Edy David Rubio Arellano

Lupus nephritis (LN) is a severe immune-mediated renal disorder causing significant morbidity and mortality in patients with systemic lupus erythematosus (SLE). Traditional biomarkers (serum complement components C3 and C4 and anti-dsDNA antibodies) have limited sensitivity and specificity for detecting renal flares; thus, new markers are needed to improve relapse detection and therapeutic response monitoring. We conducted a cross-sectional study including 71 women with SLE and 20 age- and sex-matched controls. Clinical data were collected, global activity was evaluated using the SLEDAI, and renal activity was evaluated using the renal SLEDAI (rSLEDAI). Serum syndecan-1 (SDC-1) and anti-dsDNA were measured using ELISA, and 24 h proteinuria was quantified. According to the rSLEDAI, 38 patients (53.5%) had LN flare, with a mean SDC-1 level of 108.5 ± 69.3 ng/mL and anti-dsDNA level of 113.1 ± 148.8 IU/mL. SDC-1 was correlated with the rSLEDAI (r = 0.32; p = 0.006), prednisone dose (r = 0.37; p = 0.002), proteinuria (r = 0.33; p = 0.005), and anti-dsDNA (r = 0.33; p = 0.006), while anti-dsDNA was positively correlated with proteinuria (r = 0.39; p = 0.001 and SDC-1 (r = 0.33; p = 0.006) and negatively correlated with age (r = −0.33; p = 0.006). High SDC-1 (cutoff ≥ 89 ng/mL) had higher sensitivity for detecting renal flares than anti-dsDNA (66% vs. 45%). In the multivariable analysis, high SDC-1 levels had around a 3-fold higher risk of being associated with LN flares, independently of anti-dsDNA and complement component levels. These results support serum SDC-1 as a promising biomarker for identifying renal flares in SLE patients, and it should be combined with traditional biomarkers to increase its value as a clinical tool. Follow-up studies are required to determine its value for predicting long-term renal outcomes.

Introducción: Los protocolos de Recuperación Acelerada tras la Cirugía (ERAS) han demostrado reducir la morbilidad y la estancia hospitalaria en cirugía colorrectal. No obstante, su implementación en países de ingresos medios (PIM) enfrenta desafíos particulares relacionados con los recursos disponibles, la infraestructura sanitaria y la adherencia a los protocolos. Objetivo: Sintetizar la evidencia disponible sobre los resultados clínicos y las barreras para la implementación de los protocolos ERAS en cirugía colorrectal en países de ingresos medios. Métodos: Se realizó una revisión sistemática conforme a las directrices PRISMA. Se efectuó una búsqueda bibliográfica en MEDLINE/PubMed, Embase, Scopus, Web of Science y Cochrane Library desde enero de 2005 hasta agosto de 2025. Dos revisores independientes seleccionaron los estudios, extrajeron los datos y evaluaron la calidad metodológica mediante la herramienta Cochrane RoB 2 para ensayos clínicos y la escala Newcastle-Ottawa para estudios de cohortes. Se incluyeron ensayos clínicos y cohortes comparativas que aplicaran protocolos ERAS en resecciones de colon o recto realizadas en países de ingresos medios. Debido a la heterogeneidad clínica de los estudios, se efectuó una síntesis narrativa. Resultados: La evidencia disponible en países de ingresos medios muestra una reducción consistente de la estancia hospitalaria, estimada entre uno y tres días, así como una tendencia hacia una menor tasa de complicaciones cuando la adherencia a los componentes del protocolo ERAS es elevada. La mortalidad y los reingresos no presentan diferencias significativas en comparación con el manejo convencional. Las principales barreras identificadas incluyen limitaciones de recursos —como analgesia regional, insumos para normotermia y terapia guiada por objetivos—, variabilidad en la cultura quirúrgica, ausencia de coordinadores ERAS, monitoreo insuficiente de la adherencia y restricciones logísticas para la movilización y nutrición tempranas. Conclusiones: Los protocolos ERAS son factibles y beneficiosos en cirugía colorrectal en países de ingresos medios; sin embargo, su impacto depende del grado de adherencia y de la adaptación a las condiciones locales. Su implementación requiere un enfoque escalonado, auditoría continua y priorización de intervenciones costo-efectivas

