BACKGROUND: Treatment of chronic pancreatitis (CP) is a challenging condition for surgeons. During the last decades, increasing knowledge about pathophysiology of CP, improved results of major pancreatic resections, and integration of sophisticated diagnostic methods in clinical practice have resulted in significant changes in surgery for CP.
DATA SOURCES: To detail the indications for CP surgery, the surgical procedures, and outcome, a PubMed database search was performed. The abstracts of searched articles about surgical management of CP were reviewed. The articles could be identified and further scrutinized. Further references were extracted by cross-referencing.
RESULTS: Main indications of CP for surgery are intractable pain, suspicion of malignancy, and involvement of adjacent organs. The goal of surgical treatment is to improve the quality of life of patients. The surgical approach to CP should be individualized according to pancreatic anatomy, pain characteristics, baseline exocrine and endocrine function, and medical co-morbidity. The approach usually involves pancreatic duct drainage and resection including longitudinal pancreatojejunostomy, pancreatoduodenectomy (Whipple’s procedure), pylorus-preserving pancreatoduodenectomy, distal pancreatectomy, total pancreatectomy, duodenum-preserving pancreatic head resection (Beger's procedure), and local resection of the pancreatic head with longitudinal pancreatojejunostomy (Frey's procedure). Non-pancreatic and endoscopic management of pain has also been advocated.
CONCLUSIONS: Surgical procedures provide long-term pain relief, a good postoperative quality of life with preservation of endocrine and exocrine pancreatic function, and are associated with low early and late mortality and morbidity. In addition to available results from randomized controlled trials, new studies are needed to determine which procedure is the most effective for the management of patients with CP.

BACKGROUND: Pancreatic encephalopathy (PE) is a serious complication of severe acute pancreatitis (SAP). In recent years, more and more PE cases have been reported worldwide, and the onset PE in the early stage was regarded as a poor prognosis sign of SAP, but the pathogenesis of PE in SAP still has not been clarified in the past decade. The purpose of this review is to elucidate the possible pathogenesis of PE in SAP.
DATA SOURCES: The English-language literature concerning PE in this review came from the Database of MEDLINE (period of 1991-2005), and the keywords of severe acute pancreatitis and pancreatic encephalopathy were used in the searching.
RESULTS: Many factors were involved in the pathogenesis of PE in SAP. Pancreatin activation, excessive release of cytokines and oxygen free radicals, microcirculation abnormalities of hemodynamic disturbance, ET-1/NO ratio, hypoxemia, bacterial infection, water and electrolyte imbalance, and vitamin B1 deficiency participated in the development of PE in SAP.
CONCLUSIONS: The pathogenesis of PE in SAP has not yet been fully understood. The development of PE in SAP may be a multi-factor process. To find out the possible inducing factor is essential to the clinical management of PE in SAP.

BACKGROUND: In the early period of orthotopic liver transplantation (OLT), initial poor graft function (IPGF) is one of the complications which leads to primary graft non-function (PGNF) in serious cases. This study set out to establish the clinical risk factors resulting in IPGF after OLT.
METHODS:  Eighty cases of OLT were analyzed. The IPGF group consisted of patients with alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST) above 1500 IU/L within 72 hours after OLT, while those in the non-IPGF group had values below 1500 IU/L. Recipient-associated factors before OLT analyzed were age, sex, primary liver disease and Child-Pugh classification; factors analyzed within the peri-operative period were non-heart beating time (NHBT), cold ischemia time (CIT), rewarming ischemic time (RWIT), liver biopsy at the end of cold ischemia; and factors analyzed within 72 hours after OLT were ALT and/or AST values. A logistic regression model was applied to filter the possible factors resulting in IPGF.
RESULTS: Donor NHBT, CIT and RWIT were significantly longer in the IPGF group than in the non-IPGF group; in the logistic regression model, NHBT was the risk factor leading to IPGF (P<0.05), while CIT and RWIT were possible risk factors. In one case in the IPGF group, PGNF appeared with moderate hepatic steatosis.
CONCLUSIONS: Longer NHBT is an important risk factor leading to IPGF, while serious steatosis in the donor liver, CIT and RWIT are potential risk factors.

