JOP. J Pancreas (Online) 2004; 5(4):243-246.
PANCREAS ALERTS
J Am Coll Surg 2004; 198:871-6. (PMID: 15194067)
Pancreaticogastrostomy: a novel application after central pancreatectomy.
Goldstein MJ, Toman J, Chabot JA.
Department of Surgery, New York Presbyterian Hospital, Columbia Campus. New York, NY, USA.
Limited middle segment pancreatectomy, or central pancreatectomy, has been described for sparing normal pancreatic tissue during resection of benign neoplasms of the pancreatic neck. Anatomic reconstruction after central pancreatectomy has been reported in other series with creation of a Roux-en-Y loop of jejunum for a mucosa-to-mucosa pancreaticojejunostomy.
Hospital charts and outpatient records were reviewed for 12 consecutive patients undergoing central pancreatectomy from August 1999 to November 2002. The authors performed central pancreatectomy with pancreaticogastrostomy in 12 patients: 5 with serous cystadenomas, 6 with mucinous cystadenomas, and 1 with neuroendocrine tumor. All tumors were located in the body or neck of the pancreas.
Median postoperative hospital stay was 6.5 days (range 5 to 15 days). There were no intraoperative complications. Perioperative complications included two urinary tract infections and one readmission for acute pancreatitis. There were no pancreatic leaks or fistulas in this series. Two of the 12 patients experienced endocrine insufficiency with elevated glycosylated hemoglobin levels during outpatient follow-up. None of the 12 patients experienced exocrine insufficiency.
The authors concluded that central pancreatectomy with pancreaticogastrostomy reconstruction is safe and technically advantageous over Roux-en-Y pancreaticojejunostomy, and should be considered a safe reconstruction technique after central pancreatectomy for benign disease.
Gastroenterology 2004; 126:1844-59. (PMID: 15188179)
Protease-activated receptor 2 exerts local protection and mediates some systemic complications in acute pancreatitis.
Namkung W, Han W, Luo X, Muallem S, Cho KH, Kim KH, Lee MG.
Department of Pharmacology and Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine. Seoul, South Korea.
Protease-activated receptor 2 can be stimulated by interstitially released trypsin during acute inflammation of the pancreas. The authors investigated the roles of pancreatic and circulatory protease-activated receptor 2 in the pathogenesis of acute pancreatitis by using in vitro and in vivo model systems.
Physiological and pathologic effects of protease-activated receptor 2 activation were measured in isolated pancreatic cells and in rats with experimental pancreatitis. Consequences of protease-activated receptor 2 activation on the systemic and inflammatory responses were measured after treatments with trypsin or protease-activated receptor 2-activating peptide.
Stimulation of protease-activated receptor 2 in rat pancreatic acinar cells activated short-lasting (Ca(2+) signaling) and long-lasting (extracellular signal-related kinase) signaling pathways and protected the cells against bile-induced cell damage. More importantly, protease-activated receptor 2 activation ameliorated the pathologic effects observed in the in vivo model of cerulein-induced pancreatitis. Trypsin in the circulation of rats with taurocholate-induced severe acute pancreatitis reached levels sufficient to activate endothelial and immune cells to stimulate nitric oxide and interleukin-8 production, respectively. Most notably, activation of systemic protease-activated receptor 2 by circulating protease-activated receptor 2 agonists induced a hemodynamic response pattern similar to that observed in rats with severe acute pancreatitis. The effects of protease-activated receptor 2 agonists and acute pancreatitis were not additive.
The authors concluded that these findings suggest that protease-activated receptor 2 may have a dual role in acute pancreatitis: protecting acinar and duct cells against pancreatitis-induced cell damage while mediating or aggravating the systemic complications of acute pancreatitis, which are the major cause of mortality in the early phase of necrotizing pancreatitis.
J Pediatr Surg 2004; 39:817-20. (PMID: 15185203)
Frey procedure for surgical management of chronic pancreatitis in children.
