IL10 rs1800872 Is Associated with Non-Steroidal Anti-Inflammatory Drugs Exacerbated Respiratory Disease in Mexican-Mestizo Patients

Pavón-Romero, Gandhi F.; Pérez-Rubio, Gloría; Ramírez-Jiménez, Fernando; Ambrocio-Ortiz, Enrique; Merino-Camacho, Cristian Rubén; Falfán-Valencia, Ramcés; Teran, Luis M.

doi:10.3390/biom10010104

Cited by 6 publications

(4 citation statements)

References 55 publications

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“…Although it has been reported that some genes involved in inflammation are associated with respiratory diseases [ 87 , 88 , 89 , 90 , 91 , 92 ], investigations regarding genetic factors involved in the susceptibility and severity are scanty. Two primary examples in inflammatory response genes, where genetic variability is associated with an altered phenotype, are TNF-α and IL-1β; both are pleiotropic modulators critical in regulating inflammation.…”

Section: Genetic Variants and Influenza A H1n1 Virus Infectionmentioning

confidence: 99%

Role of the Host Genetic Susceptibility to 2009 Pandemic Influenza A H1N1

Pérez-Rubio

Ponce-Gallegos

Domínguez-Mazzocco

et al. 2021

Viruses

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Influenza A virus (IAV) is the most common infectious agent in humans, and infects approximately 10–20% of the world’s population, resulting in 3–5 million hospitalizations per year. A scientific literature search was performed using the PubMed database and the Medical Subject Headings (MeSH) “Influenza A H1N1” and “Genetic susceptibility”. Due to the amount of information and evidence about genetic susceptibility generated from the studies carried out in the last influenza A H1N1 pandemic, studies published between January 2009 to May 2020 were considered; 119 papers were found. Several pathways are involved in the host defense against IAV infection (innate immune response, pro-inflammatory cytokines, chemokines, complement activation, and HLA molecules participating in viral antigen presentation). On the other hand, single nucleotide polymorphisms (SNPs) are a type of variation involving the change of a single base pair that can mean that encoded proteins do not carry out their functions properly, allowing higher viral replication and abnormal host response to infection, such as a cytokine storm. Some of the most studied SNPs associated with IAV infection genetic susceptibility are located in the FCGR2A, C1QBP, CD55, and RPAIN genes, affecting host immune responses through abnormal complement activation. Also, SNPs in IFITM3 (which participates in endosomes and lysosomes fusion) represent some of the most critical polymorphisms associated with IAV infection, suggesting an ineffective virus clearance. Regarding inflammatory response genes, single nucleotide variants in IL1B, TNF, LTA IL17A, IL8, IL6, IRAK2, PIK3CG, and HLA complex are associated with altered phenotype in pro-inflammatory molecules, participating in IAV infection and the severest form of the disease.

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Section: Genetic Variants and Influenza A H1n1 Virus Infectionmentioning

confidence: 99%

Role of the Host Genetic Susceptibility to 2009 Pandemic Influenza A H1N1

Pérez-Rubio

Ponce-Gallegos

Domínguez-Mazzocco

et al. 2021

Viruses

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“…20 However, genetic studies that evaluated approximately 100 patients with N-ERD demonstrated that the LFT and frequency of severe asthma were similar to those of asthma patients. [21][22][23] In our study, we enrolled patients who met the three clinical criteria needed for N-ERD diagnosis and not just those with asthma who were hypersensitive to NSAIDs. The N-ERD patients had similar clinical characteristics to those reported in other published series.…”

Section: Discussionmentioning

confidence: 99%

Lung Function and Asthma Clinical Control in N-ERD Patients, Three-Year Follow-Up in the Context of Real-World Evidence

Pavón-Romero,

Falfán-Valencia,

Gutiérrez-Quiroz

et al. 2023

JAA

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Purpose To describe the lung function and clinical control of asthma in patients with N-ERD during three years of medical follow-up using GINA guidelines. Methods We evaluated 75 N-ERD and 68 asthma patients (AG). Clinical control, lung function, and asthma treatment were evaluated according to GINA-2014. We compared all variables at baseline and one, two, and three years after treatment. Results At baseline, the N-ERD group had better basal lung function (LF) than the AG group ( p <0.01), and the AG group used higher doses of inhaled corticosteroids than the N-ERD group (52.4% vs 30.5%, p =0.01) and short-term oral corticosteroid (OCS) use (52.4% vs 30.5%, p <0.01). Instead, N-ERD patients needed more use of leukotriene receptor antagonists (LTRA) (29.3% vs 5.9%, p <0.01). This group had better clinical control than the AG group (62.1% vs 34.1%, p <0.01). During the medical follow-up, the LF of the N-ERD group remained at normal values; however, these parameters improved in AG from one year ( p <0.01). Likewise, there was a diminished use of high doses of ICS (52.4% vs 33%, p <0.05) and short-term OCS (67.6% vs 20.6%, p <0.01) in asthma patients. However, N-ERD patients still needed more use of LTRAs ( p <0.02) during the study. In this context, one-third of N-ERD patients had to use a combination of two drugs to maintain this control. From the second year on, clinical control of asthma was similar in both groups ( p >0.05). Conclusion According to GINA guidelines, only one-third of patients with N-ERD can gradually achieve adequate lung function and good asthma control with a high ICS dosage. Only a very small portion of patients will require the continued use of a second medication as an LTRA to keep their asthma under control.

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“…Genetic associations are likely to predispose to N‐ERD as well as to asthma, chronic rhinosinusitis, and allergic rhinitis 17 . Exploring the genotypes of the Finnish patients with N‐ERD and a positive family history may reveal more genetic risk factors than those that have been suggested as predisposing to N‐ERD 18,19 . This could offer new insights into the pathogenesis of the condition, as well as help develop novel therapeutic options.…”

Section: Discussionmentioning

confidence: 99%

Inheritance of NSAID‐Exacerbated Respiratory Disease

Suikkila

Lyly

Hafrén

et al. 2022

Otolaryngol.--head neck surg.

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Nonsteroidal anti-inflammatory drug (NSAID)–exacerbated respiratory disease (N-ERD) has been considered an acquired condition. Positive first-degree family history has been reported in 1% of cases. The geographic and genetic isolation of the Finnish population offers exceptional opportunities for inheritance studies. In this questionnaire study, we explored the familial aggregation of N-ERD in 66 Finnish families of patients with N-ERD. The majority of patients (67%) had a positive family history of NSAID intolerance, asthma, nasal polyposis, or N-ERD. Furthermore, 55% had a positive first-degree family history of asthma, 21% nasal polyposis, 20% NSAID intolerance, and 11% N-ERD. The prevalence of asthma, nasal polyposis, NSAID intolerance, and N-ERD among first-degree relatives was 13%, 5%, 4%, and 2%, respectively. We present the pedigrees of the 44 affected families. According to our findings, Finnish patients with N-ERD seem to have a genetic susceptibility to it.

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IL10 rs1800872 Is Associated with Non-Steroidal Anti-Inflammatory Drugs Exacerbated Respiratory Disease in Mexican-Mestizo Patients

Cited by 6 publications

References 55 publications

Role of the Host Genetic Susceptibility to 2009 Pandemic Influenza A H1N1

Role of the Host Genetic Susceptibility to 2009 Pandemic Influenza A H1N1

Lung Function and Asthma Clinical Control in N-ERD Patients, Three-Year Follow-Up in the Context of Real-World Evidence

Inheritance of NSAID‐Exacerbated Respiratory Disease

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