Question addressed by the studyMethotrexate (MTX) is a key anchor drug for rheumatoid arthritis (RA) management. Fibrotic interstitial lung disease (ILD) is a common complication of RA. Whether MTX exposure increases the risk of ILD in patients with RA is disputed. We aimed to evaluate the association of prior MTX use with development of RA-ILD.MethodsThrough a case-control study design with discovery and international replication samples, we examined the association of MTX exposure with ILD in 410 patients with chronic fibrotic ILD associated with RA (RA-ILD) and 673 patients with RA without ILD. Estimates were pooled over the different samples using meta-analysis techniques.ResultsAnalysis of the discovery sample revealed an inverse relationship between MTX exposure and RA-ILD (adjusted odds ratio [OR], 0.46; 95% confidence interval [CI], 0.24–0.90; p=0.022), which was confirmed in the replication samples (pooled adjusted OR, 0.39; 95% CI, 0.19–0.79; p=0.009). The combined estimate using both the derivation and validation samples revealed an adjusted OR of 0.43 (95% CI, 0.26–0.69; p=0.0006). MTX ever users were less frequent among patients with RA-ILD compared to those without ILD, irrespective of chest high resolution computed tomography pattern. In patients with RA-ILD, ILD detection was significantly delayed in MTX ever users compared to never users (11.4±10.4 years and 4.0±7.4 years, respectively; p<0.001).Answer to the QuestionOur results suggest that MTX use is not associated with an increased risk of RA-ILD in patients with RA, and that ILD was detected later in MTX treated patients.

Background Of the 14.3 million Mexicans who smoke, only a minority take advantage of evidence-based approaches to smoking cessation. Mobile health interventions have the potential to increase the reach of effective cessation interventions in Mexico. Objective This study aimed to assess the feasibility and acceptability of an innovative, personalized, and interactive smoking cessation mobile intervention developed for Mexican smokers. Methods We recruited 40 Mexican smokers to participate in Vive sin Tabaco... ¡Decídete! , a smoking cessation program that uses a tablet-based decision support software to drive a 12-week text messaging smoking cessation program and pharmacotherapy support. Outcome measures included participant text messaging interactivity with the program, participant satisfaction, and 12-week verified abstinence using urinary cotinine testing or exhaled carbon monoxide. Results Average age of the participants was 36 years (SD 10.7), and they were primarily male (65%, 26/40) with at least an undergraduate degree (62%, 25/40). Most participants (95%, 38/40) smoked daily and were interested in quitting in the next 7 days. As an indicator of participant interactivity, participants sent an average of 21 text messages during the 12-week intervention (SD 17.62). Of the 843 messages that participants sent to the program, only 96 messages (11.3%, 96/843) used keywords. At 12 weeks, 40% (16/40) of participants were biochemically verified (87%, 35/40, follow-up rate). The majority of participants (85%, 30/35) reported being very satisfied or extremely satisfied with the program. Conclusions The Vive sin Tabaco... ¡Decídete! smoking cessation mobile intervention was accepted by participants, generated high satisfaction and high text messaging interactivity, and resulted in a noteworthy cessation rate at the end of treatment. This intervention is a promising strategy for smoking cessation in Mexico. Additional testing as a formal randomized clinical trial appears warranted.

Overproduction of inflammatory cytokines is a keystone event in COVID-19 pathogenesis; TNF and its receptors (TNFR1 and TNFR2) are critical pro-inflammatory molecules. ADAM17 releases the soluble (sol) forms of TNF, TNFR1, and TNFR2. This study evaluated TNF, TNFRs, and ADAM17 at the protein, transcriptional, and gene levels in COVID-19 patients with different levels of disease severity. In total, 102 patients were divided into mild, moderate, and severe condition groups. A group of healthy donors (HD; n = 25) was included. Our data showed that solTNFR1 and solTNFR2 were elevated among the COVID-19 patients (p < 0.0001), without increasing the transcriptional level. Only solTNFR1 was higher in the severe group as compared to the mildly ill (p < 0.01), and the level was higher in COVID-19 patients who died than those that survived (p < 0.0001). The solTNFR1 level had a discrete negative correlation with C-reactive protein (p = 0.006, Rho = −0.33). The solADAM17 level was higher in severe as compared to mild disease conditions (p < 0.01), as well as in COVID-19 patients who died as compared to those that survived (p < 0.001). Additionally, a potential association between polymorphism TNFRSF1A:rs767455 and a severe degree of disease was suggested. These data suggest that solTNFR1 and solADAM17 are increased in severe conditions. solTNFR1 should be considered a potential target in the development of new therapeutic options.

The tobacco industry promotes electronic nicotine delivery systems (ENDS) and heated tobacco products (HTP) as a safer alternative to conventional cigarettes with misleading marketing sustained by studies with conflict of interest. As a result, these devices sell without regulations and warnings about their adverse effects on health, with a growing user base targeting young people. This systematic review aimed to describe the adverse effects on the respiratory system in consumers of these devices. We conducted a systematic review and bibliometric analysis of 79 studies without conflict of interest evaluating ENDS and HTP effects in the respiratory system in experimental models, retrieved from the PubMed database. We found that the damage produced by using these devices is involved in pathways related to pulmonary diseases, involving mechanisms previously reported in conventional cigarettes as well as new mechanisms particular to these devices, which challenges that the tobacco industry’s claims. The present study provides significant evidence to suggest that these devices are an emerging public health problem and that they should be regulated or avoided.

Background The influenza A H1N1/09 pandemic infected a small number of exposed individuals, which suggests the involvement of genetic factors. There are scarce data available on classical HLA class I association with the influenza A H1N1/09 pandemic. Methods We analyzed the frequency of classical HLA class I alleles and haplotypes in A H1N1/09 influenza in a case-control study including 138 influenza patients (INF-P) and 225 asymptomatic healthy contacts (INF-C) simultaneously recruited. HLA class I typing was performed by high-resolution sequence-based typing method. Results Our analysis revealed higher frequency of C∗07:02:01, B∗39:06:02, C∗03:02:01, B∗44:03:01, B∗51:01:05, and B∗73:01 (p < 0.05; OR = 1.84–9.98) and of two haplotypes—A∗68:01:02-C∗07:02:01 (p = 1.05E − 05; OR = 23.99) and B∗35:01:01-C∗07:02.01 (p = 4.15E − 04, OR = 2.15)—in A H1N1/09 influenza subjects. A∗68:01:01 was exclusively present only in the INF-P group (5/138). A decrease in the frequency of C∗03:03:01, A∗11:01:01, B∗39:01:01, A∗24:02:01, C∗03:04:01, B∗51:01:01, and C∗07:01:01 (p < 0.05; OR = 0.12–0.52) and of haplotypes A∗02:01:01-B∗35:01:01-C∗04:01:01, A∗24:02:01-B∗35:01:01, B∗39:01:01-C∗07:02:01, and B∗40:02:01-C∗03:04:01 (p < 0.05; OR = 0.08–0.22) were observed in INF-P group. Conclusion Selective classical HLA class I allele and haplotype combinations predispose individuals towards susceptibility or protection against the influenza A H1N1/09 pandemic. This work has significant implications for accessing population transmission risk for A H1N1/09 or a similar strain breakout in the future.