Randomized clinical trial demonstrates improved outcomes in COVID-19 patients, highlighting the potential of neurokinin 1 antagonism alongside corticosteroids.
Background: Corona virus infection is a respiratory infection, compromising the normal breathing in critical patients by damaging the lungs. The aim of this study was to evaluate the clinical outcomes of Substance P receptor Neurokinin 1 antagonist in COVID-19 patients against the usual treatments as controls.Methods: It is a two-arm, open-label, randomized clinical trial that was carried out at Bahria International Hospital in Lahore, Pakistan. PCR-positive, hospitalized patients older than 18 years old, all sexes, and in the critical to life-threatening stage were included. 52 patients were placed in control group A and 67 patients were placed in intervention group B out of a total 119 patients who were randomly assigned to both arms. Before and after the intervention, lab tests were conducted in both groups. Aprepitant, a neurokinin-1 receptor antagonist, was additionally administered to the other arm while the other arm got standard therapy and care. Additionally, both groups received oral administration of the corticosteroid dexamethasone.Results: Patients in group A were on average 56.05 years old, compared to 58.1 years old in group B. There were 24 women in group A and 28 in group B, while there were 28 men and 39 women in group A. Group A had three critical cases, but group B had six. The reduction in C-reactive protein in the intervention group, improvement in platelet count in group B, and normalization of ferritin and LDH levels in group B all indicated decreased inflammation in the biochemical and haematological parameters in both groups. However, because of the reduced sample size, it wasn't very significant.Conclusion: The results of this recent trial provide a solid indication of Aprepitant's medicinal potential. Patients who got a combined therapy of dexamethasone and aprepitant had better clinical results, more favourable lab results, and lower levels of C-reactive protein, an inflammatory marker.
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Mehboob et al. (2023) studied this question.
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