Pankaj Singh

Cytokines (IL-6, IL-8, TNF): early and reliable predictors of severe acute pancreatitis.

Background Severe acute pancreatitis is associated with a high mortality, especially when compared with mild acute pancreatitis. Early intervention in patients with severe acute pancreatitis has been shown to improve mortality. The value of cytokines (interleukin [IL]-6, IL-8 and tumor necrosis factor [TNF]-alpha) in diagnosing severe acute pancreatitis at an early stage was studied. Study Thirty-six patients with acute pancreatitis were prospectively evaluated. Age-matched controls were obtained from healthy volunteers. Levels of IL-6, IL-8, and TNF-alpha were obtained within 24 hours of admission. Ransons prognostic signs and Banks clinical criteria were used to differentiate patients into mild and severe pancreatitis. Results There was significant difference in IL-6 levels between controls and mild pancreatitis, controls and severe pancreatitis, and mild and severe pancreatitis. IL-8 levels were significantly different between controls and severe pancreatitis and mild and severe pancreatitis. There was no significant difference between controls and mild pancreatitis. The results for TNF-alpha were similar to the findings for IL-8. Conclusion IL-6, IL-8, and TNF can be used independently in differentiating mild acute pancreatitis from early severe acute pancreatitis.

Evaluation of factors that have reduced mortality from acute pancreatitis over the past 20 years

Background The mortality associated with acute pancreatitis varies markedly in different studies, with most frequently reported mortality rates of 10% to 15% for all cases and 15% to 90% for attacks regarded as “severe.” More recently, various centers have recorded lower mortality rates of 4% to 7% for all attacks of acute pancreatitis and 20% to 50% for those regarded as severe. Goals To investigate whether there has been a reduction in mortality associated with acute pancreatitis over the past 20 years and the reasons for this reduction. Study Intended as a review, this study included the authors 20-year prospective assessment of mortality as it relates to the severity of the disease, complications, and current therapy. For the mortality results, the study was divided into four 4-year periods from 1977 to 1998 and the past 3 years (i.e., 1998–2001). For comparison, the mortality figures from some other large studies are presented. Results This study showed that the initial reduction in mortality related to acute pancreatitis coincided with the recognition and application of the signs of severity, either Ransons prognostic signs or Banks clinical criteria. These signs dictated admission to intensive care unit (ICU) therapy, the intensity of ICU monitoring, and the importance of organ-specific emergent therapy. Further mortality reduction in the 1990s could be attributed to either a more select study sample or earlier and more selective endoscopic or surgical debridement of infected tissue, endoscopic cyst drainage, and angiographic control of gastrointestinal bleeding. Improved nutritional support by jejunal feeding, earlier use of antibiotic therapy, gut sterilization, early endoscopic retrograde cholangiopancreatography for common bile duct stones and necrosectomy for noninfected necrosis have reduced the overall mortality associated with acute pancreatitis to a mean of 5% (range, 3.8–7%) for all cases and 20% (range, 15–25%) for severe cases. However, it is clear that the greater the number of signs denoting severity of organ failure, the higher the mortality. Conclusions There has been considerable reduction in the mortality associated with acute pancreatitis over the past 20 years. The reasons are multifactorial, but recognition of severity signs, early implementation of organ-specific therapy, and newer endoscopic, surgical, and angiographic therapy for infection cyst and bleeding appear to have been the major factors in reducing mortality.

Pylephlebitis—diagnosis and management

1. Dusheiko G. Side effects of alpha interferon in chronic hepatitis C. Hepatology 1997;26(suppl 1):112S–21S. 2. Mellstedt H, Osterborg A, Bjorkholm M, et al. Induction treatment witha-interferon in multiple myeloma: An interim report from MGCS. Eur J Haematol 1989;43:124–8. 3. Marcellin P, Pouteau M, Martinot-Peignoux M, et al. Lack of benefit of escalating dosage of interferon alpha in patients with chronic hepatitis C. Gastroenterology 1995;109:156–65. 4. Jett GK. Captopril-induced angioedema. Ann Emerg Med 1984;13:489–90. 5. Israili ZH, Hall WD. Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy. A review of the literature and pathophysiology. Ann Intern Med 1992;117:234–42. 6. Messerli FH, Nussberger J. Vasopeptidase inhibition and angio-oedema. Lancet 2000;356:608–9. 7. Naldi L, Ferri C, Locati T, et al. Cutaneous reactions to analgesic-antipyretics and nonsteroidal anti-inflammatory drugs. Dermatology 1993;186:164–9. 8. Chin HL, Buchan DA. Severe angioedema after long-term use of an angiotensin-converting enzyme inhibitor. Ann Intern Med 1990;112:312–3. 9. Shionoiri H, Takasaki I, Hirawa N, et al. A case report of angioedema during long-term (66 months) angiotensin converting enzyme inhibition therapy with enalapril. Jpn Circ J 1996;60:166–70. 10. Schiller PI, Messmer SL, Haefeli WE, et al. Angiotensinconverting enzyme inhibitor-induced angioedema: Late onset irregular course, and potential role of triggers. Allergy 1997; 52:432–5. 11. Anderson MW, deShazo RD. Studies of the mechanism of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema: The effect of an ACE inhibitor on cutaneous responses to bradykinin, codeine, and histamine. J Allergy Clin Immunol 1990;85:856–8. 12. Nussberger J, Cugno M, Amstutz C, et al. Plasma bradykinin in angio-oedema. Lancet 1998;351:1693–7. 13. Blais C Jr, Rouleau JL, Brown NJ, et al. Serum metabolism of bradykinin and des-Arg9-bradykinin in patients with angiotensin-converting enzyme inhibitor-associated angioedema. Immunopharmacology 1999;43:293–302. Reprint requests and correspondence:Kenji Ohmoto, M.D., Division of Gastroenterology, Department of Medicine, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan. Received Nov. 28, 2000; accepted Dec. 6, 2000.

