Effect of Somatostatin, Ulinastatin and Gabexate on the Treatment of Severe Acute Pancreatitis

Wang, Guiliang; Liu, Yan; Zhou, Shu-Feng; Qiu, Ping; Xu, Li; Wen, Ping; Wen, Jianbo; Xiao, Xianzhong

doi:10.1016/j.amjms.2016.03.013

Cited by 40 publications

(30 citation statements)

References 21 publications

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“…As a commonly used clinical drug, ulinastatin is mainly used for acute pancreatitis and chronic recurrent pancreatitis ( Ohwada et al, 1997 ; Wang et al, 2016 ). Recent studies show that ulinastatin is also beneficial in treatment of cerebral ischemia/reperfusion injury ( Cao et al, 2011 ; Liu M. et al, 2017 ), early cardiopulmonary resuscitation, lung injury induced by hip fracture and pulmonary fibrosis as well as others ( Liu Q. et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Ulinastatin Inhibits Osteoclastogenesis and Suppresses Ovariectomy-Induced Bone Loss by Downregulating uPAR

et al. 2018

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Recent studies indicate that uPAR acts a crucial part in cell migration and the modulation of bone homeostasis. As a natural serine protease inhibitor, ulinastatin owns the capacity to reduce proinflammatory factors, downregulate the activation of NF-κB and mitogen-activated protein kinases (MAPKs) signaling pathways. Osteoclastogenesis has been demonstrated to be related with low-grade inflammation which involves cell migration, thus we speculate that ulinastatin may have a certain kind of impact on uPAR so as to be a potential inhibiting agent of osteoclastogenesis. In this research, we investigated the role which ulinastatin plays in RANKL-induced osteoclastogenesis both in vivo and in vitro. Ulinastatin inhibited osteoclast formation and bone resorption in a dose-dependent manner in primary bone marrow-derived macrophages (BMMs), and knockdown of uPAR could completely repress the formation of osteoclasts. At the molecular level, ulinastatin suppressed RANKL-induced activation of cathepsin K, TRAP, nuclear factor-κB (NF-κB) and MAPKs, and decreased the expression of uPAR. At the meantime, ulinastatin also decreased the expression of osteoclast marker genes, including cathepsin K, TRAP, RANK, and NFATc1. Besides, ulinastatin prevented bone loss in ovariectomized C57 mice by inhibiting the formation of osteoclasts. To sum up, this research confirmed that ulinastatin has the ability to inhibit osteoclastogenesis and prevent bone loss, and uPAR plays a crucial role in that process. Therefore, ulinastatin could be chosen as an effective alternative therapeutics for osteoclast-related diseases.

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Section: Discussionmentioning

confidence: 99%

Ulinastatin Inhibits Osteoclastogenesis and Suppresses Ovariectomy-Induced Bone Loss by Downregulating uPAR

et al. 2018

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“…According to Working Group IAP/APA Acute Pancreatitis Guidelines, oral feeding can be initiated as soon as the pain decreases and inflammatory markers are lowering [ 19 ]. Octreotide is a synthetic analogue of somatostatin that is effective for the treatment of AP via the inhibition of the release of exocrine secretions of the pancreas [ 20 ]. Steroid administration has been controversial in the treatment of AP over the past few decades.…”

