Objectives This study aims to describe the clinical presentation and outcome of patients diagnosed with acute ileitis in our pediatric emergency department. Methods We performed a retrospective study of all patients diagnosed with terminal ileitis by abdominal ultrasonography findings in our pediatric emergency department, over the years 2013 and 2014. Patients with previous diagnosis of inflammatory bowel disease (IBD) were excluded. Data collected were clinical, radiological, and laboratory data at diagnosis; outcome including hospitalization care; and outpatient follow-up in pediatric gastroenterology and/or primary care. Results A total of 20 cases were retrieved and studied. All of them presented with abdominal pain, 65% located in the right lower quadrant. Leukocyte count, C-reactive protein, and fibrinogen levels (means, 12,889; 4/μL; 50.1 mg/L; and 575 mg/dL, respectively) were above normal range. Hemoglobin and platelet count were normal. A microbial cause of ileitis was found in 3 cases (Yersinia enterocolitica, Campylobacter jejuni, and Adenovirus). Nine patients were referred to a pediatric gastroenterology unit. No cases of IBD were found. Conclusions Acute ileitis is a rare and benign cause of abdominal pain in the pediatric emergency department. The main intervention on initial assessment is to rule out potentially severe causes of abdominal pain that could benefit of an emergency surgical procedure. In contrast with adults and adolescents, acute ileitis in children does not have a clear association with development of IBD.

Pyogenic sacroilitis is an infrequent osteoarticular infection, and its diagnosis is a challenge in young children. A series of 20 cases is described. The median age was 15 months, 75% of them being under 2 years old. Fourteen (70%) reported fever. Refusal to sit was the main reason for consultation. Final diagnosis was confirmed by bone scintigraphy. All patients achieved a complete resolution without sequelae.

Background Data about safety and efficacy of the mRNA SARS-CoV-2 vaccine in adolescents with rheumatic diseases (RD) is scarce and whether these patients generate a sufficient immune response to the vaccine remains an outstanding question. Objective To evaluate safety and humoral and cellular immunity of the BNT162b2 vaccine in adolescents 12 to 18 years with RD and immunosuppressive treatment compared with a healthy control group. Methods Adolescents from 12 to 18 years with RD followed at Hospital La Paz in Madrid (n = 40) receiving the BNT162b2 mRNA vaccination were assessed 3 weeks after complete vaccination. Healthy adolescents served as controls (n = 24). Humoral response was measured by IgG antiSpike antibodies, and cellular response by the quantity of IFN-γ and IL-2 present in whole blood stimulated with SARS-CoV-2 Spike and M proteins. Results There were no differences in spike-specific humoral or cellular response between groups (median IFN-γ response to S specific protein; 528.80 pg/ml in controls vs. 398.44 in RD patients, p 0.78, and median IL-2 response in controls: 635.68 pg/ml vs. 497.30 in RD patients, p 0.22. The most frequent diagnosis was juvenile idiopathic arthritis (26/40, 65%) followed by Lupus (6/40, 15%). 60% of cases (23/40) received TNF inhibitors and 35% (14/40) methotrexate. 40% of patients (26/64) had previous SARS-CoV-2 infection, 9 in the control group and 17 in the RD patients without differences. Of note, 70% of infections were asymptomatic. A higher IFN-γ production was found in COVID-19 recovered individuals than in naive subjects in both groups (controls: median 859 pg/ml in recovered patients vs. 450 in naïve p 0.017, and RD patients: 850 in recovered vs. 278 in naïve p 0.024). No serious adverse events or flares were reported following vaccination. Conclusions We conclude that standard of care treatment for adolescents with RD including TNF inhibitors and methotrexate did not affect the humoral and the cellular immunity to BNT162b2 mRNA vaccination compared to a healthy control group. The previous contact with SARS-CoV-2 was the most relevant factor in the immune response.

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