A Case for Chloroquine or Hydroxychloroquine in COVID-19

A lot has been said about the potential of hydroxychloroquine or chloroquine, as a standalone monotherapy or combined with azithromycin and, perhaps, zinc supplement, in the treatment of COVID-19 patients.

While claims of treatment effectiveness have been touted by physicians in China, and South Korea, in the West a lot of skepticism about this treatment continues to linger in the minds of many health professionals who are hesitant or even reluctant to use either drug in treating SARS-CoV-2 patients with only mild symptoms, due to the lack of reliable data and the apparent availability of only sketchy evidence of its effectiveness, because of the limitations of studies carried out so far, in this respect.

Given the anecdotal nature of claims of treatment effectiveness by some physicians here and there in the USA, the limited sample size and the lack of a control group in a study conducted by a renown French professor of infectious diseases, Didier Raoult, rather than stoking clarity in people’s minds has instead sown more seeds of doubts.

Skepticism about chloroquine has grown, and it has been made the more confounding by premature stoppages, in different parts of the country, of clinical trial studies which had earlier set out to determine the effectiveness of hydroxychloroquine in COVID-19, amidst claims that high mortality rates are increasingly registered in patients being administered this drug, and, these, supposedly, arising from the rising incidence of the toxic effects of hydroxychloroquine or chloroquine observed in these patients.

Here is my take on the issue:

Hydroxychloroquine or chloroquine should be prescribed to treat the novel coronavirus when COVID-19 symptoms are still mild, in the early infection. Given late, when the pathology is fully set, does not only fail to reverse the course of the disease but it, unfortunately, gives rise to severe toxicity, mindful of the underlying hypoxic heart conduction problems resulting from the consolidated lungs and the ensuing respiratory distress.

Once the chloroquine treatment protocol is supplemented with azithromycin, the likelihood of the Q-T interval prolongation, cardiac conduction block, supraventricular tachycardias, torsades de pointes and the deadly ventricular fibrillation, is increased. Each of these drugs causes Q-T prolongation, and cardiac conduction toxicity, in its own right.

Low plasma potassium, magnesium or calcium that cause conduction problems and any lingering, intrinsic cardiac tissue-derived conduction problems make the hydroxychloroquine or chloroquine /azithromycin combo treatment potentially more toxic. Preferably, ionic deficiences should be corrected beforehand, if the aforementioned drug combination treatment must be given. A well thought out risk/benefit analysis should be carried out and accompanying palliative and vital support must be nearby, and handy, for the high risk cardiac conduction defect patients.

The problem is that in the Western World, this therapeutic drug combination has traditionally been given to severely ill patients who already are having acute respiratory distress syndrome and are on ventilatory support. This means that they are more likely to have cardiac conduction problems from low tissue oxygen (hypoxia). In Senegal where early, and still mild cases of COVID-19, have been selected for treatment as proposed by professor Didier Raoult, the outcomes have been amazing.

Chloroquine prevents coronaviruses from entering and infecting human cells. It is also anti-inflammatory, thus preventing the excess inflammation and oxidative stress that make the novel coronavirus more deadly.

Chloroquine also carries zinc into the cell. Many plants also produce quercetin which transports zinc into the cell. Both molecules are called ionophores.

Zinc is an interesting and useful partner in this game. It does not only regulate and boost your immune system by inhibiting excessive calcium influx into the cell, but it proves to be antiviral through many mechanisms, as outlined below.

The diverse stages of viral replication cycles that are inhibited by zinc. In vitro studies have demonstrated a number of mechanisms by which zinc interferes with the viral replication cycle. These include free virus inactivation (1), inhibition of viral uncoating (2), viral genome transcription (3), and viral protein translation and polyprotein processing (4). No studies to date, however, have demonstrated zinc-mediated inhibition of virus assembly and/or particle release. CV, coronavirus; DdDp, DNA-dependent DNA polymerase; EMCV, encephalomyocarditis virus; FMDV, foot and mouth disease virus; HCV, hepatitis C virus; HIV, human immunodeficiency virus; HPV, human papilloma virus; HRV, human rhinovirus; HSV, herpes simplex virus; PV, polio virus; RdRp, RNA-dependent RNA polymerase; RT, reverse transcriptase; SARS, severe acute respiratory syndrome coronavirus; SFV, Semliki Forest virus; SV, sindbis virus; VZV, varicella-zoster virus; Zn, zinc.

Dr. Oliver Verbe  Birnso, MD.