Treatment options for chronic pancreatitis

Issa, Yama; Bruno, Marco J.; Bakker, Olaf J.; Besselink, Marc G.; Schepers, Nicolien J.; Santvoort, Hjalmar C. van; Gooszen, Hein G.; Boermeester, Marja A.

doi:10.1038/nrgastro.2014.74

Cited by 48 publications

(38 citation statements)

References 112 publications

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“…Currently, the main treatment methods for chronic pancreatitis are focused on pain management, the management of complications (i.e., pseudocysts), and the correction of pancreatic insufficiency. [3] Intractable abdominal pain is the main surgical indication for chronic pancreatitis. Pancreatic hyperplasia is also a potential carcinogen.…”

Section: Introductionmentioning

confidence: 99%

Surgical strategies in the treatment of chronic pancreatitis

et al. 2017

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Background:Chronic pancreatitis (CP) is a common and frequently occurring disease. Pancreaticoduodenectomy (PD), pylorus-preserving pancreaticoduodenectomy (PPPD), and duodenum-preserving pancreatic head resection (DPPHR) are important treatment options for patients with chronic pancreatitis. The Beger and Frey procedures are 2 main duodenum-preserving techniques in duodenum-preserving pancreatic head resection (DPPHR) strategies. We conducted this systematic review and meta-analysis to compare the clinical efficacy of DPPHR versus PD, the Beger procedure versus PD, the Frey procedure versus PD, and the Beger procedure versus the Frey procedure in the treatment of pancreatitis. The optimal surgical option for chronic pancreatitis is still under debate. The aim of this systematic review and meta-analysis was to evaluate the clinical efficacy of different surgical strategies for chronic pancreatitis.Methods:Five databases (PubMed, Medline, SinoMed, Embase, and Cochrane Library) were searched with the limitations of human subjects and randomized controlled trials (RCTs) text. Data were extracted by 2 of the coauthors independently and analyzed using the RevMan statistical software, version 5.3. Weighted mean differences (WMDs), risk ratios (RRs), and 95% confidence intervals (CIs) were calculated. Cochrane Collaboration's Risk of Bias Tool was used to assess the risk of bias.Results:Seven studies involving a total of 385 patients who underwent the surgical treatments were assessed. The methodological quality of the trials ranged from low to moderate and included PD (n = 134) and DPPHR (n = 251 [Beger procedure = 100; Frey procedure = 109; Beger or Frey procedure = 42]). There were no significant differences between DPPHR and PD in post-operation mortality (RR = 2.89, 95% CI = 0.31–26.87, P = 0.36), pain relief (RR = 1.09, 95% CI = 0.94–1.25, P = 0.26), exocrine insufficiency (follow-up time > 60 months: RR = 0.91, 95% CI = 0.72–1.15, P = 0.41), and endocrine insufficiency (RR = 0.75, 95% CI = 0.52–1.08, P = 0.12). Concerning the follow-up time < 60 months, the DPPHR group had better results of exocrine insufficiency (RR = 0.22, 95% CI = 0.08–0.62, P = 0.04). However, operation time (P < 0.0001), blood transfusion (P = 0.02), hospital stay (P = 0.0002), postoperation morbidity (P = 0.0007), weight gain (P < 0.00001), quality of life (P = 0.01), and occupational rehabilitation (P = 0.007) were significantly better for patients who underwent the DPPHR procedure compared with the PD procedure. The comparison results of the Frey procedure and PD showed that both procedures had an equal effect in the pain relief, postoperation mortality, exocrine and endocrine function, and quality of life (QoL) (P > 0.05), whereas patients who underwent the Frey procedure had significantly reduced operative times (P < 0.05) and less blood transfusions (P < 0.05). Comparing the Beger procedure to the PD procedure, there were no significant differences in hospital stay, blood transfusion, postoperation morbidity or mortality, pain ...

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Section: Introductionmentioning

confidence: 99%

Surgical strategies in the treatment of chronic pancreatitis

et al. 2017

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“…The strongest predictor of poor quality of life and disability among complications of CP is constant pain (1). Recent studies have addressed the quality of life (2, 8), and comparative effectiveness of treatment for neuropathic pain (9, 10) and outcomes of both endoscopic and surgical treatments (11, 12). Finally, there is growing use of total pancreatectomy with islet autotransplantation (TPIAT) for control of pain (13–15).…”