BACKGROUND: Retransplantation of the liver is required for several complications of primary grafting, such as primary allograft non-function, hepatic artery thrombosis, biliary problems, or chronic ductopenic rejection. Surgeons usually take regrafting as the only pathway to treat those patients who are considered to have a poor outcome after the first operation. Whether the retransplantation is early or late, further attempts at rescue with a second or more grafts are associated with higher mortality and morbidity. However, retransplantation plays a role in improving survival of the patients. Therefore, it is necessary to summarize the experiences in liver retransplantation, as well as the factors influencing operative effects.
METHOD: The clinical data of 8 patients who received liver retransplantation in our center were analyzed retrospectively.
RESULTS: Complications of the biliary tract occurred in 5 of the 8 patients, chronic rejection in 2, and embolism in the hepatic artery in 1. Infections occurred in 7 patients before engraftment. Patient 1 had developed renal failure before the surgery, and he died of severe infection and multi-organ failure after transplantation. Patient 4 had a massive hemorrhage during the operation and also died of multi-organ failure after transplantation. Patient 7 developed intracranial hemorrhage and abdominal infection and died soon after transplantation. The other 5 patients recovered and discharged from the hospital.
CONCLUSIONS: Liver retransplantation is the only measure that can be taken to save the lives of patients whose liver allograft fails to function. It is very important that the indications and time of retransplantation are carefully selected. Factors leading to harmful effects on retransplantation include the preoperative condition of the recipient, a difficult and prolonged operation, massive hemorrhage during the operation, and severe complications after the surgery.

BACKGROUND: The past several decades have witnessed increasingly successful rates of liver transplantation. However, retransplantation remains the only choice for patients with irreversible graft failure after primary transplantation. This article aimed to summarize our clinical experience in liver retransplantation.
METHODS: From June 2002 to December 2005, a total of 185 cases of liver transplantation including 8 cases of retransplantation were performed in our hospital. The clinical data were analyzed retrospectively.
RESULTS: The rate of liver retransplantation was 4.32%. Retransplantation was indicated for the following reasons: biliary complication (3 cases), chronic rejection (2), hepatic artery thrombosis (1), uncontrollable acute rejection (1) and hepatitis B recurrence (1). The mean model of end-stage liver disease (MELD) scores before primary transplantation and retransplantation were 15.6 and 23.9, respectively (P<0.05). The MELD score reflected the severity of liver disease more precisely than the Child classification. The mean interval between the first and second transplantation was 316 days (78-725 days). The first three patients, with mean interval of 101 days, died of severe infection combined with multiple organ failure after retransplantation. The patients who underwent retransplantation more than six months after the first transplant had better outcomes. The one-year survival rate for retransplantation in our group was 62.5%.
CONCLUSIONS: Liver retransplantation is the only means of saving the patient with hepatic allograft failure. Understanding of the indications for retransplantation, careful selection of operation timing, excellent surgical skills and meticulous postoperative management all contribute to the success of each case of retransplantation.

