por ciento) e inestabilidad hemodinámica grave tras la intubación (70 por ciento). Tanto la mortalidad asociada a la ventilación mecánica como la mortalidad intrahospitalaria fueron del 100 por ciento. CONCLUSIÓN: El desencadenante de la insuficiencia respiratoria y el deterioro clínico no son identificables en una proporción significativa de pacientes a pesar de una aproximación diagnóstica sistemática. La ventilación mecánica y las medidas de soporte vital agresivo no parecen ofrecer ningún beneficio a los pacientes con fibrosis pulmonar que ingresan en UCI por insuficiencia respiratoria (AU)

Transforming growth factor-beta1 gene polymorphisms are associated with disease progression in idiopathic pulmonary fibrosis.

Transforming growth factor-beta1 (TGF-beta1) is a cytokine that plays a key role in the development of idiopathic pulmonary fibrosis. There have been reports on the presence of two genetic polymorphisms in the DNA sequence encoding the leader sequence of the TGF-beta1 protein, located in codons 10 and 25. The objective of this study was to investigate the association between TGF-beta1 gene polymorphisms in codons 10 and 25 and the susceptibility to idiopathic pulmonary fibrosis and the progression of the disease. Compared with healthy control subjects (n = 140), patients with idiopathic pulmonary fibrosis (n = 128) showed no significant deviations in genotype or allele frequencies. One hundred and ten patients with idiopathic pulmonary fibrosis were followed up for 30.3 +/- 25 months. The presence of a proline allele at codon 10 was independently associated with a significant increase in alveolar arterial oxygen tension difference during follow-up, after controlling for the effect of treatment (coefficient = 0.59; 95% confidence intervals, 0.23 to 0.96; p = 0.002). These findings suggest that (1) TGF-beta1 gene polymorphisms in codons 10 and 25 do not predispose to the development of idiopathic pulmonary fibrosis; and (2) TGF-beta1 gene polymorphisms may affect disease progression in patients with idiopathic pulmonary fibrosis.