Opinion: Missoula doctor promotes new COVID anti-inflammatory protocols

Since COVID-19 prevention with vaccines and elimination with anti-virals has not been yet sufficiently achieved, and the recent recognition that the majority of the risk in the sickest COVID-19 patients derives from an excessive viral induced hyper-immune response, rather than the virus itself and because multiple subsequent attempts to reduce COVID-19 mortality with traditional anti-inflammatories have failed, we now have a pandemic.

There may be a solution. Peschel has developed and tested his most efficacious 4-drug anti-inflammatory (Peschel Protocol) which has consistently improved adverse clinical courses in both acute and chronic diseases much better than when compared to traditional anti-inflammatories.

Now Peschel in a small off-label study simply repeated a previous failed COVID-19 experiment, substituting his protocol for the single agent anti-inflammatory use.

To better understand the experiment and to appreciate the unprecedented protection of eliminating the disease risk end-points (need for hospitalization and death) consider the following.

There is a continuum of risk varying from low-risk, young 30 year old, without chronic disease, a moderate immune response, mostly out-patient clinical course with a 3% mortality. To high-risk elderly, 60 year old, especially poorly controlled diabetes, a most intense immune response, with a 50% need for hospitalization and 30% mortality most often from lung failure.

The disease has a sequence. First, viral activation of the immune response which when activated damages the lung. Subsequent lung failure is responsible for the disease end-points, need for hospitalization and death. To decrease these end-points if you cannot eliminate the virus it makes sense to attenuate the immune response.

Following viral inhalation and lung entry, released blood-born injury mediators travel to and activate the immune system to produce and release cytokines.

Cytokines are potential toxic effector proteins and an essential part of the immune arsenal for fighting disease. The toxicities are non-specific, injuring and eliminating both pathogens and innocent by-stander cells (collateral damage), while stimulating hepatic production of CRP. CRP is an accepted marker for the intensity of the immune response; the amount of cytokine release, the amount of collateral damage, and the morbidity and mortality of the disease.

The cytokines have survival value if released briefly and in modest amount where the benefit of insult reduction outweighs the risk of collateral injury. They can also contribute to acute mortality as they do in the sick COVID-19 patients where they are released excessively, acutely, or if released persistently, even at low levels, they can slowly and systemically decrease organ reserve resulting in a different chronic disease presentation as each organ fails.

In most cases of COVID-19 the initial clinical course driven by the virus alone is mild; consisting of fever, cough, loss of taste and smell. To be followed in the second and third week by an added cytokine driven toxic immune overlay. Now having 2 sources of injury. Low-risk young patients without chronic disease usually have a modest amount of cytokine and CRP elevation. With the immune contribution to the clinical course minimal followed by a self-limited out-patient disease with recovery.

What a differentiates the high-risk group (60 years of age with chronic disease) from the low-risk group is that following a similar mild viral induced clinical course the subsequent cytokine release is excessive, delivered in a storm. CRP levels sometimes 200 times normal, with marked collateral damage to the heart, kidney, and lung (acute respiratory distress syndrome) often requiring hospitalization and ventilator assist; increasing the mortality to 80%. The majority of lung damage coming from the immune response not the virus.

The increase in immune intensity is measured by an increase in the CRP and the increase in lung injury by the decrease in O2 saturation. To compare the efficacy of a proposed treatment one can record and monitor serial changes in the CRP and O2 stat through the clinical course and compare the percentage change and disease end-points between treated and untreated patients best done in a high-risk group.

The untreated high-risk patient, hyper active immune response can be documented by serial increases in the CRP from a normal baseline of 3 upward to 30 and sometimes as high as 400. This is the highest I’ve seen in clinical medicine; the associated lung injury measured by decreasing O2 stat from normal of 96 downward. At 89 risk is increased, diagnosis of lung failure with need for hospitalization and ventilator support with progression the mortality increases to 80%. It is important to keep the O2 stats above 89.

A similar high-risk patient treated with Peschel Protocol, both CRP and O2 stats remained normal at 3 and 98 respectively throughout the clinical course, with the exception of a brief increase of CRP to 8 and decrease of O2 stats to 93 in the third week of a one month clinical course. The patient emerged from an out-patient flu like illness probably self-immunized. This is an inexpensive and safe way toward herd immunity. This compares to a normal non-afflicted patient maintaining a CRP of 3 and an O2 stat of 96.

Since the high-risk and low-risk patients respond with different immune intensities they were separated non-randomly into low-risk and high-risk groups, then randomly separated to treated and non-treated in each groups. Protocol meds were given daily soon after diagnosis, measuring serial CRPs and O2 stats and quantitative comparisons to the end-points at the end of the clinical course within each group.

Results:

Un-Treated High-Risk Group

Treated High-Risk Group

Normal Non-Afflicted

For $3.00 a day with no side-effects the high-risk end-points of 50% hospitalization and 30% mortality were completely eliminated. The entire clinical course was out-patient. Drugs are deemed safe and can be administered today off-label by your own physician. They are ready for use off-the shelf and are carried at your local pharmacy.

They most likely mix well with any COVID or non-COVID treatments this is to be confirmed by the pharmacy or MEDEX. Many people can benefit from this treatment while awaiting vaccination and even after.