Respiratory failure & ventilation
Temporal stability of phenotypes of acute respiratory distress syndrome: clinical implications for early corticosteroid therapy and mortality
Authors' conclusion
Characterization of inflammatory ARDS phenotypes using clinical surrogate data allows physicians to monitor patients throughout the course of the disease and guide clinical treatment. Corticosteroids may be beneficial in hyperinflammatory ARDS and harmful in hypoinflammatory ARDS.
Study context
- Population
- Patients with acute respiratory distress syndrome (ARDS); six multicentre RCTs (development n = 1207; validation n = 2751) and a retrospective investigation cohortretrospective investigation cohort
- Participants
- 5,578 patients
- Comparison
- Corticosteroids vs no corticosteroids by inflammatory ARDS phenotype
- Hyperinflammatoryn = 2,169
- Hypoinflammatoryn = 3,409
- Primary endpoint
- Corticosteroid effect on 30-day mortality depending on phenotype
- Follow-up
- 30 days
Methodological detailsindividual patient data, AI clinical classifier development and validation, discrete-time Bayesian Markov model, target trial emulation, longitudinal logistic regression
- Individual patient data
- AI clinical classifier development and validation
- Discrete-time Bayesian Markov model
- Target trial emulation
- Longitudinal logistic regression
Primary result
As reported in the abstract
Further findings
30-day mortality by phenotype
P < 0.001
Phenotype transition from baseline · Over 30 days
P < 0.001
Transitioned to hypoinflammatory Hyperinflammatory 1072/2169
Transitioned to hyperinflammatory Hypoinflammatory 229/3409
Corticosteroid response at day 3 in patients who remained hyperinflammatory
| aOR (95% CI) | P value | ||
|---|---|---|---|
| Remained hyperinflammatoryPositive response only persisted in this subgroup | 0.51 (0.32–0.80) | P = 0.004 | |
| 0.20.5125Adjusted odds ratio (log scale) |
Original publication
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