Skip to main content
Erschienen in: Inflammation 3-4/2007

01.08.2007

High Macrophage Migration Inhibitory Factor Levels in Disseminated Intravascular Coagulation Patients with Systemic Inflammation

verfasst von: Satoshi Gando, Atsushi Sawamura, Mineji Hayakawa, Hirokatsu Hoshino, Nobuhiko Kubota, Jun Nishihira

Erschienen in: Inflammation | Ausgabe 3-4/2007

Einloggen, um Zugang zu erhalten

Abstract

To determine the relationship between macrophage migration inhibitory factor (MIF) and disseminated intravascular coagulation (DIC) in patients with systemic inflammatory response syndrome (SIRS) and sepsis, and their relationship to multiple organ dysfunction syndrome (MODS) and prognosis, we conducted a prospective cohort study. Forty-eight patients with SIRS or sepsis were classified as 20 DIC and 28 non-DIC patients. MIF, tumor necrosis factor-alpha (TNF-alpha), soluble fibrin, protein C activity (protein C), and plasminogen activator inhibitor-1 (PAI-1) were all measured within 24 h after the patients met the criteria of SIRS or sepsis (day 0), and on days 1 to 4. The number of SIRS criteria that the patients met and the DIC scores were determined simultaneously. In DIC patients, significantly higher levels of MIF, TNF-alpha, soluble fibrin, PAI-1 were found compared with non-DIC patients. We also found significantly lower protein C levels in the DIC patients than in the non-DIC patients. Significant correlations were found between the peak levels of MIF and soluble fibrin in the DIC patients (rs = 0.496, p < 0.0407). All DIC patients had MODS and also showed a higher number of dysfunctioning organs and a poorer prognosis than the non-DIC patients. A simple logistic regression analysis showed the peak MIF levels and DIC significantly to be related to the patients’ death (odds ratio 1.016 and 40.5; p < 0.0409, p < 0.0009, respectively). In conclusion, DIC patients with elevated levels of MIF and TNF-alpha had more organ dysfunctions leading to a poor prognosis in a population of SIRS and sepsis patients. MIF may therefore play a role in the inflammatory and thrombotic processes in DIC patients.
Literatur
1.
Zurück zum Zitat Calandra, T., J. Bernhagen, C. N. Metz, L. A. Spiegel, M. Bacher, T. Donnelly, A. Cerami, and R. Bucala. 1995. MIF as a glucocorticoid-induced modulator of cytokine production. Nature 377:68–71.PubMedCrossRef Calandra, T., J. Bernhagen, C. N. Metz, L. A. Spiegel, M. Bacher, T. Donnelly, A. Cerami, and R. Bucala. 1995. MIF as a glucocorticoid-induced modulator of cytokine production. Nature 377:68–71.PubMedCrossRef
2.
Zurück zum Zitat Bucala, R., and MIF rediscovered. 1996. Cytokine, pituitary hormone, and glucocorticoid-induced regulator of the immune response. FASEB J. 10:1607–1613.PubMed Bucala, R., and MIF rediscovered. 1996. Cytokine, pituitary hormone, and glucocorticoid-induced regulator of the immune response. FASEB J. 10:1607–1613.PubMed
3.
Zurück zum Zitat Calandra, T., and T. Roger. 2003. Macrophage migration inhibitory factor. A regulator of innate immunity. Nature Rev. 3:791–800.CrossRef Calandra, T., and T. Roger. 2003. Macrophage migration inhibitory factor. A regulator of innate immunity. Nature Rev. 3:791–800.CrossRef
4.
Zurück zum Zitat Members of American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference. 1992. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit. Care Med. 20:864–874.CrossRef Members of American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference. 1992. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit. Care Med. 20:864–874.CrossRef
5.
Zurück zum Zitat Bernhagen, J., T. Calandra, R. A. Mitchell, S. B. Martin, K. J. Tracey, W. Voelter, K. R. Manogue, A. Cerami, and R. Bucala. 1993. MIF is a pituitary-derived cytokine that potentiates lethal endotoxemia. Nature 365:756–759.PubMedCrossRef Bernhagen, J., T. Calandra, R. A. Mitchell, S. B. Martin, K. J. Tracey, W. Voelter, K. R. Manogue, A. Cerami, and R. Bucala. 1993. MIF is a pituitary-derived cytokine that potentiates lethal endotoxemia. Nature 365:756–759.PubMedCrossRef
