Friday, March 26, 2021 3:39:38 PM
https://www.mayoclinicproceedings.org/article/S0025-6196(20)30989-7/fulltext
Targeting individual cytokines downstream in the inflammatory cascade of CRS, such as IL-6, have not shown improved clinical outcomes in COVID-19. However, the clinical benefit observed with broad immunosuppression with dexamethasone suggests that a hyper-inflammatory immune response is pathologic in latter stages of COVID-19. Neutralization of GM-CSF, which is upstream in the CRS cascade, may provide better suppression of the hyper-inflammatory immune response than IL-6 receptor antagonists alone while sparing the lympholytic effects of broad immunosuppression with steroids.
That is good, not bad. Why wait until they are in bad shape to treat? There is considerable evidence that treating critical patients is too late. They are too far gone by that time.
https://www.mayoclinicproceedings.org/article/S0025-6196(20)30989-7/pdf
The time to clinical improvement was significantly shorter for the
lenzilumab-treated group compared with the untreated cohort with a median of 5 days versus 11 days
(P¼.006). Similarly, the proportion of patients with acute respiratory distress syndrome (oxygen
saturation/fraction of inspired oxygen<315 mm Hg) was significantly reduced over time when treated
with lenzilumab compared with untreated (P<.001). Significant improvement in inflammatory
markers (C-reactive protein and interleukin 6) and markers of disease severity (absolute lymphocyte
count) were observed in patients who received lenzilumab, but not in untreated patients. Cytokine
analysis showed a reduction in inflammatory myeloid cells 2 days after lenzilumab treatment. There
were no treatment-emergent adverse events attributable to lenzilumab.
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