Literature DB >> 15689677

Chronic pancreatitis.

Matthew J DiMagno1, Eugene P DiMagno.   

Abstract

PURPOSE OF REVIEW: Clinicians are learning more about chronic pancreatitis but are entering an era of some confusion, primarily driven by uncovering new etiologies of chronic pancreatitis. Ideally, this knowledge will lead to better diagnosis and treatment, and abandonment of ill-conceived treatments. In contrast with previous reviews, this review highlights select contributions this year that may develop into true advances in chronic pancreatitis. RECENT
FINDINGS: Small steps have been made to understand better the molecular basis of chronic pancreatitis. Diagnosis of early chronic pancreatitis remains challenging. Rapid diagnosis by combining endoscopy and a direct stimulatory test of pancreatic function may lead to more widespread use of function testing, but this test is not ready for clinical use. Application of microarray and proteomic technologies may aid future diagnosis of chronic pancreatitis. The failure to account clearly for the phenotype of patients with chronic pancreatitis may confound delineating the etiologies of chronic pancreatitis. Clinical description and studies of autoimmune pancreatitis have led to the realization that steroids are an effective treatment for this form of chronic pancreatitis. Genetic-based studies have provided insight into the pathogenic mechanisms of chronic pancreatitis. Investigation of the role of stellate cells, an essential component fibrogenesis, has led to identification of potential novel treatments for chronic pancreatitis.
SUMMARY: Ongoing basic and clinical research this past year has characterized further the histologic, genetic, molecular, and clinical aspects of chronic pancreatitis, efforts that may translate into novel therapies once well-designed, controlled studies have been performed.

Entities:  

Year:  2004        PMID: 15689677     DOI: 10.1097/00001574-200409000-00005

Source DB:  PubMed          Journal:  Curr Opin Gastroenterol        ISSN: 0267-1379            Impact factor:   3.287


  3 in total

1.  Inhibition of acinar apoptosis occurs during acute pancreatitis in the human homologue DeltaF508 cystic fibrosis mouse.

Authors:  Matthew J DiMagno; Sae-Hong Lee; Chung Owyang; Shi-yi Zhou
Journal:  Am J Physiol Gastrointest Liver Physiol       Date:  2010-06-03       Impact factor: 4.052

2.  K-ras and Dpc4 mutations in chronic pancreatitis: case series.

Authors:  Marijana Popović Hadzija; Marina Korolija; Jasminka Jakić Razumović; Pajica Pavković; Mirko Hadzija; Sanja Kapitanović
Journal:  Croat Med J       Date:  2007-04       Impact factor: 1.351

3.  Mononuclear cells modulate the activity of pancreatic stellate cells which in turn promote fibrosis and inflammation in chronic pancreatitis.

Authors:  Christoph W Michalski; Andre Gorbachevski; Mert Erkan; Carolin Reiser; Stefanie Deucker; Frank Bergmann; Thomas Giese; Markus Weigand; Nathalia A Giese; Helmut Friess; Jörg Kleeff
Journal:  J Transl Med       Date:  2007-12-05       Impact factor: 5.531

  3 in total

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