Important Roles Played In Severe Acute Pancreatitis By Large Dose Dexamethasone

Main Category: GastroIntestinal / Gastroenterology
Also Included In: Biology / Biochemistry;  Immune System / Vaccines
Article Date: 05 Nov 2007 - 2:00 PDT

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Severe acute pancreatitis (SAP) is a fatal systemic disease featuring acute onset, serious conditions, high incidence of complications and 20 - 30% mortality, mainly due to multiple organ failure at its early stage. The pathogenesis of SAP is closely related to factors such as activation of pancreatin, release of inflammatory mediators, microcirculation disturbance and apoptosis. However, excessive inflammatory mediators release was regarded as a vital role in the development of SAP. In recent years, it has been found that both inflammatory mediators and pancreatic acinar cell apoptosis are participants in the onset of SAP. The apoptosis of pancreatic acinar cells may be a reaction beneficial to the body after the occurrence of SAP.

The effect of glucocorticoid (represented by dexamethasone) on AP/SAP has been an issue in dispute. In 1952, Stephensen for the first time reported the effect of glucocorticoid in AP treatment. Many empirical studies show glucocorticoid can improve the survival of AP animals. Its mechanisms mainly are: inhibiting the generation of inflammatory mediators and/or inhibiting the effects of inflammatory mediators, enhancing body stress, improving microcirculation, alleviating endotoxemia, cleaning free radicals, inhibiting nitric oxide (NO) and expression of NF- kappa B. In terms of administration and dose, many studies also found a large dose of dexamethasone was obviously superior to the small dose dexamethasone in therapeutic effect, and early use of dexamethasone was superior to dexamethasone of the same dose.

The research team, led by Dr. Zhang Xi-Ping from the First People¡¯s Hospital of Hangzhou and 2nd Affiliated Hospital of Zhejiang University, found that the large dose dexamethasone treatment rats' survival rate, ascites/body weight ratio, plasma amylase and endotoxin content and inflammatory mediators (such as TNF-A and IL-6) were lower than in SAP rats. With the application of tissue microarray technique, it was shown that pathological change of pancreatic tissue and its severity scores were also greatly alleviated with large dose dexamethasone treatment. Compared with the SAP rats, the pancreatic acinar cell apoptosis was induced and the apoptotic index was significantly promoted with the large dose dexamethasone treatment.

The article clarified that large dose dexamethasone therapeutic mechanisms in SAP may be related to the inhibition of inflammatory mediators and the induction of pancreatic acinar cell apoptosis, demonstrated by the application of tissue microarray technique.

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Reference: Zhang XP, Chen L, Hu QF, Tian H, Xu RJ, Wang ZW, Wang KY, Cheng QH, Yan W, Li Y, Li QY, He Q, Wang F.Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis. World J Gastroenterol2007; 13(41): 5506-5511 1007-9327/13/5506.asp

Correspondence to: Xi-ping Zhang, MD,Department of General Surgery, Hangzhou First People's Hospital,261 Huansha Road. Hangzhou 310006, Zhejiang province, China.

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World Journal of Gastroenterology (World J Gastroenterol, WJG), a leading international journal in gastroenterology and hepatology, has an established reputation for publishing fi rst class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection, providing a forum for both clinicians and scientists, and has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by The WJG Press. The publication date is 7th, 14th, 21st, and 28th every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No.30424812, which was founded with a name of China National Journal of New Gastroenterology on October 1, 1995, and renamed as WJG on January 25, 1998.

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Source: You-De Chang
World Journal of Gastroenterology

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