BACKGROUND: Budd-Chiari syndrome (BCS) refers to posthepatic portal vein hypertension and/or inferior vena cava hypertension syndrome caused by obstruction of the blood flow at the portal cardinal hepatic vein and/or posterior hepatic inferior vena cava. The main surgical treatments of BCS include operations on pathological lesioned membrane, shunt, and combined operations. There are more than ten treatments available and reports on their therapeutic effects vary. As to operations on lesioned membrane, there are Kimura's finger rupture, balloon dilatation and membrane removal. With reference to our experience, the clinical value of membrane resection at normal temperature and under direct vision is discussed.
METHODS: A total of 292 patients with BCS undergoing membrane resection at normal temperature and under direct vision from June 1996 to June 2005 were retrospectively analyzed.
RESULTS: The short-term therapeutic effect in 256 patients was satisfactory and the effective rate was 87.7% (256/292). Within a week, ascitic fluid disappeared, the liver shrank and edema of the lower extremities was greatly relieved or even disappeared. Perioperative death occurred in 14 patients (4.8%). Of these, 3 had acute heart failure (one during the operation, one after 6 hours and one 7 days later). Six patients had thoracic cavity bleeding within 12 hours after the operation, 3 had acute respiratory distress syndrome (ARDS), 2 had disseminated intravascular coagulation (DIC), and 1 had pulmonary embolism. 158 patients were followed up for 6 months to 12 years, and 12 (7.6%) had recurrences.
CONCLUSIONS:  After membrane resection at normal temperature and under direct vision, hemodynamics was found to be close to normal, damage was slight, effectiveness was evident and the recurrence rate low. So this method is effective in treating BCS.

BACKGROUND: Combined hepatocellular carcinoma and cholangiocarcinoma (cHCC-CC) is a rare subtype of primary liver cancer, and clinicopathological features of cHCC-CC have seldom been reported in detail. This study was undertaken to explore the diagnosis and clinicopathological characteristics of cHCC-CC in comparison with hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC), respectively.
METHODS: The clinical data from 15 patients with cHCC-CC, 132 patients with HCC and 44 patients with CC who had undergone hepatic resection were analyzed retrospectively. Clinicopathological characteristics of cHCC-CC, HCC and CC such as hepatitis B viral infection, serum hepatitis C virus (HCV) antibody, serum alpha-fetoprotein (AFP) level, cirrhosis, vascular invasion, lymph node metastasis, surgical procedure and adjuvant treatment were also analyzed. Follow up was carried out in the patients, and their 1-, 3-, and 5-year survival rates were calculated.
RESULTS: Two patients with cHCC-CC were correctly diagnosed by enhanced CT before operation, the other 13 patients were diagnosed by histology and immunohistochemistry after operation. Radical (8/15) and conservative hepatectomy (7/15) for cHCC-CC was similar to that for HCC and CC (P>0.05). Pathologically cHCC-CC showed more significantly vascular invasion and lymph node metastasis than HCC (P<0.05), and a similarity to CC (P>0.05). Hepatitis B viral infection, serum HCV antibody, cirrhosis, and serum AFP level of cHCC-CC patients were similar to those of HCC patients (P>0.05) but different from CC patients (P<0.05). The cumulative 1-, 3-, and 5-year survival rates in patients with cHCC-CC were poorer than in patients with HCC or CC (P<0.05).
CONCLUSIONS: Patients with cHCC-CC are seldom diagnosed before operation. The progression of cHCC-CC is more rapid than that of HCC or CC. Survival rate of patients with cHCC-CC after hepatic resection is poorer than that of patients with HCC or CC.

BACKGROUND: Much evidence demonstrates that the genotypes of hepatitis B virus (HBV) present differences in pathogenicity and outcomes owing to differences in genetic structure. This study aimed to investigate the influences of HBV genotypes on the anti-viral therapeutic efficacy of interferon-α (IFN-α) in chronic hepatitis B patients, and to determine the relationship between HBV genotypes and levels of viral replication or gene variations.
METHODS: The chronic hepatitis B patients who were treated with IFN-α were selected randomly. Anti-viral therapeutic efficacy was monitored in these patients. The HBV genotypes were detected by PCR microplate hybridization ELISA. The levels of serum HBV-DNA were determined by fluorescence quantitative PCR. HBV gene variation at pre-C and basic core promoter (BCP) regions were assayed by gene chip technology.
RESULTS: Genotypes B and C were predominant in 94 chronic hepatitis B patients. A, E and F genotypes were not found in these patients. The HBV-DNA levels of genotype C and mixed genotypes were significantly higher than those of genotype B. The response to IFN-α in patients with genotype B was markedly better than in those with genotypes C and D, and the complete response to IFN-α was only observed in genotype  B. The response to IFN-α in patients with mixed genotypes was the least sensitive. The negative transition of HBeAg was correlated with variations in the HBV pre-C and BCP regions in patients with partial or no response to IFN-α. The variation rates of HBV pre-C and BCP regions were clearly higher in genotype C than in genotype B.
CONCLUSIONS: The results suggest that HBV genotype is correlated with the serum levels of HBV-DNA, HBV gene variations and therapeutic efficacy of IFN-α. The regular detection of HBV genotypes in the clinic will be of benefit for disease prognosis and planning of anti-viral therapeutic strategies.

