皮质类固醇治疗严重急性胰腺炎

Int J Clin Exp Pathol 2015;8(7):7654-7660

/ISSN:1936-2625/IJCEP0007864

Review Article

Corticosteroid therapy for severe acute pancreatitis: a meta-analysis of randomized, controlled trials

Li-Hua Dong1,2, Zhong-Min Liu1, Shi-Ji Wang1, Shu-Jie Zhao1, Dong Zhang1, Ying Chen1, Yu-Shan Wang1

1Intensive Care Unit, First Affiliated Hospital of Jilin University, Changchun 130021, China; 2Intensive Care Unit, Second Affiliated Hospital of Jilin University, Changchun 130041, China

Received March 12, 2015; Accepted June 10, 2015; Epub July 1, 2015; Published July 15, 2015

Abstract: Background: Recent reports about the benefits of corticosteroid therapy in patients with severe acute pancreatitis (SAP) have shown conflicting results. We aimed to explore the effects of corticosteroid therapy in SAP patients on patient outcomes by performing a meta-analysis. Methods: Databases (Medline, EMBASE, Web of Sci-ence, PubMed, Cochrane Library, Chinese Biomedicine Database, and China Academic Journal Full-Text Database) were queried for all relevant, randomized, controlled trials investigating corticosteroid therapy in patients with SAP. Results: Six randomized, controlled trials including 430 SAP patients were identified. Corticosteroid therapy for SAP was associated with reductions in the length of hospital stay, the need for surgical intervention, and the mortality rate (weighted mean difference[WMD]: -9.47, 95% confidence interval [CI]: -16.91 to -2.04, P = 0.01; odds ratio [OR]: 0.35, 95% CI: 0.18-0.67, P = 0.002; OR: 0.45, 95% CI: 0.22-0.94, P = 0.03). There were no significant differ-ences in the complication rates or Physiology and Chronic Health Evaluation II (APACHE II) scores in patients with or without corticosteroid therapy. Conclusion: Corticosteroid therapy may improve outcomes in patients with SAP. Keywords: Corticosteroid, severe acute pancreatitis, meta-analysis

Introduction

Acute pancreatitis (AP) is initiated by autodiges-tion, defined as the activation of proteolytic and lipolytic enzymes within acinar cells and/or pancreatic ducts, which leads to inflammation and destruction of the pancreatic tissue. AP is associated with a high mortality rate, and its incidence has been increasing in recent years. Standard therapy for AP includes bowel rest, pain control, intravenous fluids, and correction of electrolyte and metabolic abnormalities. Patients with more severe presentations are treated with early enteral nutrition and are closely monitored to maintain adequate organ perfusion.

Despite these therapeutic interventions, ap- proximately 20% of patients with severe acute pancreatitis (SAP) will progress to systemic inflammatory response syndrome (SIRS), com-plicated by shock, multiorgan failure, and even death, within the first 72 hours after admission [1, 2]. SIRS is a response to the widespread systemic effects of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interleukin (IL)-β, IL-6, and phospholipase A

2 (PLA

2

). These circulating cytokines play major roles in SAP progression to a systemic process by activating the vascular endothelium, increas-ing capillary permeability, and triggering the migration of leukocytes into tissues throughout the entire body [3, 4]. Inhibitors of these proin-flammatory cytokines can be beneficial for reducing the severity of SAP. Corticosteroids have shown beneficial effects in animal models of AP and SAP [5-7], poten-tially due to their effects on inflammatory medi-ators, such as cytokines, endotoxins, and free radicals [8, 9]. Corticosteroids were initially reported to induce pancreatitis in susceptible patients [10]. However, in 1952, corticosteroids were used successfully as nonspecific anti-inflammatory agents to treat AP [11]. Following this report, additional studies showed that cor-ticosteroids suppress the release of inflamma-tory cytokines in AP [12-14]. In 1997, Lazar and colleagues found that rats treated with hydro-cortisone showed diminished IL-6 levels [15].