What is EARLY TREATMENT for COVID? Is there scientific evidence?
April 16, 2023
Currently, much controversy has been created around the so-called early treatment of COVID. The political connotation and power struggle have led v
Early treatment, as the name suggests, means intense, regular, and as rapid as possible medical monitoring, ideally in PHASE 1 of the disease (first 5 days).
COVID is a serious inflammatory pathology that generates various metabolic changes that may require rapid adjustments and the inclusion of new drugs within a very short period.
The political connotation and power struggle have led media outlets to adopt partial positions, where only one side of the story is heard. Various medical societies also speak out against a treatment that addresses patient care from the onset of the disease with the best available scientific evidence. The claim is that early treatment lacks scientific evidence; below, we will present our viewpoint on this.
Early treatment is based on the use of a protocol that employs a cocktail of drugs whose use was proposed due to in vitro studies that progressed to case reports, “expert” opinions, observational studies, case-control studies, and so on.
It is logical and rational to expect that clinical monitoring of disease phases and intervention in pathophysiology with the tools we currently have available will be more efficient than solely using symptomatic treatments and not clinically monitoring the patient.
The most powerful scientific evidence is called IA evidence, which refers to the highest scale and comprises systematic reviews, a compilation of several randomized, controlled, and double-blind studies. However, only 10% of medical practices, in general, possess this level of evidence.
The principles of outpatient EARLY TREATMENT for COVID-19 include:
A FDA-approved antiparasitic, previously shown to have broad-spectrum antiviral activity in vitro, is an inhibitor of the causative virus (SARS-CoV-2), with a single addition to Vero-hSLAM cells 2 hours post-infection with SARS-CoV-2 capable of effecting a ~5,000-fold reduction in viral RNA at 48 h.
Ivermectin is an FDA-approved broad-spectrum antiparasitic agent that, in recent years, along with other groups, we have shown to have antiviral activity against a wide range of viruses in vitro. Originally identified as an inhibitor of the interaction between human immunodeficiency virus-1 (HIV-1) integrase protein (IN) and the importin α/β1 (IMP) heterodimer responsible for nuclear import of IN, ivermectin has since confirmed inhibition of nuclear IN import and HIV-1 replication. Other actions of ivermectin have been reported, but ivermectin has been shown to inhibit the nuclear import of host and viral proteins, including the simian virus SV40 tumor antigen (T-ag) and dengue virus (DENV) 5 non-structural protein. Importantly, it has been shown to limit infection by RNA viruses such as DENV 1-4, West Nile virus, Venezuelan equine encephalitis virus (VEEV), and influenza, with this broad-spectrum activity believed to be due to the dependence of many different RNA viruses on IMPα/β1 during infection. Ivermectin has also been shown to be effective against pseudo-DNA virus (PRV) in vitro and in vivo, with ivermectin treatment demonstrating increased survival in mice.
Ivermectin, therefore, warrants further investigation for potential benefits in humans, but due to the chaotic nature of the pandemic, it may be one of the tools to be used with appropriate medical supervision.
Vitamin D appears to interact with the immune system through its action on the regulation and differentiation of cells such as lymphocytes, macrophages, and natural killer (NK) cells, in addition to interfering with cytokine production in vivo and in vitro. Among the demonstrated immunomodulatory effects are: decreased production of interleukin-2 (IL-2), interferon-gamma (INFγ), and tumor necrosis factor (TNF); inhibition of IL-6 expression; and inhibition of the secretion and production of autoantibodies by B lymphocytes.
Vitamin D may simply be a marker of severity in critically ill patients. However, the literature reports several physiological mechanisms dependent on vitamin D, suggesting that 25(OH)D deficiency may be implicated in the pathogenesis of organ dysfunction and mortality in critical patients, perhaps mediated by its effects on immunity and the cardiovascular system.
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