Pediatric Allergy Immunology and Pulmonology最新文献

Objective: Previous reports have indicated the close association of allergy with adenoid hypertrophy (AH). The aim of this study was to evaluate whether the inflammatory cells and total immunoglobulin E (IgE) in blood could be useful in the diagnosis of allergy in AH. Methods: Two hundred thirty-four children who underwent adenoidectomy were retrospectively enrolled in this study. Blood routine parameters were recorded, and total IgE as well as specific IgE (sIgE) of common allergens were tested perioperatively. The diagnostic utility of blood inflammatory cells and total IgE compared with serum sIgE testing was assessed. Results: In our study, 35.47% of AH children were atopic. Dermatophagoides farinae (d2), Dermatophagoides pteronyssinus (d1), and mold (mx2) were the most common sensitizing allergens. Significantly elevated eosinophil count, eosinophil to lymphocyte value, and total IgE were found in allergic AH children. As a result of receiver operating characteristic analysis, systemic total IgE could be a method to diagnose allergy in AH with a cutoff value of 46.55 and higher (area under curve [AUC] = 0.837; P < 0.001). Peripheral eosinophil count and eosinophil to lymphocyte were also able to predict positive allergy test result in AH children, with a cutoff value of 0.295 (AUC = 0.721; P < 0.001) and 0.082 (AUC = 0.685; P < 0.001), respectively. Conclusion: The presence of allergy can be distinguished by looking at peripheral total IgE and/or blood eosinophils in AH, which will guide us to the precise treatment of AH and also reduce the cost considerably.

Background: Studies suggest that children with asthma experienced improved symptom control and less frequent inpatient admission during the COVID-19 (coronavirus disease 2019) pandemic. The characteristics of hospitalized children remain less well defined. Methods: This retrospective cohort study compared patients admitted for asthma during the pandemic with patients hospitalized the year prior at a children's hospital in the Bronx, New York. Results: In the year before the pandemic, 667 children were hospitalized for asthma, compared with 177 children the following year. Children admitted during the pandemic were older (7.8 versus 7.0 years, P = 0.04), more likely underweight (P < 0.01), and more likely to have public insurance (P = 0.02). Additionally, children hospitalized during the pandemic required intensive care (P = 0.03) and magnesium sulfate (P = 0.05) more frequently. Despite this, length of stay remained similar. Conclusion: While inpatient utilization for asthma decreased during the pandemic, children hospitalized were sicker on presentation. The cause of this is likely multifactorial and requires further study.

Background: Most cases of food-dependent exercise-induced anaphylaxis (FDEIA) are caused by eating wheat or crustaceans. However, fruits or vegetables may rarely act as allergens for FDEIA. We report a rare case of FDEIA caused by eating carrots. Case Presentation: An 8-year-old boy developed an anaphylactic reaction while playing, after eating lunch that included cooked carrots. Serum carrot-specific immunoglobulin E level was 0.19 UA/mL. The prick-by-prick test for raw carrots was positive (wheal diameter: 4 mm). The patient developed urticaria after exercise provocation tests following ingestion of raw carrots. Carrot proteins were analyzed by 2-dimensional Western blotting to identify the causative allergens. Nine proteins were identified as candidate antigens at 21-66 kDa. Conclusions: Our patient presented with FDEIA symptoms after ingesting both raw and cooked carrots. Both raw and cooked carrots contain 9 proteins that may induce FDEIA.

