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Introduction Because many aspects of the management of esophageal atresia (EA) are still controversial, we evaluated the practice patterns of this condition across Europe. Methods A survey was completed by 178 delegates (from 45 [27 European] countries; 88% senior respondents) at the EUPSA-BAPS 2012. Results Approximately 66% of respondents work in centers where more than five EA repairs are performed per year. Preoperatively, 81% of respondents request an echocardiogram, and only 43% of respondents routinely perform preoperative bronchoscopy. Approximately 94% of respondents prefer an open approach, which is extrapleural in 71% of respondents. There were no differences in use of thoracoscopy between Europeans (10%) and non-Europeans (11%, p ¼ nonsignificant). Approximately 60% of respondents measure the gap intraoperatively. A transanastomotic tube (90%)

Biliary atresia (BA) is the most frequent indication for paediatric liver transplantation. We tested the hypothesis of a viral aetiology of this disease by screening liver samples of a large number of BA patients for the common human hepatotropic viruses. Moreover, we correlated our findings to the expression of Mx protein, which has been shown to be significantly up-regulated during viral infections. Seventy-four liver biopsies (taken during Kasai portoenterostomy) were tested by polymerase chain reaction (PCR) for DNA viruses (herpes simplex virus [HSV], Epstein-Barr virus [EBV], varicella zoster virus [VZV], cytomegalovirus [CMV], adenovirus, parvovirus B19 and polyoma BK) and RNA viruses (enteroviruses, rotavirus and reovirus 3). Mx protein expression was assessed by immunohistochemistry. Virus DNA/RNA was found in less than half of the biopsies (8/74 CMV, 1/74 adenovirus; 21/64 reovirus, 1/64 enterovirus). A limited number presented with double infection. Patients that had detectable viral RNA/DNA in their liver biopsies were significantly older than virus-free patients (P = 0.037). The majority (54/59) of the liver biopsies showed expression of Mx proteins in hepatocytes, bile ducts and epithelium. Our data suggest that the known hepatotropic viruses do not play a major role in the aetiology and progression of BA. Their incidence appears to be, rather, a secondary phenomenon. Nonetheless, the inflammatory response in the livers of BA patients mimics that observed during viral infections.

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The acute respiratory distress syndrome (ARDS) is a major cause of morbidity after injury. We hypothesized that alveolar macrophage (AMΦ) chemokine and cytokine release after hemorrhage and sepsis is regulated by NF-κB and MAPK. Adult male rats underwent soft tissue trauma and hemorrhagic shock (∼90 min) followed by crystalloid resuscitation. Sepsis was induced by cecal ligation and puncture (CLP) 20 h after resuscitation. AMΦ were harvested, and TNF-α, IL-6, and macrophage inflammatory protein (MIP)-2 release and serum IL-6 and TNF-α levels were measured at 5 h after HCLP. Lung tissues were analyzed for activation of NF-κB, myeloperoxidase activity, and wet/dry weight ratio. In control animals, AMΦ were stimulated with LPS with or without inhibitors of NF-κB and MAPK. Serum TNF-α and IL-6 levels and spontaneous AMΦ TNF-α and MIP-2 release were elevated ( P < 0.05) after HCLP, concomitantly with the development of lung edema and leukocyte activation. Activation of NF-κB increased in lungs from the hemorrhage and CLP group compared with shams. Inhibition of NF-κB or the upstream MAPK significantly decreased LPS-stimulated AMΦ activation. Because enhanced release of inflammatory mediators by AMΦ may contribute to ARDS after severe trauma, inhibition of intracellular signaling pathways represents a target to attenuate organ injury under those conditions.

In livers of mice with BA, γδ T cells produce IL17, which is required for inflammation and destruction of the biliary system. IL17 is up-regulated in liver tissues from patients with BA, compared with controls, and might serve as a therapeutic target.

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