Serious complications after button battery ingestion in children

Serious and fatal complications after button battery ingestion are increasing worldwide. The aim of this study is to describe serious complications after battery ingestion in children in the Netherlands. All pediatric gastroenterologists in the Netherlands performing upper endoscopies were asked to report all serious complications after battery ingestion in children (0–18 years) between 2008 and 2016 retrospectively. Sixteen serious complications were reported: death after massive bleeding through esophageal-aortal fistula (n = 1), esophageal-tracheal fistula (n = 5), stenosis after (suspected) perforation and mediastinitis (n = 5), (suspected) perforation and mediastinitis (n = 3), vocal cord paralysis (n = 1), and required reintubation for dyspnea and stridor (n = 1). The median time interval between ingestion and presentation was 5 (IQR 2–258) h. All children were ≤ 5 (median 1.4; IQR 0.9–2.1) years. Vomiting (31.3%), swallowing/feeding problems (31.3%), and fever (31.3%) were the most common presenting symptoms; however, 18.8% of the patients were asymptomatic (n = 1 missing). All batteries were button batteries (75% ≥ 20 mm; 18.8% < 20 mm; n = 1 missing). The batteries were removed by esophagogastroduodenoscopy (50%) and rigid endoscopy (37.5%) or surgically (12.5%). Conclusion: Sixteen serious complications occurred after small and large button batteries ingestion between 2008 and 2016 in both symptomatic and asymptomatic children in the Netherlands. Therefore, immediate intervention after (suspected) button battery ingestion is required.(Table presented.

Proposed model for the interaction between intestinal and lung impairment in cystic fibrosis (CF).

<p>Intestinal alterations due to CFTR dysfunction may result in malnutrition with consistent respiratory muscle weakness and comprised innate lung defences [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0138062#pone.0138062.ref054" target="_blank">54</a>], an impaired barrier function with consequent bacterial translocation to the lungs, and release of inflammatory mediators (cytokines such as interleukin (IL)-8, IL-1 and tissue necrosis factor (TNF)-a, immunoglobulins, lactoferrin, neutrophil elastase, and calprotectin [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0138062#pone.0138062.ref011" target="_blank">11</a>–<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0138062#pone.0138062.ref017" target="_blank">17</a>]) into the systemic circulation, contributing to lung inflammation and impaired lung function. Inflammatory mediators in the lung (cytokines such as IL-8, IL-6, IL-1 and TNF-a, complement factor 5A, neutrophils, proteases (elastase), oxigen radicals, and leukotriene B4 [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0138062#pone.0138062.ref058" target="_blank">58</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0138062#pone.0138062.ref059" target="_blank">59</a>]) are released into the systemic circulation and will reach the intestine or, alternatively, can be swallowed with sputum (together with lung bacteria) and enter the gastrointestinal tract. Further, impaired lung function may result in splanchic hypoperfusion and intestinal hypoxia affecting the intestine. Taken together, this may contribute to intestinal inflammation and impairment and explain the complex interrelationship between CF enteropathy and lung function.</p

A Pilot Study on the Noninvasive Evaluation of Intestinal Damage in Celiac Disease Using I-FABP and L-FABP

Background and Goals: In the clinical management of celiac disease, new noninvasive tools for evaluation of intestinal damage are needed for diagnosis and for follow-up of diet effects. Fatty acid binding proteins (FABP) are potentially useful for this purpose as these arc small cytosolic proteins present in enterocytes and sensitive markers for intestinal mucosal damage. First, the distribution and microscopic localization of FABP in the healthy human intestine was examined. Second. levels of circulating FABP were measured in patients with celiac disease before and after introducing a gluten-free diet (GFD) and in healthy controls. Study: The distribution and microscopic localization of FABP in normal human intestinal tissue was assessed using surgical intestinal specimens of 39 patients. Circulating levels of intestinal (I)-FABP and liver (L)-FABP were determined in 26 healthy volunteers and 13 patients with biopsy proven celiac disease. Ten of these patients were reevaluated within 1 year after starting GFD. Results: I-FABP and L-FABP are predominantly present in the small intestine, mainly the jejunum. Moreover, FABP are expressed in cells on the upper part of the villi, the initial site of destruction in celiac disease. Circulating levels of FABP are significantly elevated in untreated patients with biopsy proven celiac disease compared with healthy controls (I-FABP: 784.7 pg/mL vs. 172.7 pg/mL, P <0.001: L-FARP: 48.4 ng/mL vs. 10.4 ng/mL, P <0.001). In response to GFD, these concentrations normalize. Conclusions: Results of this pilot study strongly suggest that FABP can be used as a noninvasive method for assessment of intestinal damage in celiac disease. Besides an additional role in the diagnosis of celiac disease. FABP potentially enable noninvasive monitoring of the GFD effects

Serum I-FABP levels were significantly elevated in cystic fibrosis patients as compared with control subjects.

<p>Boxplot of serum I-FABP concentrations in the study groups, showing the median, the 25^th percentile, the 75^th percentile and the range of values. * Significant difference, p<0.001.</p

Distribution of faecal calprotectin levels in patients with cystic fibrosis (CF).

<p>The upper normal limit for faecal calprotectin (50 ug/g) is indicated by the dashed line.</p