The role of unexplained high serum alpha-fetoprotein (AFP) and human chorionic gonadotropin (hCG) levels in the second trimester to determine poor obstetric outcomes.

OBJECTIVE: To investigate the relationship between gestational complications and high levels of maternal serum alfa-fetoprotein (MSAFP) and/or beta human chorionic gonadotropin (hCG) and to determine whether these markers are effective predictors of poor pregnancy outcomes. MATERIALS AND METHODS: In this study, we enrolled a total of 679 women at 15-20 gestational weeks with MSAFP and hCG below or above 2.0 multiples of the median (MoM); of those, 200 women with normal MSAFP and hCG MoM formed the control group. Pre-eclampsia, intrauterine growth retardation (IUGR), preterm labor, preterm delivery, placental abruption, placenta previa, placenta accreta, preterm premature rupture of the membranes (PPROM), intrauterine fetal death, as well as neonatal and perinatal morbidity rates were evaluated. RESULTS: A significant relationship was found between adverse pregnancy outcomes and abnormal elevation of hCG and AFP levels in the second trimester. In cases of isolated elevation of hCG, preeclampsia and preterm labor/spontaneous preterm birth rate were slightly higher than in the control group (p=0.043, p=0.015), while IUGR, PPROM, placental abruption, and intrauterine fetal death rates were all similar (p=0.063, p=0.318, p=1.00, p=0.556). In case having an elevation in both markers, increased rate of obstetric complications have been observed. A significant relationship was found between the high levels of maternal serum AFP and hCG MoM and poor pregnancy outcomes like preeclampsia, IUGR, PPROM, intrauterine fetal death (p=0.003, p=0.001, p=0.040, p=0.006). CONCLUSION: To our knowledge, up to now, no definitive follow-up and treatment protocols have been established for patients at increased risk. In light of these findings, it is recommended to inform and educate patients about the most likely signs and symptoms of complications, to make more often antenatal visits, to perform more frequent ultrasound examination (fetal growth, AFI, etc.), NST, arterial/venous doppler, biophysical profile, and cervical length measurements in high-risk group.

Elevated plasma advanced oxidation protein products in children with Henoch-Schonlein purpura.

Henoch-Schonlein purpura (HSP) is a systemic vasculitis characterized by involvement of skin, joints, gastrointestinal tract (GIT), and kidney; its pathogenesis is still controversial. The aim of our study was to investigate the role of oxidative stress in the pathogenesis of HSP. Plasma advanced oxidation protein products (AOPP) level was measured in 29 children with HSP at the onset of the disease and during remission in comparison with 30 healthy subjects. Patients at the active stage had significantly higher AOPP levels than those at the remission stage of HSP and the controls (42.9 ± 25.7, 30.6 ± 11.8, 27.9 ± 11.2 mmol/l; P = 0.027 and P = 0.023 respectively). The mean AOPP levels of the patients with arthritis and/or arthralgia were significantly higher those than without joint involvement (48.3 ± 26.0 and 22.3 ± 9.3, P = 0.036 respectively). However, AOPP levels were similar in patients with and without gastrointestinal involvement. Plasma AOPP levels were positively correlated with leukocyte and thrombocyte count at disease onset, whereas they were found to be negatively correlated with serum glucose and sodium levels. The mean thrombocyte count was the only independent predictor of increased level of AOPP in regression analysis (ß = 0.407; P = 0.029). In conclusion, this study showed that increased oxidative stress may play an important role in the pathogenesis of HSP. Also, we suggest that higher platelet count might be an indirect indicator of oxidative stress in these patients. Further research is required to identify the potential association between oxidative stress and increased thrombocyte count in children with HSP.

Hemodialysis and protein oxidation products.

The presence of a chronic inflammatory state has also been widely documented in end-stage renal disease patients receiving maintenance hemodialysis (HD). It is commonly attributed to the constantly renewed activation of circulating neutrophils and monocytes following blood passage through dialysis circuits and subsequent generation of activated complement components due to contact of plasma with bioincompatible membranes and/or transfer of endotoxins from the dialyzate to the blood compartment. This conjunction leads to a massive generation of reactive oxygen species (ROS), for example, superoxide anion, hydrogen peroxide, hydroxyl radical, and chlorinated oxidants, such as hypochlorous acid by activated neutrophils. The exquisite vulnerability of proteins to ROS is now well documented. Oxidation of amino acid residues, such as tyrosine, leads to the formation of dityrosine, protein aggregation, cross-linking, and fragmentation. Dityrosine-containing protein cross-linking products in the plasma of dialysis patients are named as advanced oxidation protein products (AOPP). In addition, advanced glycation end-products (AGE) is a protein carbonyl compound and produced by protein-ROS interaction. We investigated both the effect of the renewed activation of the immune cells, due to blood-dialyzer interaction over protein oxidation products like AOPP and AGE, among chronic renal failure (CRF) patients receiving maintenance HD, and choice of dialyzers like high flux or the other group on protein oxidation product levels.