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Reparixin improves survival in critically ill and transplant patients: A meta-analysis

Background: Reparixin, an anti-inflammatory drug that inhibits interleukin 8 (IL-8) activity, might be life-saving for high-risk in-hospital patients without increasing the risk of infection according to a previous meta-analysis. With the increasing availability of randomised data the aim of the current study is to update previous findings by including any randomised control trials (RCTs) investigating the impact of reparixin on survival of critically ill or transplant patients.

Methods: A search strategy was developed to identify all RCTs involving reparixin in critically ill or transplant patients, with the exclusion of oncological patients. Two trained and independent authors conducted a thorough search of relevant databases. In addition, backward snowballing was employed. Language restrictions were not imposed.

Results: Our analysis included a total of nine studies involving 733 patients: 437 received reparixin and 296 the comparator. The reparixin group had a significantly lower all-cause mortality rate compared to the control group [15/437 (3.4%) vs. 19/294 (6.4%), odds ratio = 0.47 (95% confidence interval 0.23-0.96), p-value for effect .04, I2 = 22%, number needed to treat = 33]. These findings had the same direction and magnitude of effect across COVID-19 patients (n = 325) and non-COVID-19 patients (n = 408). Furthermore, there were no significant differences in the rate of pneumonia, sepsis or non-serious infections between the two groups.

Conclusions: The findings of this meta-analysis indicate that reparixin, an anti-inflammatory drug, improved survival in critically ill or transplant patients (including both COVID-19 and non-COVID-19 patients) without increasing the risk of infection.

 

Comments:

The results of the current study, which included a meta-analysis of nine randomized controlled trials (RCTs), suggest that reparixin, an anti-inflammatory drug that inhibits interleukin 8 (IL-8) activity, may improve the survival of critically ill or transplant patients. The study included a total of 733 patients, with 437 receiving reparixin and 296 receiving a comparator drug.

The analysis revealed that the group receiving reparixin had a significantly lower all-cause mortality rate compared to the control group. Specifically, the mortality rate in the reparixin group was 3.4%, while it was 6.4% in the control group. The odds ratio for mortality in the reparixin group compared to the control group was 0.47, with a 95% confidence interval of 0.23-0.96. This suggests that patients receiving reparixin had a 53% lower odds of mortality compared to those in the control group. The p-value for this effect was 0.04, indicating statistical significance.

The analysis also assessed the impact of reparixin on COVID-19 patients (n = 325) and non-COVID-19 patients (n = 408) separately. The findings showed that reparixin had a similar direction and magnitude of effect on both groups, suggesting that it may be beneficial for critically ill or transplant patients regardless of COVID-19 status.

Importantly, the use of reparixin did not appear to increase the risk of pneumonia, sepsis, or non-serious infections when compared to the control group. This indicates that reparixin may provide survival benefits without compromising patient safety in terms of infection risk.

In conclusion, this meta-analysis suggests that reparixin, as an anti-inflammatory drug, improved survival in critically ill or transplant patients, including both COVID-19 and non-COVID-19 patients. These findings support the potential life-saving benefits of reparixin for high-risk in-hospital patients and warrant further investigation and clinical consideration.

Related Products

Cat.No. Product Name Information
S8640 Reparixin (Repertaxin) Reparixin (Repertaxin, DF 1681Y) is a potent and specific inhibitor of CXCR1 with IC50 of 1 nM. Reparixin (Repertaxin) inhibits PMN migration induced by CXCL8 (IC50 = 1 nM) and rodent PMN chemotaxis induced by CXCL1 and CXCL2. Repertaxin inhibits the response of human PMN to CXCL1, which interacts with CXCR2 (IC50 = 400 nM).

Related Targets

CXCR