C-reactive protein value in organophosphate-poisoned patients – Promises and pitfalls

To the Editor:

We were intrigued by the recent article of Lee et al.¹ Although difference in C-reactive protein (CRP) values between initial and 24-h follow-up in organophosphate (OP) poisoning appears to be a promising independent prognostic indicator, these observations have to be interpreted cautiously in view of the “5Ps” we faced in our study.² These are Poisonous agent, Polymorphism of gene(s), Physiological factors including habits, Pathological status, and Pharmacotherapeutic agents.

CRP is a critical component of the immune system; however, variations in the levels of CRPs between different people are genetically determined. In addition, the concentration may be affected by polymorphisms in the CRP gene, so it is necessary to interpret any CRP concentration in the context of an individual's genotype.³ Despite the fact that identical CRP thresholds were suggested for men and women,⁴ we have observed statistically significant gender differences in spite of perfect matching for age and BMI. These differences should be considered while assessing the prognosis. Similarly, we also found that CRP levels are elevated in women using oral contraceptives and oral estrogen replacement. Their plasma CRP levels were increased by 60–90% (adjusted for fat-free mass) compared to those of the women who are not on hormone therapy, so the risk prediction for such women may need to be calibrated downward. In our study, we found that patients who smoked, were diabetic, hypertensive, had high BMI, abdominal obesity, sedentary lifestyle or belonged to low socio-economic status had increased odds of repeatedly elevated CRP similar to Ishii et al.'s⁵ report. These risk factors should be taken into account in order to avoid bias.

During the acute phase response, the levels of CRP rapidly increase within 2 h of acute insult, reaching a peak at 48 h and with effective treatment. The concentration decreases at a rate that is dependent on its half-life (first-order elimination kinetics), so the influence of time lapse between the consumption of poison and the presentation to the emergency department plays an important role. We noted that there was a considerable variation in the time delay and the CRP values in our study. Moreover, each organophosphorus insecticide has a substantial variability in clinical course and outcome.⁶ These factors should be reflected in guidelines for the risk stratification in OP-poisoned victim. Interestingly, high-sensitivity CRP analysis in our OP-poisoned patients had different values compared to traditional CRP test in the same patient. It is important to assess the sensitivity and specificity of each assay before recommending it; otherwise, it will create chaos. The authors are not sure why elevated CRP levels are linked to worse prognosis.

CRP is a good indicator, but optimal cut-off points should be developed for a specific population. Unfortunately, data obtained from this region are sparse, so any generalization in these patients should be made with caution because a different prevalence of risk factors, quantity of the compound, and concurrent subclinical infections could alter the CRP concentration. It is dubious in our study as to which of these risk factors are considered as confounders and which might actually be mediators of any CRP effect.

Despite these limitations, it may be worth investigating CRP in OP poisoning further. As experience with large, multiethnic, population-based study grows, a critical appraisal of the strengths and limitations may become clearer.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.