Journal of hepato-biliary-pancreatic surgery最新文献

We report herein a case of recurrent mucosal cancer of the extrahepatic bile duct, with superficial flat spread, 12 years after operation. A 67-year-old woman had undergone common bile duct (CBD) resection and Roux-en-Y reconstruction. Histologically, the tumor was papillary adenocarcinoma, with superficial flat spread, with no invasive component. The epithelium at the distal margin had been exfoliated, so the absence or presence of any remnant cancerous lesion was unclear. But the superficial flat spread had expanded to within at least 3 mm from the distal margin. About 12 years postoperatively, she was hospitalized with upper abdominal pain, and duodenoscopy demonstrated a tumor in the second portion of the duodenum. Biopsy identified adenocarcinoma. Computed tomography showed a low-density mass between the duodenum and pancreatic head. Pancreatoduodenectomy was performed. Histologically, papillary adenocarcinoma was found within the whole of the intrapancreatic bile duct, and its histological appearance resembled that of the original tumor. Moderately differentiated tubular adenocarcinoma had invaded around the tissue of the intrapancreatic CBD. These findings suggest that remnant intramucosal flat carcinoma within the intrapancreatic bile duct had developed into invasive carcinoma over the course of 12 years. This case suggests that remnant intraepithelial flat carcinoma within the CBD may develop a late local recurrence.

Pancreatic leakage is one of the most common complications following pancreatic surgery. Although several surgical techniques and several devices for the management of pancreatic ducts have been advocated to prevent pancreatic leakage, its incidence is still not acceptable. We report our new surgical technique, a gastric-wall-covering method, for the prevention of pancreatic leakage in the enucleation of insulinoma in the pancreas, along with intraoperative pancreatography for navigation surgery of the pancreatic duct. Our novel techniques help to prevent pancreatic leakage following pancreatic surgery, including partial resection of the pancreas.

A 45-year-old man with recurrent episodes of hematemesis caused by extensive varices in the esophagus and stomach was admitted. He had a history of liver cirrhosis with hepatitis C virus infection. Computed tomography revealed a conglomeration of small strong nodular stains in the pancreatic head. Angiography revealed a racemose vascular network at the same site and early appearance of the portal venous system in the arterial phase. With a diagnosis of pancreatic arteriovenous malformation with portal hypertension, he underwent pylorus-preserving pancreaticoduodenectomy, preceded, 2 days earlier, by transcatheter arterial embolization of some of the feeding arteries. The varices observed preoperatively in the esophagus and stomach disappeared, and he has been well for 6 years after the operation. We reviewed 47 cases of pancreatic arteriovenous malformation previously reported in the English-language literature, with a focus on the clinical manifestations, treatment approaches, and etiological relationship with portal hypertension and liver cirrhosis.

A case of undifferentiated spindle-cell carcinoma of the gallbladder is described. A 72-year-old man presented with right hypochondralgia and fever. Imaging studies revealed a well-demarcated solid tumor (with a necrotic center) in the gallbladder that invaded the liver and transverse colon. On gross examination of the surgical specimen, the cut surface of the polypoid tumor showed nodular invasive growth. Microscopically, the tumor was composed of atypical spindle-shaped tumor cells that proliferated in a whirling or interlacing pattern. The tumor also showed foci with a malignant epithelial component that simulated a carcinosarcoma. Immunohistochemically, the biphasic differentiation of the tumor was highlighted by the different immunoreactivity to antibodies against cytokeratins, epithelial membrane antigen (EMA), and vimentin shown by the malignant epithelial components and the spindle-cell components. However the latter showed faint positivity for cytokeratin antibody. These results suggested that the spindle-cell carcinoma of the gallbladder originated from cholecystic mucosa and showed sarcomatous reaction or dedifferentiation, as indicated by the presence of vimentin-positive cells. The proliferation index, as detected by ki-67, in the spindle-cell component was higher than that in the epithelial component, which may account for the more aggressive biological behavior of the spindle-cell component.

A 39-year-old woman was admitted to hospital due to perforated relapsing duodenal ulcer. Clinical, laboratory, and surgical examinations revealed a peripancreatic lymph node gastrinoma as the cause of Zollinger-Ellison syndrome. Further examinations established multiple endocrine neoplasia type 1 (MEN1) with a germline mutation at codon 1153 (T->A) in exon 7, causing an amino-acid change, from isoleucine to asparagine (Ile348Asn), in the MEN1 gene. The following findings strongly supported a diagnosis of primary lymph node gastrinoma: a rapid fall of the serum gastrin level after operation, the continuous normalization of the serum gastrin level before and after secretin stimulation, the lack of any symptoms, and the absence of another tumor for 13 years after surgical resection of the tumor-bearing lymph node. A review of similar cases in the world literature reveals that not all gastrinomas in lymph nodes are the result of metastastic spread. A long-term symptom-free follow-up after the excision of a lymphnode gastrinoma is the only reliable criterion for the diagnosis of a primary lymph node tumor. To our knowledge, this is the only well-documented case of a primary lymph node gastrinoma in a patient with MEN1. Our case supports the idea that any gastrinoma in patients with MEN1 should be surgically resected for cure if possible.

Background/purpose: Mirizzi syndrome is a rare complication of gallstone disease (GSD). The association of Mirizzi syndrome and gallbladder carcinoma (GBC) is not well understood. We report our experience of gallbladder carcinoma in patients with Mirizzi syndrome.

