Dispepsia no investigada y los factores de riesgos relacionados en estudiantes universitarios / Uninvestigated dyspepsia and related risk factorsin collegestudents

Introducción. La dispepsia no investigada es un síndrome que se caracteriza por la sensación de plenitud, molestias epigástricas, náuseas, entre otros síntomas, ya sea de forma recurrente o episodios aislados, para lo cual no se ha realizado una endoscopia para determinarla etiología. Para el diagnóstico clínico se utilizan los criterios de Roma IV. Materiales y Métodos. Estudio observacional descriptivo de corte transversal. Los alumnos del ciclo preclínico de la Universidad del Pacífico fueron sometidos al test diagnóstico OnSite H. PyloriAb Combo Rapid Test de CTK Biotech inc, que consiste en la técnica de inmunoensayo cromatográfico para detectar de forma cualitativa la presencia de anticuerpos en sangre. Los estudiantes completaron un cuestionario sobre los síntomas y factores de riesgo para adquirir dispepsia. Resultados. Se estudiaron 156 estudiantes con una edad media fue de 22,1 años, el 65% del sexo femenino, 55,1% del departamento Central. La prevalencia de dispepsia no investigada fue de 32,7%; y de anticuerpos anti H. Pylori14%. El 13% informó ser fumador de al menos 1 cigarrillo/día, el 71% refirió beber alcohol, y el 45% consumir AINES con una elevada frecuencia. Conclusión.La prevalencia de la dispepsia no investigada es elevada y seria imperativo adjudicarle una causa, o categorizarla como dispepsia funcional para poder emplear medidas terapéuticas. También es importante la identificación y control de posibles factores de riesgo para la patología. Palabras clave: dispepsia; helicobacter pylori; gastroenterología

Introduction. Uninvestigated dyspepsia is a syndrome characterized by a feeling of fullness, epigastric discomfort, nausea, among other symptoms, whether recurrent or isolated episodes, for which an endoscopy has not beenperformed to determine the etiology. For clinical diagnosis,the Rome IV criteria are used. Material and Methods.A cross-sectional descriptive observational study.Students from the preclinical cycle of the Universidad del Pacíficowere subjected to the OnSite H. PyloriAb Combo Rapid Test diagnostic test, from CTK Biotech inc, consistingin the chromatographic immunoassay technique to qualitatively detect the presence of antibodies in the blood.The students filled out a questionnaireon symptoms and risk factors to acquire dyspepsia. Results.A total of 156 students were studied with anaverage age of22.1 years, 65% female, 55,1% from the Central department. The prevalence of uninvestigated dyspepsia was 32,7%andof anti-H. Pyloriantibodies 14%;13% claimedto be a smoker of at least 1 cigarette/day, 71% reporteddrinking alcohol, and 45% consuming NSAIDs with a high frequency. Conclusion.The prevalence of uninvestigated Dyspepsia is high and it would be imperative to assign a cause or categorize it as functional dyspepsia in order to usetherapeutic measures. It is also important to identifyand control possible risk factors for the pathology. Key words: dyspepsia; helicobacter pylori; gastroenterology

Human PIK3R1 mutations disrupt lymphocyte differentiation to cause activated PI3Kδ syndrome 2.

Heterozygous loss-of-function (LOF) mutations in PIK3R1 (encoding phosphatidylinositol 3-kinase [PI3K] regulatory subunits) cause activated PI3Kδ syndrome 2 (APDS2), which has a similar clinical profile to APDS1, caused by heterozygous gain-of-function (GOF) mutations in PIK3CD (encoding the PI3K p110δ catalytic subunit). While several studies have established how PIK3CD GOF leads to immune dysregulation, less is known about how PIK3R1 LOF mutations alter cellular function. By studying a novel CRISPR/Cas9 mouse model and patients' immune cells, we determined how PIK3R1 LOF alters cellular function. We observed some overlap in cellular defects in APDS1 and APDS2, including decreased intrinsic B cell class switching and defective Tfh cell function. However, we also identified unique APDS2 phenotypes including defective expansion and affinity maturation of Pik3r1 LOF B cells following immunization, and decreased survival of Pik3r1 LOF pups. Further, we observed clear differences in the way Pik3r1 LOF and Pik3cd GOF altered signaling. Together these results demonstrate crucial differences between these two genetic etiologies.

Tracking the clonal dynamics of SARS-CoV-2-specific T cells in children and adults with mild/asymptomatic COVID-19.

Children infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) develop less severe coronavirus disease 2019 (COVID-19) than adults. The mechanisms for the age-specific differences and the implications for infection-induced immunity are beginning to be uncovered. We show by longitudinal multimodal analysis that SARS-CoV-2 leaves a small footprint in the circulating T cell compartment in children with mild/asymptomatic COVID-19 compared to adult household contacts with the same disease severity who had more evidence of systemic T cell interferon activation, cytotoxicity and exhaustion. Children harbored diverse polyclonal SARS-CoV-2-specific naïve T cells whereas adults harbored clonally expanded SARS-CoV-2-specific memory T cells. A novel population of naïve interferon-activated T cells is expanded in acute COVID-19 and is recruited into the memory compartment during convalescence in adults but not children. This was associated with the development of robust CD4+ memory T cell responses in adults but not children. These data suggest that rapid clearance of SARS-CoV-2 in children may compromise their cellular immunity and ability to resist reinfection.