Section: Discussionmentioning

confidence: 99%

Henoch-Schönlein purpura with acute pancreatitis: analysis of 13 cases

et al. 2018

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BackgroundHenoch-Schönlein purpura is a common small vessel vasculitis in children. Acute pancreatitis rarely presents as a complication of Henoch-Schönlein purpura and has not been well characterized.MethodsWe retrospectively reviewed 13 cases of Henoch-Schönlein purpura with acute pancreatitis among 3212 patients who attended our hospital between January 2003 and June 2016 and analyzed their clinical characteristics, laboratory findings, imaging findings, treatment and overall prognosis.ResultsAll patients had abdominal manifestations, including significant abdominal pain (13/13), vomiting (9/13), abdominal distension (3/13) and melena (6/13). Serum amylase level significantly increased in all patients, and urine amylase was increased in 7 cases (7/10). However, increased urine lapse was only noted in 2 cases (2/5), and diffuse swelling of the pancreas was seen in 2 cases (2/13) by abdominal ultrasonography. Although all patients had typical skin purpura (13/13), 5 patients (5/13) with acute pancreatitis initially experienced acute abdominal pain in clinical onset of Henoch-Schönlein purpura. Glucocorticoid therapy was effective in alleviating abdominal symptoms of Henoch-Schönlein purpura patients with acute pancreatitis. All patients were in good general condition without any abdominal complications 6–12 months after discharge.ConclusionsAcute pancreatitis is rarely observed in Henoch-Schönlein purpura children and has no specific clinical features that differentiate it from abdominal manifestations of Henoch-Schönlein purpura. Therefore, in Henoch-Schönlein purpura patients with severe abdominal pain, serum amylase levels should be assessed to confirm the diagnosis of acute pancreatitis. Early diagnose of Henoch-Schönlein purpura with acute pancreatitis and treatment timely was very important for good clinical outcomes.

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“…The major cause of intestinal mucosal injury during AP has been reported to be the excessive secretion of inflammatory mediators (29). A possible mechanism involved is that of somatostatin, which suppresses the production of pancreatic enzymes and represses the motor activity of Oddi's sphincter and Oddi basal pressure, while protecting gastrointestinal mucosal cells and stimulating the reticulo-endothelial system (30). Furthermore, patients with Crohn's disease, a chronic inflammatory bowel disease, who have increased serum CRP levels, demonstrate more active inflammation are more susceptible to a high clinical efficacy of infliximab (anti-TNF-α monoclonal antibody) when compared with those patients with low serum CRP levels (31).…”

Section: Discussionmentioning

confidence: 99%

Predicative values of C‑reactive protein for the therapeutic effects of ulinastatin combined with somatostatin in severe acute pancreatitis and for the severity of gastrointestinal failure

Wang

2018

Exp Ther Med

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Severe acute pancreatitis (SAP) is a serious systemic disease with high mortality. Ulinastatin is a drug widely used for patients with SAP and multiple organ failure syndrome. The present study aimed to investigate the capacity of the serum C-reactive protein (CRP) levels to predict the therapeutic effects of ulinastatin combined with somatostatin as well as determine the severity of SAP. SAP patients were treated with ulinastatin combined with somatostatin and serum CRP levels were measured. The computed tomography severity index (CTSI), acute physiology and chronic health evaluation II (APACHE II) and gastrointestinal failure scores were used to determine the therapeutic effects. All patients were assigned to the effective group and the ineffective group. Receiver operating characteristic curve analysis was performed to determine the sensitivity and specificity of CRP levels in predicting the severity of SAP and patient prognosis. Logistic regression analysis was adopted to investigate the factors influencing the therapeutic effects. Prior to and after treatment, serum CRP levels in patients of the effective and ineffective groups were significantly different. After treatment, serum CRP levels in patients of the effective group exhibited a more obvious reduction. The sensitivity and specificity of serum CRP levels in predicting the therapeutic effects of ulinastatin combined with somatostatin in SAP patients upon hospital admission were 0.813 and 0.934, respectively. Serum CRP levels were positively correlated with APACHE II, CTSI and gastrointestinal failure scores of SAP patients. The logistic regression demonstrated that serum albumin, creatinine and CRP levels on admission were factors influencing the therapeutic effects of ulinastatin combined with somatostatin in SAP patients. These results indicate that serum CRP levels may have a predictive value regarding the therapeutic effects of ulinastatin combined with somatostatin and are an indicator of the severity of gastrointestinal failure in SAP.

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Effect of Somatostatin, Ulinastatin and Gabexate on the Treatment of Severe Acute Pancreatitis

Cited by 40 publications

References 21 publications

Ulinastatin Inhibits Osteoclastogenesis and Suppresses Ovariectomy-Induced Bone Loss by Downregulating uPAR

Ulinastatin Inhibits Osteoclastogenesis and Suppresses Ovariectomy-Induced Bone Loss by Downregulating uPAR

Henoch-Schönlein purpura with acute pancreatitis: analysis of 13 cases

Predicative values of C‑reactive protein for the therapeutic effects of ulinastatin combined with somatostatin in severe acute pancreatitis and for the severity of gastrointestinal failure

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