Gender as an independent predictor of severe acute pancreatitis

Purpose: It is unclear whether men are at a higher risk of developing severe acute pancreatitis as compared to women. Previous studies have revealed conflicting results. There is speculation that estrogens may be protective towards the pancreas, causing a diminished severity of pancreatitis. Basic science experiments on male and female rats are currently underway to prove this hypothesis, To determine whether men are at a higher risk of developing severe acute pancreatitis as compared to women.

Family history of inflammatory bowel disease is uncommon among African Americans

Background: Infectious agents were implicated in the pathogenesis of 1BD. Such infections may be seasonal. However, no information is available regarding the linkage between the month of birth of the patient and the risk to develop CD or UC in Israel. Aim: To determine the risk of developing CD and UC according to the momh of birth. Methods: Birth dates of CD and UC patients in three medical centers were recorded. Data from 576 CD and 268 UC patients born in Israel were available. The risk to develop disease was determined using the standard mortality ratio (SMR). Results: The SMRs for CD and UC according to the month of birth showing significant differences are depicted in the table. Compared to the general population, a sigmficant risk to develop CD but not UC is associated with birth during the winter period, November to February. By contrast, birth during the spnng was found to be protective for onset of CD. Conclusion: These data show that the risk to develop CD, but not UC, vanes significantly by season. These findmgs may support the notion that infectious agents are involved in the pathogenesis of CD,

Bacterial infection in cirrhotic patients and its relationship with alcohol

TO THE EDITOR: We read with interest the study by Rosa et al. on bacterial infection in cirrhotic patients and its relationship with alcohol (1). Their study included 128 cirrhotic patients, 78 of whom were alcoholic and 50 of whom were nonalcoholic. The infection and mortality rate was greater in alcoholic cirrhotics, but the difference in infection rate did not reach statistical significance. The authors concluded that bacterial infections are more common in cirrhotics irrespective of etiology.

7101 Choledocho-duodenostomy rendezvous : an approach to solo biliary rendezvous for performance of biliary sphincterotomy in a case of sump syndrome.

Introduction Sump syndrome is an infrequent complication of side-to-side choledocho-duodenostomy (CDD). Endoscopic sphincterotomy with removal of the debris has been shown to be an effective means of treating sump syndrome. However, cases arise in which standard sphincterotomy is not possible because of distal CBD impaction, ampullary stenosis or stricture.We describe a technique of solo biliary rendezvous for performance of biliary sphincterotomy in patients with side-to-side CDD. Case A 63 year old female was referred to our institution for ERCP for treatment of probable sump syndrome that developed following CDD. An ERCP was performed. Endoscopy revealed a patent double-barrel CDD but the ampulla appeared small with no clearly visible papilla. Cannulation of the ampulla with a cannulotome or wire was unsuccessful. Pre-cut was not performed due to a very short intramural segment. Cholangiography of the lower limb of the CDD revealed distal CBD blockage and no flow into the duodenum. Given the lack of easy access to the distal duct for standard sphincterotomy, we proceeded with antegrade wire and cannula access through the CDD. Under fluroscopic guidance, a Zebra wire was passed via the lower limb into the distal CBD through the ampulla and into the duodenum. The endoscope was carefully withdrawn to the ampulla while maintaining the postion of Zebra wire in its location in the duodenum. At this point, a regular snare was passed alongside the Zebra wire through the therapeutic channel of the endoscope. The soft tip of the Zebra wire was snared. Under fluroscopic guidance, the endoscope was carefully withdrawn, while feeding the Zebra wire and maintaining a large loop of wire through the lower limb of the CDD, ampulla and duodenum. After removal of the endoscope from the patient, the soft tip of this wire was then threaded through the distal end of the therapeutic channel of the ERCP endoscope. The endoscope was then re-inserted and passed to the ampulla. At this point the endoscopists visualized the wire exiting the ampulla. Thereafter, standard wire-guided sphincterotomy was easily performed. Adequate biliary drainage of the distal sump segment was achieved and the patient remains asymptomatic. Discussion The preceding case illustrates a technique for solo biliary rendezvous for performance of biliary sphincterotomy in patients with side-to-side choledocho-duodenostomy and tough access to the distal CBD.