ARTYKUŁ PRZEGLĄDOWY
Właściwości reologiczne erytrocytów u pacjentów zakażonych Clostridium difficile
Jacek Czepiel 1 , Artur Jurczyszyn 2 , Grażyna Biesiada 1 , Iwona Sobczyk-Krupiarz 1 , Izabela Jałowiecka 3 , Magdalena Świstek 3 , William Perucki 3 , Aneta Teległów 4 , Jakub Marchewka 4 , Zbigniew Dąbrowski 4 , Tomasz Mach 1 , Aleksander Garlicki 11. Department of Infectious Diseases, Jagiellonian University Medical College, Krakow, Poland
2. Department of Hematology, University Hospital, Krakow, Poland
3. Students’ Scientific Society Jagiellonian University Medical College, Krakow, Poland
4. Motoral Pathology Laboratory, Department of Clinical Rehabilitation, University School of Physical Education, Krakow, Poland
Opublikowany: 2014-12-04
DOI: 10.5604/17322693.1130558
GICID: 01.3001.0003.1380
Dostępne wersje językowe: pl en
Wydanie: Postepy Hig Med Dosw 2014; 68 : 1397-1405
Abstrakt
Przypisy
- 1. Ananthakrishnan A.N.: Clostridium difficile infection: epidemiology,risk factors and management. Nat. Rev. Gastroenterol. Hepatol.,2011; 8: 17-26
Google Scholar - 2. Assayag E.B., Bornstein N., Shapira I., Mardi T., Goldin Y., TolshinskiT., Vered Y., Zakuth V., Burke M., Berliner S., Bonet D.S.:Inflammation-sensitive proteins and erythrocyte aggregation inatherothrombosis. Int. J. Cardiol., 2005; 98: 271-276
Google Scholar - 3. Astiz M.E., De Gent G.E., Lin R.Y., Rackow E.C.: Microvascularfunction and rheologic changes in hyperdynamic sepsis. Crit. CareMed., 1995; 23: 265-271
Google Scholar - 4. Barmparas G., Fierro N., Lamb A.W., Lee D., Nguyen B., Tran D.H.,Chung R., Ley E.J.: Clostridium difficile increases the risk for venousthromboembolism. Am. J. Surg., 2014; 208: 703-709
Google Scholar - 5. Baskurt O.K., Gelmont D., Meiselman H.J.: Red blood cell deformabilityin sepsis. Am. J. Respir. Crit. Care Med., 1998; 157: 421-427
Google Scholar - 6. Baskurt O.K., Temiz A., Meiselman H.J.: Red blood cell aggregationin experimental sepsis. J. Lab. Clin. Med., 1997; 130: 183-190
Google Scholar - 7. Beppu M., Inoue M., Ishikawa T., Kikugawa K.: Presence of membrane-boundproteinases that preferentially degrade oxidativelydamaged erythrocyte membrane proteins as secondary antioxidantdefense. Biochim. Biophys. Acta, 1994; 1196: 81-87
Google Scholar - 8. Bernstein C.N., Blanchard J.F., Houston D.S., Wajda A.: The incidenceof deep venous thrombosis and pulmonary embolism amongpatients with inflammatory bowel disease: a population-based cohortstudy. Thromb. Haemost., 2001; 85: 430-434
Google Scholar - 9. Beutler E.: Red cell metabolism: a manual of biochemical methods.Grune and Stratton, New York, San Francisco and London 1984
Google Scholar - 10. Biesiada G., Krzemień J., Czepiel J., Teległów A., Dąbrowski Z.,Spodaryk K., Mach T.: Rheological properties of erythrocytes in patientssuffering from erysipelas. Examination with LORCA device.Clin. Hemorheol. Microcirc., 2006; 34: 383-390
Google Scholar - 11. Borovikova L.V., Ivanova S., Zhang M., Yang H., Botchkina G.I.,Watkins L.R., Wang H., Abumrad N., Eaton J.W., Tracey K.J.: Vagusnerve stimulation attenuates the systemic inflammatory responseto endotoxin. Nature, 2000; 405: 458-462