Rollins MD, Meyers RL.
Division of Pediatric Surgery, Primary Children's Medical Center. Salt Lake City, UT, USA.
The authors adopted the Frey procedure for the surgical management of chronic pancreatitis after one of their patients had recurrent disease in the head of the gland after a longitudinal pancreaticojejunostomy.
A retrospective chart review was performed of all children undergoing a drainage or resection procedure for chronic pancreatitis from 1995 to 2002.
Eleven children underwent either the longitudinal pancreatic jejunostomy (3) or Frey (8) procedure. Etiologies included: idiopathic, familial, congenital anomaly of the major papilla, pancreatic head mass, short bowel syndrome, and pancreatic divisum. Before surgical therapy, patients had been symptomatic 2.3 years (range, 1 month to 6 years) and had been hospitalized for pancreatitis 4 times (range, 1 to 10).
Four patients did not respond to endoscopic stenting, and 5 had a pancreatic pseudocyst. Patients were followed up in clinic an average of 2.5 years, with total time elapsed since surgery averaging 4.6 years. Eight of 11 patients experienced excellent or good results subsequent to surgical intervention.
The authors concluded that the Frey procedure is effective for children who have not responded to conservative management of chronic pancreatitis and may prevent recurrent disease in the head of the gland.
Clin Cancer Res 2004; 10:3780-7. (PMID: 15173085)
Down-regulation of BRCA1 in chronic pancreatitis and sporadic pancreatic adenocarcinoma.
Beger C, Ramadani M, Meyer S, Leder G, Kruger M, Welte K, et al.
Department of Pediatric Hematology, Hannover Medical School. Hannover, Germany.
BRCA1 and BRCA2 are considered to be breast cancer susceptibility genes that may also contribute to pancreatic cancer development because family studies revealed mutation carriers to have an increased risk of developing pancreatic cancer. However, as demonstrated for breast and ovarian cancer, inactivation of BRCA in sporadic diseases is based on alteration in gene expression or functional alteration.
To study a potential correlation of BRCA1 and BRCA2 to chronic pancreatitis and development of sporadic pancreatic adenocarcinoma, the authors have analyzed the expression of these genes by quantitative PCR and performed immunohistochemical analyses in normal pancreatic tissues, chronic pancreatitis, and pancreatic cancer specimens.
BRCA1 expression was down-regulated in chronic alcoholic pancreatitis, in particular on the RNA level. Furthermore, the data indicate suppressed BRCA1 expression in pancreatic cancer on both the RNA and protein levels. Quantitative analysis of BRCA1 protein expression demonstrated regular staining in 50% of tumor specimens tested and reduced staining in 50% of tumor specimens tested. Correlation with the clinical outcome revealed a significantly better 1-year overall survival for patients with BRCA1-regular as compared with BRCA1-reduced or BRCA1-absent tumors. In contrast, no substantial differences in BRCA2 expression were found in chronic pancreatitis and pancreatic cancer samples.
The authors concluded that the data demonstrate alteration of BRCA1 expression in chronic pancreatitis and sporadic pancreatic adenocarcinoma.
Am J Surg Pathol 2004; 28:813-20. (PMID: 15166675)
Ductuloinsular tumors of the pancreas: endocrine tumors with entrapped nonneoplastic ductules.
van Eeden S, de Leng WW, Offerhaus GJ, Morsink FH, Weterman MA, de Krijger RR, et al.
Department of Pathology, Academic Medical Center. Amsterdam, The Netherlands.
Rare pancreatic neoplasms have been reported that show both endocrine and exocrine differentiation in the neoplastic components. In addition, pancreatic endocrine tumors may contain small, cytologically bland ductules intimately admixed with the endocrine component. It was recently suggested that these ductules represent an intrinsic part of the tumor, i.e., that the ductules are neoplastic, and the term "ductulo-insular tumors of the pancreas" was proposed.
