Publication: The role of prostacyclin (PGI<inf>2</inf>) and thromboxane A<inf>2</inf>(TXA<inf>2</inf>) in pathogenesis of dengue hemorrhagic fever (DHF)
No. of Pages/File Size
Journal of the Medical Association of Thailand. Vol.82, No.SUPPL. (1999)
Chawalit Preeyasombat, Suporn Treepongkaruna, Arporn Sriphrapradang, Lulin Choubtum (1999). The role of prostacyclin (PGI<inf>2</inf>) and thromboxane A<inf>2</inf>(TXA<inf>2</inf>) in pathogenesis of dengue hemorrhagic fever (DHF). Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/25522.
The role of prostacyclin (PGI<inf>2</inf>) and thromboxane A<inf>2</inf>(TXA<inf>2</inf>) in pathogenesis of dengue hemorrhagic fever (DHF)
In previous studies it has been demonstrated that the levels of plasma 6 keto-prosta-glandin F1α (6-K-PGF1), the stable metabolite of PGI2were elevated in DHF patients during shock. In this study it is hypothesized that excessive PGI2production plays a very important role in developing serious clinical manifestations of dengue shock syndrome (DSS) patients. In addition, an attempt was made to determine whether TXA2has any significant role in such patients. Plasma 6-K-PGF1and thromboxane B2(TXB2), the stable metabolites of TXA2were determined in 43 normal healthy children (NC) and 54 DHF patients without shock (DHF-N) and 33 DHF patients with shock (DHF-S). Subjects aged between 2 and 14 years. Plasma 6-K-PGF1and TXB2were measured by radioimmunoassay and the ratio of TXB2/6-K-PGF1were also calculated. In 43 NC the values of plasma TXB2, 6-K-PGF1and TXB2/6-K-PGF1ratio were (mean ± SE) 372.3 ± 17.1, 150.1 ± 2.4 and 2.52 ± 0.12 pg/ml, respectively. In 54 DHF-N patients the corresponding values were 409.1 ± 16.0, 278.4 ± 11.6 and 1.54 ± 0.06 pg/ml; whereas those in 33 DHF-S patients were 254.3 ± 26.2, 349.1 ± 20.5 and 0.757 ± 0.073 pg/ml, respectively. Plasma 6-K-PGF1levels of DHF-N and DHF-S patients were significantly greater than those in normal children (p < 0.001, p < 0.01 respectively). The plasma 6-K-PGF1levels seem to be greater in DHF-S patients than in the DHF-N patients, however the difference in values were not statistically significant (p > 0.05). These findings indicate that plasma PGI2level is significantly increased in DHF particularly during shock. Plasma TXB2levels of DHF-N had no significant statistical difference from those of NC (p > 0.05); however, those in DHF-S patients were significantly lowered (p < 0.001) than those of NC and DHF-N patients. The findings suggest the important role of TXA2to compensate for excessive PGI2secretion in DHF patients. The failure or inadequate TXA2production may eventually lead to shock. The ratios were significantly reduced in both DHF-N and DHF-S patients when compared to those of NC (p < 0.001 both). The ratio in DHF-S patients was also significantly lowered than that in DHF-N patients (p < 0.001). It is suggested that the imbalance between TXA2and PGI2production exists during DHF infection. The more reduction of plasma TXA2/PGI2ratio leads to more overt and serious clinical manifestations of the disease.