6.
Zurück zum Zitat Bozza, M., A. R. Satoskar, G. Lin, B. Lu, A. A. Humbles, C. Gerard, and J. R. David. 1999. Targeted disruption of migration inhibitory factor gene reveals its critical role in sepsis. J. Exp. Med. 189:341–346.PubMedCrossRef Bozza, M., A. R. Satoskar, G. Lin, B. Lu, A. A. Humbles, C. Gerard, and J. R. David. 1999. Targeted disruption of migration inhibitory factor gene reveals its critical role in sepsis. J. Exp. Med. 189:341–346.PubMedCrossRef
7.
Zurück zum Zitat Calandra, T., B. Echtenacher, D. L. Roy, J. Pugin, C. N. Metz, L. Hültner, D. Heumann, D. Männel, R. Bucala, and M. P. Glauser. 2000. Protection from septic shock by neutralization of macrophage migration inhibitory factor. Nature Med. 6:164–170.PubMedCrossRef Calandra, T., B. Echtenacher, D. L. Roy, J. Pugin, C. N. Metz, L. Hültner, D. Heumann, D. Männel, R. Bucala, and M. P. Glauser. 2000. Protection from septic shock by neutralization of macrophage migration inhibitory factor. Nature Med. 6:164–170.PubMedCrossRef
8.
Zurück zum Zitat Gando, S., J. Nishihira, S. Kobayashi, Y. Morimoto, S. Nanzaki, and O. Kemmotsu. 2001. Macrophage migration inhibitory factor is a critical mediator of systemic inflammatory response syndrome. Intensive Care Med. 27:1187–1193.PubMedCrossRef Gando, S., J. Nishihira, S. Kobayashi, Y. Morimoto, S. Nanzaki, and O. Kemmotsu. 2001. Macrophage migration inhibitory factor is a critical mediator of systemic inflammatory response syndrome. Intensive Care Med. 27:1187–1193.PubMedCrossRef
9.
Zurück zum Zitat Lehmann, L. E., U. Novender, S. Schroeder, T. Pietsch, C. Putensen, A. Hoeft, and F. Stüber. 2001. Plasma levels of macrophage migration inhibitory factor are elevated in patients with severe sepsis. Intensive Care Med. 27:1412–1415.PubMedCrossRef Lehmann, L. E., U. Novender, S. Schroeder, T. Pietsch, C. Putensen, A. Hoeft, and F. Stüber. 2001. Plasma levels of macrophage migration inhibitory factor are elevated in patients with severe sepsis. Intensive Care Med. 27:1412–1415.PubMedCrossRef
10.
Zurück zum Zitat Beishuizen, A., L. G. Thijs, C. Haanen, and I. Vermes. 2001. Macrophage migration inhibitory factor and hypothalamo-pituitary-adrenal function during critical illness. J. Clin. Endocrinol. Metab. 86:2811–2816.PubMedCrossRef Beishuizen, A., L. G. Thijs, C. Haanen, and I. Vermes. 2001. Macrophage migration inhibitory factor and hypothalamo-pituitary-adrenal function during critical illness. J. Clin. Endocrinol. Metab. 86:2811–2816.PubMedCrossRef
11.
Zurück zum Zitat Bozza, F., R. N. Gomes, A. M. Japiassu, M. Soares, H. C. Castro-Faria-Neto, P. T. Bozza, and M. T. Bozza. 2004. Marophage migration inhibitory factor levels correlate with fatal outcome in sepsis. Shock 22:309–313.PubMedCrossRef Bozza, F., R. N. Gomes, A. M. Japiassu, M. Soares, H. C. Castro-Faria-Neto, P. T. Bozza, and M. T. Bozza. 2004. Marophage migration inhibitory factor levels correlate with fatal outcome in sepsis. Shock 22:309–313.PubMedCrossRef
12.
13.
Zurück zum Zitat Nishihira, J., Y. Mizue, and W. Sakamoto. 1999. Induction of T-kininogen and tumor necrosis factor-alpha by macrophage migration inhibitory factor in vivo. Semin. Thromb. Haemost. 25:557–562. Nishihira, J., Y. Mizue, and W. Sakamoto. 1999. Induction of T-kininogen and tumor necrosis factor-alpha by macrophage migration inhibitory factor in vivo. Semin. Thromb. Haemost. 25:557–562.
14.
Zurück zum Zitat Shimizu, T., J. Nishihira, H. Watanabe, R. Abe, A. Honda, T. Ishibashi, and H. Shimizu. 2004. Macrophage migration inhibitory factor is induced by thrombin and factor Xa in endothelial cells. J. Biol. Chem. 279:13729–13737.PubMedCrossRef Shimizu, T., J. Nishihira, H. Watanabe, R. Abe, A. Honda, T. Ishibashi, and H. Shimizu. 2004. Macrophage migration inhibitory factor is induced by thrombin and factor Xa in endothelial cells. J. Biol. Chem. 279:13729–13737.PubMedCrossRef
15.
