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2007 | 2 | 1 | 26-36
Tytuł artykułu

Monocyte and neutrophil direct counts correlate with C-reactive protein plasma concentration in patients with acute pancreatitis

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Języki publikacji
EN
Abstrakty
EN
Acute pancreatitis (AP) is associated with the intensive inflammatory response in white blood cells (WBC) and C-reactive protein (CRP). This paper presents the relationship between the CRP plasma concentration and the direct counts of peripheral WBC in AP during the initial five days. The study consisted of 56 patients with AP, 36 patients with mild form of AP and 20 patients with severe form of AP. ABX VegaRetic hematological analyzer was used to perform the count of blood cells, and the immunonephelometric method was performed to measure the CRP concentration levels. AP patients presented with WBC count values in the range of 3.2 − 22.4 × 103/µl and CRP concentration levels in the range 3.3 − 599.8 mg/l. The WBC count correlates with CRP levels during the entire observation period. The relationship of CRP and WBC is expressed in the following regression equation: WBC (103/µl) = 3.66 + 1.40 × logeCRP (mg/l). The highest median neutrophil count (8.15 × 103/µl) was observed on the first day. The count decreased to 5.27 × 103/µl on the fifth day. The most substantial finding in this study involved the values found for the monocytes and CRP (r= 0.53; p<0.001). Day two and day three were the highest (r=0.59, p<0.001). On day two, the regression equation for this relationship is: Monocytes (103/µl) = −0.34 + 0.21 × logeCRP(mg/l). The correlation between direct monocyte count and plasma CRP concentration in AP reflect a CRP-dependent stimulation of IL-6 release from activated blood monocytes.
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Wydawca

