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Revista Brasileira de Ginecologia e Obstetrícia. 1999;21(2):91-98
DOI 10.1590/S0100-72031999000200006
Purpose: placental alterations were evaluated in macrosomatia and fetal growth retardation in pregnancy complicated by diabetes. Three groups of rats, used as experimental models, were studied: control, moderate and severe diabetes. Material and Method: cesarian sections were carried out on the 18th or 21st day of pregnancy. Maternal and fetal glycemia, newborn weight, placental weight, relationship between placental and fetal weight, DNA, RNA and protein contents and the glycogen deposited on placental membranes were analyzed. Results: there was a higher number of macrosomic newborns in the moderate diabetes group, whose placentas were rich in DNA with progressive decrease of glycogen in their membranes towards the end of pregnancy. There was a predominance of small for date newborns in the severe diabetes group. Their placentas showed a small DNA proportion, an increase in RNA synthesis and a tendency to higher protein production, with no change in the glycogen deposit. Conclusions: we conclude that fetal growth deviation in moderate and severe maternal diabetes between the 18th and 21st days of pregnancy is related to several placental alterations. In the moderate form there were only cellular hyperplasia and disappearance of placental glycogen at the end of pregnancy. In the severe diabetes group there was thickening of maternal-fetal membranes during this period. There was cellular hyperplasia and hypertrophy associated with the maintenance of glycogen reserves in the placental membranes.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 1999;21(2):91-98
DOI 10.1590/S0100-72031999000200006
Purpose: placental alterations were evaluated in macrosomatia and fetal growth retardation in pregnancy complicated by diabetes. Three groups of rats, used as experimental models, were studied: control, moderate and severe diabetes. Material and Method: cesarian sections were carried out on the 18th or 21st day of pregnancy. Maternal and fetal glycemia, newborn weight, placental weight, relationship between placental and fetal weight, DNA, RNA and protein contents and the glycogen deposited on placental membranes were analyzed. Results: there was a higher number of macrosomic newborns in the moderate diabetes group, whose placentas were rich in DNA with progressive decrease of glycogen in their membranes towards the end of pregnancy. There was a predominance of small for date newborns in the severe diabetes group. Their placentas showed a small DNA proportion, an increase in RNA synthesis and a tendency to higher protein production, with no change in the glycogen deposit. Conclusions: we conclude that fetal growth deviation in moderate and severe maternal diabetes between the 18th and 21st days of pregnancy is related to several placental alterations. In the moderate form there were only cellular hyperplasia and disappearance of placental glycogen at the end of pregnancy. In the severe diabetes group there was thickening of maternal-fetal membranes during this period. There was cellular hyperplasia and hypertrophy associated with the maintenance of glycogen reserves in the placental membranes.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2005;27(11):691-697
DOI 10.1590/S0100-72032005001100010
This is both a synthesis and a review of the major research findings, with the aim of validating Rudge's group IB. In this group of pregnants, screening for gestational diabetes was positive while the diagnosis was negative (normal 100 g-oral glucose tolerance test 100 g-OGTT). Nonetheless, the variations in glucose levels observed throughout the day, and confirmed by the glycemic profile (GP), characterized diurnal hyperglycemia, which accounts for maternal risk and adverse perinatal outcome. The description of this group is unique for both the establishment of the diagnosis during gestation and the follow-up of both the mother and the infant. These pregnancies have been erroneously classified as "low risk" and have not been diagnosed or treated. The IB group corresponds to 13.8% of the pregnant women screened in our service. This rate, added to the 7% of pregnancies complicated by diabetes, increase the occurrence of hyperglycemic disorders during gestation to up to 20.0%. In Rudge's group IB: a) perinatal mortality rate is 41‰, which is similar to that observed among diabetic pregnant women and 10 times higher than that found among non-diabetics; b) the observed placental abnormalities (both morphological and functional) differed from those seen in non-diabetic and diabetic pregnant women, indicating an adjustment to maintain functional activities that facilitated the passage of glucose to the fetus and explained fetal macrosomia (53.8% in non-treated pregnancies); c) maternal risk for hypertension, obesity and hyperglycemia was high and seemed to reproduce a model of metabolic syndrome, favoring the potential risk for future diabetes; d) 10 years after the index-pregnancy, type 2 diabetes was confirmed in 16.7% of the women in group IB. The authors suggest the development of multicentric studies in order to identify biomarkers specific for Rudge's group IB and establish protocols for the diagnosis of gestational hyperglycemic disorders using the combination GP + 100g-GTT as a standard. This procedure may cause an impact on the morbidity/mortality rate among pregnancies complicated by diurnal hyperglycemia.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2005;27(11):691-697