La reconstrucción de defectos complejos de la extremidad inferior (EEI) tiene como objetivos lograr una cobertura estable, prevenir osteomielitis e infecciones y restaurar la función de la extremidad. La elección entre colgajos locales o regionales y colgajos libres microquirúrgicos continúa siendo motivo de debate. El objetivo de este estudio fue comparar los resultados clínicos, las complicaciones y los criterios de selección entre colgajos locales y microcirugía para la cobertura de defectos de EEI. Se realizó una revisión sistemática conforme a PRISMA mediante búsqueda en PubMed/MEDLINE, Embase, Scopus y Cochrane Library de estudios comparativos y series relevantes relacionadas con trauma, infección y resección oncológica de EEI. Se incluyeron investigaciones en adultos que reportaran desenlaces de colgajos locales —musculares, fasciocutáneos, perforantes, sural reverso y propeller— frente a colgajos libres, como ALT, latissimus dorsi, fibular y gracilis. Los resultados muestran tasas de supervivencia global más altas y consistentes para los colgajos libres (aproximadamente 94–97%) en comparación con los colgajos locales o regionales (85–95%), especialmente en defectos extensos, distales o con exposición ósea e implantes. Los colgajos libres demostraron mayor durabilidad en defectos complejos, mientras que los colgajos locales presentaron menor tiempo operatorio y menor demanda de recursos. Se concluye que los colgajos libres constituyen la principal alternativa en defectos extensos o distales de alta complejidad, mientras que los colgajos locales continúan siendo estratégicos en defectos pequeños o medianos y en entornos sin microcirugía

MicroRNAs (miR) have emerged as key regulatory molecules in immune response and inflammation. This study investigated the association between the plasma expression levels of miR-146a-5p, miR-143-3p, miR-145-5p and rheumatoid arthritis (RA) clinical activity measured by standard tools such as the Simplified Disease Activity Index (SDAI). Forty-eight RA patients fulfilling the EULAR/ACR 2010 criteria and 39 clinical apparently healthy subjects (HS) were included. Patients were categorized based on disease clinical activity using standard scores. Expression levels of miR were determined by RT-qPCR to be analyzed in the context of disease clinical activity, serum inflammation markers and autoantibodies such as rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibodies (anti-CCP). Bioinformatic analysis was performed to assess gene interactions and signaling pathways. The expression of miR-146a-5p showed higher expression in patients with low or moderate clinical disease activity. In addition, miR-145-5p was negatively correlated with both RF and anti-CCP antibodies. Bioinformatic analysis revealed that the miRs could simultaneously regulate myosin VI (MYO6) and connective tissue growth factor (CTGF) genes. Our findings suggest that the plasma levels of the analyzed miR are associated with key serological markers and low to moderate disease clinical activity in RA patients according to SDAI score. The bioinformatics data supports the potential for these miRs to regulate genes involved in RA pathology.

Th17 cells are known for producing IL-17 and their role in the pathogenesis of various autoimmune diseases, including myositis. Likewise, the participation of the IL-23/IL-17 pathway in autoimmunity has been confirmed. In this study, we aimed to evaluate the behavior of cytokines in myositis, focusing on the autoantibodies profile and the myositis core set measures. Twenty-five myositis patients were enrolled in this cross-sectional study. An expert rheumatologist evaluated the myositis core set measures. Serum levels of cytokines and chemokines were quantified using the LEGENDplex Multi-Analyte Flow Assay Kit from BioLegend. The autoantibodies detection was carried out using the line-blot assay kit Euroline: Autoimmune Inflammatory Myopathies from EUROIMMUN. We found higher serum levels of IL-33, CXCL8, IL-6, IL-23, and IL-12p70 in seronegative patients. A multiple linear regression analysis revealed that MYOACT scores could be predicted by the increment of IL-23 and the decrement of CCL2, IL-10, and CXCL8 serum levels. These findings suggest that the immune response in seronegative myositis patients exhibits an IL-23-driven Th17 immune response. The relevance of this discovery lies in its potential therapeutic implications. Insights into the IL-23-driven Th17 immune response in seronegative patients highlight the potential for targeted therapies aimed at modulating Th17 activity.

