Helmut Friess
Yale University
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Annals of Surgery | 1999
Hans G. Beger; Wolfgang Schlosser; Helmut Friess; Markus W. Büchler
OBJECTIVEnTo present preoperative and early postoperative data for 504 patients who underwent duodenum-preserving pancreatic head resection (DPPHR) for severe chronic pancreatitis (CP).nnnBACKGROUNDnThe pancreatic head is considered to be the pacemaker of the disease in alcohol-induced CP. Indications for surgery in CP are intractable pain and local complications. DPPHR offers the advantage of treating the complications related to the inflammatory process in the head, relieving the pain syndrome, and preserving the bilioduodenal anatomy, and it may have the potential to change the natural course of chronic pancreatitis.nnnMETHODSnBetween November 1972 and December 1998, 504 patients with chronic pancreatitis and an inflammatory mass in the pancreatic head were treated surgically after medical pain treatment for a median of 3.6 years. The procedure resulted in a hospital mortality rate of 0.8%. A continuous follow-up investigation lasting up to 26 years was conducted, during which the patients were reevaluated four times (1983, 1987, 1994, 1996). Between November 1982 and October 1996, 388 patients treated surgically were reinvestigated to evaluate the late outcome; the follow-up rate was 94% (25 patients were lost to follow-up). The reinvestigation evaluation included glucose tolerance test, exocrine pancreatic function test, pain status, physical status, professional and social rehabilitation, and quality of life.nnnRESULTSnAfter an observation period of up to 14 years, 78.8% of the patients were completely pain-free and 12.5% had (yearly) pain. 91.3% were considered as pain-free; 8.7% had continuing abdominal pain; 12% had abdominal complaints. During the 14 years of follow-up, only 9% were admitted to the hospital for acute episodes of chronic pancreatitis. Endocrine function was improved in 11%; in 21%, diabetes developed de novo. The rate of hospital admission for acute episodes decreased from 69% before surgery to 9% after surgery. In the clinical management period of 9 years (median), the frequency of hospital admission dropped from 5.4 per patient before surgery to 2.7 after surgery. Fourteen years after surgery, 69% of the patients were professionally rehabilitated; in 72%, the quality of life index (Karnofsky criteria) was 90 to 100 and in 18%, it was <80.nnnCONCLUSIONnIn patients with alcoholic chronic pancreatitis in whom an inflammatory mass has developed in the pancreatic head, DPPHR results in a change in the natural course of the disease in terms of pain status, frequency of acute episodes, need for further hospital admission, late death, and quality of life.
Archive | 2004
Shailesh V. Shrikhande; Helmut Friess; Jan Schmidt; Jens Werner; Waldemar Uhl; Markus W. Büchler
Acute necrotizing pancreatitis is possibly the most severe form of acute pancreatitis. While results have improved significantly in the past decade, acute necrotizing pancreatitis still carries a high morbidity and mortality. However, it is the infected necrosis of acute necrotizing pancreatitis that accounts for a major share of this high morbidity and mortality.1 On the other hand, management of sterile necrosis has evolved considerably in recent years with improved results. This article discusses the current understanding of sterile necrosis and the approach to its management.
Archive | 2004
Robert Sutton; Deborah D. Stocken; Janet A. Dunn; Helen Hickey; Michael Raraty; Paula Ghaneh; John A. C. Buckels; Mark Deakin; Clement W. Imrie; Helmut Friess; Markus W. Büchler; John P. Neoptolemos
Pancreatic cancer is amongst the top ten fatal cancers of the Western world, accounting for 57 000 deaths per year in Europe and 29 000 deaths per year in the United States.1 It is particularly difficult to treat because of its inaccessible location, late presentation, and frequently aggressive tumour biology. Five-year survival in the 10–15% of affected patients who undergo potentially curative surgery is limited to 17–24%,2,3 whilst overall 5-year survival in all patients is less than 0.5%.4 Although significant improvements in surgical outcome have been obtained with increasing specialisation and case-load,3,5 and further benefits may be anticipated with earlier investigation and referral of high risk groups, 6 the role of adjuvant and neo-adjuvant treatment accompanying surgery remains uncertain.7-10 Interestingly, chemotherapy is the principal modality in the treatment of advanced pancreatic cancer.11
Archive | 2011
Niels Teich; Jörg Kleeff; Herbert Lochs; Joachim Mössner; Volker Keim; Helmut Friess; Johann Ockenga
Copyright information: Taken from The presence of the proteolysis-inducing factor in urine does not predict the malignancy of a pancreatic tumourBMC Gastroenterology 2005;5():20-20.Published online 21 Jun 2005PMCID:PMC1184069.Copyright
Archive | 2007
Lars Fischer; Jörg Kleeff; Helmut Friess; Markus W. Büchler
Das Pankreaskarzinom mit seinem aggressiven Tumorwachstum, fruhen Metastasierung und Therapieresistenz und daraus resultierend schlechten Prognose bestimmtwesentlich die Bauchspeicheldrusen-Chirurgie. In rund einem Drittel der Falle sind jedoch gutartige Erkrankungen (chronische Entzundung, gutartige Tumore) die Indikation fur eine Pankreasoperation, und stellen damit andere, nicht weniger komplexe Herausforderungen an die behandelnden Arzte.
