Background It is known that severe acute respiratory coronavirus 2 (SARS-CoV-2) is the viral strain responsible for the recent coronavirus disease 2019 (COVID-19) pandemic. Current documents have demonstrated that the virus causes a PGE2 storm in a substantial proportion of patients via upregulating cyclooxygenase-2 (COX-2) and downregulating prostaglandin E2 (PGE2)-degrading enzymes within the host cell. Aim Herein, we aimed to study how short-term treatment with celecoxib (Celebrex), a selective COX-2 inhibitor, affects demographic features, early symptoms, O 2 saturation, and hematological indices of cases with COVID-19. Methods A total of 67 confirmed COVID-19 cases with a mild or moderate disease, who had been referred to an institutional hospital in south-eastern Iran from October 2020 to September 2021, were enrolled. Demographic characteristics, symptoms, and hematological indices of the patients were recorded within different time periods. One-way ANOVA or Kruskal–Wallis tests were used to determine differences between data sets based on normal data distribution. Results O 2 saturation was statistically different between the control group and patients receiving celecoxib ( p = 0.039). There was no marked difference between the groups in terms of the symptoms they experienced ( p > 0.05). On the first days following Celebrex therapy, analysis of complete blood counts showed that white blood cell (WBC) counts were markedly lower in patients treated with a high dose of celecoxib (0.4 g/day) than in controls ( p = 0.026). However, mean lymphocyte levels in patients receiving a high dose of celecoxib (0.4 g/day) were markedly higher than in patients receiving celecoxib with half of the dose (0.2 g/day) for one week or the untreated subjects ( p = 0.004). Changes in platelet count also followed the WBC alteration pattern. Conclusion Celecoxib is a relatively safe, inexpensive, and widely available drug with non-steroidal anti-inflammatory properties. The therapeutic efficacy of celecoxib depends on the administrated dose. Celecoxib might improve disease-free survival in patients with COVID-19.
Abstract. The current study aimed to examine the possible association between the interferon-induced transmembrane protein-3 (IFITM3) gene polymorphisms and risk of pulmonary tuberculosis (PTB) in a sample population. This case-control study was conducted on 188 PTB patients and 169 healthy subjects. The rs7478728 and rs3888188 variants of IFITM3 were genotyped using polymerase chain reaction-restriction fragment length polymorphism. The findings showed no significant association between rs7478728 polymorphism and risk of PTB. Regarding rs3888188 polymorphism, the TG genotype as well as G allele significantly increased the risk of PTB [odds ratio (OR)=2.48, 95% confidence interval (CI): 1.42-4.53; P=0.002, and OR=2.26, 95% CI: 1.33-3.86; P= 0.003, respectively]. In conclusion, the findings revealed that rs3888188 polymorphism increased the risk of PTB in a sample of Iranian population. Additional investigation with larger sample sizes and different ethnicities are needed to verify our findings. IntroductionTuberculosis (TB), caused by Mycobacterium tuberculosis (MTB) infection, is a public health problem globally (1,2). According to the WHO report on the worldwide control of TB, approximately 8.6 million new cases occurred in 2012 (3). Although almost 33% of the population is infected with TB, only 5-10% of infected cases develop active TB (3), which suggests a major role of genetic factors in host immunity.Interferon-γ (IFNγ) is produced and released by host cells in response to the presence of numerous pathogens (4). It plays a key role in macrophage activation during MTB infection (5).Individuals defective in the genes for IFNγ or IFNγ receptor (IFNγR) have been indicated to be susceptible for mycobacterial infections including MTB (6). Previously, we showed an association between IFNγ and IFNγR variants and risk of pulmonary TB (PTB) (7,8).Interferon-induced transmembrane protein-3 (IFITM3) is a double transmembrane protein that can be upregulated by IFNs and participates in INF-triggered processes, such as homotypic cell adhesion, anti-proliferative activities in tumor pathogenesis, and the innate immune response to virus infections (9-13). The IFITM3 gene is mapped to an IFITM gene cluster on chromosome 11p15.5 (14). In a genome wide scan, Stein et al (15) identified that one of the TB-linked loci was located in this chromosome region. To the best of our knowledge, there is only one report regarding the impact of IFITM gene polymorphisms on the risk of TB (16). Therefore, the present study aimed to examine the possible associations between polymorphisms of IFITM3 gene and susceptibility to PTB in a sample of Iranian population. Materials and methodsPatients. This case-control study was performed on 188 PTB patients and 169 age-and gender-matched healthy individuals. The enrollment process and study design are described elsewhere (17-23). Briefly, the cases were chosen from PTB patients admitted to a University-Affiliated Hospital (Bou-Ali Hospital, Zahedan, Iran, referral center for TB) with no clinical sy...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.