Methods: We performed a retrospective analysis of the records of patients with Mirizzi syndrome who underwent cholecystectomy at a tertiary care hospital with special emphasis on patients who were found to harbor GBC. Patients with Mirizzi syndrome with associated GBC were compared with those who had Mirizzi syndrome alone and those with uncomplicated GSD.

Results: Out of 4,800 cholecystectomies, Mirizzi syndrome was found in 133 (2.8%). Seven (5.3%) patients with Mirizzi syndrome had associated GBC, as compared to only 1% in patients with GSD. GBC was detected on final histology after cholecystectomy in 5 patients, and was detected preoperatively and intraoperatively in 1 patient each. Patients with Mirizzi syndrome with associated GBC were older (60 vs 50 years; P

Conclusions: There was a higher incidence of GBC in patients with Mirizzi syndrome than in patients with uncomplicated GSD. There were no clinical features to differentiate these patients with GBC from those with Mirizzi syndrome alone, except that they were a decade older and had longer duration of symptoms. In the majority, the diagnosis of GBC was made on final histology, after cholecystectomy; hence, this group of patients with GBC are to be treated like any other patients with incidental GBC.

The past several years have witnessed an explosive increase in our knowledge about epigenetic features in human cancers. It has become apparent that pancreatic cancer is an epigenetic disease, as it is a genetic disease, characterized by widespread and profound alterations in DNA methylation. The introduction of genome-wide screening techniques has accelerated the discovery of a growing list of genes with abnormal methylation patterns in pancreatic cancer, and some of these epigenetic events play a role in the neoplastic process. The detection and quantification of DNA methylation alterations in pancreatic juice is likely a promising tool for the diagnosis of pancreatic cancer. The potential reversibility of epigenetic changes in genes involved in tumor progression makes them attractive therapeutic targets, but the efficacy of epigenetic therapies in pancreatic cancer, such as the use of DNA methylation inhibitors, remains undetermined. In this review, we briefly summarize recent research findings in the field of pancreatic cancer epigenetics and discuss their biological and clinical implications.

Diabetes remains a major burden, with more than 200 million people affected worldwide, representing 6% of the population. New technology, known as protein transduction technology, has been recently developed. A variety of peptides, known as protein transduction domains or cell-penetrating peptides, have been characterized for their ability to translocate into live cells. There are numerous examples of biologically active full-length proteins and peptides that have been delivered to cells and tissues both in vitro and in vivo, suggesting new avenues for the treatment of several diseases. Some studies have shown that this technology is useful for the treatment of diabetes. In islet isolation and transplantation, cell-permeable peptides deliver anti-apoptotic molecules to protect islets. Another peptide provides immunosuppression for fully mismatched islet allografts in mice. These findings suggest that peptide drugs could lead to outcome improvement for pancreatic islet transplantation. In mice with type 2 diabetes, a cell-penetrating peptide markedly improves insulin resistance and ameliorates glucose tolerance. Moreover, the technology facilitates the differentiation of stem cells into insulin-producing cells. Protein transduction technology has opened up several possibilities for the development of new peptide/protein drugs for the treatment of diabetes.

Background/purpose: The postoperative recovery of gastric motility with various reconstructions after pancreatic head resection has been reported. However, little is known about this recovery after pancreatic head resection with segmental duodenectomy (PHRSD). Some have attributed gastric stasis after pylorus-preserving pancreatoduodenectomy (PPPD) to tube gastrostomy, but its effect on gastric motility has not been investigated. In this study, the postoperative recovery after PHRSD and PPPD, and gastric motility with and without gastrostomy after PPPD were investigated.

Methods: We analyzed the first appearance of gastric phase III motility, postoperative systemic status, and body weight (BW; n = 32). The Imanaga PPPD and PHRSD were compared because the procedures differ only in the length of the remaining duodenum. Traverso and Roux-en-Y PPPDs were compared because the two procedures are similar except for the creation of gastrostomy.

Results: (1) Times to first appearance of gastric phase III motility and BW recovery were significantly better after PHRSD than after the Imanaga PPPD (P < 0.05). (2) Times to first gastric phase III motility and resumption of a regular diet as well as periods of gastric sump tube use and postoperative hospital stay were significantly shorter after the Roux-en-Y than after the Traverso PPPD (P < 0.05).

Conclusions: Preservation of as long a portion of the duodenum as possible, the choice of a Roux-en-Y duodenojejunostomy, and the avoidance of peritoneal fixation of the gastric wall may be factors that improve the recovery of gastric motility and BW after pancreatic head resection.

Background/purpose: We provide an initial report of the indications and procedure for three-port laparoscopic partial hepatectomy.

Methods: Three-port laparoscopic partial hepatectomy was performed in nine patients (age, 49 to 73 years) at our department. Eight patients (seven men and one woman) had hepatocellular carcinoma (HCC); six of these patients had liver cirrhosis (LC) and two had chronic hepatitis (CH). The ninth patient, a woman had a single metastatic liver tumor from colon cancer. The tumors were located in regons S(2), S(3), S(4), S(5), S(6), and S(8). Preoperative liver function assessment revealed Child-Pugh classification A or B. All the tumors were located superficially, and their diameter averaged approximately 3 cm. Hepatectomy was performed laparoscopically, using an ultrasonically activated device (USAD) with or without microwave coagulation therapy (MCT).

Results: The operative time was 50 to 168 min, and the intraoperative blood loss ranged from 32 to 158 g. The postoperative hospital stay was 5 to 17 days. No recurrences, including local relapse, were observed.

Conclusions: Three-port laparoscopic partial hepatectomy is safe and feasible for patients with Child-Pugh liver function classification A or B if the tumor is located superficially and is less than 3 cm in diameter.