Diagnostic and therapeutic strategies to manage post-pancreaticoduodenectomy hemorrhage.

OBJECTIVE: To explore the causes, diagnosis and treatment of post-pancreaticoduodenectomy hemorrhages (PPHs). METHODS: A database of 703 pancreaticoduodenectomy patients in our institution (January 2008-July 2013) was analyzed retrospectively. RESULTS: PPHs occurred in 62 patients of which, 38 had clear causes and 15 died because of uncontrolled bleeding and multiple organ failure. Pancreatic fistula and abdominal infection rates were significantly higher in the PPH group compared to the group who did not experience hemorrhages (P < 0.05) but did not significantly increase the mortality of PPH patients. Hemostasis was attempted by endotherapy in 7 patients and was successful in 4 (57.1 %). Angioembolization was performed in 12 patients and was successful in 10 (83.3 %) and relaparotomy in 24 patients successful in 13 (54.2 %). All deceased patients belonged to International Study Group of Pancreatic Surgery clinical grade C and sentinel bleeding occurred in 60 % of PPH mortalities (9/15) (P = 0.005). CONCLUSION: Pancreatic fistulae and abdominal infections are associated with PPH. Control of early mild upper gastrointestinal hemorrhages could be attempted by endotherapy, but angiography with intervention or surgical treatments were always required for delayed bleeding. The mortality in cases with sentinel bleedings was obviously increased.

Recurrence of Hepatocellular Carcinoma With Epithelial-Mesenchymal Transition After Spontaneous Regression: A Case Report.

Hepatocellular carcinoma (HCC) is one of the most malignant cancers and ranks as the third leading cause of cancer-related death in the world. However, some patients with untreated HCC can experience spontaneous regression, a rare phenomenon that has been observed in various malignancies. Here, we report a unique case with untreated HCC, who first underwent a spontaneous cancer regression after the spontaneous clearing of chronic hepatitis B virus (HBV) infection from the liver as evidenced by hepatitis B virus surface antigen (HBsAg) seroconversion; then developed the recurrent HCC with epithelial-mesenchymal transition (EMT) after 14 years. We hypothesized that a strengthened immune system in response to HBV infection may have led to immune-mediated spontaneous cancer regression. The later recurrence of HCC may suggest the host's immune system was no longer able to contain HCC since aging and other chronic diseases may have significantly weakened the immune surveillance.

Comparative survival analysis of adjuvant therapy with iodine-131-labeled lipiodol to hepatic resection of primary hepatocellular carcinoma: a meta-analysis.

OBJECTIVE: Adjuvant therapies play an important role in delaying the recurrence of hepatocellular carcinoma (HCC) in patients with resectable tumor. Among the available options, use of radionuclides is an effective strategy. This meta-analysis aims to examine the evidence pertaining to the effectiveness of adjuvant therapy with intra-arterial iodine-131-labeled lipiodol ((131)I-lipiodol) to hepatic resection of HCC. METHODS: A literature survey was conducted of multiple electronic databases including PubMed/Medline, Embase, CINAHL, Cochrane library, and Google Scholar using various combinations of the most relevant key terms. The odds ratio-based meta-analysis of recurrence and survival rates was performed with RevMan software (version 5.2) using a random-effect model. Heterogeneity was assessed by χ(2) and I(2) statistics. RESULTS: When compared with the resection-only group, recurrence rates at 2 and 5 years were significantly lower in patients who received adjuvant therapy with intra-arterial I-lipiodol, with a corresponding odds ratio (95% confidence interval) of 0.45 (0.29-0.70) and 0.52 (0.32-0.85), respectively. The 3- and 5-year overall survival rates were found to be significantly higher in patients who received adjuvant therapy with (131)I-lipiodol than in patients who were not given any adjuvant therapy. Between-study statistical heterogeneity was moderate. CONCLUSION: Postoperative adjuvant therapy with intra-arterial (131)I-lipiodol to hepatic resection of HCC significantly improves overall and disease-free survival rates and reduces recurrence rates. However, well-designed randomized trials are needed to arrive at conclusive evidence.

Protective effect of nitric oxide on hepatopulmonary syndrome from ischemia-reperfusion injury.

AIM: To evaluate immunological protection of nitric oxide (NO) in hepatopulmonary syndrome and probable mechanisms of ischemia-reperfusion (IR) injury in rat liver transplantation. METHODS: Sixty-six healthy male Wistar rats were randomly divided into three groups (11 donor/recipient pairs). In group II, organ preservation solution was lactated Ringer's solution with heparin 10, 000/µL at 4 °C. In groups I and III, the preservation solution added, respectively, L-arginine or N(G)-L-arginine methyl ester (L-NAME) (1 mmol/L) based on group II, and recipients were injected with L-arginine or L-NAME (50 mg/kg) in the anhepatic phase. Grafted livers in each group were stored for 6 h and implanted into recipients. Five rats were used for observation of postoperative survival in each group. The other six rats in each group were used to obtain tissue samples, and executed at 3 h and 24 h after transplantation. The levels of alanine aminotransferase (ALT), tumor necrosis factor (TNF)-α and NO metabolites (NOx) were detected, and expression of NO synthase, TNF-α and intercellular adhesion molecule 1 (ICAM-1) was examined by triphosphopyridine nucleotide diaphorase histochemical and immunohistochemical staining. RESULTS: By supplementing L-arginine to strengthen the NO pathway, a high survival rate was achieved and hepatic function was improved. One-week survival rate of grafted liver recipients in group I was significantly increased (28.8 ± 36.6 d vs 4 ± 1.7 d, P < 0.01) as compared with groups II and III. Serum levels of ALT in group I were 2-7 times less than those in groups II and III (P < 0.01). The cyclic guanosine monophosphate (cGMP) levels in liver tissue and NOx in group I were 3-4 times higher than those of group II after 3 h and 24 h reperfusion, while in group III, they were significantly reduced as compared with those in group II (P < 0.01). The levels of TNF-α in group I were significantly lower than in group II after 3 h and 24 h reperfusion (P < 0.01), while being significantly higher in group III than group II (P < 0.01). Histopathology revealed more severe tissue damage in graft liver and lung tissues, and a more severe inflammatory response of the recipient after using NO synthase inhibitor, while the pathological damage to grafted liver and the recipient's lung tissues was significantly reduced in group I after 3 h and 24 h reperfusion. A small amount of constitutive NO synthase (cNOS) was expressed in liver endothelial cells after 6 h cold storage, but there was no expression of inducible NO synthase (iNOS). Expression of cNOS was particularly significant in vascular endothelial cells and liver cells at 3 h and 24 h after reperfusion in group II, but expression of iNOS and ICAM-1 was low in group I. There was diffuse strong expression of ICAM-1 and TNF-α in group III at 3 h after reperfusion. CONCLUSION: The NO/cGMP pathway may be critical in successful organ transplantation, especially in treating hepatopulmonary syndrome during cold IR injury in rat orthotopic liver transplantation.