DOI 10.1590/S0100-72032005001100010
This is both a synthesis and a review of the major research findings, with the aim of validating Rudge's group IB. In this group of pregnants, screening for gestational diabetes was positive while the diagnosis was negative (normal 100 g-oral glucose tolerance test 100 g-OGTT). Nonetheless, the variations in glucose levels observed throughout the day, and confirmed by the glycemic profile (GP), characterized diurnal hyperglycemia, which accounts for maternal risk and adverse perinatal outcome. The description of this group is unique for both the establishment of the diagnosis during gestation and the follow-up of both the mother and the infant. These pregnancies have been erroneously classified as "low risk" and have not been diagnosed or treated. The IB group corresponds to 13.8% of the pregnant women screened in our service. This rate, added to the 7% of pregnancies complicated by diabetes, increase the occurrence of hyperglycemic disorders during gestation to up to 20.0%. In Rudge's group IB: a) perinatal mortality rate is 41‰, which is similar to that observed among diabetic pregnant women and 10 times higher than that found among non-diabetics; b) the observed placental abnormalities (both morphological and functional) differed from those seen in non-diabetic and diabetic pregnant women, indicating an adjustment to maintain functional activities that facilitated the passage of glucose to the fetus and explained fetal macrosomia (53.8% in non-treated pregnancies); c) maternal risk for hypertension, obesity and hyperglycemia was high and seemed to reproduce a model of metabolic syndrome, favoring the potential risk for future diabetes; d) 10 years after the index-pregnancy, type 2 diabetes was confirmed in 16.7% of the women in group IB. The authors suggest the development of multicentric studies in order to identify biomarkers specific for Rudge's group IB and establish protocols for the diagnosis of gestational hyperglycemic disorders using the combination GP + 100g-GTT as a standard. This procedure may cause an impact on the morbidity/mortality rate among pregnancies complicated by diurnal hyperglycemia.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2000;22(7):401-411
DOI 10.1590/S0100-72032000000700002
Purpose: to analyze the relationship between White's classification and the histopathological, changes occurring in the placentas of diabetic pregnant women, performing a qualitative comparison of histopathological changes in the placentas of nondiabetic pregnant women with those in diabetic ones (classes A and A/B), clinical, short duration (classes B and C), and clinical with vasculopathy (classes D to FRH), studying the influence of the quality of glycemic control and of gestational age on placental changes in the three groups of diabetic pregnant women. Patients and methods: specimens of placentas were collected from all diabetic pregnant women seen between 1991 and 1996 in the Maternity Section of the Hospital das Clínicas, Faculdade de Medicina de Botucatu, stained using the hematoxylin-eosin technique, and submitted to a histopathological examination. The quality of glycemic control was analyzed by the glycemia average of gestation and classified as adequate or inadequate, with a limit of 120 mg/dl. Gestational age was individualized as term and preterm. Results: forty-two newborns (43.3%) were born at term and the remaining were preterm (56.7%). The prematurity rate was higher for women with clinical diabetes (classes B and C; D to FRH). Some histopathological alterations were observed only in placentas from diabetic pregnant women: cystoid degeneration, chorial edema, intima edema, dysmaturity, Hofbauer cell hyperplasia, villitis, ghost cells, two vessels in the umbilical cord, and endarteritis. Conclusions: histopathological changes in the placentas of pregnant women with gestational diabetes (classes A and A/B), clinical, short duration (classes B and C), and clinical with vasculopathy (classes D to FRH) were similar to those in the nondiabetic ones, and, therefore, were independent of White's clinical classification. The histopathological changes in the placentas of pregnant women with gestational diabetes (classes A and A and B), clinical, short duration (classes B and C), and clinical with vasculopathy (classes D to FRH) were not related to gestational age at birth and to the quality of glycemic control of the mother. The comparison between histopathological changes and the increased number of preterm newborns in clinical diabetes, class D to FRH, suggest early placental ageing in clinical diabetes patients.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2000;22(7):401-411
DOI 10.1590/S0100-72032000000700002
