Year 2017 Vol. 25 No 6

GENERAL & SPECIAL SURGERY

A.T. SHCHASTNY

CHRONIC PANCREATITIS: CORRELATION BETWEEN PAIN SYNDROME INTENSITY AND PANCREAS NERVE TISSUE CHANGES

Vitebsk State Medical University, Vitebsk
The Republic of Belarus

Objective. To study interrelation between pain syndrome intensity and nerve tissue marker neurofilament (NF) expression in pancreas at chronic pancreatitis.
Methods. The research included 45 patients with chronic pancreatitis who needed surgical intervention because of abdominal pain that could not be stopped by medications. For assessment of a pain syndrome a visual analogue scale (VAS) was used. Involvement of nervous tissue was estimated by a NF expression in the serial histological sections of resected pancreas head stained with Anti-Neurofilament Monoclonal Antibody. Control group for morphological research included 7 pancreas head samples without any pancreas pathology from age comparable people died by accidents.
Results. In patients with chronic pancreatitis the pain syndrome intensity index, estimated by VAS, varied from 2 to 10 points. A mild pain (from 1 to 3 points) was noted by 4 (9%), moderate pain (4-6 points) 17 (38%), severe pain (7-10 points) 24 (53%) patients.
Statistical assessment of a pain syndrome intensity and NF expression showed a moderate linear relationship (r=0,3, p=0,04). The research of a pain syndrome intensity and positively NF-expressing nervous elements percent also showed a moderate correlation (r=0,33; p=0,03).
Conclusions. Chronic pancreatitis is associated with a different intensity pain syndrome (from 2 to 10 points). At the same time the intensity of the pain syndrome estimated by visual analogue scale (VAS) was associated with nervous tissue qualitative characteristics changes that was confirmed by high rates of NF expression and percent of NF- positively expressing nervous elements at the severe pain syndrome.

Keywords: chronic pancreatitis, immunohistochemistry, nerve tissue, neurofilament, abdominal pain, visual analog scale
p. 567-573 of the original issue
References
  1. Teo K, Johnson MH, Truter S, Pandanaboyana S, Windsor JA. Pain assessment in chronic pancreatitis: A comparative review of methods. Pancreatology. 2016 Nov-Dec;16(6):931-39. doi: 10.1016/j.pan.2016.09.006.
  2. Talukdar R, Reddy DN. Pain in chronic pancreatitis: managing beyond the pancreatic duct. World J Gastroenterol. 2013 Oct 14; 19(38): 6319-28.Published online 2013 Oct 14. doi: 10.3748/wjg.v19.i38.631.
  3. Toma H, Winston J, Micci MA, Shenoy M, Pasricha PJ. Nerve growth factor expression is up-regulated in the rat model of L-arginine-induced acute pancreatitis. Gastroenterology. 2000 Nov;119(5):1373-81. doi: 10.1053/gast.2000.19264.
  4. Friess H, Zhu ZW, di Mola FF, Kulli C, Graber HU, Andren-Sandberg A, Zimmermann A, Korc M, Reinshagen M, Büchler MW. Nerve growth factor and its high-affinity receptor in chronic pancreatitis. Ann Surg. 1999 Nov;230(5):615-24.
  5. Mascetta G, di Mola FF, Tavano F, Selvaggi F, Giese N, Bassi C, Büchler MW, Friess H, di Sebastiano P. Substance P and neprilysin in chronic pancreatitis. Eur Surg Res. 2012;48(3):131-38. doi: 10.1159/000337869.
  6. Zhu Y, Colak T, Shenoy M, Liu L, Pai R, Li C, Mehta K, Pasricha PJ. Nerve growth factor modulates TRPV1 expression and function and mediates pain in chronic pancreatitis. Gastroenterology. 2011 Jul;141(1):370-77. doi: 10.1053/j.gastro.2011.03.046.
  7. Liu L, Shenoy M, Pasricha PJ. Substance P and calcitonin gene related peptide mediate pain in chronic pancreatitis and their expression is driven by nerve growth factor. JOP. 2011 Jul 8;12(4):389-94. doi: 10.6092/1590-8577/3226.
  8. Michalski CW, Shi X, Reiser C, Fachinger P, Zimmermann A, Büchler MW, Di Sebastiano P, Friess H. Neurokinin-2 receptor levels correlate with intensity, frequency, and duration of pain in chronic pancreatitis. Ann Surg. 2007 Nov;246(5):786-93.
  9. Farkas G Jr, Hofner P, Balog A, Takács T, Szabolcs A, Farkas G, Mándi Y. Relevance of transforming growth factor-beta1, interleukin-8, and tumor necrosis factor-alpha polymorphisms in patients with chronic pancreatitis. Eur Cytokine Netw. 2007 Mar;18(1):31-37.
  10. Wick EC, Hoge SG, Grahn SW, Kim E, Divino LA, Grady EF, Bunnett NW, Kirkwood KS. Transient receptor potential vanilloid 1, calcitonin gene-related peptide, and substance P mediate nociception in acute pancreatitis. Am J Physiol Gastrointest Liver Physiol. 2006 May;290(5):G959-69.
  11. Hutter MM, Wick EC, Day AL, Maa J, Zerega EC, Richmond AC, Jordan TH, Grady EF, Mulvihill SJ, Bunnett NW, Kirkwood KS. Transient receptor potential vanilloid (TRPV-1) promotes neurogenic inflammation in the pancreas via activation of the neurokinin-1 receptor (NK-1R). Pancreas. 2005 Apr;30(3):260-65.
  12. Liddle RA. The role of Transient Receptor Potential Vanilloid 1 (TRPV1) channels in pancreatitis. Biochim Biophys Acta. 2007 Aug;1772(8):869-78.
  13. Breivik H, Borchgrevink PC, Allen SM, Rosseland LA, Romundstad L, Hals EK, Kvarstein G, Stubhaug A. Assessment of pain. Br J Anaesth. 2008 Jul;101(1):17-24. doi: 10.1093/bja/aen103.
  14. Yuan A, Rao MV, Sasaki T, Chen Y, Kumar A, Veeranna, Liem RKH, Eyer J, Peterson AC, Julien JP, Nixon RA. &alfa;-internexin is structurally and functionally associated with the neurofilament triplet proteins in the mature CNS. J Neurosci. 2006;26(39). doi: 10.1523/JNEUROSCI.2580-06.2006.
  15. Gnanapavan S, Grant D, Pryce G, Jackson S, Baker D, Giovannoni G. Neurofilament a biomarker of neurodegeneration in autoimmune encephalomyelitis. Autoimmunity. 2012 Jun;45(4):298-303. doi: 10.3109/08916934.2012.654865.
Address for correspondence:
210023, The Republic of Belarus,
Vitebsk, Frunze ave., 27,
EE Vitebsk State Medical University,
Department of Surgery
of the Faculty of Advanced Training and Retraining,
Tel.: +375 29 654-45-99,
E-mail: anatol1961@bk.ru,
Anatoliy T. Shchastny
Information about the authors:
Shchastny A.T., MD., Ass. Professor, Rector of Vitebsk State Medical University
Contacts | ©Vitebsk State Medical University, 2007-2023