ABSTRACT
Biliary atresia is a serious congenital malformation that threatens the life of newborns.At present, the treatment of biliary atresia mainly relies on Kasai portoenterostomy which is also named hepatoportoenterostomy to correct the dysplastic biliary system.Cholangitis is the most common and intractable complication after Kasai portoenterostomy.The pathogenesis is still unidentified.Many factors including ascending infection of intestinal bacteria, abnormal development of intrahepatic bile duct, surgical injury, reflux of intestinal contentscan and so on can affect the occurrence and development of the disease.The initial time and frequency of cholangitis can affect the postoperative primary liver function, so it is especially important to diagnose and treat it timely.The diagnosis of post-Kasai cholangitis is lack of specificity, mainly based on clinical manifestations, biochemical abnormalities and surgical history.For intractable cholangitis should consider completing radioisotope hepatobiliary imaging, percutaneous cholangiography and single or double-balloon enteroscopy.The main focus of prevention and treatment lies in preoperative care, surgical improvement and postoperative care, as well as drug prevention during disease follow-up.
ABSTRACT
Biliary atresia is a serious congenital malformation that threatens the life of newborns.At present, the treatment of biliary atresia mainly relies on Kasai portoenterostomy which is also named hepatoportoenterostomy to correct the dysplastic biliary system.Cholangitis is the most common and intractable complication after Kasai portoenterostomy.The pathogenesis is still unidentified.Many factors including ascending infection of intestinal bacteria, abnormal development of intrahepatic bile duct, surgical injury, reflux of intestinal contentscan and so on can affect the occurrence and development of the disease.The initial time and frequency of cholangitis can affect the postoperative primary liver function, so it is especially important to diagnose and treat it timely.The diagnosis of post-Kasai cholangitis is lack of specificity, mainly based on clinical manifestations, biochemical abnormalities and surgical history.For intractable cholangitis should consider completing radioisotope hepatobiliary imaging, percutaneous cholangiography and single or double-balloon enteroscopy.The main focus of prevention and treatment lies in preoperative care, surgical improvement and postoperative care, as well as drug prevention during disease follow-up.
ABSTRACT
OBJECTIVE： To study therapeutic effects of Spider toxin oral ulcer powder on recurrent aphthous ulcer （RAU） model rats and its mechanism. METHODS： In vitro antimicrobial activity of the powder was determined by disk diffusion method. 50 healthy SD rats were randomly divided into normal group， model group， positive group （Guilin watermelon frost， 100 mg/kg） and oral ulcer powder high-dose and low-dose groups （70， 35 mg/kg）， with 10 rats in each group. Except for normal group， RAU model was established in the right oral submucosa of rats in other groups by acetic acid method. After modeling， administration groups were smeared with corresponding drugs on ulcers for 3 days. Normal group and model group were not treated. The ulcer surface of rats was observed and the ulcer area was measured on the 1st and 3rd days after administration. The morphological changes of ulcer tissues were observed. The serum levels of SOD， MDA， GSH， TNF-α， IL-1， IL-6 and IFN-γ were detected. The protein expressions of MMP-9， NF-κB， Caspase-3 and PARP in ulcer tissues of rats were detected by immunohistochemistry. RESULTS： The oral ulcer powder showed obvious in vitro bacteriostasis effect. Compared with blank group， oral ulcer and histopathological changes were obvious in model group； serum levels of TNF-α， IL-1， IL-6 and MDA were increased significantly， while the levels of IFN-γ， SOD and GSH were decreased significantly （P＜0.01）； the expression of MMP-9， NF-κB， Caspase-3 and PARP in ulcer tissue were increased significantly （P＜0.05 or P＜0.01）. Compared with model group， the ulcer area of rats in each dosage group was significantly reduced （P＜0.05 or P＜0.01） or nearly healed， the pathological changes of tissue were significantly alleviated； serum levels of MDA， TNF-α， IL-1 and IL-6 were decreased significantly， while the levels of SOD， GSH and IFN-γ were increased significantly （P＜0.05 or P＜0.01）； the expression of MMP-9， NF-κB， Caspase-3 and PARP in ulcer tissue were decreased significantly （P＜0.01）. CONCLUSIONS： Spider toxin oral ulcer powder shows strong bacteriostasis， detumescence and repair effects， and has obvious therapeutic effect on RAU model rats. Its mechanism may be related to reducing the level of inflammatory factors， mediating the expression of apoptotic factors and regulating immune imbalance.