BACKGROUND: Many methods are used to treat liver cancer. Among them, radiofrequency ablation (RFA) is a hot topic because of its advantages. This study was designed to determine the significance of blood alpha-fetoprotein mRNA (AFPmRNA) changes in patients with hepatocellular carcinoma (HCC) treated with RFA.
METHODS: The AFPmRNA content in blood samples from HCC patients was determined by reverse transcriptase-polymerase chain reaction (RT-PCR) before RFA and 48 hours, 72 hours, 1 week and 2 weeks later. 
RESULTS: The blood of 183 patients was negative for AFPmRNA before RFA, but that of 62 of them was positive 72 hours later, then returned to negative after 2 weeks. The blood of 129 patients was positive for AFPmRNA before RFA, but that of 112 of them became negative 2 weeks later; 17 patients were still AFPmRNA positive 2 weeks after RFA.
CONCLUSIONS: Blood AFPmRNA, which is increased temporarily after RFA, can be used as an objective index for the persistence and recurrence of HCC after RFA.

BACKGROUND: Liver fibrosis is the result of an imbalance between synthesis and degradation of extracellular matrix proteins of the liver. At the cellular and molecular levels, this progressive process is mainly characterized by activation of hepatic stellate cells (HSCs). Schistosoma japonica is one of the most prevalent causes of liver fibrosis in China. It is characterized by hepatocyte damage, inflammation, and chronic parasite egg-induced granuloma formation leading to fibrosis. This study aimed to investigate the inhibitory effects of prostaglandin E1 (PGE1) on activation of HSCs and the alteration of type I and III collagen in rabbits with schistosomiasis. The study may promote the clinical application of praziquantel and PGE1 as a combined therapy to reverse hepatic fibrosis caused by schistosomiasis.
METHODS: Rabbits were percutaneously infected with cercaria of S. japonicum. Seven rabbits were subjected to intravenous injections of PGE1 (2.5 µg/kg daily) from days 60 to 120 after infection. The ultrastructural changes in activated HSCs were observed under transmission electron microscopy. The expression of α-smooth muscle actin (α-SMA) was detected by immunohistochemistry. Fibril-forming collagens were detected by picrosirius staining. 
RESULTS: Activation of HSCs was a characteristic alteration in schistosome-induced hepatic fibrosis. The expression of contraction-related α-SMA and the content of collagens were increased. Exogenous PGE1 markedly inhibited the activation of HSCs and reduced the expression of α-SMA around the hepatic sinusoids (P<0.01). The contents of type I and III collagens were significantly attenuated. The ratio of staining area to the whole field (10×3.3) under a polarized light microscope in the untreated and treated groups was 37.25±9.71 vs. 13.38±4.24 (P<0.01) and 9.66±3.52 vs. 6.23±1.81 (P<0.05), respectively.
CONCLUSIONS: Activation of HSCs may play a key role in the progress of schistosome-induced hepatic fibrosis. PGE1 effectively protects rabbit liver from fibrosis, at least in part by inhibiting the activation of HSCs.

