The kinetics of endotoxin and cytokines in dengue hemorrhagic fever

Endotortnwas detected in 63lo among 120 dengue hemorrhagicfever (DHF) cases. The proportion of endotoxemia in shock group were higher than that non-shock as well as serum endotoxin level (13.9 and 4.3 pg/ml respectively, p=0.0008). Shock group has 3.0 times isk to have endotoxemia than that non-shock DHF group (OR 3.0; 1.29-7.05 95Vo CI). Serum end.otoin concentration increased at the time of shock and decrease after shock recovered. Patients with endotoxemia has 5.8 times higher risk to develop severe dengue infectioncomparedtonon-endotoxemiagroup(OR5.5; 1.72-2I.7495VoCI).Pre-inflammatorymediatorTNF-acanbedetectedatthe beginningofrhediseaseanddisappearedonconvalescencesta7e,whilelL-6titerincreased attheearly convalescencephaseasafeed back mechanisû, to endotoxin andTNF-x. Keyw ords : endoloxin, cytokines, dengue hemorrhagic fever Dengue hemorrhagic fever (DHF) has been already known in Indonesia since two decades ago. As an endemic disease, dengue infection did not appear as a health problem at that time, but during the last 20 years many fatal cases were reported.' Government's effort has been succesful to decrease the mortality rate; however, this disease through national health proqram, the mortality rate in several hospitals is still high.'-'Better case management is needed, especially for shock syndrome. Shock is the primary evidence in severe DHF, other vital organ involvement are secondary to shock.6 Hospital data show that mortality of shock cases is 3 to 10 times compared to non shock group. On the other hand, the severity of shock sy.ndrome depends on the pathogenesis of the disease.' A group of scientist hypothesized that four pathways were activated during the course of illness, i.e. complement, endothel, platelets, and cytokine pathway. These four pathways work synergistically. Complement and cytokines promote hypovolemic shock via anaphylatoxin substance (C3a, C5a) release.o Cytokine as pre-inflammatory mediators of infectious agents^ seems to play a role in the pathogenesis of DHF.e The cytokine production is needed for natural and specific host immunity against infection. Contrarily, overproduction of cytokine by monocytes as the subsequent target organ in DHF induced cell damage. Other effects of increased vascular permeability and shock are ischemia, reperfusion, and damage of intestinal mucosa integrity.l0'll Th"*" condifio;s promote bacterial/endotoxin translocation from intestinal lumen to lymphatic duct and finally to the blood circulation.l2il3'Endotoxin as an outér capsul of Gram negative bacteria has a biological activity to stimulate cardiovascular and respiratory system, complement, coagulation, metabolic, and cytokine cascades.'" Tumor necrosis factor-cx, interleukin-1, and interDepartment of Child Health Faculty of Medicine University of Indonesia./Dr. Cipto M angunkusumo H ospital, Jakarta, Indonesia Vol 8, No 3, July September 1999 leukin-6 are the most common cvtokines that are activated by endotoxemia.l5 Finaliy, endotoxemia will induce severe shock and hemorrhage in DHF cases. Concerning the matter mentioned above, the roles of endotoxin and cytokine in DHF should be further studied.