Objectives: Mechanism of action of biological and synthetic disease-modifying antirheumatic drugs (DMARDs) includes the inhibition of specific proinflammatory cytokines. This study aimed to elucidate the cytokines and chemokines inhibited by different treatments (conventional synthetic DMARD [csDMARD], biological and targeted synthetic DMARD) in rheumatoid arthritis (RA). Methods: Fifty-nine RA patients with low disease activity or remission included in a cross-sectional study were classified by treatment in groups: abatacept, certolizumab, rituximab (RTX), tocilizumab, tofacitinib (TOF), baricitinib (BAR), and csDMARD. Cytokine and chemokine serum levels were measured by LEGENDplex Human Inflammation panel. Quantitative variables were compared using Student t or Mann-Whitney U test as appropriate, whereas qualitative variables were compared using χ² or Fisher exact test. p < 0.05 was considered significant. Results: Certolizumab, RTX, tocilizumab, and TOF showed that most cytokine pathways inhibited: tumor necrosis factor α, interferon γ, interleukin 1β (IL-1β), IL-12, IL-18, and IL-23; in addition, csDMARDs showed a similar inhibition patron except for IL-23. Serum level of tumor necrosis factor α pathway was one of the most inhibited being undetectable in RTX, TOF, and BAR groups. Interleukin 6 was shown to be inhibited by abatacept, RTX, and TOF; however, higher levels were observed in 3 patients treated with tocilizumab. Abatacept, certolizumab, RTX, and TOF downregulated IL-10 in this group of patients but remained detectable in almost half of the subjects, with the highest levels in the BAR group. The active pathways that remained the most were CC chemokine ligand 2, IL-8, IL-17, and IL-33. Conclusions: Understanding the cytokine chemokine pathways inhibition could help rheumatologists to prescribe a tailored therapy using the arsenal of DMARDs for individualized RA treatment in an evidence-based decision manner.

Anterior disc displacement with reduction (DDWR) is considered one of the most common disorders within the temporomandibular joint (TMJ), with a prevalence of 41% in adults. Matrix metalloproteinases play an important role in the degradation of the TMJ and the matrix metalloproteinase 1 (MMP1) 1607 1G/2G polymorphism increases the local expression of MMP1 thus leading to accelerated degradation of the extracellular matrix. The objective of this study was to evaluate the association between the 1607 1G/2G polymorphism of MMP1 gene and DDWR in a group of Mexican individuals from western Mexico. A total of 67 unrelated individuals, between the ages of 18 and 36 years, of both genders, were included in this study. Study participants with DDWR were required to meet the Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD), while a second control group of 90 individuals without DDWR were also included. Both groups were required to have paternal and maternal ancestry (grandparents) of the same geographic and ethnic region. Genotypes were determined using the nested PCR technique. The 1G/2G polymorphism was found in 68.7%, followed by 2G/2G in 25.4% and 1G/1G in 6.0% of the cases group. While the prevalence in the control group was 55.5% for the 1G/2G polymorphism, 26.6% for 1G/1G and 17.7% for 2G/2G. An association was found between the 2G allele of the 1607 1G/2G polymorphism of MMP1 gene and the presence of DDWR in the patients of western Mexico.

Background . Neuropeptide Y (NPY) is a sympathetic neurotransmitter with effects on the regulation of inflammatory cells. The role of NPY on autoimmune inflammatory diseases such as rheumatoid arthritis (RA) is not completely understood. Therefore, we evaluate if NPY levels are markers of disease activity in RA and if there is a correlation between NPY levels and tumor necrosis factor‐alpha (TNF‐ α ), leptin, and interleukin 6 (IL‐6) levels. Methods . Cross‐sectional design, including 108 women with RA. We assessed disease activity by DAS28‐ESR (considering active disease a score of ≥2.6). Serum NPY levels and anti‐CCP2 antibody, TNF‐ α , IL‐6, and leptin levels were quantified (ELISA). Results . Sixty‐eight RA had an active disease (RA‐active), and 40 were in remission (RA‐remission). RA‐active patients had higher NPY levels vs. RA‐remission (22.8 ± 13.6 vs. 17.8 ± 10.3; p = 0.04). NPY levels correlated with increased TNF‐ α levels ( r = 0.32, p = 0.001). Leptin or IL‐6 did not correlate with NPY levels. In the logistic regression analysis, NPY increased the risk of disease activity (OR: 1.04, 95% CI 1.006‐1.09, and p = 0.03). Conclusion . Higher NPY levels are an independent marker of disease activity in RA. This study encourages the quantification of NPY levels as a surrogate marker for RA‐active. Future studies evaluating the role of NPY levels interacting with other proinflammatory cytokines are required.