Operative and non-operative management of endoscopic retrograde cholangiopancreatography-associated duodenal injuries.

INTRODUCTION: Endoscopic retrograde cholangiopancreatography (ERCP) is indispensable in everyday surgical practice. Despite this, as an invasive procedure, it has its own mortality and morbidity, the most feared of which is periduodenal perforations. Our experience with ERCP related periduodenal perforations and its treatment strategies are presented. Additionally, a rarely encountered subtype is highlighted. METHODS: Patients who underwent ERCP and sustained a periduodenal perforation between August 2008 and October 2011 were reviewed. RESULTS: During the period from August 2008 to October 2011, 597 ERCP procedures were performed in our hospital. Ten of these patients (3 male, 7 female) had a perforation. The mean patient age was 56.6 years. During the procedure, injury was suspected in four patients; it passed unnoticed in the remaining six. The decision to operate or follow a conservative policy was based on a combination of clinical and radiological findings. Operative intervention was required in three patients, with one mortality, while conservative treatment was followed in the remaining seven. A laparotomy was performed early in two patients whereas it was performed after an initial period of conservative treatment in one. The presence of periduodenal fluid collection, contrast extravasation or free intraperitoneal air were decisive factors for performing laparotomy. CONCLUSIONS: ERCP-related periduodenal perforations include different categories. Certain types require operative repair while others should be treated conservatively. The choice of the management approach should be individualised, depending on the clinical picture and radiological findings. Although rare, these are potentially serious complications that may end fatally. Early recognition and appropriate intervention is the only way to avert a fatal outcome.

The incapability of interleukin-4 to induce AP-1 activity in murine mast cells.

The results presented in this study shed new light on the molecular mechanism responsible for the control of interleukin (IL)-3- and IL-4 mediated mast cell proliferation. By measurements of AP-1 DNA-binding activity, it was found that IL-3 induced such activity while IL-4 did not. This difference in the pattern of AP-1 DNA-binding activity induced by each lymphokine indicates the differential involvement of AP-1 in the different proliferative responses of mast cells to IL-3 and IL-4.

Enhancement of interleukin-3-dependent mast cell proliferation by suppression of c-jun expression.

We have previously shown that protein kinase C (PKC) depletion is associated with an increase in the proliferation of interleukin 3 (IL-3)-induced mast cells. Here we show that the AP-1 components c-Jun and c-Fos are induced by IL-3. While c-Jun's induction by IL-3 is totally dependent on PKC, c-Fos induction by IL-3 is only attenuated by PKC depletion. AP-1 binding activity was also induced by IL-3 but this induction was PKC independent. These results indicated a possible involvement of c-Jun in the inhibition of IL-3-induced growth regulation. A support for this assumption came from experiments in which an increase in thymidine incorporation into mast cells was noted when c-jun antisense oligomers were administered to IL-3-treated cells. Since the only known effect of direct inhibition of c-Jun on proliferation rates in several cellular systems was a reduction of proliferation, we verified that our c-jun antisense oligomer could also inhibit proliferation rates in fibroblasts where such a repression was previously reported. Thus c-Jun has an inhibitory effect on IL-3 induction of mast cells proliferation that is distinct from its role in several other cellular environments. These observations reveal the involvement of AP-1 and its components in IL-3-induced signal transduction and the importance of the mast cell environment in determining their specific cellular function.