Ultrasound, MRCP and endoscopic retrograde cholangiopancreatography in combination with choledochoscope procedure in operation could improve the diagnostic sensitivity of Mirizzi syndrome. Intraoperative choledochoscope is effective to confirm Mirizzi syndrome during operation. Open surgery is the current standard for managing patients with Mirizzi syndrome. Laparoscopic surgery should be confined to Mirizzi syndrome type I and patients should be selected very strictly.
To investigate patients with severe acute pancreatitis (SAP) by dynamic levels of pro-/anti-inflammatory cytokines and endotoxin (ET) in plasma and the relationship between immunity and infection, organ dysfunction. Seventy-two patients with SAP were recruited. The ET, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-10 (IL-10), and interleukin-4 (IL-4) were determined on admission and days 3, 7, and 14. For comparison, patients were analyzed through infection group versus non-infection group, multiple organ dysfunction syndrome (MODS) group versus non-MODS group. There were sixteen patients with secondary infection, twenty-two with MODS, and nine deaths. The infection group had higher levels of ET than the non-infection group on days 3 and 7. The dynamic cytokine levels of patients in the MODS group were unanimous with those outcomes in the infection group. The levels of cytokines in the infection group were different from the non-infection group, with more levels of TNF-α, IL-6 on days 3 and 7 and less on days 14, and more levels of IL-10, IL-4 on days 7 and 14. The levels of TNF-α, IL-6 in the MODS group were different from the non-MODS group, with more levels on days 3 and 7, and less levels on days 14. Immune dysregulation may play an important role in infection and organ dysfunction for patients with SAP.
The predominant infections were gram-negative bacterium, gram-positive bacterium, and fungi concomitantly or consecutively. Most of the infected patients had polyinfection. There were many patients with hospital-acquired infection and opportunistic infection. Multiple factors affected the outcome.
may remain asymptomatic. With the progress of the radiological techniques, the incidence of this finding and the knowledge on the pathogenetic relation between IPMT and PD will probably increase.
Within 24 h after admission, moderate elevation of TC level seemed to increase the resistance to inflammation and hence improved the survival rate in patients with SAP, and reduced the in-hospital mortality. Inflammatory reaction (with or without infection), hypoalbuminemia and TC were prognostic factors for in-hospital mortality; both high levels of CRP and low ALB levels were associated with in-hospital mortality in patients with SAP.
Objective
To describe the differential diagnosis and treatment options for xanthogranulomatous cholecystitis (XGC), the presentations and management of 68 patients were described.
Subjects and Methods
Demographical and clinical data from 68 cases of XGC treated between January 2004 and January 2010 were analyzed. Clinical characteristics, radiological and surgical findings, histopathological features and postoperative recoveries were recorded. Clinical features of laparoscopic cholecystectomy versus open surgery and XGC versus gallbladder (GB) cancer were compared.
Results
The CA19-9 levels of XGC and coexisting GB cancer were significantly different (p = 0.0034). In radiological findings, focal thickening of the GB wall was more frequent in coexisting GB cancer, early enhancement of the GB was observed more often in coexisting GB cancer, and lymph node enlargement was seen more often in coexisting GB cancer (p < 0.05). There were also significant differences between laparoscopic and open surgery for CA19-9, intramural hypoattenuated nodule, pericholecystic invasion, lymph node enlargement and maximum thickness, focal thickening, heterogeneous enhancement and early enhancement of the GB wall (p < 0.05). These findings were confirmed by multivariate analysis.
Conclusions
Ultrasound, computed tomography scan and intraoperative frozen section were the helpful modalities for XGC diagnosis. CA19-9 (>37 kU/l), pericholecystic invasion, lymph node enlargement (>10 mm), and focal thickening and early enhancement of the GB wall were the criteria for open surgery. In some selected cases, laparoscopic cholecystectomy was preferable.
BackgroundLithogenic bile is the major cause of cholesterol gallstone, but its pathogenesis is not well understood. The hypersecretion of biliary cholesterol is believed to be an important cause of lithogenic bile. Sterol Carrier Protein 2 (SCP2) participates in cholesterol trafficking and lipid metabolism in hepatocytes and may play a key role in cholesterol gallstone formation.Methods21 cholesterol gallstone genealogies were studied to investigate the expression of SCP2 gene in liver tissue of hereditary and non-hereditary cholesterol gallstone patients as well as non-gallstone patients. The mRNA expression of liver SCP2 in 28 hereditary patients, 30 non-hereditary cholesterol gallstone patients and 32 non-gallstone patients was measured by Reverse Transcription Polymerase Chain Reaction (RT-PCR). The protein expression of liver SCP2 was also detected in all the patients by Western blotting. At the same time, the bile was also analyzed with biochemical techniques and the Cholesterol Saturation Index (CSI) was calculated.ResultsThe mRNA and protein expression of SCP2 was significantly increased in cholesterol gallstone patients compared to those of non-gallstone patients. Moreover, SCP2 was expressed at higher levels in hereditary cholesterol gallstone patients than that of non-hereditary cholesterol gallstone patients. There was significant difference observed in CSI between cholesterol gallstone patients and non-gallstone patients, but not in CSI between hereditary and non-hereditary cholesterol gallstone patients.ConclusionsSCP2 was overexpressed in hereditary cholesterol gallstone patients compared to non-hereditary cholesterol gallstone patients. This finding indicated that SCP2 might be one of the genetic factors contributing to cholesterol gallstone formation, which was always accompanied by the increase of bile lithogenicity.
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