BACKGROUND: Reversal of liver fibrosis is one of the key steps in the prevention and treatment of alcoholic liver disease (ALD), but the mechanism is unknown. This study was to investigate the effects of the Chinese medicine Kang Xian Fu Fang I (KXI) on prophylaxis and treatment of ALD in rats and its possible mechanism of action. 
METHODS: Eighty male Wistar rats were randomly divided into four groups: normal control; ALD model; treatment of ALD with KXI; and prophylaxis of ALD by KXI. At the end of 4, 8, 12 and 16 weeks, five rats from each group were anesthetized and their livers were removed for pathological studies using hematoxylin-eosin and Masson stain, immunohistochemical studies, and flow cytometry for matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9). Blood samples were taken for hyaluronic acid (HA) assay. 
RESULTS: Serum HA level and liver collagen content were lower in the groups given KXI for prophylaxis and treatment than in ALD model group (P<0.05). The levels of MMP-2 and MMP-9 were also decreased in the prophylaxis and treatment groups (P<0.05). Immunohistochemistry showed immunoreactive MMP-2 in endothelial cells of the hepatic artery and portal vein, sinusoidal endothelial cells, and sinusoidal cells. Immunoreactive MMP-9 occurred in the hepatic cells around the veins and sinusoidal cells. 
CONCLUSIONS: KXI can effectively inhibit or reverse the course of ALD. This may be attributable to its capacity to inhibit the expression of MMP-2 and MMP-9.

BACKGROUND: Biliary atresia, the etiology of which still remains unclear, occurs exclusively in newborns and most are infected with rotavirus. In this study, we aimed to investigate the histopathological patterns of different kinds of rotavirus in the liver and biliary tract of neonatal mice and the expression of NF-κB in the liver and biliary tract of infected mice.
METHODS: Twenty-three adult mice (8 were male and 15 female) were divided into 8 breeding pairs, and each pair (1 male and 2 females) was housed in a cage in a laminar flow hood. Newborn mice, 24-48 hours old were randomly divided into A, B and C groups. The A and B groups were respectively inoculated with MMU18006 and SA11 rotavirus through the intraperitoneal route, while group C as blank control was only inoculated with culture medium. The liver was dissected after 5, 10, 15, 21 and 28 days; the weight of each mouse and the histopathological patterns in the liver were recorded. The expression of NF-κB in the liver and intrahepatic bile ducts was detected by immunohistochemical staining and the expression intensity was analyzed with a GT-2 imaging instrument.  
RESULTS: The average increase in weight of infected mice was significantly slower than that of the normal control, while the growth rate of group A (injected with MMU18006 rotavirus) was slower than that of group B (SA11 rotavirus). In infected mice, the acute and chronic inflammation of liver and intra- and extra-hepatic bile ducts was more significant in group A. Stenosis was found in most intrahepatic bile ducts, and sporadically in extrahepatic bile ducts. The expression of NF-κB in infected mice was dramatically higher than that of the normal control, while the expression in group A was higher than in group B.
CONCLUSIONS: Significant damage to the liver and biliary tract of neonatal mice can be induced by inoculating MMU18006 rotavirus through the intraperitoneal route, which is very similar to the pathology of biliary atresia in the newborn human. Similar inoculation with SA11 rotavirus can only result in moderate impairment that disappears quickly. The difference of pathogenicity between the two rotaviruses may depend on their differing capacities to increase the expression of NF-κB in the liver and biliary tract.

BACKGROUND: Hydrophobic bile acids lead to the generation of oxygen free radicals in mitochondria. Accordingly, this study is to investigate if gene delivery of superoxide dismutase (SOD) will reduce hepatocyte injury caused by experimental cholestasis.
METHODS: The recombinant of pLNCX-SOD gene packaged with lipofection of AMINE was transfected into hepatocytes in vitro, which stably expressed the SOD gene.
RESULTS: After transfection, hepatocytes enhanced the protective effect against injury to bile and the toxicity of serum in obstructive jaundice. The inhibition of bile at the concentration of 2% (v:v, bile: DMEM 1:50) decreased obviously from (78.80±12.35)% to (43.35±9.69)% in 12 hours, from (82.55±11.27)% to (-26.64±7.66)% in 24 hours, and from (83.83±18.69)% to (-19.27±14.38)% in 48 hours, compared with that of the untransfected cells (P<0.01). The inhibition of serum at the obstructive jaudice concentration of 2.5% was obviously decreased from (89.72±1.52)% to (14.68±14.33)% in 12 hours, from (92.2±11.27)% to (41.39±7.66)% in 24 hours, and from (94.25±8.96)% to (22.71±4.38)% in 48 hours (P<0.01).
CONCLUSION: Hepatocytes transfected with the pLNCX-SOD gene could obviously be resistant to the toxicity of bile and serum from rat with obstructive jaundice.

