RESUMO
BACKGROUND: Gallbladder perforation and gastrointestinal fistula are rare but serious complications of severe acute pancreatitis (SAP). However, neither spontaneous gallbladder perforation nor cholecysto-colonic fistula has been reported in acalculous acute pancreatitis patients. CASE SUMMARY: A 31-year-old male presenting with epigastric pain was diagnosed with hypertriglyceridemia-related SAP. He suffered from multiorgan failure and was able to leave the intensive care unit on day 20. Three percutaneous drainage tubes were placed for profound exudation in the peripancreatic region and left paracolic sulcus. He developed spontaneous gallbladder perforation with symptoms of fever and right upper quadrant pain 1 mo after SAP onset and was stabilized by percutaneous drainage. Peripancreatic infection appeared 1 mo later and was treated with antibiotics but without satisfactory results. Then multiple colon fistulas, including a cholecysto-colonic fistula and a descending colon fistula, emerged 3 mo after the onset of SAP. Nephroscopy-assisted peripancreatic debridement and ileostomy were carried out immediately. The fistulas achieved spontaneous closure 7 mo later, and the patient recovered after cholecystectomy and ileostomy reduction. We presume that the causes of gallbladder perforation are poor bile drainage due to external pressure, pancreatic enzyme erosion, and ischemia. The possible causes of colon fistulas are pancreatic enzymes or infected necrosis erosion, ischemia, and iatrogenic injury. According to our experience, localized gallbladder perforation can be stabilized by percutaneous drainage. Pancreatic debridement and proximal colostomy followed by cholecystectomy are feasible and valid treatment options for cholecysto-colonic fistulas. CONCLUSION: Gallbladder perforation and cholecysto-colonic fistula should be considered in acalculous SAP patients.
RESUMO
OBJECTIVE: To analyze the immunological characteristics of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model and examine the therapeutic effects and mechanisms of Astragalus polysaccharides (APS) treatment. METHODS: Thirty-two male specific pathogen free Spragne-Dawley rats were randomly equally assigned to four groups: control, TNBS, APS and prednisone groups. Experimental colitis was induced by enema administration of TNBS. Then rats were treated with APS (0.5 gâ¢kg-1â¢day-1, once daily) or prednisone (1.0 mgâ¢kg-1â¢day-1, once daily) by gavage for 14 days. Macroscopic lesion and histological damage were determined, and activity of myeloperoxidase (MPO) was measured in the colonic tissues. Expressions of T-box expressed in T-cells (T-bet) and GATA-binding protein-3 (GATA-3) were determined by immunohistochemistry analysis and western blot. RESULTS: Both macroscopic lesion and histological colonic damage induced by TNBS were reduced by APS and prednisone treatment. These were accompanied by significant attenuation of MPO activity (P=0.03). TNBS intervention enhanced the expression of both GATA-3 and T-bet, but the expression of T-bet was significantly enhanced than that of GATA-3, resulting in significant reduction of GATA-3/T-bet ratio (P=0.025). APS administration enhanced the expression of T-bet (P=0.04) and GATA-3 (P=0.019) in comparison to TNBS group, and resulting in an up-regulated GATA-3/T-bet ratio. Prednisone treatment inhibited both expressions; however it also resulted in up-regulation of the GATA-3/T-bet ratio. CONCLUSIONS: These results demonstrated that APS exerted a beneficial immune regulatory effect on experimental colitis. It promoted the expression of T helper cell 1 (Th1) and T helper cell 2 (Th2) specific transcription factors but ultimately favor a shift toward Th2 phenotype, suggesting that APS possessed therapeutic potential in experimental colitis.