Pain management in chronic pancreatitis

Andrén‐Sandberg, Åke; Hoem, Dag; Gíslason, Hjörtur

doi:10.1097/00042737-200209000-00006

Cited by 85 publications

(65 citation statements)

References 111 publications

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“…Quality of life is low in approximately 85% of the patients with chronic pancreatitis, especially the younger patients, with social consequences [10][11][12] . Chronic pain is the main deteriorator of the quality of life of these patients, more so than other Rev.…”

Section: Introductionmentioning

confidence: 99%

Alcoholic chronic pancreatitis: A quality of life study

et al. 2016

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A B S T R A C T ObjectiveTo compare the quality of life between patients with alcoholic chronic pancreatitis and controls, and between diabetic and non-diabetic patients, correlating clinical, sociodemographic, and nutritional factors with their quality of life scores. MethodsForty-three outpatients of the pancreas and biliary tract clinic diagnosed with alcoholic chronic pancreatitis were assessed. Quality of life was measured by the Brazilian version of the Short Form-36. The control group consisted of 43 healthy companions. Nutritional status was classified according to body mass index and triceps, biceps, suprailiac, and subscapular skinfold thicknesses, using the appropriate methods. The percentage of body fat was given by adding the four skinfold thicknesses and by bioelectrical impedance analysis. The statistical tests included the Chi-square, Mann-Whitney, and Spearman's correlation tests, with the significance level set at p<0.05. ResultsThe sociodemographic variables of the case and control groups did not differ. Quality of life was lower in alcoholic chronic pancreatitis patients than in controls. The only quality of life domain that differed between diabetics and non-diabetics was functional capacity, lower in diabetics (p=0.022). Smoking duration, alcohol intake in grams, and time since pancreatic surgery correlated negatively with the quality of life of alcoholic chronic pancreatitis patients. Old age, skinfold thicknesses, and percentage of body fat correlated positively with quality of life.

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Section: Introductionmentioning

confidence: 99%

Alcoholic chronic pancreatitis: A quality of life study

et al. 2016

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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%

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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“…Pancreatic enzyme supplementation may help. Non-narcotic analgesics should be tried first, but many need narcotic analgesics; patient comfort takes precedence over concerns of addiction (Ahmad et.al., 2006;Andren-Sandberg et al, 2002;Fasanella et al, 2007). Some patients need escalating doses, with the addition of fentanyl patches or even parenteral administration.…”

Section: Wwwintechopencommentioning

confidence: 99%