Introduction: Macrosomia in diabetic pregnancy is an ubiquitous finding and implies both maternal and fetal issues. Its incidence surpasses other critical obstetrical morbidity in diabetic pregnancy with increased placental size and polyhydramnios as comorbidity. The studies on the underlying factors contributing to macrosomia have focused on growth stimuli like IGF, glycemia, and insulin and their effects on regional organ function. IGF-I and -II in maternal serum are associated with birth weight and the bioavailabiliy is modulated by IGF-binding-proteins (IGFBP) and phosporylated isoforms of IGFBP and the presence of proteases and IGF split products. Human placental growth hormone regulates the effect of IGF-I in pregnancy. Methods: The literature on the IGF system′s possible effect on fetal growth in diabetic pregnancy is reviewed before our current studies and updated with respect to later findings. Regulation on bioavailability by proteolysis and phosporylation is described. The review discusses briefly the studies on pregnant women with type 1 diabetes with respect to vasculopathy. Results: The data show good correlation of IGF-1/2 levels with birth weight. No such correlation with IGFBP-1 and -3 is found. Fetal growth deviation in diabetic pregnancy is not uniform. In first trimester, growth delay is documented in fetal growth curves compared to non-diabetic controls. Accordingly, a shift in IGF-IGFBP regulation in second trimester is found with less proteolysis of IGFBPs and relative increase in total binding capacity. In third trimester, free IGF further increases as IGFBP binding decreases by proteolysis and modulation. The first trimester values may be used as predictor of fetal weight at term. Diabetic women show a two-to threefold increase in the in vitro IGFBP-3 proteolytic activity during pregnancy as compared to post-partum values. Conclusions: Prominent proteolysis of binding proteins and the modulation by insulin account for the mechanism leading to macrosomia. The two factors combined guarantee the stimulation by more bioavailable IGF and the glycemic levels reveal whether insulin dose are optimal. Structural factors of diabetes i.e. microangiopathy further modulate the sum of effects on fetal growth. In contrast to macrosomia, fetal growth restriction is associated with prominent maternal vascular endothelial complications, such as overt nephropathy, proliferative retinopathy, preeclampsia, and hypertension. In parallel to the growth inhibition, stimulatory effects are exerted by the GH axis including the placental growth hormones and occur probably as compensatory mechanism, similar to the increased IGFBP-3 proteolysis in late pregnancy found in growth retardation. This influence may in part explain the disproportionate growth in different tissue components occurring in the various stages of diabetic pregnancy.
IntroductionCervical cancer is staged preoperatively and the postoperative treatment depends on the combination of staging with histopathological finding. Survival is related to certain histopathological factors, most importantly lymph node status and other findings indicating that tumor may have spread i.e. parametrium and the lymph-vascular space. Other factors like tumor size and depth of stromal invasion indicate aggressive biological behavior. Poorer survival depending on histological type of tumor is reported in adenocarcinoma compared to squamous carcinoma [1][2][3][4][5][6][7]. The concurrent increasing incidence of adenocarcinoma associated with use of oral contraceptives in the Western World is a concern to that it may reverse the positive effect of screening [6,7]. However, the survival relates heavily on different pre-and postoperative treatment regimens and stage of disease [1,3,4]. Adverse histopathological factors are often present simultaneously and reviewed heterogeneously.The aim of our study was to evaluate independent histopathological factors for women with radical hysterectomy with focus on standardized histopathological diagnosis combined with similar pre-and postoperative treatment. Material and Methods141 women were diagnosed with cervical cancer stage 1b and operated with radical hysterectomy during 24 years at Holstebro Hospital. The hospital served as centre for the county with a population of approximately 275.000. The stage, pre-and postoperative treatment was registered as the data charts were reviewed. The local patient registry provided information of survival, relapse, and re-admittance. None of the women was lost to follow-up. Data charts or post mortem sections confirmed the cause of death. AbstractBackground: Evaluation of histopathological factors for women with radical hysterectomy a.m. Okabayashi for cervical cancer in stage 1bwith similar pre-and postoperative treatment Methods: Data on 141 women with cervical cancer stage 1b were revised. The local patient registry, data charts, and post mortem sections provided follow-up on survival, relapse, and re-admittance. Histopathological evaluation was performed by the same pathologist. Results: Histological evaluation showed that adenosquamous cervical cancer in stage 1b was associated with poorer survival than the pure squamous and adenomatous type (p<0.001, mixed versus pure type). Five year's survival rate was 40 % (2-78 %) for mixed type and 92 % (87-97 %) for pure type. The mixed type was associated with glandular metastasis (p<0.02). The relapse free survival after 5 and 10 years was 88 % (82-94 %) and 83 % (75-91 %), respectively, while survival was found to be 89 % (83-95 %) and 86 % (79-93 %), respectively. The women's age at diagnosis showed no association with histology type or survival.
Aim: The arterial wall elasticity and genetic setting is a potential risk factor for dysfunction of vas¬cular endothelial cells and the clinical expression of retinopathy. The prevalence was evaluated of polymorphism in the genes of methylene-tetrahydro-folate-reductase (MTFHR), Factor V, glycoprotein IIb/IIIa (Gp2b3a), and prothrombin in a cohort of pregnant women with type 1 diabetes. The role of hyperhomo¬cysteinemia in microangiopathy in diabetes mellitus has been debated and is mainly seen with reduced activity of the MTHFR gene. The arterial resistance index (AASI) has been used to detect arterial dysfunction and correlate with cardiovascular morbidity and mortality in patients with hypertension.Design: Two-hundred-and-thirty-three women with type 1 diabetes mellitus were analyzed for MTHFR gene polymorphism and Factor V Leiden. In 176 of these women AASI was further evaluated. In a sub-cohort of 40 women with preeclampsia, mutations in glycoprotein IIb/IIIa (Gp2b3a) and prothrombin was measured. The pregnancy and ophthalmological examination data charts were reviewed retrospectively.Results: Retinopathy was associated with higher AASI during pregnancy (p<0.01, in all three trimesters) and preeclampsia (p<0.05). The stiffness increased with higher grades of retinopathy. AASI in women with simplex and proliferative retinopathy followed different patterns during the three trimesters, even when adjusted for age, BMI, and glycemic regulation (p<0.01). None of the studied coagulation genes (MTHFR, Factor V, Gp2b3a, and prothrombin) were found associated with retinopathy or preeclampsia. Conclusion:Retinopathy showed a strong association with AASI during pregnancy and not outside pregnancy in women with type 1 diabetes. This suggests a pregnancy-related functional change in the vascular bed.A common polymorphism in methylene-tetrahydro-folate-reductase (MTFHR 677C>T, a C to T substitution at nucleotide 677, which converts alanine to a valine residue) has been identified as responsible for reduced MTHFR activity and increased plasma homocysteine [10,11].Factor V Leiden is a mutated form of human factor V that causes an increase in blood clotting. With this mutation, the anticoagulant protein secreted is inhibited, leading to an increased tendency to form dangerous, abnormal blood clots. Factor V Leiden is the most common hereditary hypercoagulability disorder amongst ethnic Europeans and linked with increased risk of preeclampsia, abortions, intrauterine growth restriction, placental abruption, and thrombosis [12][13][14].Glycoprotein IIb/IIIa (Gp2b3a, also known as integrin αIIbβ3) is a complex found on platelets. It is a receptor for fibrinogen and von Lauszus FF (2017) Retinopathy in pregnancy in women with type 1 diabetes -a study of associations with arterial wall elasticity and mutation in coagulation genes
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