ABSTRACT
INTRODUCTION: Double-layer dermal grafts are used for the management of complicated abdominal wall hernias in obese, high risk patients. The method has not yet been used in case of emergency in septic/dirty environment. CASE REPORT: A 76-year old female patient (BMI 36.7kg/m2) was admitted with mechanical bowel obstruction and sepsis caused by a third time recurred, incarcerated and eventrated abdominal wall hernia. During the emergency surgery perforation of the terminal ileum and the ascending colon was detected, along with a feculent peritonitis and extended abdominal wall necrosis. Extended right hemicolectomy and necrectomy of the abdominal wall were performed. The surgery resulted in an abdominal wall defect measuring 223cm2, for the management of which direct closure was not possible. Using a specific method, an autologous dermal graft was prepared from the redundant skin. The first dermal graft was placed under the abdominal wall with 5cm overlap, and the second layer was placed onto the first layer with 3cm overlap in a perforated fashion. The operating time was 250min. No significant intra-abdominal pressure elevation was measured. No reoperation was performed. On the fifth postoperative day, the patient was mobilised. She was discharged in satisfactory general condition on the 18th postoperative day. There is no recurrent hernia 8 months after the surgery. DISCUSSION: Abdominal wall reconstruction was possible in a necrotic, purulent environment by using a de-epithelised autologous double layer dermal graft, without synthetic or biological graft implantation. The advantage of the procedure was cost-effectivity, and the disadvantage was that only in an obese patient is the sufficient quantity of dermal graft available. CONCLUSION: A homogeneous internal and perforated outer dermal graft was suitable for bridging the abdominal gap in the case of an obese, high risk patient. Autologous dermal grafts can be a safe and feasible alternative to biological meshes in emergency abdominal wall surgeries. Evaluation of a case series can be the next cornerstone of the method described above.
ABSTRACT
AIMS: Doxorubicin (DOX) is widely used in cytostatic treatments, although it may cause cardiovascular dysfunction as a side effect. DOX treatment leads to enhanced free radical production that in turn causes DNA strand breakage culminating in poly(ADP-ribose) polymerase (PARP) activation and mitochondrial and cellular dysfunction. DNA nicks can activate numerous enzymes, such as PARP-2. Depletion of PARP-2 has been shown to result in a protective phenotype against free radical-mediated diseases, suggesting similar properties in the case of DOX-induced vascular damage. METHODS AND RESULTS: PARP-2(+/+) and PARP-2(-/-) mice and aortic smooth muscle (MOVAS) cells were treated with DOX (25 mg/kg or 3 µM, respectively). Aortas were harvested 2-day post-treatment while MOVAS cells were treated with DOX for 7 hours. Aortas from PARP-2(-/-) mice displayed partial protection against DOX toxicity, and the protection depended on the conservation of smooth muscle but not on the conservation of endothelial function. DOX treatment evoked free radical production, DNA breakage and PARP activation. Importantly, depletion of PARP-2 did not quench any of these phenomena, suggesting an alternative mechanism. Depletion of PARP-2 prevented DOX-induced mitochondrial dysfunction through SIRT1 activation. Genetic deletion of PARP-2 resulted in the induction of the SIRT1 promoter and consequently increased SIRT1 expression both in aortas and in MOVAS cells. SIRT1 activation enhanced mitochondrial biogenesis, which provided protection against DOX-induced mitochondrial damage. CONCLUSION: Our data identify PARP-2 as a mediator of DOX toxicity by regulating vascular SIRT1 activity and mitochondrial biogenesis. Moreover, to the best of our knowledge, this is the first report of SIRT1 as a protective factor in the vasculature upon oxidative stress.
