Nuclear transcription factor-kappa beta-dependent ultrastructural alterations within the placenta and systemic inflammatory activation in pregnant patients with hemolysis, elevated liver functions and low thrombocyte count (HELLP) syndrome: a case-control study

SIMSEK Y., GÜL M. , CELIK O., AYDIN N. E. , DUZ S. A. , CELIK E., ...Daha Fazla

HYPERTENSION IN PREGNANCY, cilt.32, ss.281-291, 2013 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 32 Konu: 3
  • Basım Tarihi: 2013
  • Doi Numarası: 10.3109/10641955.2013.806538
  • Sayfa Sayıları: ss.281-291


Objective: Preeclampsia appears to be associated with a higher extent of inflammation than in uncomplicated pregnancies. We aimed to test whether this was the case in patients with hemolysis, elevated liver functions and low platelet count (HELLP) syndrome and to clarify the contribution of placental and systemic inflammatory variables in the development of this syndrome. Materials and methods: Thirty healthy pregnant women (control group) and 20 patients with HELLP syndrome (study group) were included in the study. Placental inflammatory activity was evaluated by quantifying immunohistochemically the levels of p65/RelA expression of nuclear transcription factor-kappa beta (NF-kB) in paraffin-embedded tissue samples. In addition, ultrastructural changes in placental morphology in HELLP patients were evaluated by transmission electron microscopy (TEM). The serum concentrations of myeloperoxidase (MPO) and C-reactive protein (CRP) were also measured and compared. Results: p65/RelA immunoexpression and serum MPO and CRP levels were significantly higher in patients with HELLP syndrome (p < 0.05). TEM of placenta in the study group revealed severely vacuolized syncytiotrophoblasts, irregular basal lamina and damaged capillary endothelium when compared with the placenta of control subjects. Conclusion: Our results suggest that over-expression of placental NF-kB is correlated with elevation of serum inflammatory markers and placental ultrastructural changes, which may point to an important role of local and systemic inflammatory activation in the pathogenesis of HELLP syndrome.