Handbook of Immunohistochemistry and in Situ Hybridization of Human Carcinomas | 2005
Irene Esposito; Frank Bergmann; Markus W. Büchler; Helmut Friess
Mast cells play a key role in immediate hypersensitivity (type I) immune reactions. Binding of a specific antigen to two adjacent immunoglobulin E (IgE) molecules expressed on mast cell plasma membrane initiates the process of degranulation, which is the release of preformed mediators of the inflammatory reaction contained in mast cell granules (e.g., histamine, adenosine, heparin, various proteases). At the same time, the synthesis of new mediators (e.g., prostaglandins, leukotrienes, cytokines, and growth factors) is initiated. Through this and other IgE-independent mechanisms, mast cells exert their function as major cell mediators of the allergic reactions. At the same time, they are also involved in acute and, at a higher level, chronic fibrogenic inflammatory processes in which they directly induce fibrosis through the production of fibroblast growth factor, platelet-derived growth factor, and transforming growth factor-β. The differentiation of mast cells from bone marrow precursors and their proliferation is promoted by stem cell factor (SCF), which binds to c-kit, a type-3 tyrosine-kinase receptor.
Bildverarbeitung für die Medizin | 2005
Lars Fischer; Matthias Thorn; Jan-Oliver Neumann; Tobias Heimann; Lars Grenacher; Hans-Peter Meinzer; Helmut Friess; Markus W. Büchler
Die exakte Definition von Lebervenensegmenten und deren Lagebeziehung zu den klassischen Couinaud-Segmenten spielt vor dem Hintergrund der Leberlebendspende eine zunehmende Bedeutung im klinischen Alltag. Unter Zuhilfenahme des vom DKFZ entwickelten Operationsplanungsprogramm LENA werteten wir die CT-Daten von 64 Patienten aus, bei denen in Vorbereitung auf eine Leberresektion routinemasig eine CT-Untersuchung durchgefuhrt wurde. Das Drainagegebiet der rechten Lebervene umfasst mit 47,1% das groste Volumen. Die mittlere Lebervene drainiert 32,5% und die linke Lebervene 20,4%. Innerhalb dieser venosen Segmente nehmen die Couinaud- und portalen Segmente 2, 3, 5, 7 und 8 identische raumliche Positionen ein. Das Drainagengebiet der venosen Subsegmente reicht von 79,3 ml bis zu 337 ml. Es besteht keine Lageubereinstimmung zwischen venosen Subsegmenten und Couinaud/portalen Segmenten (kappa 0,8).
Archive | 1998
Helmut Friess; Pascal O. Berberat; Markus W. Büchler
Chronic pancreatitis is an inflammatory disease of the pancreas that leads to persistent and progressive morphological and functional alterations of the whole organ and in its terminal state severe exocrine and endocrine insufficiencies are present. (1, 2, 3). Morphologically, chronic inflammation of the pancreas is also associated with pancreatic head enlargement, calcifications of the parenchyma, cysts, necrosis, and pancreatic stones (4, 5, 6). The continuous tissue destruction and subsequent remodeling causes finally the two major clinical symptoms: upper abdominal pain and maldigestion.
Journal of Surgical Research | 1999
Seth A. Spector; Eric T. Olson; Andrew A. Gumbs; Helmut Friess; Markus W. Büchler; Neal E. Seymour
Clinical Pancreatology: For Practising Gastroenterologists and Surgeons | 2007
Pierluigi Di Sebastiano; Markus A. Weigand; Jörg Köninger; Fabio F. di Mola; Helmut Friess; Markus W. Büchler