Zurück zum Zitat Knaus, W. A., E. A. Draper, D. P. Wanger, and J. E. Zimmerman. 1985. APACHE II: a severity classification system. Crit. Care Med. 13:818–829.PubMedCrossRef Knaus, W. A., E. A. Draper, D. P. Wanger, and J. E. Zimmerman. 1985. APACHE II: a severity classification system. Crit. Care Med. 13:818–829.PubMedCrossRef
16.
Zurück zum Zitat Murray, J. F., M. A. Matthay, J. M. Luce, and M. R. Flick. 1988. An expanded definition of the adult respiratory distress syndrome. Am. Rev. Respir. Dis. 138:720–723.PubMed Murray, J. F., M. A. Matthay, J. M. Luce, and M. R. Flick. 1988. An expanded definition of the adult respiratory distress syndrome. Am. Rev. Respir. Dis. 138:720–723.PubMed
17.
Zurück zum Zitat Gando, S., T. Kameue, S. Nanzaki, and Y. Nakanishi. 1996. Disseminated intravascular coagulation is a frequent complication of systemic inflammatory response syndrome. Thromb. Haemost. 75:224–228.PubMedCrossRef Gando, S., T. Kameue, S. Nanzaki, and Y. Nakanishi. 1996. Disseminated intravascular coagulation is a frequent complication of systemic inflammatory response syndrome. Thromb. Haemost. 75:224–228.PubMedCrossRef
18.
Zurück zum Zitat Taylor, F. B. Jr., C. H. Toh, W. K. Hoots, H. Wada, and M. Levi. 2001. Toward definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. Thromb. Haemost. 86:1327–1330.PubMed Taylor, F. B. Jr., C. H. Toh, W. K. Hoots, H. Wada, and M. Levi. 2001. Toward definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. Thromb. Haemost. 86:1327–1330.PubMed
19.
Zurück zum Zitat Onodera, S., K. Suzuki, K. Kaneda, M. Fuinaga, and J. Nishihira. 1999. Growth factor-induced expression of macrophage migration inhibitory factor in osteoblasts: relevance to the plasminogen activator system. Semin. Thromb. Haemost. 25:563–567.CrossRef Onodera, S., K. Suzuki, K. Kaneda, M. Fuinaga, and J. Nishihira. 1999. Growth factor-induced expression of macrophage migration inhibitory factor in osteoblasts: relevance to the plasminogen activator system. Semin. Thromb. Haemost. 25:563–567.CrossRef
20.
Zurück zum Zitat Schmidt-Supprian, M., C. Murphy, B. While, M. Lawler, A. Kapurniotu, W. Voelter, O. Smith, and J. Bernhagen. 2000. Activated protein C inhibits tumor necrosis factor and macrophage migration inhibitory factor production in monocytes. Eur. Cytokine. Netw. 11:407–413.PubMed Schmidt-Supprian, M., C. Murphy, B. While, M. Lawler, A. Kapurniotu, W. Voelter, O. Smith, and J. Bernhagen. 2000. Activated protein C inhibits tumor necrosis factor and macrophage migration inhibitory factor production in monocytes. Eur. Cytokine. Netw. 11:407–413.PubMed
21.
Zurück zum Zitat Hamano, S., S. Tanaka, Y. Takeda, M. Umeda, and Y. Sakata. 2002. A novel monoclonal antibody to fibrin monomer and soluble fibrin for the detection of soluble fibrin in plasma. Clin. Chim. Acta 318:25–32.PubMedCrossRef Hamano, S., S. Tanaka, Y. Takeda, M. Umeda, and Y. Sakata. 2002. A novel monoclonal antibody to fibrin monomer and soluble fibrin for the detection of soluble fibrin in plasma. Clin. Chim. Acta 318:25–32.PubMedCrossRef
22.
Zurück zum Zitat Levi, M., and H. ten Cate. 1999. Disseminated intravascular coagulation. N. Engl. J. Med. 341:586–592.PubMedCrossRef Levi, M., and H. ten Cate. 1999. Disseminated intravascular coagulation. N. Engl. J. Med. 341:586–592.PubMedCrossRef
23.
Zurück zum Zitat Furukawa, M. 2004. Anti-MIF monoclonal antibody inhibits LPS-stimulated expression of tissue factor. Hokkaido Medical Journal. 79: 523–532. (In Japanese). Furukawa, M. 2004. Anti-MIF monoclonal antibody inhibits LPS-stimulated expression of tissue factor. Hokkaido Medical Journal. 79: 523–532. (In Japanese).
Metadaten
Titel
High Macrophage Migration Inhibitory Factor Levels in Disseminated Intravascular Coagulation Patients with Systemic Inflammation
verfasst von
Satoshi Gando
Atsushi Sawamura
Mineji Hayakawa
Hirokatsu Hoshino
Nobuhiko Kubota
Jun Nishihira
Publikationsdatum
01.08.2007
Erschienen in
Inflammation / Ausgabe 3-4/2007
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-007-9027-1

