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Acute Pancreatitis (AP) is an inflammatory condition with cumbersome side effects. Gastrointestinal (GI) fistula is a rare complication seen in cases with infected pancreatic or peripancreatic necrosis. GI fistulas can result in severe haemorrhage and septicemia. Hereby, the authors present a case of 36-year-old male with a chief complaint of abdominal pain associated with abdominal distension and non bilious vomiting after binge consumption of alcohol for the past 10 days. Computed Tomography (CT) scan showed the presence of free gas in the abdomen. Contrast-Enhanced CT (CECT) imaging revealed diffuse enlargement affecting the head, uncinate process, body, and tail of the pancreas. There were also a few necrotic peripancreatic fluid collections with extensive peripancreatic fat stranding. Based on these findings, the diagnosis of acute necrotising pancreatitis was suggested. Despite treatment with antibiotics and necrosectomy with drainage of the abscess collection, the patient showed no improvement. A repeat CECT examination was performed due to the deterioration of the patient's clinical condition, which showed a complete non enhancing pancreas. Additionally, a large defect measuring approximately 16 mm was observed in the posteroinferior wall of the stomach at the middle third of the body, with extravasation of contrast material into the pancreatic collection, suggestive of fistula formation. Subsequently, the patient underwent pancreatic necrosectomy with closure of the gastric perforation using feeding jejunostomy. A follow-up CT examination was performed four days later due to the deteriorating status of the patient, as well as new onset haematemesis and bloody discharge from the surgical drain. The CT scan revealed a few peripancreatic soft tissue infiltrates adjacent to the pancreatic head. Persistent collections were noted along the anterolateral surface of the right psoas, extending to the adjoining right anterior pararenal space and the left anterolateral abdominal wall in the left hypochondriac region. Thickening of the bilateral lateroconal fascia and anterior and posterior renal fascia was observed, likely due to inflammation. Following this, the patient underwent another surgery, and percutaneous drainage was performed with antibiotic coverage. The patient showed a significant reduction in the collection and improved clinical condition after 10 days. Imaging plays a crucial role in diagnosing such complications, enabling early detection and reducing mortality in these patients. [ABSTRACT FROM AUTHOR]

Peripancreatic necrosis (PPN) is considered as a distinct entity with a better outcome when compared with combined pancreatic and peripancreatic necrosis (CPN), but there is no systematic review to summarize the evidence. Our study aimed to perform a meta-analysis of existing observational studies comparing the outcomes of PPN with CPN. Studies in adult patients comparing the outcomes of PPN and CPN from PubMed, Medline, and Scopus databases from inception to November 2018 were systematically searched. The primary outcome was mortality, and secondary outcomes included multi-organ failure, persistent organ failure, infected necrosis, need for interventions including open necrosectomy. Pooled adjusted odds ratios, and 95% confidence intervals (CI) were obtained by the random-effects model. Forrest plots were constructed to show the summary pooled estimate. Heterogeneity was assessed by using I2 measure of inconsistency. A total of 6 studies involving 1851 patients (1295 (70%) with CPN and 556 (30%) with PPN) were included. Patients with CPN had a significantly higher mortality (OR 2.49, 95% CI: 1.61–3.87), risk for multi-organ failure (OR 3.24, 95% CI: 2.38–4.43), persistent organ failure (OR 2.79, 95% CI: 1.53–5.08), and infected necrosis (OR 6.21, 95% CI: 3.85–10.03). They underwent more interventions (OR 5.86, 95% CI: 3.69–9.32), including open necrosectomy (OR 5.04, 95% CI: 3.33–7.63). Heterogeneity was low (I2 = 18.1, p = 0.296), and there was no publication bias. Isolated peripancreatic necrosis portends an overall better prognosis when compared to necrosis involves pancreatic parenchyma. Clinicians should recognize this distinction for management decisions. [ABSTRACT FROM AUTHOR]

Macrophages are crucially involved in the pathophysiology of acute pancreatitis. Soluble CD163 (sCD163) is specifically released from macrophages and systemic levels are increased in inflammatory diseases. Here, sCD163 was measured in serum of 50 patients with acute pancreatitis to find out possible associations with disease activity. Admission levels of systemic sCD163 were nearly three-fold higher in patients with acute pancreatitis compared to controls. In patients sCD163 did not correlate with C-reactive protein and leukocyte count as established markers of inflammation. Levels were not associated with disease severity assessed by the Schroeder score, Balthazar score, Acute Physiology, Age, and Chronic Health Evaluation (Apache) II score and peripancreatic necrosis score. Soluble CD163 was not related to complications of acute pancreatitis. These data show that serum sCD163 is increased in acute pancreatitis indicating activation of macrophages but is not associated with disease severity and outcome. [ABSTRACT FROM AUTHOR]

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Abstract: The progression of acute pancreatitis to necrotizing pancreatitis which often results in high morbidity and mortality is difficult to predict. Here we report that serum concentrations of sCD137 are increased in patients with acute pancreatitis. Admission levels and 10-day median sCD137 levels positively correlate with markers of biliary pancreatitis and the 10-day sCD137 median is significantly higher in metabolic than in alcoholic pancreatitis. Serum concentrations of sCD137 at time of admission and the 10-day median of sCD137 correlate with the Ranson and APACHE II disease scores but not with the radiological Balthazar and Schroeder scores that reflect pancreatic and peripancreatic necrosis. Further, sCD137 levels correlate with the probability of complications and lethality. The association of sCD137, a product of activated T cells, with the severity of acute pancreatitis suggests that T cells contribute to the pathogenesis of acute pancreatitis. [Copyright &y& Elsevier]

A case of peripancreatic fat necrosis, after an episode of acute pancreatitis, which mimicked pancreatic cancer with lymph node metastases, is presented. We describe the imaging findings with helical CT scanning and with unenhanced and mangafodipir-enhanced MR imaging, with special emphasis on the differential diagnoses. [ABSTRACT FROM AUTHOR]