Google Scholar - 12. Chari S.N., Nath N.: Sialic acid content and sialidase activityof polymorphonuclear leukocytes in diabetes mellitus. Am. J. Med.Sci., 1984; 288: 18-20
Google Scholar - 13. Cicha I., Tateishi N., Suzuki Y., Maeda N.: Rheological changesin human red blood cells under oxidative stress: effects of thiolcontainingantioxidants. Pathophysiology, 1999; 6: 121-128
Google Scholar - 14. Cooke B.M., Stuart J.: Automated measurement of plasma viscosityby capillary viscometer. J. Clin. Pathol., 1988; 41: 1213-1216
Google Scholar - 15. de Almeida J.P., Saldanha C.: Nonneuronal cholinergic system inhuman erythrocytes: biological role and clinical relevance. J. Membr.Biol., 2010; 234: 227-234
Google Scholar - 16. Deplaine G., Safeukui I., Jeddi F., Lacoste F., Brousse V., Perrot S.,Biligui S., Guillotte M., Guitton C., Dokmak S., Aussilhou B., SauvanetA., Cazals Hatem D., Paye F., Thellier M. et al.: The sensing of poorlydeformable red blood cells by the human spleen can be mimickedin vitro. Blood, 2011; 117: e88-e95
Google Scholar - 17. Donner M., Mills P., Stoltz J.F.: Influence of plasma proteins onerythrocyte aggregation. Clin. Hemorheol., 1989; 9: 715-721
Google Scholar - 18. Eichelbrönner O., Sielenkämper A., Cepinskas G., Sibbald W.J.,Chin-Yee I.H.: Endotoxin promotes adhesion of human erythrocytesto human vascular endothelial cells under conditions of flow. Crit.Care Med., 2000; 28: 1865-1870
Google Scholar - 19. Fumery M., Xiaocang C., Dauchet L., Gower-Rousseau C., PeyrinBirouletL., Colombel J.F.: Thromboembolic events and cardiovascularmortality in inflammatory bowel diseases: a meta-analysis of observationalstudies. J. Crohns Colitis, 2014; 8: 469-479
Google Scholar - 20. Gamzu R., Rotstein R., Fusman R., Zeltser D., Berliner A.S., Kupferminc M.J.: Increased erythrocyte adhesiveness and aggregationin peripheral venous blood of women with pregnancy-induced hypertension.Obstet. Gynecol., 2001; 98: 307-312
Google Scholar - 21. Ghigo D., Todde R., Ginsburg H., Costamagna C., Gautret P., BussolinoF., Ulliers D., Giribaldi G., Deharo E., Gabrielli G., PescarmonaG., Bosia A.: Erythrocyte stages of Plasmodium falciparum exhibit ahigh nitric oxide synthase (NOS) activity and release an NOS-inducingsoluble factor. J. Exp. Med., 1995; 182: 677-688
Google Scholar - 22. Grando S.A., Kawashima K., Kirkpatrick C.J., Wessler I.: Recentprogress in understanding the non-neuronal cholinergic system inhumans. Life Sci., 2007; 80: 2181-2185
Google Scholar - 23. Hardeman M.R., Dobbe J.G., Ince C.: The laser-assisted opticalrotational cell analyzer (LORCA) as red blood cell aggregometer. Clin.Hemorheol. Microcirc., 2001; 25: 1-11
Google Scholar - 24. Ho H.Y., Cheng M.L., Weng S.F., Chang L., Yeh T.T., Shih S.R., ChiuD.T.: Glucose-6-phosphate dehydrogenase deficiency enhances enterovirus 71 infection. J. Gen. Virol., 2008; 89: 2080-2089
Google Scholar - 25. Ismail N.H., Cohn E.J.Jr., Mollitt D.L.: Nitric oxide synthase inhibitionnegates septic-induced alterations in cytoplasmic calciumhomeostasis and membrane dynamics. Am. Surg., 1997; 63: 20-23