Section: Introductionmentioning

confidence: 99%

Mechanism, assessment and management of pain in chronic pancreatitis: Recommendations of a multidisciplinary study group

et al. 2016

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Description Pain in patients with chronic pancreatitis (CP) remains the primary clinical complaint and source of poor quality of life. However, clear guidance on evaluation and treatment is lacking. Methods Pancreatic Pain working groups reviewed information on pain mechanisms, clinical pain assessment and pain treatment in CP. Levels of evidence were assigned using the Oxford system, and consensus was based on GRADE. A consensus meeting was held during PancreasFest 2012 with substantial post-meeting discussion, debate, and manuscript refinement. Results Twelve discussion questions and proposed guidance statements were presented. Conference participates concluded: Disease Mechanism: Pain etiology is multifactorial, but data are lacking to effectively link symptoms with pathologic feature and molecular subtypes. Assessment of Pain: Pain should be assessed at each clinical visit, but evidence to support an optimal approach to assessing pain character, frequency and severity is lacking. Management: There was general agreement on the roles for endoscopic and surgical therapies, but less agreement on optimal patient selection for medical, psychological, endoscopic, surgical and other therapies. Conclusions Progress is occurring in pain biology and treatment options, but pain in patients with CP remains a major problem that is inadequately understood, measured and managed. The growing body of information needs to be translated into more effective clinical care.

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“…Pain is a cardinal feature of CP, featured as burning, intermittent, and shooting pain (13). It is, not only the most frequent and dominant symptom of patients with CP, but also the most difficult to treat (1,3,22,35). Our lack of knowledge about what causes pain in pancreatitis has been a serious obstacle to treatment on these patients, with pain frequently relapsing or persisting (1, 31).…”

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confidence: 99%

“…difficult to treat (1,3,22,35). Our lack of knowledge about what causes pain in pancreatitis has been a serious obstacle to treatment on these patients, with pain frequently relapsing or persisting (1,31).…”

mentioning

confidence: 99%

Adrenergic signaling mediates mechanical hyperalgesia through activation of P2X3 receptors in primary sensory neurons of rats with chronic pancreatitis

Wang

Zhu

Jin

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Adrenergic signaling mediates mechanical hyperalgesia through activation of P2X3 receptors in primary sensory neurons of rats with chronic pancreatitis. Am J Physiol Gastrointest Liver Physiol 308: G710 -G719, 2015. First published January 29, 2015; doi:10.1152/ajpgi.00395.2014.-The mechanism of pain in chronic pancreatitis (CP) is poorly understood. The aim of this study was designed to investigate roles of norepinephrine (NE) and P2X receptor (P2XR) signaling pathway in the pathogenesis of hyperalgesia in a rat model of CP. CP was induced in male adult rats by intraductal injection of trinitrobenzene sulfonic acid (TNBS). Mechanical hyperalgesia was assessed by referred somatic behaviors to mechanical stimulation of rat abdomen. P2XR-mediated responses of pancreatic dorsal root ganglion (DRG) neurons were measured utilizing calcium imaging and whole cell patch-clamp-recording techniques. Western blot analysis and immunofluorescence were performed to examine protein expression. TNBS injection produced a significant upregulation of P2X3R expression and an increase in ATP-evoked responses of pancreatic DRG neurons. The sensitization of P2X3Rs was reversed by administration of ␤-adrenergic receptor antagonist propranolol. Incubation of DRG neurons with NE significantly enhanced ATPinduced intracellular calcium signals, which were abolished by propranolol, and partially blocked by protein kinase A inhibitor H-89. Interestingly, TNBS injection led to a significant elevation of NE concentration in DRGs and the pancreas, an upregulation of ␤ 2-adrenergic receptor expression in DRGs, and amplification of the NE-induced potentiation of ATP responses. Importantly, pancreatic hyperalgesia was markedly attenuated by administration of purinergic receptor antagonist suramin or A317491 or ␤ 2-adrenergic receptor antagonist butoxamine. Sensitization of P2X3Rs, which was likely mediated by adrenergic signaling in primary sensory neurons, contributes to pancreatic pain, thus identifying a potential target for treating pancreatic pain caused by inflammation. chronic pancreatitis; dorsal root ganglion; purinergic receptors; norepinephrine; protein kinase A CHRONIC PANCREATITIS (CP) is a progressive inflammatory disorder characterized by repeated attacks of abdominal pain, fibrosis, and destruction of the glandular pancreas (15,29,39). Pain is a cardinal feature of CP, featured as burning, intermittent, and shooting pain (13). It is, not only the most frequent and dominant symptom of patients with CP, but also the most difficult to treat (1,3,22,35). Our lack of knowledge about what causes pain in pancreatitis has been a serious obstacle to treatment on these patients, with pain frequently relapsing or persisting (1, 31). Basic research of pancreatic nerves and experimental human pain studies have provided evidence that pain processing is abnormal in these patients and in many conditions resembles that seen in neuropathic pain disorders (34). Despite much speculation, little is known about the detailed pathophysiology of pain in ...

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Treatment options for chronic pancreatitis

Cited by 48 publications

References 112 publications

Surgical strategies in the treatment of chronic pancreatitis

Surgical strategies in the treatment of chronic pancreatitis

Mechanism, assessment and management of pain in chronic pancreatitis: Recommendations of a multidisciplinary study group

Adrenergic signaling mediates mechanical hyperalgesia through activation of P2X3 receptors in primary sensory neurons of rats with chronic pancreatitis

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