In the present study, the nature of the ductular component of 16 cases of ductule-containing pancreatic endocrine tumors was investigated at the molecular level.
Molecular genetic changes often present in ductal pancreatic neoplasms were not found by immunohistochemistry for DPC4, p53, and ERBB2 and by sequence analysis of KRAS codon 12. An X-chromosome inactivation clonality assay of one such tumor from a female patient indicated that the neuroendocrine component was monoclonal, contrasting with the ductular component that was polyclonal. The lymph node and liver metastases from three patients only contained the neuroendocrine component, and no ductules were observed. Although certain morphologic features of ductule-containing endocrine tumors are reminiscent of the embryonic development of the human pancreas, none of the tumors expressed PDX-1, a transcription factor essential in pancreatic organ development.
Based on these results, it is suggested that the ductular component occasionally found in pancreatic endocrine tumors is the result of entrapment of preexisting nonneoplastic ductules and that the tumors are otherwise not distinctive from conventional pancreatic endocrine tumors. Although the phenomenon is rare, it is important to recognize and to distinguish these tumors from true mixed ductal-endocrine neoplasms, which are generally more clinically aggressive. "Pancreatic endocrine tumors with entrapped ductules" would be the preferred nomenclature since it better reflects the nonneoplastic nature of the ductules
Adv Skin Wound Care 2004; 17:232-8. (PMID: 15192491)
The use of telemedicine in the management of diabetes-related foot ulceration: a pilot study.
Wilbright WA, Birke JA, Patout CA, Varnado M, Horswell R.
Medical Informatics and Telemedicine Program, Biostatistics Section, School of Public Health and Preventive Medicine, Louisiana Health Sciences Center. New Orleans, LA, USA.
The authors determined if the management of forefoot ulcerations through telemedicine is medically equivalent to ulcer care at a diabetes foot program.
Nonrandomized comparison of forefoot ulcer healing rates was performed. Twenty consecutive patients with diabetes were treated for neuropathic forefoot ulcerations via telemedicine consultation and 120 consecutive patients with diabetes were treated face-to-face at a diabetes foot program. Management of forefoot ulcers by a certified wound care nurse trained in the use of a staged management approach algorithm and alternative off-loading methods, supported by real-time interactive telemedicine consultation. Forefoot ulcer healing time in days, percentage of wounds healed in 12 weeks, and healing time ratio (adjusted for age, gender, ulcer duration, location, size, crossover, and grade).
No differences were found between the telemedicine and diabetes foot program groups in the average forefoot ulcer healing time, the percent of forefoot ulcers healed in 12 weeks and the adjusted healing time ratio.
These data appear to support the effectiveness of real-time interactive telemedicine consultation in the management of diabetes-related forefoot ulceration.
Am J Epidemiol 2004; 159:1160-7. (PMID: 15191933)
Diabetes mellitus as a predictor of cancer mortality in a large cohort of US adults.
Coughlin SS, Calle EE, Teras LR, Petrelli J, Thun MJ.
Epidemiology and Applied Research Branch, Division of Cancer Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention. Atlanta, GA, USA.
Several studies have suggested that diabetes mellitus may alter the risk of developing a variety of cancers, and the associations are biologically plausible.
To learn more about the relation between diabetes and cancer mortality, the authors examined associations with selected cancers in a large, prospective US cohort of 467,922 men and 588,321 women who had no reported history of cancer at enrollment in 1982.
After 16 years of mortality follow-up, diabetes was significantly associated with fatal colon cancer in men and women and with pancreatic cancer in men and women. For men, diabetes was significantly associated with liver cancer and bladder cancer. In addition, diabetes was significantly associated with breast cancer in women. These associations were not explained by high body mass.
The authors concluded that these findings suggest that diabetes is an independent predictor of mortality from cancer of the colon, pancreas, female breast, and, in men, of the liver and bladder.