Endoscopic retrograde appendicitis treatment for periappendiceal abscess: A case report.

BACKGROUND: Acute appendicitis is the most common abdominal emergency. At present, the main treatments for periappendiceal abscess include antibiotics and surgery. However, the complications and mortality of emergency surgery are high. The preferred therapy is conservative treatment with antibiotics first, ultrasound-guided puncture drainage or surgical treatment is followed when necessary. Endoscopic retrograde appendicitis therapy (ERAT) for acute uncomplicated appendicitis have been proved clinically effective, but it is rarely used in periappendiceal abscess. CASE SUMMARY: We report a patient admitted to hospital because of "right lower abdominal pain for six days". The computerized tomography (CT) of patient showed that appendicitis with fecaliths and abscess in the pelvis. The patient was treated by CT-guided puncture and drainage of abdominal abscess combined with ERAT to remove appendiceal fecaliths, irrigation and stent placement. CONCLUSION: The patient did not receive surgery because of impoverished family. Abdominal pain did not recur during the follow-up period. This case confirms the value of ERAT in the treatment of periappendiceal abscess.

Left hepatic artery pseudoaneurysm complicating endoscopic retrograde cholangiopancreatography: A case report.

BACKGROUND: Pseudoaneurysms of the hepatic artery or its branches have been reported following abdominal trauma, iatrogenic injury at the time of many operations such as percutaneous transhepatic biliary drainage and cholecystectomy. Hepatic artery pseudoaneurysms after endoscopic retrograde cholangiopancreatography (ERCP) are uncommon and potentially life threatening and should be identified and treated rapidly. CASE SUMMARY: We report a case of intra-abdominal hemorrhage secondary to a left hepatic artery pseudoaneurysm resulting from guide wire injury at ERCP. The patient primary diagnosis was acute biliary pancreatitis with cholangitis, he underwent ERCP on the third day of admission. During ERCP, the left intrahepatic bile duct was cannulated three times. Over the sixth day, Contrast enhanced computed tomography scan demonstrated left hepatic lobe contusion and a pseudoaneurysm formation. The patient was successfully treated with the embolization of a small branch of left hepatic artery angiographically. CONCLUSION: The common complications of ERCP are pancreatitis, bleeding and perforation. False aneurysms occur as a result of damage to the wall of an artery. As far as we know, it is rare complication has been reported following ERCP. We advise urgent referral for angiographic embolization in this situation to avoid aneurysm rupture.

Theoretical Study of Hydrogen Production from Ammonia Borane Catalyzed by Metal and Non-Metal Diatom-Doped Cobalt Phosphide.

The decomposition of ammonia borane (NH3BH3) to produce hydrogen has developed a promising technology to alleviate the energy crisis. In this paper, metal and non-metal diatom-doped CoP as catalyst was applied to study hydrogen evolution from NH3BH3 by density functional theory (DFT) calculations. Herein, five catalysts were investigated in detail: pristine CoP, Ni- and N-doped CoP (CoPNi-N), Ga- and N-doped CoP (CoPGa-N), Ni- and S-doped CoP (CoPNi-S), and Zn- and S-doped CoP (CoPZn-S). Firstly, the stable adsorption structure and adsorption energy of NH3BH3 on each catalytic slab were obtained. Additionally, the charge density differences (CDD) between NH3BH3 and the five different catalysts were calculated, which revealed the interaction between the NH3BH3 and the catalytic slab. Then, four different reaction pathways were designed for the five catalysts to discuss the catalytic mechanism of hydrogen evolution. By calculating the activation energies of the control steps of the four reaction pathways, the optimal reaction pathways of each catalyst were found. For the five catalysts, the optimal reaction pathways and activation energies are different from each other. Compared with undoped CoP, it can be seen that CoPGa-N, CoPNi-S, and CoPZn-S can better contribute hydrogen evolution from NH3BH3. Finally, the band structures and density of states of the five catalysts were obtained, which manifests that CoPGa-N, CoPNi-S, and CoPZn-S have high-achieving catalytic activity and further verifies our conclusions. These results can provide theoretical references for the future study of highly active CoP catalytic materials.

