The Novel Coronavirus 2019, was first reported on in Wuhan, China in late December 2019.  The outbreak was declared a public health emergency of international concern in January 2020 and on March 11th, 2020, the outbreak was declared a global pandemic.  The spread of this virus is now global with lots of media attention.  The virus has been named SARS-CoV-2 and the disease it causes has become known as coronavirus disease 2019 (COVID-19).  This new outbreak has been producing lots of hysteria and false truths being spread, however the data surrounding the biology, epidemiology, and clinical characteristics are growing daily, making this a moving target.

REBEL COVID-19

will serve as a summary of what is currently known, how to screen, when to test, and how to prevent spread, and any new data/information on COVID-19.

June 24, 2021

Background: Antibodies targeted at the SARS-CoV2 spike protein are an essential part of the body’s immune response to COVID19 infection. Infection with SARS-CoV2 stimulates the immune system to produce a polyclonal spike protein antibody response in the host. Vaccines have similar results and recent studies show that the antibody response is even more robust than with natural infection. These antibodies bind to numerous locations on the SARS-CoV2 spike protein limiting the virus’s ability to enter and infect host cells. 

One of the many massive challenges of the COVID19 pandemic has been the lack of targeted therapeutics. Extensive efforts have been invested into research with only glimmers of benefit for most drugs. The exception to this has been dexamethasone which was shown in the RECOVERY trial to have remarkable impacts on death in patients requiring O2 (NNT = 29) and in those requiring invasive ventilation (NNT = 8.5).  The RECOVERY Group has continued to perform excellent research but most of the investigated therapeutics including azithromycin, convalescent plasma, aspirin and colchicine have all fallen flat.

Monoclonal antibody infusions have gained national attention as a potential therapeutic in COVID patients and have been touted by medical experts. The goal of these drugs is to give patients antibodies prior to their body mounting a response in an effort to prevent progression of disease. We have previously reviewed the EUA drug bamlanivimab (LY-CoV555) - a monoclonal antibody. In that review, we note the absence of any difference in patient centered outcome as well as serious methodological flaws. We have also reviewed REGN-COV2 (casirivimab/imdevimab) noting the lack of any evidence of benefit as well as the suspect methodology. In January, in a post for Brief 19, I concluded that “there is no convincing data that monotherapy or a cocktail of antibodies improves meaningful outcomes in patients with COVID19.” However, the RECOVERY group has submitted a new study that was released as a preprint on June 16th, 2021.

June 14, 2021

Background: Outside of vaccines, effective pharmaceuticals for COVID19 continue to be evasive. Steroids have been a success (in patients who require supplemental O2) leading to additional studies investigating optimal drug and dose. Despite early excitement, we’ve seen high-quality studies demonstrate a lack of benefit for numerous drugs including colchicine, hydroxychloroquine, ritonavir etc. Some meds, like remdesivir and monoclonal antibodies (mAbs) targeting the spike protein of SARS-CoV2, are being widely used despite an absence of robust data supporting their use (Bamlanivimab, REGN-COV2, Remdesivir). 

Still, continued research and investigation is vital. One area research continues to focus on is the hyperactive inflammatory response that occurs as COVID19 progresses. Janus kinase-inhibitors (JAK-inhibitors) work by targeting and suppressing cytokine pathways. The ACTT-2 Trial published in the NEJM in December 2020 demonstrated a small decrease in time to recovery in patients treated with baricitinib (one day) that was barely statistically significant (PulmCrit 2020). Secondary outcomes (hypothesis generating) demonstrated improvements in progression of oxygen requirement and intubation as well as a non-significant trend towards decreased mortality. However, the majority of patients in this study did not receive steroids which became standard care in those with hypoxemia after the RECOVERY study. This raised questions about the utility of baricitinib when added to steroids. 

May 31, 2021

Earlier this year, my home shop began administering the Johnson & Johnson COVID-19 vaccine to patients in the emergency department (ED). Thirteen years of experience in emergency medicine has afforded me many opportunities to counsel patients on lifestyle modifications, death and dying, tPA administration, and many other complex medical issues. However, I’ve never experienced a more polarizing topic than the COVID-19 vaccination. My initial attempts were met with a few quick wins. While in fast-track, a middle-aged Hispanic man presented with an injury to his left knee. I suspected a patellar tendon rupture, and while we waited for the orthopedist to evaluate his knee, I offered him the COVID-19 vaccine. He smiled acceptingly and slapped his left shoulder with his right hand, signaling the location he wished to receive his vaccine and said: “Yeah! I’ll take it.” “I want it too!” His wife exclaimed. Though not yet a patient, she sat patiently at her husband’s bedside, awaiting the orthopedists. She was quickly registered and vaccinated. 

May 27, 2021

Background: We have all seen the wide spectrum of illness caused by COVID-19 ranging from asymptomatic disease on one extreme all the way up to critical illness, acute respiratory disease and ultimately death at the other extreme.  In the most critically ill there are thoughts that a viral-induced hyperinflammatory immune response (i.e. cytokine storm) is the culprit.  The main gatekeeper of the cytokine storm is, granulocyte-macrophage colony-stimulating factor (GM-CSF) which in turn can stimulate increases in inflammatory markers such as IL-6, CRP, d-dimer, and ferritin.  Medications that can inhibit or slow down upstream effects of GM-CSF could have beneficial effects. However, there is a lack of robust evidence to support this claim. Now we have the newest kid on the block…Lenzilumab. Lenzilumab is an anti-human GM-CSF monoclonal antibody that directly binds to GM-CSF and prevents signaling through its receptor.

May 13, 2021

Background Information: Over one year into the pandemic many therapies to treat COVID-19 have targeted innumerable aspects of the virus. Most recently, the use of corticosteroids to treat the virus’ excessive inflammatory effects has become the front and center of therapy in patients requiring oxygen therapy.1 The RECOVERY trial showed a mortality benefit when using Dexamethasone in severe cases where oxygen therapy or mechanical ventilation was required.2 Interestingly, compared to other corticosteroids, high doses of Methylprednisolone are actually the preferred agent for anti-inflammation in pulmonary diseases as it achieves a more direct effect on cell membrane associated proteins.3 The authors of the following paper sought to investigate the effectiveness of methylprednisolone compared to Dexamethasone in hypoxemic ICU patients with COVID-19.
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