Background: Necrotizing pneumonia rarely occurs in children, but when it does it can be complicated by bronchopleural fistula, empyema, pneumothorax, sepsis, and acute respiratory distress syndrome (ARDS). Antimicrobial therapy is the cornerstone of its management; however, surgery is necessary in some cases. Ideally, surgical interventions are kept to a minimum, but this is not always possible if there is a mass effect from air and fluid in the pleural space, pulmonary necrosis leading to massive hemoptysis, uncontrolled sepsis, or difficulties with assisted ventilation. Case Presentation: Herein we present a patient with refractory pyopneumothorax and ARDS due to pneumococcal necrotizing pneumonia complicated by a bronchopleural fistula. The patient's clinical condition deteriorated despite antibiotics, surgical drainage, and assisted ventilation. Owing to pneumothorax with a high percentage of air leakage, bilateral diffuse collapse of the lungs, and insufficient oxygenation, surgical treatment was considered, but because of the patient's lack of tolerance for surgery due to hemodynamic reasons and the complications associated with surgery, medical treatment was determined to be more appropriate. Surfactant treatment was administered to the patient, resulting in significant clinical improvement. Conclusion: To the best of our knowledge, this is the first report of the use of surfactant to treat ARDS due to necrotizing pneumonia. Based on the presented case, we think surfactant can be considered as a salvage treatment for such patients.

Background: Previously, lipopolysaccharide-responsive beige-like anchor (LRBA) deficiency was categorized as a subtype of common variable immune deficiency. Research shows that LRBA deficiency is caused by dysregulation of T cell activation and expansion; it is placed under the category of immune dysregulation with cytotoxic T lymphocyte-associated protein 4 (CTLA-4) haploinsufficiency. Cohort studies have revealed a broad spectrum of clinical manifestations and variable phenotype expression, including immune dysregulation [enteropathy, autoimmune cytopenia, interstitial lung disease (ILD), etc.] on 1 hand and immune deficiency (hypogammaglobulinemia, recurrent infections, bronchiectasis, etc.) on the other hand. Chronic lung disease is frequently seen in LRBA deficiency and is associated with poor outcomes. Case Presentation: This case report evaluates a female who presented with recurrent pneumonia and bronchiectasis but did not respond to treatment; she was lastly diagnosed with ILD with detailed clinical, radiological, and pathological workup. Conclusions: The respiratory characteristics of patients with LRBA deficiency should be investigated, monitored, and treated from the time of its diagnosis. The awareness and involvement of pulmonologists to pulmonary morbidity of patients with LRBA deficiency in workup and clinical decision making are crucial.

Background: Mutations in the ATP-binding cassette transporter A3 (ABCA3) gene are one of the most common surfactant disorders leading to interstitial lung diseases (ILD). The clinical spectrum and severity of lung disease caused by ABCA3 deficiency due to missense variants is variable. Case Presentations: A novel ABCA3 c.3135G>C (p.Gln1045His) mutation was identified at the homozygous state in 3 subjects from 2 unrelated families: one 19-month-old boy with severe ILD and his homozygous pauci-symptomatic mother, and one 10-year-old girl with moderate late-onset ILD. Corticosteroid pulses associated with hydroxychloroquine were beneficial for both children. Conclusion: We illustrate here the huge intra- and interfamilial phenotypic variability associated with the same homozygous missense ABCA3 mutation, and the benefit of identifying the disease for treatment, follow-up, and appropriate genetic counseling.

Introduction: Sideroblastic anemia with B cell immunodeficiency, periodic fevers, and developmental delay (SIFD) syndrome is caused by biallelic TRNT1 mutations. TRNT1 gene encodes a CCA-adding tRNA nucleotidyl transferase enzyme. Mutant TRNT1 results in immunodeficiency and anemia in various degrees, accompanied by several organ involvement. Case Presentation: We present here a 15-month old male, demonstrated brittle hair, growth hormone deficiency, recurrent fever, arthritis, recurrent infections, mild anemia, and hypogammaglobulinemia. The patient did not respond to colchicine treatment, and after establishing SIFD diagnosis with the presence of homozygote c.948-949delAAinsGG (p.Lys317Glu) mutation in TRNT1 gene, we commenced monthly intravenous immunoglobulin replacement and weekly subcutaneous etanercept. A rapid resolution of fever episodes and infections occurred after initiation of this treatment regimen. Afterward, both anemia and growth parameters have improved during follow-up. Conclusion: SIFD syndrome should be considered in patients with recurrent fever, arthritis, and growth retardation even in the absence of severe anemia and prominent hypogammaglobulinemia.