Friend of mine (not local to me) presented at 77% SpO2, dyspnea, cough, febrile and asked for help after refusing to contact his PCP. I convinced him to arrange for emergency transport to a nearby hospital due to pending respiratory failure and hypoxemia while advocating for 5-HT antagonism with cyproheptadine due to likely excessive pulmonary serotonin levels causing localized vasoconstriction and perfusion abnormalities. Classic bilateral ground glass opacities were confirmed via CXR consistent with COVID pathophysiology (of course we already expected this to be the case). Absence of pulmonary thrombi confirmed via CTPE.
Instantly landed in ICU, stabilized with bipap initially and ultimately high flow nasal cannula 85% FiO2 (unsure of flow rate). Over the course of several days, hospital ran typical dex/remdesivir/toci/enoxaparin stack that didn’t provide any noticeable clinical improvement other than reducing FiO2 to 60%.
I began advocating on his behalf for ivermectin by conveying to his ICU doctors the late stage mechanism of action centered around inhibiting an aberrant JAK/STAT pathway likely driven primarily by NF-kB transcription factor. The fact that ivermectin has a strong affinity for multiple viral proteins, human proteases, and BSG (thus potentially inhibiting RBC clumping & clotting probably due to sialic acid binding) was simply gravy at this point (he continued to test positive on nasopharyngeal PCR).
They refused the cyproheptadine but agreed to begin dosing ivermectin at typical 0.2mg/kg.
Within 48 hours of beginning ivermectin dosing, friend went from 60% FiO2 high flow to discharge.