Czasopismo
Rocznik
Tom
2
Numer
1
Strony
26-36
Opis fizyczny
Daty
wydano
2007-03-01
online
2007-03-01
Twórcy
  • Department of Clinical Biochemistry, Collegium Medicum Jagiellonian University, 31-501, Kraków, Poland, mbnaskal@cyf-kr.edu.pl
  • Department of Clinical Biochemistry, Collegium Medicum Jagiellonian University, 31-501, Kraków, Poland
  • Department of Clinical Biochemistry, Collegium Medicum Jagiellonian University, 31-501, Kraków, Poland
  • Department of Clinical Biochemistry, Collegium Medicum Jagiellonian University, 31-501, Kraków, Poland
  • IInd Department of General Surgery, Collegium Medicum, Jagiellonian University, 31-501, Kraków, Poland
Bibliografia
  • [1] J. Norman: “The role of cytokines in the pathogenesis of acute pancreatitis”, Am. J. Surg., Vol. 175, (1998), pp. 76–83. http://dx.doi.org/10.1016/S0002-9610(97)00240-7[Crossref]
  • [2] Z. King, J. Gauldie and G. Cox. “IL-6 is an anti-inflammatory cytokine required for controlling local or systemic acute inflammatory response”, J. Clin. Invest., Vol. 101, (1998), pp. 311–320.
  • [3] M.T. Hamalainen, P. Gronroos and J.M. Gronroos: “Do normal leukocyte count and C-reactive protein on admission to hospital exclude a life-threatening attack of acute pancreatitis?”, Scand. J. Surg., Vol. 91, (2002), pp. 353–356.
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  • [5] L. Thomas: “Tests for diagnosis of inflammation”, In: L. Thomas (Ed.): Clinical laboratory diagnostics. Use and assessment of clinical laboratory results, TH Books Verlaggesselschaft, Frankfurt, 1999, pp. 697–700.
  • [6] R. Pezzilli, P. Billi and F. Miniero: “Serum interleukin 6, interleukin 8 and beta-microglobulin in early assessment of severity of acute pancreatitis. Comparison with C-reactive protein”, Dig. Dis. Sci., Vol. 40, (1995), pp. 2341–2348. http://dx.doi.org/10.1007/BF02063235
  • [7] C.H. Weakfield, G.R. Barcley, K.C. Fearon, A.S. Goldie, J.A. Ross, I.S. Grant, G. Ramsay and J.C. Howie: “Proinflammatory mediator activity, endogenous and systemic inflammatory response in intra abdominal sepsis”, Br. J. Surg., Vol. 85, (1998), pp. 818–825. http://dx.doi.org/10.1046/j.1365-2168.1998.00710.x[Crossref]
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  • [9] U.A. Wittel, B. Rau, F. Gensauge, S. A.K. Nussler, H.G. Beger and B. Poch: “Influence of PMN leukocyte mediated pancreatic damage on the systemic immune response in severe acute pancreatitis in rats”, Dig. Dis. Sci., Vol. 49, (2004), pp. 1348–1357. http://dx.doi.org/10.1023/B:DDAS.0000037833.16433.77[Crossref]
  • [10] V. Pasceri and J.T. Willerson: “Direct proinflammatory effect of C-reactive protein in human endothelial cells by antisclerosis drugs”, Circulation, Vol. 102, (2000), pp. 2165–2168. [Crossref]
  • [11] B. Ray, U. Prall, M.H. Schonenber and H.G. Berger: “Management of sterile necrosis in instances of severe acute pancreatitis”, J. Am. Coll. Surg., Vol. 181, (1995), pp. 279–288.
  • [12] R. Pezzilli, B. Barakat and M. Maldini: “Acute pancreatitis: Enhancement of early phase lymphocyte activation”, Pancreatology, Vol. 2, (2002), pp. 217–361. http://dx.doi.org/10.1159/000058036[Crossref]
  • [13] C. de Beaux, J.A. Ross, J.P. Maingay, K.C. Fearon and D.C. Carter: “Proinflammatory cytokine release by peripheral blood mononuclear cells from patients with acute pancreatitis”, Br. J. Surg., Vol. 83, (1996), pp. 1071–1075.
  • [14] P. Mentula, E. Kylanpaa, E. Kemapinen, S.E. Jansson, S. Sarna, P. Puolakkainen, R. Haapiainen and H. Repo: “Plasma anti-inflammatory cytokines and monocytes human leukocyte antigen-DR expression in patients in patients with acute pancreatitis”, Scand. J. Gastroenterol., Vol. 39, (2004), pp. 178–187. http://dx.doi.org/10.1080/00365520310008278[Crossref]
  • [15] K. Kimura, A. Masamura, T. Yamagiwa and T. Shimosagawa: “HLA DR expression on peripheral blood monocytes as a predictive of sepsis during acute pancreatitis”, Pancreatology, Vol. 2, (2002), pp. 217–361. http://dx.doi.org/10.1159/000058036[Crossref]
  • [16] J.J. Li and X.J. Chen: “Simvastatin inhibits interleukin 6 releases in human cultures monocytes stimulated by C-reactive protein and liposaccharide”, Coron. Artery. Dis., Vol. 14, (2003), pp. 329–334. http://dx.doi.org/10.1097/00019501-200306000-00009[Crossref]
  • [17] J.J. Li, H.R. Wang, C.X. Huang and G.S. Li: “Enhanced inflammatory response of blood monocytes to C-reactive protein in patients with unstable angina”, Clin. Chim. Acta., Vol. 352, (2005), pp. 127–133. http://dx.doi.org/10.1016/j.cccn.2004.08.019[Crossref]
  • [18] T. Lesse and D. Show: “Comparison of three Glasgow multifactor prognostic scoring systems in acute pancreatitis”, World. J. Surg., Vol. 75, (1988), pp. 460–462.
  • [19] B. Kusnierz-Cabala, J.W. Naskalski, B. Kedra and J. Panek: “Comparison of sensitivity and specificity of serum poly-C ribonuclease activity and C-reactive protein concentration in detection of mild and severe acute pancreatitis”, Clin. Chem. Lab. Med., Vol. 42, (2004), pp. 549–555. http://dx.doi.org/10.1515/CCLM.2004.093[Crossref]
  • [20] U.C. Weber and G. Adler: “Acute pancreatitis”, Curr. Opin. Gastroenterol., Vol. 19, (2003), pp. 441–445. http://dx.doi.org/10.1097/00001574-200309000-00002[Crossref]
  • [21] R. Pezzilli, R. Ceciliato, B. Barakat and R. Cordinalesi: “Immune manipulation of the inflammatory response in acute pancreatitis. What could be expected?” JOP, Vol. 5, (2004), pp. 115–121.
  • [22] R. Lavenda, J. Martinez and C. Munoz: “Different profile of cytokine synthesis according to the severity of acute pancreatitis”, World. J. Gastroenterol., Vol. 34, (2005), pp. 5309–5313.
  • [23] K. Ohmoto and S. Yamamoto: “Serum interleukin-6 and interleukin-10 in patients with acute pancreatitis: clinical implications”, Hepatogastroenterology, Vol. 64, (2005), pp. 990–994.
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.-psjd-doi-10_2478_s11536-007-0008-4
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