Preprint IL-6 Receptor Antagonists and Severe Post-COVID-19 Outcomes: An Emulated Target Trial, 2026, Butzin-Dozier et al.

SNT Gatchaman

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IL-6 Receptor Antagonists and Severe Post-COVID-19 Outcomes: An Emulated Target Trial
Zachary Butzin-Dozier; Manav Kumar; Yunwen Ji; Lin-Chiun Wang; A Jerrod Anzalone; Eric Hurwitz; Rena C Patel; Rachel Wong; Carolyn Bramante; Benjamin Sines; on behalf of the National Clinical Cohort Collaborative

BACKGROUND
Interleukin-6 (IL-6) is a cytokine that plays a key role in systemic hyperinflammation and may mediate the relationship between acute COVID-19 and severe long-term outcomes such as Long COVID or death. IL-6 modulating drugs may reduce patients risk of severe post-COVID-19 outcomes.

METHODS
We conducted an emulated target trial in a retrospective cohort of patients with moderate-to-severe rheumatoid arthritis who were prescribed IL-6 receptor antagonists (sarilumab or tocilizumab, pooled treatment) or other biologic agents (anakinra or baricitinib, pooled comparator) in 2022. We compared the 12-month cumulative incidence of mortality and Long COVID (diagnosed and probable) between groups using Super Learner and targeted maximum likelihood estimation, adjusting for covariates of interest.

RESULTS
In our cohort of 3,553 patients, we found that prescription of IL-6 receptor antagonists was associated with a lower 12-month cumulative mortality (adjusted relative risk (aRR) 0.40, 95% CI 0.27, 0.59), diagnosed Long COVID (aRR 0.42, 95% CI 0.23, 0.78), and probable Long COVID (aRR 0.71, 95% CI 0.61, 0.83), compared to prescription of other biologic agents among rheumatoid arthritis patients.

CONCLUSIONS
IL-6 receptor antagonists may prevent the incidence of severe post-COVID-19 outcomes such as Long COVID or mortality. This supports the hypothesis that IL-6 may be a mechanistic biomarker of COVID-19 sequelae and that acute COVID-19 severity may mediate this relationship.

Web | DOI | PDF | Preprint: MedRxiv | Open Access
 
I haven't read the paper - if it is methodologically sound it's yet another hint that trying to figure out ME/CFS without taking into account the acute phase, by only starting to investigate at the 6 months mark, is ridiculous. Biobanks more or less ignoring the temporal dimension of this disease is not helping either. I find it honestly hard to believe how hardly anyone seems to be talking about this. If ME/CFS is 'injury-like', then obviously we have to understand the nature of the original insult better. If the injury/setpoint change is mostly neurological and without clear focal damage that's the best way forward.
 
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