RESUMO
BACKGROUND AND AIMS: Severe Ovarian Hyperstimulation Syndrome (OHSS) forms with very aggressive clinical evolution are still common, despite prophylactic measures. Besides the Vascular Endothelial Growth Factor (VEGF), there are other angiogenic factors, like Renin-Angiotensin-Aldosterone System (RAS), that might be associated with this disorder. Our study aims to evaluate the role of VEGF and Angiotensin II (ANG II) in the development of early severe OHSS, in high risk patients under prophylactic Cabergoline therapy. MATERIAL AND METHODS: We recruited 192 patients undergoing in vitro fertilization (IVF) procedures with high risk for OHSS development. Out of these, 106 patients with OHSS were enrolled in the study, of which 28 subjects had a severe form of disease (group I), and 78 patients had a mild/moderate form (group II). We collected blood and follicular fluid from our study participants and determined serum and follicular VEGF and ANG II levels using Enzyme-Linked Immunosorbent Assay (ELISA) technique. RESULTS: Follicular VEGF, ANG II, and serum VEGF levels were significantly higher in group I versus group II. Serum VEGF titers were 645.97 versus 548.62 (p = 0.0008), follicular VEGF titers were 2919.52 versus 1093.68 (p < 0.0001), and follicular ANG II levels were 281.64 versus 65.76 (p < 0.0001). No significant differences have been shown between the two groups for serum ANG II levels. CONCLUSION: Our study results provide evidence of a OHSS phenotype that is more prone to undergo severe clinical forms of disease, despite treatments with VEGF receptor blockers, and show that ANG II appears to play a major role alongside VEGF, in the development of these severe forms of disease.
RESUMO
AIM: To investigate the biochemical and genetic thyroid status in women with preeclampsia by the determination of serum FT3 and FT4 levels in association with D1-C785T genotypes. METHODS: We genotyped using PCR-RFLP methods 50 women with preeclampsia and 50 normotensive pregnant women. RESULTS: FT3 levels (pg/ml, 2.63 ± 0.56 vs. 2.91 ± 1.41) were low, and FT4 levels (ng/dl, 1.11 ± 0.3 vs. 0.88 ± 0.14) were high in women with preeclampsia compared to normal pregnant women. The association with severe preeclampsia was stronger for the homozygous T/T genotype (OR 6.57, p = 0.029). Women with preeclampsia with the D1-T785 mutated allele had lower FT3 levels (pg/ml, 2.31 ± 0.81 vs. 3.04 ± 0.39, p < 0.001), higher FT4 levels (ng/dl, 1.32 ± 0.87 vs. 0.84 ± 0.24, p = 0.009) than women with preeclampsia with the D1-C/C genotype. Significant decrease in serum FT3 levels in positive women with severe preeclampsia compared to women negative for this genetic variation (pg/ml, 1.59 ± 0.74 vs. 2.77 ± 0.23, p = 0.003) was observed. Women with severe preeclampsia, positive for the mutated T785 allele, delivered at a significantly lower gestational age (31.75 ± 3.69 vs. 38.66 ± 3.21 weeks, p = 0.035) neonates with a lower birth weight (1861.11 ± 869.9 vs. 3500 ± 424.26 g, p = 0.023) compared to women negative for the same allele. CONCLUSIONS: Thyroid hormone levels and the D1-C785T polymorphism, alone or in combination, correlate with the severity of preeclampsia. The D1-C785T polymorphism influences the outcome of pregnancy in severe preeclampsia.