Google Scholar - 26. Kletzien R.F., Harris P.K., Foellmi L.A.: Glucose-6-phosphate dehydrogenase:a “housekeeping” enzyme subject to tissue-specificregulation by hormones, nutrients, and oxidant stress. FASEB J.,1994; 8: 174-181
Google Scholar - 27. Konturek P.C., Brzozowski T., Konturek S.J.: Stress and the gut:pathophysiology, clinical consequences, diagnostic approach andtreatment options. J. Physiol. Pharmacol., 2011; 62: 591-599
Google Scholar - 28. Korbut R., Gryglewski R.J.: Nitric oxide from polymorphonuclearleukocytes modulates red blood cell deformability in vitro. Eur.J. Pharmacol., 1993; 234: 17-22
Google Scholar - 29. Lam C., Tyml K., Martin C., Sibbald W.: Microvascular perfusionis impaired in a rat model of normotensive sepsis. J. Clin. Invest.,1994; 94: 2077-2083
Google Scholar - 30. Machiedo G.W., Powell R.J., Rush B.F.Jr., Swislocki N.I., DikdanG.: The incidence of decreased red blood cell deformability in sepsisand the association with oxygen free radical damage and multiple–system organ failure. Arch. Surg., 1989; 124: 1386-1389
Google Scholar - 31. Mesquita R., Pires I., Saldanha C., Martins-Silva J.: Effects ofacetylcholine and spermineNONOate on erythrocyte hemorheologicand oxygen carrying properties. Clin. Hemorheol. Microcirc.,2001; 25: 153-163
Google Scholar - 32. Milligan T.W., Baker C.J., Straus D.C., Mattingly S.J.: Associationof elevated levels of extracellular neuraminidase with clinical isolatesof type III group B streptococci. Infect. Immun., 1978; 21: 738-746
Google Scholar - 33. Mohandas N., Chasis J.A.: Red blood cell deformability, membranematerial properties and shape: regulation by transmembrane,skeletal and cytosolic proteins and lipids. Semin. Hematol., 1993;30: 171-192
Google Scholar - 34. Moutzouri A.G., Skoutelis A.T., Gogos C.A., Missirlis Y.F., AthanassiouG.M.: Red blood cell deformability in patients with sepsis: amarker for prognosis and monitoring of severity. Clin. Hemorheol.Microcirc., 2007; 36: 291-299
Google Scholar - 35. Nguyen G.C., Sam J.: Rising prevalence of venous thromboembolismand its impact on mortality among hospitalized inflammatorybowel disease patients. Am. J. Gastroenterol., 2008; 103: 2272-2280
Google Scholar - 36. Novacek G., Weltermann A., Sobala A., Tilg H., Petritsch W.,Reinisch W., Mayer A., Haas T., Kaser A., Feichtenschlager T., FuchssteinerH., Knoflach P., Vogelsang H., Miehsler W., Platzer R., et al.:Inflammatory bowel disease is a risk factor for recurrent venousthromboembolism. Gastroenterology, 2010; 139: 779-787.e1
Google Scholar - 37. Ortiz-Carranza O., Miller M.E., Adragna N.C., Lauf P.K.: AlkalinepH and internal calcium increase Na+ and K+ effluxes in LK sheep redblood cells in Cl–free solutions. J. Membr. Biol., 1997; 156: 287-295
Google Scholar - 38. Perrotta S., Gallagher P.G., Mohandas N.: Hereditary spherocytosis.Lancet, 2008; 372: 1411-1426
Google Scholar - 39. Piagnerelli M., Boudjeltia K.Z., Brohee D., Piro P., Carlier E., VincentJ.L., Lejeune P., Vanhaeverbeek M.: Alterations of red blood cellshape and sialic acid membrane content in septic patients. Crit. CareMed., 2003; 31: 2156-2162