Purpose: to analyze the relationship between White's classification and the histopathological, changes occurring in the placentas of diabetic pregnant women, performing a qualitative comparison of histopathological changes in the placentas of nondiabetic pregnant women with those in diabetic ones (classes A and A/B), clinical, short duration (classes B and C), and clinical with vasculopathy (classes D to FRH), studying the influence of the quality of glycemic control and of gestational age on placental changes in the three groups of diabetic pregnant women. Patients and methods: specimens of placentas were collected from all diabetic pregnant women seen between 1991 and 1996 in the Maternity Section of the Hospital das Clínicas, Faculdade de Medicina de Botucatu, stained using the hematoxylin-eosin technique, and submitted to a histopathological examination. The quality of glycemic control was analyzed by the glycemia average of gestation and classified as adequate or inadequate, with a limit of 120 mg/dl. Gestational age was individualized as term and preterm. Results: forty-two newborns (43.3%) were born at term and the remaining were preterm (56.7%). The prematurity rate was higher for women with clinical diabetes (classes B and C; D to FRH). Some histopathological alterations were observed only in placentas from diabetic pregnant women: cystoid degeneration, chorial edema, intima edema, dysmaturity, Hofbauer cell hyperplasia, villitis, ghost cells, two vessels in the umbilical cord, and endarteritis. Conclusions: histopathological changes in the placentas of pregnant women with gestational diabetes (classes A and A/B), clinical, short duration (classes B and C), and clinical with vasculopathy (classes D to FRH) were similar to those in the nondiabetic ones, and, therefore, were independent of White's clinical classification. The histopathological changes in the placentas of pregnant women with gestational diabetes (classes A and A and B), clinical, short duration (classes B and C), and clinical with vasculopathy (classes D to FRH) were not related to gestational age at birth and to the quality of glycemic control of the mother. The comparison between histopathological changes and the increased number of preterm newborns in clinical diabetes, class D to FRH, suggest early placental ageing in clinical diabetes patients.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2001;23(1):9-14
DOI 10.1590/S0100-72032001000100002
Purpose: to evaluate the effects of maternal diabetes on the fetal lung phospholipid profiles of rats with moderate and severe diabetes measuring lecithin (L), sphingomyelin (S), phosphatidyl-glycerol (PG), phosphatidyl-inositol (PI), and the relationships between L/S and PG/PI. Methods: fifty-four mature Wistar rats were submitted to experimental diabetes and pregnancy¹. Diabetes was induced by alloxan (42 mg/kg of weight, iv) and three groups were formed: control; moderate diabetes (MD), with glycemia levels between 120 and 200 mg/dl, and severe diabetes (SD), with glycemia levels higher than 200 mg/dl. On the 21st day, cesarian section was performed, and the fetal lungs were macerated and pooled. The phospholipids were measured by unidirectional thin-layer chromatography. Results: 1) the fetal lungs of the rats with moderate diabetes showed higher weight (0.159 g) and lower concentration of PG (3.0 µg/ml) and PI (3.4 µg/ml) than the controls, and the same relationship between L/S (2.2) and PG/PI (2.0). The fetal lungs of the rats with severe diabetes showed lower weight (0.145 g), the same values of L/S (1.9) and PG/PI (2.1), and lower PI (5.1 µg/ml) value than the controls. Conclusions: 1) the pulmonary maturity retardation in the pups of rats with moderate diabetes is explained by the higher pulmonary weight associated with lower concentration of PG and PI; 2) the pulmonary maturity acceleration in the pups of rats with severe diabetes is explained by the lower pulmonary weight associated with the same concentration of PG and PI.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2001;23(1):9-14
DOI 10.1590/S0100-72032001000100002
Purpose: to evaluate the effects of maternal diabetes on the fetal lung phospholipid profiles of rats with moderate and severe diabetes measuring lecithin (L), sphingomyelin (S), phosphatidyl-glycerol (PG), phosphatidyl-inositol (PI), and the relationships between L/S and PG/PI. Methods: fifty-four mature Wistar rats were submitted to experimental diabetes and pregnancy¹. Diabetes was induced by alloxan (42 mg/kg of weight, iv) and three groups were formed: control; moderate diabetes (MD), with glycemia levels between 120 and 200 mg/dl, and severe diabetes (SD), with glycemia levels higher than 200 mg/dl. On the 21st day, cesarian section was performed, and the fetal lungs were macerated and pooled. The phospholipids were measured by unidirectional thin-layer chromatography. Results: 1) the fetal lungs of the rats with moderate diabetes showed higher weight (0.159 g) and lower concentration of PG (3.0 µg/ml) and PI (3.4 µg/ml) than the controls, and the same relationship between L/S (2.2) and PG/PI (2.0). The fetal lungs of the rats with severe diabetes showed lower weight (0.145 g), the same values of L/S (1.9) and PG/PI (2.1), and lower PI (5.1 µg/ml) value than the controls. Conclusions: 1) the pulmonary maturity retardation in the pups of rats with moderate diabetes is explained by the higher pulmonary weight associated with lower concentration of PG and PI; 2) the pulmonary maturity acceleration in the pups of rats with severe diabetes is explained by the lower pulmonary weight associated with the same concentration of PG and PI.
