![]() Although used in the reference trial,6 the main role in the beneficial outcome of CQ/HoCQ- poisoned patients among all administered treatments should go to early tracheal intubation, mechanical ventilation, and epinephrine infusion.Ĭhloroquine leaves the consciousness clear. Similarly, in a double-blind placebo-controlled study, diazepam did not reverse CQ-induced clinical andĮlectrocardiographic effects in moderate intoxication.4 Altogether, these findings strongly suggested not administering high-dose diazepam in spontaneously breathing CQ/HoCQ-poisoned patients due to its ineffectiveness and to the elevated risk of aspiration pneumonia.5 Clearly and in contrast to what is stated in the review paper, the belief that diazepam may improve CQ/HoCQ-induced-vasodilation or dysrhythmic effects is illusive. Recently, in vivo rat models of CQ toxicity used to assess diazepam, clonazepam and Ro5-4864 administered prior, during and after CQ, and high-dose diazepam eventually co-administered with epinephrine, demonstrated that neither diazepam nor other ligands for benzodiazepine-binding sites were effective to protect against or attenuate CQ-induced cardiotoxicity.3 Diazepam-attributed augmentation of co- administered positive inotrope effects was the only effect that contributed to reduce cardiotoxicity. The results were clear none of the tested benzodiazepines succeeded at this task (Hughes, 2020): In 2020, a well-conducted experimental study on rats that tested the efficacy of diazepam, clonazepam and 4’-chlorodiazepam on reducing the cardiac toxicity of chloroquine poisoning was published in the British Journal of Pharmacology (Hughes, 2020). ![]() Failing that, we have to rely on experimental studies on animals. Of course, on ethical grounds, one cannot run a RCT of chloroquine poisoning so we are forced to rely on case-control studies. In general, case-control studies cannot infer causation, and this is even more true when they contain an inadequate control group - unfortunately, this often happens. It would then be wrong to conclude that the observed association between celery juice consumption and heart size is caused by the former. Here, fitness level is a confounding variable because it is an unmeasured factor that influences the results of the study. As a result, even if the participants are well matched on age, sex and weight, increased fitness is much more likely to explain a larger heart than drinking celery juice (the heart is a muscle, so it grows by working out). Generally, celery juice is associated with wellness so fit people are more likely to drink it. The investigators record other measures like age, sex and weight, and eventually find that those who drink celery juice have a larger heart. Imagine that a case-control study investigates the effect of celery juice on heart size. ![]() This lack of randomization makes case-control studies prone to systematic bias(es), as illustrated below. In contrast, participants are not assigned to one treatment or another in a case-control study the investigators only observe how much and how often they use a treatment (if at all). In other words, randomization allows for a reliable comparison between both groups. confounders, see below) that could influence the results of the trial. The crucial point is that randomizing patients to receiving either the drug or the placebo / other drug ensures that both the active and control groups are well matched in terms of age, sex, weight, ethnicity, disease severity, comorbidities and other unmeasured factors (a.k.a. The active treatment group receives the drug, while the control group receives either a placebo or another drug that is considered the standard of care at the time the trial is conducted (since it would be unethical not to give it to patients in need). Normally, to investigate the efficacy of a drug, one needs to run a randomized controlled trial (RCT). A note about the control group in the study by Riou et al.
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