Google Scholar - 40. Piagnerelli M., Boudjeltia K.Z., Vanhaeverbeek M., Vincent J.L.:Red blood cell rheology in sepsis. Intensive Care Med., 2003; 29:1052-1061
Google Scholar - 41. Piagnerelli M., Cotton F., Van Nuffelen M., Vincent J.L., GulbisB.: Modifications in erythrocyte membrane protein content are notresponsible for the alterations in rheology seen in sepsis. Shock,2012; 37: 17-21
Google Scholar - 42. Powell R.J., Machiedo G.W., Rush B.F.Jr., Dikdan G.: Oxygen freeradicals: effect on red cell deformability in sepsis. Crit. Care Med.,1991; 19: 732-735
Google Scholar - 43. Rampling M.W., Pearson M.J.: Enzymatic degradation of the redcell surface and its effect on rouleaux formation. Clin. Hemorheol.Microcirc., 1994; 14: 531-538
Google Scholar - 44. Reggiori G., Occhipinti G., De Gasperi A., Vincent J.L., PiagnerelliM.: Early alterations of red blood cell rheology in critically illpatients. Crit. Care Med., 2009; 37: 3041-3046
Google Scholar - 45. Schechner V., Shapira I., Berliner S., Comaneshter D., HershcoviciT., Orlin J., Zeltser D., Rozenblat M., Lachmi K., Hirsch M., BeigelY.: Significant dominance of fibrinogen over immunoglobulins, C–reactive protein, cholesterol and triglycerides in maintaining increasedred blood cell adhesiveness/aggregation in the peripheralvenous blood: a model in hypercholesterolaemic patients. Eur. J.Clin. Invest., 2003; 33: 955-961
Google Scholar - 46. Schmid-Schönbein H.: Blood rheology and physiology of microcirculation.Ric. Clin. Lab., 1981; 11 (Suppl. 1) : 13-33
Google Scholar - 47. Todd J.C. 3rd, Mollitt D.L.: Effect of sepsis on erythrocyte intracellularcalcium homeostasis. Crit. Care Med., 1995; 23: 459-465
Google Scholar - 48. Todd J.C. 3rd, Mollitt D.L.: Leukocyte modulation inhibits endotoxin-induceddisruption of intracellular calcium homeostasis. J.Trauma, 1995; 39: 1148-1151
Google Scholar - 49. Todd J.C.3rd, Mollitt D.L.: Sepsis-induced alterations in the erythrocytemembrane. Am. Surg., 1994; 60: 954-957
Google Scholar - 50. Vaishnavi C.: Clinical spectrum & pathogenesis of Clostridiumdifficile associated diseases. Indian J. Med. Res., 2010; 131: 487-499
Google Scholar - 51. van Aken B.E., Reitsma P.H., Rosendaal F.R.: Interleukin 8 andvenous thrombosis: evidence for a role of inflammation in thrombosis.Br. J. Haematol., 2002; 116: 173-177
Google Scholar - 52. Wang H., Yu M., Ochani M., Amella C.A., Tanovic M., Susarla S.,Li J.H., Wang H., Yang H., Ulloa L., Al-Abed Y., Czura C.J., Tracey K.J.:Nicotinic acetylcholine receptor α7 subunit is an essential regulatorof inflammation. Nature, 2003; 421: 384-388
Google Scholar - 53. Wessler I., Kirkpatrick C.J.: Acetylcholine beyond neurons: thenon-neuronal cholinergic system in humans. Br. J. Pharmacol., 2008;154: 1558-1571
Google Scholar - 54. Wu Y.H., Tseng C.P., Cheng M.L., Ho H.Y., Shih S.R., Chiu DT.:Glucose-6-phosphate dehydrogenase deficiency enhances humancoronavirus 229E infection. J. Infect. Dis., 2008; 197: 812-816
Google Scholar