[Risk factors and prevention of incisional hernia--what is evidence-based?]. / Risikoprofil und Rezidivprophylaxe der Narbenhernie--was ist evidenzbasiert?

Incisional hernia is a late complication of laparotomy for which an evidence-based prohylactic approach is still lacking. Postoperatively, incisional hernias occur because of multiple factors. Preoperative comorbidities belong to these risk factors. A risk reduction related to concomitant diseases mostly does not succeed. There is a range of studies comparing the techniques of surgical wound closure. A consensus of these is that a running suture of the fascia with slowly absorbable or non-absorbable sutures results in the lowest incidence of incisional hernias. A one-cm distance between the stitches and a minimal distance of one cm to the fascial margin as well as a 4:1 suture length to wound length ratio are still valid principles. In any case, solely optimising the surgical technique of the abdominal wall closure is not able to reduce the incidence of incisional hernias. Prevention of postoperative complications by adequate pain management, respiratory training and early mobilisation are procedures to reduce the incidence of incisional hernias. However, systematic studies are lacking. To avoid an incisional hernia, only a practical approach remains which, however, does not meet the requirements of evidence-based medicine.

MMP-9 in serum correlates with the development of pulmonary complications in experimental acute pancreatitis.

INTRODUCTION: The prediction of the course of acute pancreatitis and its arising complications is of clinical importance. The aim of this study was to judge the time course and relevance of matrix metalloproteinase-9 (MMP-9), a PMN-derived protease, for the development of pulmonary complications in two models of acute pancreatitis. METHODS: MMP-9 was evaluated in a standardized experimental model of acute pancreatitis. Mild edematous (n = 12) and severe necrotizing pancreatitis (n = 48) were induced by intravenous cerulein or intravenous cerulein and intraductal application of glycodeoxycholic acid and compared to control animals. 1, 6, 9, 12, 24 and 72 h after induction, rats were sacrificed and damage to the lung and the pancreas was quantified by histology and extravasation of Evans blue. At 1, 6, 9, 12, 24 and 72 h, we determined MMP-9 in serum by ELISA. RESULTS: In our model, MMP-9 in serum was increased in the group with severe acute pancreatitis in comparison to mild edematous pancreatitis and controls at each evaluated time point (p < 0.05). The maximum release of MMP-9 preceded the development of pulmonary complications, verified by histology and extravasation of Evans blue. MMP-9 showed a negative predictive value of 96.2% and a positive predictive value of 100% for the development of pulmonary complications. CONCLUSION: MMP-9 in serum allows a valid grouping to severe and mild courses of experimental acute pancreatitis with a good predictive value for the development of pulmonary complications. MMP-9 should be evaluated as a valid single marker for the prediction of progression and the development of pulmonary complications in acute pancreatitis in clinical studies.

Oxidized lipoproteins increase reactive oxygen species formation in microglia and astrocyte cell lines.

Lipoproteins exist in the central nervous system and surrounding vasculature possibly mediating effects upon cells in the brain during times of oxidative stress or compromised blood-brain barrier. The focus of the present study was to determine the effect of unmodified and oxidatively modified lipoproteins on astrocytes and microglia. Application of oxidized low-density lipoprotein resulted in an increase in DCF fluorescence, which was inhibited by pretreatment with antioxidants, consistent with the formation of reactive oxygen species (ROS). Low-density at concentrations below 20 microg/ml likewise increased ROS formation. Because ROS are associated with numerous astrocyte and microglia activities including proliferation, activation, and cytokine production it is possible that lipoproteins may mediate such effects on glial cells in the central nervous system.

Opposing actions of native and oxidized lipoprotein on motor neuron-like cells.

Lipoproteins are present in the central nervous system and surrounding vasculature and possibly mediate effects relevant to neuronal physiology and pathology. To determine the effects of lipoproteins on motor neurons, native low density lipoproteins (LDL) and oxidized LDL (oxLDL) were applied to a motor neuron cell line. Oxidized LDL, but not native LDL, resulted in a dose- and time-dependent increase in reactive oxygen species and neuron death. Oxidized LDL-induced toxicity was attenuated by a calcium chelator, antioxidants, caspase inhibitors, and inhibitors of macromolecular synthesis. In addition to being nontoxic, application of native LDL attenuated reactive oxygen species formation and neuron loss following glucose deprivation injury. Together, these data demonstrate a possible neuroprotective role for unmodified lipoproteins and suggest oxidized lipoproteins may amplify oxidative stress and neuron loss.