Weitere Artikel der Ausgabe 3-4/2007

Inflammation 3-4/2007 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Erhebliches Risiko für Kehlkopfkrebs bei mäßiger Dysplasie

29.05.2024 Larynxkarzinom Nachrichten

Fast ein Viertel der Personen mit mäßig dysplastischen Stimmlippenläsionen entwickelt einen Kehlkopftumor. Solche Personen benötigen daher eine besonders enge ärztliche Überwachung.

Nach Herzinfarkt mit Typ-1-Diabetes schlechtere Karten als mit Typ 2?

29.05.2024 Herzinfarkt Nachrichten

Bei Menschen mit Typ-2-Diabetes sind die Chancen, einen Myokardinfarkt zu überleben, in den letzten 15 Jahren deutlich gestiegen – nicht jedoch bei Betroffenen mit Typ 1.

15% bedauern gewählte Blasenkrebs-Therapie

29.05.2024 Urothelkarzinom Nachrichten

Ob Patienten und Patientinnen mit neu diagnostiziertem Blasenkrebs ein Jahr später Bedauern über die Therapieentscheidung empfinden, wird einer Studie aus England zufolge von der Radikalität und dem Erfolg des Eingriffs beeinflusst.

Costims – das nächste heiße Ding in der Krebstherapie?

28.05.2024 Onkologische Immuntherapie Nachrichten

„Kalte“ Tumoren werden heiß – CD28-kostimulatorische Antikörper sollen dies ermöglichen. Am besten könnten diese in Kombination mit BiTEs und Checkpointhemmern wirken. Erste klinische Studien laufen bereits.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.