BACKGROUND: Stone recurrence is a major problem in the medication of gallstones with gallbladder preservation. The aim of this study was to determine the long-term recurrence rate of gallstones and the clinical outcome after successful percutaneous cholecystolithotomy (PCCL) treatment, and to investigate the possible risk factors for gallstone recurrence.
METHODS: After successful PCCL for gallstones, 439 patients were followed up during a 10-year period. The long-term gallstone recurrence rate and clinical outcome were evaluated. Risk factors associated with stone recurrence were identified.
RESULTS: Gallstone recurrence was detected in 182 of 439 PCCL patients, giving an overall recurrence rate of 41.46%. The cumulative gallstone recurrence rate for each of the 10 post-operative years was 9.57%, 18.91%, 27.33%, 34.14%, 37.59%, 39.86%, 41.90%, 42.73%, 42.85%, and 43.21%, respectively. Among these recurrent patients, 94 were asymptomatic, 80 suffered from nonspecific upper gastrointestinal symptoms and 8 suffered from abdominal pain or biliary colic. Thirty-eight of the 182 patients were retreated with cholecystectomy. The risk factors for stone recurrence included a family history of gallstones, preference for fatty food, accompanying liver disease, multiple stones and poor gallbladder function pre-PCCL.
CONCLUSIONS: In this study, the overall recurrence rate of gallstone was 41.46% during a 10-year period. The highest frequency of gallstone recurrence was during the 5th to 6th postoperative years and then continued to slowly increase. Risk factors for stone recurrence varied. We suggest that the use of PCCL in patients with gallstones should be considered carefully because of stone recurrence.

BACKGROUND: Spinal cord injury (SCI) is associated with increased prevalence of gallstones and acute acalculous cholecystitis. A possible explanation for the increased prevalence of gallstones in SCI patients is decreased gallbladder motility causing gallbladder stasis. In this study, we investigated gallbladder function in patients with SCI. 
METHODS: Eighteen normal controls, 16 trauma controls and 46 SCI patients were included in this study. Gallbladder function was measured by technium 99m-labeled imino-diacetic acid analogue (⁹⁹Tc^m-DISIDA) hepatobiliary imaging and represented by filling fraction (FF) and ejection fraction (EF). The data from SCI patients were analyzed according to old versus young, female versus male, heavy versus light body weight, ASIA A & B versus ASIA C & D classification, high- versus low-level injury, and long versus short injury duration. 
RESULTS: Fifty-two percent of SCI patients had abnormal FF and 59% had abnormal EF. Significantly decreased FF and EF values were found in SCI patients, especially in female patients with severe and high-level injuries.
CONCLUSION: Quantitative ⁹⁹Tc^m-DISIDA cholescinti-graphy showed that SCI can significantly impair gallbladder function.

