Dokumen Artikel Penelitian ini milik penulis/penelliti yang diserahkan sebagian (judul dan Abstrak) hak ciptanya

kepada Universitas Airlangga untuk digunakan referensi dalam penulisan artikel ilmiah. Penulis : SUHARTONO TAAT PUTRA Fakultas : Kedokteran Tim Peneliti : A. GUNTUR HERMAWAN,

Abstrak :

The purpose of this study was intended to explain a shock septic mechanism in immunocompromise (IC) and Non immuno-compromise (NIC). This study contains two phases of observational analysis. First phase applied cross sectional design to differentiate iznmune response for IC and NIC in non-sepsis condition. Second phase applied Cohort design to differentiate immune response for IC and NIC in sepsis and septic shock condition. First and second phases of this study used a separate sample. The variables of immune response were determined by analyzing IgG, C3, C4, IL-10, IFNg. TNF-a and IL-1b. A multivariate analysis (Manova) was applied in this study for statistical analysis. Result of this study showed that there was a significant difference (p<0.05) in immune response toward an IC and NIC non-sepsis condition marked by increasing on IL-10, TNF-a, IgG and decreasing on C3 variable. However, there was no significant (p>0.05) difference on the result for IC and NIC in sepsis condition. No significant difference also found for IC and NIC in septic shock condition (p>0.05). Then it is concluded that IC and NIC groups showed no difference in septic and shock condition. Therefore, those two groups together are considered into one group to analyse the difference between IC-NIC in septic shock and IC-NIC in non-septic shock that showed a significant difference (p<0.05). Furthermore, due to immune response differences above, the study was continued with discriminant analysis (discriminator). For IC-N1C septic shock and IC-NIC sepsis, there were four variables as discriminators, IL-10, IL-b, IgG and C3. To explain the immunopathobiogenesis, a narration of conceptual framework has been done using discriminant pattern. Based on such method, immunogene stimulation to macrophage (APC) could influence Th2, inducing the increase of IL-10 contribution that accelerating B lymphocyte maturity to become IgG-producing plasma cells. IgG with toxin fortned a toxin complex which precipitated on the wall of endothelial cells in blood vessels, and activated C3 complement, leading to endothelial destruction through a process called antibody dependent cellular cytotoxicity (ADCC). Thl stimulation increased IFNg. IFNg stimulated macrophage, inducing the increase of IL 1b which stimulated endothelial cells to induce 1CAM-l. As an adhesive substance, ICAM-1 would be bound with neutrophyl, leading to endothelial destruction in blood vessels through DTH process. Both processes caused leakage of the wall of blo vessel, leading to produce the occurrence of septic shock. In conclusion, the immunopathobiogenesis of septic shock c be caused by the mechanisms of ADCC and DTH. Keyword : Immunocompromise (IC), Non-Immunocompromise (NIC), Sepsis, Septic Shock, ADCC, DTH

Page 1

Sign up to vote on this title
UsefulNot useful