Effect of Nafamostat Mesilate on Disseminated Intravascular Coagulation (DIC) in Patients with Systemic Inflammatory Response Syndrome (SIRS)

• Published in: Nihon Kyukyu Igakukai Zasshi 1996/03/15, Vol.7(3), pp.120-127
• Main Authors: Gando, Satoshi, Kameue, Takashi, Nanzaki, Satoshi, Igarashi, Miyuki, Sakai, Hiroto, Makise, Hiroshi, Nakanishi, Yoshimi
• Format: Article
• Language: English
• Subjects: disseminated Intravascular coagulation (DIC); nafamostat mesilate; outcome; plasminogen activator inhibitor-1 (PAI-1); systemic inflammatory response syndrome (SIRS)
• ISSN: 0915-924X; 1883-3772
• DOI: 10.3893/jjaam.7.120

We conducted a pilot study to determine the effect of nafamostat mesilate (FUT) on disseminated Intravascular coagulation (DIC) in patients with systemic inflammatory response syndrome (SIRS). Sixteen SIRS patients with DIC served as subjects and were classified into a DIC-recovery group (n=7) and non-DIC-recovery group (n=9). Fibrinopeptide A (FPA), flbrinopeptide Bβ15-42 (FPBβ15-42), D-dimer, tissue plasminogen activator (t-PA) antigen concentration, t-PA activity, plasminogen activator inhibitor-1 (PAI-1) antigen concentration, and PAI-1 activity were measured on the day of DIC diagnosis, and on the 1st, 3rd, 5th days of FUT therapy. The results of these measurements, demographic data, mortality, and frequencies of multiple organ dysfunction syndrome (MODS) were compared between the groups and the effect of FUT on the various molecular markers was assessed. PAI-1 increased markedly in the SIRS patients. Although continuous FUT infusion resulted in a statistically significant decrease in FPA in the DIC-recovery patients, the FPA levels of the non-DIC-recovery patients were unaffected. FPBβ15-42 and D-dimer remained at consistently high levels throughout the testing period in all patients and no statistically differences in these markers were noted between the groups. A significant correlation was found between the FPBβ15-42 and the D-dimer. The number of dysfunctioning organs, the mortality rate, and the PAI-1 levels were higher in the non-DIC-recovery group. These results suggest that FUT may be a beneficial anticoagulant in the treatment of DIC in patients with SIRS, however, in spite of FUT treatment some patients continued to produce thrombin and PAI-1, with subsequent MODS and death. To elucidate the exact mechanism of action of FUT on DIC in the SIRS patients an additional randomized double-blind study involving a large number of patients will be neccessary.