BACKGROUND: Pancreatic duct stone is a rare disease, but there appears to be a rising trend in its incidence in recent years. Its pathogenesis remains unknown. The causes, diagnosis and treatment of pancreatic duct stone are reviewed through a retrospective analysis of the cases treated in our hospital. 
METHODS: The medical records of 88 patients with pancreatic duct stone treated in West China Hospital, Sichuan University from January 1, 1998 to November 30, 2004 were analyzed retrospectively in terms of clinical characteristics, diagnosis and treatment. 
RESULTS: Epigastric pain was the most common symptom in the 88 patients with an average age of 45.44±6.72 years. Various other symptoms were also observed. Eighty-one patients were subjected to B-ultrasonography, 51 to CT, and 47 to magnetic resonance cholangiopancreatography (MRCP). Fifty-six patients (63.64%) were operated on, 25 (28.41%) were treated with Chinese and Western medicine, and 7 (7.95%) abandoned treatment. Chronic pancreatitis was pathologically confirmed in all patients undergoing operation. 
CONCLUSIONS: B-ultrasonography is the first choice to check for pancreatic duct stone, while MRCP proves instructively useful for the diagnosis and treatment. Chronic pancreatitis is the most important cause of pancreatic duct stone, but whether there is not a direct correlation between stone formation and alcohol abuse needs further study in China. Surgery is the most curative method for pancreatic duct stone patients with severe symptoms or suspected pancreatic carcinoma, while individual treatment is emphasized, and microtraumatic surgery may be a developing option for treating pancreatic stone.

BACKGROUND: Acute necrotizing pancreatitis (ANP) leads to a systemic inflammatory response characterized by widespread leukocyte activation and, as a consequence, distant organ injury. The aim of this study was to explore the relationship between gastric microcirculatory impairment and inflammatory mediators released in rats and to evaluate the therapeutic effect of ligustrazine extracted from Rhizoma ligusticum wallichii on gastric mucosa injury in a rat model of ANP.
METHODS: Ninety-six Sprague-Dawley rats were randomly divided into three groups: normal control (group C); ANP without treatment (group P); and ANP treated with ligustrazine (group T). The ANP model was induced by injection of 50 g/L sodium taurocholate under the pancreatic membrane (4 ml/kg). Group C was given isovolumetric injection of 9 g/L physiological saline by the same route. Group T was injected with ligustrazine (10 ml/kg) via the portal vein. The radioactive biomicrosphere technique was used to measure the blood flow 2 and 12 hours after the induction of ANP. Samples of the pancreas and stomach were taken to assess pathological changes by a validated histology score; meanwhile, the levels of serum interleukin-1β (IL-1β) were determined. Gastric tissues were also used to measure the level of myeloperoxidase (MPO), which is expressed intracellularly in the azurophilic granules of neutrophils.
RESULTS: Blood flow in group P was significantly lower than that in group C (P<0.01). Pathological changes were significantly aggravated in group P. The gastric MPO activity in group P was significantly higher than that in group C (P<0.01). The level of serum IL-1β in group P increased more significantly than that in group C (P<0.01). Blood flow of the stomach in group T was significantly higher than that in group P after 2 hours (P<0.01). The pathological changes were significantly alleviated in group T. The MPO activity of group T was significantly lower than that of group P (P<0.01). Although serum IL-1β level of group T, was higher than of group C (P<0.01), it was lower than that of group P (P<0.01). There was a negative correlation between gastric blood flow and MPO activity (r=-0.983, P<0.01), and between gastric blood flow and pathological score (r=-0.917, P<0.05).
CONCLUSIONS: Decreased gastric blood flow and increased inflammatory mediators can be seen early in ANP, and both are important factors for gastric and mucosal injury. Ligustrazine can ameliorate microcirculatory disorder and alleviate the damage to the pancreas and stomach.

BACKGROUND: Diaphragmatic hernia of the liver is a rare clinical entity, usually found after trauma in adults.  This study was undertaken to elucidate a misdiagnosis of non-traumatic diaphragmatic hernia of the liver in an adult.
METHOD: The clinical data of one patient with non-traumatic diaphragmatic hernia of the liver was analyzed.
RESULTS: A tumor in the right lower thorax was revealed by chest X-ray and computed tomography. Non-traumatic diaphragmatic hernia of the liver was not identified until the operation. Pathological analysis confirmed the finding. The patient recovered well.
CONCLUSIONS:  Non-traumatic diaphragmatic hernia of the liver in an adult is a rare right-sided diaphragmatic hernia, which can move up into the chest cavity. It should be distinguished from lung cancer. The diagnosis and evaluation of non-traumatic diaphragmatic hernia of the liver can help optimize surgical management.