19 research outputs found

    Peritonitis secondary to traumatic duodenal laceration in the presence of a large pancreatic pseudocyst: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>A pancreatic pseudocyst is a common sequela of severe acute pancreatitis. Commonly, it presents with abdominal pain and a mass in the epigastrium several weeks after the acute episode and can be managed conservatively, endoscopically or surgically. We report a patient with a pancreatic pseudocyst awaiting endoscopic therapy who developed a life-threatening complication following a rather innocuous trauma to the abdomen.</p> <p>Case presentation</p> <p>A 23-year-old Asian male student presented as an emergency with an acute abdomen a week after a minor trauma to his upper abdomen. The injury occurred when he was innocently punched in the abdomen by a friend. He experienced only moderate discomfort briefly at the time. His past medical history included coeliac disease and an admission four months previously with severe acute pancreatitis. He was hospitalized for 15 days; his pancreatitis was thought to be due to alcohol binge drinking on weekends. Ultrasound scanning showed no evidence of gallstone disease. Five days after the trauma, he became anorexic, lethargic and feverish and started vomiting bilious content. Seven days post-trauma, he presented to our emergency department with severe abdominal pain. An emergency laparotomy was performed where a transverse linear duodenal laceration was found at the junction of the first and second part of his duodenum, with generalized peritonitis. His stomach and duodenum were stretched over a large pancreatic pseudocyst posterior to his stomach. It was postulated that an incomplete duodenal injury (possibly a serosal tear) occurred following the initial minor trauma, which was followed by local tissue necrosis at the injury site resulting in a delayed presentation of generalized peritonitis.</p> <p>Conclusion</p> <p>This is the first reported case of a traumatic duodenal laceration following minor blunt trauma in the presence of a large pancreatic pseudocyst. Minor blunt abdominal trauma in a normal healthy adult would not be expected to result in a significant duodenal injury. In the presence of a large pseudocyst, however, the stretching of the duodenum over the pseudocyst had probably predisposed the duodenum to this injury. Patients awaiting therapeutic interventions for their pancreatic pseudocysts should be warned about this unusual but life-threatening risk following minor blunt abdominal trauma.</p

    The effect of sulindac, a non-steroidal anti-inflammatory drug, attenuates inflammation and fibrosis in a mouse model of chronic pancreatitis

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    <p>Abstract</p> <p>Background</p> <p>Chronic pancreatitis is characterized by progressive fibrosis, pain and loss of exocrine and endocrine functions. The long-standing chronic pancreatitis and its associated pancreatic fibrosis are the most common pathogenic events involved in human pancreatic carcinogenesis, but the therapeutic strategies to chronic pancreatitis and the chemoprevention of pancreatic carcinogenesis are very limited.</p> <p>Methods</p> <p>We investigated the effect of sulindac, a non-steroidal anti-inflammatory drug (NSAID), on inhibition of chronic pancreatitis in a caerulein induced chronic pancreatitis mouse model.</p> <p>Results</p> <p>Sulindac significantly reduced the severity of chronic pancreatitis including the extent of acini loss, inflammatory cell infiltration and stromal fibrosis. The protein expression of phosphorylation of MEK/ERK was inhibited in the chronic pancreatic tissues by sulindac treatment as measured by Western blot assay. The levels of inflammatory cytokines including TNF-α and MCP-1 were also significantly decreased with sulindac treatment, as well as the expression of TGF-β, PDGF-β, SHH and Gli in the chronic pancreatic tissue detected by qPCR assay and confirmed by western blot assay. The activation of pancreatic satellet cells was also inhibited by sulindac as measured by the activity of α-smooth muscle actin (α-SMA) in the pancreatic tissue of chronic pancreatitis.</p> <p>Conclusions</p> <p>Sulindac is a promising reagent for the treatment of chronic pancreatitis via inhibition of inflammatory cell infiltration and stromal fibrosis, the inhibitory effect of sulindac on chronic pancreatitis may through targeting the activation ERK/MAPK signaling pathway.</p
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