Level of hepatitis B surface antigen might serve as a new marker to predict hepatocellular carcinoma recurrence following curative resection in patients with low viral load.

To investigate the association between preoperative HBsAg (hepatitis B surface antigen) level and risk of HCC (hepatocellular carcinoma) recurrence following curative resection, we enrolled 826 HBV-related HCC patients who underwent curative resection and received long-term follow-up at the Eastern Hepatobiliary Surgery Hospital (Shanghai, China). Multivariate analyses showed that serum HBsAg ≥ 2000 S/CO, seropositive hepatitis B e antigen (HBeAg), γ-glutamyl transpeptidase > 61 U/L, prothrombin time > 13 s, multinodularity, lager tumor size, and major portal vein invasion were independently associated with a increased risk of HCC recurrence. Compared with HCC patients with HBsAg level < 2000 S/CO, HCC patients with HBsAg level ≥ 2000 S/CO had a higher prevalence of seropositive HBeAg, antiviral therapy, and cirrhosis; were younger; and had a higher levels of alanine transaminase (ALT), aspartate aminotransferase (AST), and HBV viral load. Multivariable stratified analyses showed HCC patients with HBsAg level < 2000 S/CO tended to have a lower incidence of HCC recurrence in following subgroups of patients, including for noncirrhotic (HR, 0.561; 95% CI, 0.345-0.914), HBV DNA < 2000 IU/mL (HR, 0.604; 95% CI, 0.401-0.912), ALT ≤ 41 U/L (HR, 0.643; 95% CI, 0.440-0.942), AST ≤ 37 U/L (HR, 0.672; 95% CI, 0.459-0.983), and seronegative HBeAg (HR, 0.682; 95% CI, 0.486-0.958). When we evaluated HBeAg-negative patients with HBV DNA < 2000 IU/mL, HBsAg level still determined risk of HCC recurrence (p = 0.014), but not HBV DNA (p = 0.550) and ALT (p = 0.186). These results suggest high levels of HBsAg increase risk of HCC recurrence following curative resection. HBsAg level might serve as a new marker to complement HBV DNA level in predicting HCC recurrence, especially in HBeAg-negative patients with low viral load.

Protective effects of polydatin against CCl(4)-induced injury to primarily cultured rat hepatocytes.

AIM:To investigate the protective effects of polydatin (PD) against injury to primarily cultured rat hepatocytes induced by CCl(4).METHODS:Rat hepatocytes were separated by methods of liver infusion in vivo and cultured medium (7.5X10(5) cells/mL). Two mL or 0.2mL was added into 24-well or 96-well plates respectively. Twenty-four hours after cell preculture, PD at concentrations of 10(-7) mol/L-10(-4)mol/L was added into each plate. At the same time injury to hepatocytes was induced by adding 10mmol/L CCl(4).Then, 0.1mL or 1mL culture solution was removed from the 96-well or 24-well plates at 6h, 12h, 24h and 48h after CCl14 intoxication respectively for the determination of GPT, GSH and MDA. At 48h, the survivability of rat hepatocytes was assayed by the MTT colormetric method.RESULTS:After CCl(4) challenge, the release of GPT and the formation of MDA in rat hepatocytes markedly increased and maintained at a high level in 48h, whereas PD with different concentrations could markedly inhibit this elevation with 10(-5)mol/L PD having the strongest effects and inhibiting rate was over 50%. PD could also improve the decreased content of GSH caused by CCl(4) in accordance with the doses used. CCl(4) evidently decreased the hepatocyte survivability from 91.0% ± 7.9% to 35.4% ± 3.8%. On the other hand, PD at 10(-7)mol/L-10(-4)mol/L could reverse this change and improve the cell survival rates to 56.1% ± 5.2%, 65.8% ± 5.0%, 88.7% ± 6.8% and 75.2% ± 7.3%, respectively.CONCLUSION: PD at 10(-7)mol/L-10(-4)mol/L could protect primarily cultured rat hepatocytes against CCl(4) induced injury.