Asthma is a common pulmonary disease with chronic inflammation of the airways, and obesity is a chronic state of low-grade inflammation. Toll-like receptors (TLRs) are involved in the innate immune response. This study was designed to analyze whether obesity has an effect on the immune response of patients with asthma. We included obese asthmatic, obese, asthmatic, and healthy children. Biochemical and anthropometric analyses were performed. Interleukin (IL)-2, interferon (IFN) gamma, IL-4, IL-10, IL-1beta, and tumor necrosis factor alpha were measured. Peripheral blood mononuclear cells were analyzed by immunostaining with anti-TLR2 and anti-TLR9 antibodies. The data were expressed as means ± SEM or medians and percentiles. Kruskal-Wallis test and Dunn's multiple comparison test were applied. Asthmatic patients, both obese and nonobese, exhibited a mild asthma phenotype; none had infectious process, exacerbation, or acute symptoms during the 30 days before the inclusion in the study. The IL-2 and IFN-gamma levels in the obese asthmatic group were lower than in the other three groups. IL-4 levels in the obese asthmatic group were almost equal to those of the asthmatic group and more than in the other two groups, without significant difference. There were higher levels of TLR2 and TLR9 in obese asthmatic patients than in the other three groups. There is a decrease in Th1 cytokines in obese asthmatic patients, and we only found a trend to an increased Th2 profile. Patients studied do not appear to fit into any of the endotypes described until now. This is the first study showing the high expression of TLR2 and TLR9 in obese asthmatic patients. It is necessary to study other cytokines in obese asthmatic patients to see if it is possible to fit them into any of the already described endotypes or if it is a distinct endotype.
Antecedentes: El síndrome de enterocolitis inducida por proteínas de los alimentos es una alergia alimentaria poco frecuente no mediada por IgE. El síntoma principal son los vómitos una a cuatro horas después del consumo del alimento causal.Caso clínico: Varón de ocho meses, sin antecedentes heredofamiliares de alergia, con antecedentes personales patológicos de alergia a la proteína de la leche de vaca. A los siete meses había presentado gastroenteritis aguda con choque mixto y a los ocho meses, gastroenteritis aguda y deshidratación moderada; en ambos eventos hubo consumo de arroz previo al inicio de los síntomas. Al descartar etiología infecciosa y otras causas de vómitos y deshidratación, se formuló el diagnóstico de síndrome de enterocolitis inducida por proteínas de los alimentos, secundario a proteína de arroz, que se corroboró con prueba de parche.Conclusión: El síndrome de enterocolitis inducida por proteínas de los alimentos debe ser considerado en el diagnóstico diferencial de gastroenteritis recurrente, principalmente en cuadros graves sin causa infecciosa identificada.
INTRODUCCIÓNLas inmunodeficiencias primarias son enfermedades hereditarias generalmente causadas por alteraciones monogénicas. Pueden afectar el sistema inmunitario en su desarrollo, su función, o en ambos.1 Se clasifican de acuerdo con la afección particular del sistema inmuno-
ABSTRACTPrimary immunodeficiencies (PID) are genetic diseases affecting immunological normal response. In the great majority of cases affected individual sare predisposed to recurrent and / or severe infections with impaired quality of life (QoL). The most frequent PID are defects in the production of antibodies. When diagnosis and treatment are not done properly, permanent damage may occur in affected organs and further affecting QoL.Objective: To evaluate QoL in patients with antibody PID compared with QoL of healthy controls.
Methods:Cross-sectional study with the application of the instrument "Pediatric Quality of Life Inventory" (PedsQL) in its Mexican Spanish validated version. The PedsQL score difference between children with PID and healthy children was determined by the Student t test. The effect of a delayed in diagnosis was evaluated by analysis in a covariance model. 28 patients were included. The median age was 5 years and 5 months.
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