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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Perinatal morbidity and mortality are increased in both overt and gestational diabetes. Since retardation of placental development has been documented in overt diabetes, we, thus, examined morphometrically the terminal villi of 26 patients with gestational diabetes in order to determine if there is an immaturity of placental development. Investigation of villous surface, degree of vascularization, and development of epithelial plates yielded values lying somewhere between those of non-diabetic patients and those of patients with overt diabetes. Only the surface areas of the vessels were reduced to levels lower than in overt diabetes. Our findings appear to explain the occasional development of acute placental insufficiency.
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PMID:Morphohistometric investigations in placentas of gestational diabetes. 321 Jan 5

To observe the influence of gestational diabetes over placental morphology, a prospective study was taken for 28 gestational diabetic pregnancies and 25 non-diabetic control subjects. Placental net weight in diabetic group is 549.38 +/- 143.01 g; in control group 458.75 +/- 60.98 g, significant difference was found between above two groups. The changes of diabetic placentas in light microscopy shows villous immaturity, proliferation of small fetal vessels, syncytiotrophoblast knots, cytotrophoblast and vessel syncytiotrophoblast membrane increased. Morphohistometric investigations showed that the changes of placenta in gestational diabetes are significant.
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PMID:[Placental pathology in gestational diabetes]. 813 39

The relationship between young maternal age and preterm delivery was investigated in a subsample of 605 primigravidas enrolled in the Camden (New Jersey, US) Study. Included were 366 adolescents under 16 years of age (cases) and 239 women 18-29 years of age (controls). 36.3% of young mothers had a low gynecological age (i.e., their chronological age was 2 or fewer years more than their age at menarche). After adjustment for ethnicity, cigarette smoking, weight gain rate, height, fetal sex, gestational diabetes mellitus, and pregnancy-induced hypertension, the odds ratio (OR) of preterm labor among young adolescents was 1.74 (95% confidence interval (CI), 1.07-2.84) and that of preterm delivery was 2.08 (95% CI, 1.08-4.00). There was a modest decreased risk of preterm delivery attributable to other causes (e.g., premature rupture of the membranes) among the youngest women (OR, 0.70; 95% CI, 0.28-1.75). Young age with low gynecological age was associated with a 2.15 OR (95% CI, 1.19-3.89) of preterm labor and a 2.64 OR (95% CI, 1.23-5.65) of preterm delivery with preterm labor. The risk associated with young age and higher gynecological age was increased only moderately. These findings suggest that it is the biological immaturity often associated with young age, rather than young maternal age per se, that increases the risks of adolescent pregnancy. The association between low gynecological age and preterm labor is presumed to reflect an irritability of the adolescent uterus, a sensitivity to dehydration, and/or an altered hormonal milieu that promotes maternal development at the expense of fetal well-being.
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PMID:Young maternal age and preterm labor. 927 49

Several groups have reported a risk of fetal macrosomia in pregnancies with maternal glucose intolerance which is intermediate between gestational diabetes (GDM) and normal glucose tolerance. The present study was designed to determine whether these pregnancies are also at risk for fetal obesity, hyperinsulinism and placental villous immaturity. 325 women with risk factors for GDM underwent a 75 g OGTT interpreted according to the O'Sullivan criteria. All women who met the criteria for GDM were managed with diet therapy. Insulin therapy was added for women with a mean serum glucose value > 100 mg/dl on a 24 hour glucose profile. Patients not meeting the GDM criteria were managed without special intervention. Primary outcome variables were measures of neonatal weight and skinfold thickness, fetal and neonatal insulin and glucose concentration, and placental villous maturation. Outcome parameters were compared among three groups: pregnancies with normal OGTT (control, n = 95), 1 abnormal value in the OGTT (1 abnl, n = 76) and GDM (n = 154). The outcome of pregnancies with 1 abnormal value in the OGTT was different from those with normal OGTT. Regarding fetal growth, rates of LGA were approximately twice as high in groups with one abnormal value and GDM (21% and 24%) compared to women with normal OGTTs (11%: p < 0.05 vs GDM and p = 0.07 vs 1 abnormal value). The percent of infants with skinfold thickness > 90th percentile was also greater in the 1 abnormal value and GDM groups (31.1 and 31.6% respectively) compared to controls (19.2%; p < 0.05 for GDM vs control only). Regarding fetal hyperinsulinism, AFI concentrations were similar in control and GDM groups (3.1 +/- 0.4 and 3.4 +/- 0.8 microU/ml, respectively), but were higher in the group with one abnormal OGTT value (4.3 +/- 1.2 microU/ml, p < 0.05 vs controls). Cord blood insulin: glucose ratios were elevated in both the 1 abnormal value and GDM groups (0.22 +/- 0.05 and 0.20 +/- 0.02 microU/ml per mg/dl), compared to controls (0.12 +/- 0.01 microU/ml per mg/dl, p < 0.05 vs 1 abnormal value). Neonatal glycemia < 30 mg/dl was significantly more common in the one abnormal value than in the control group (49% vs 34% of infants) and intermediate in the GDM group (40%). Severe placental villous immaturity was more than twice as frequent in the 1 abnormal value group compared to controls (24% vs 9%, p < 0.05) and the most frequent in the GDM group (33%; p < 0.001 vs controls). Pregnancies with glucose intolerance below the thresholds for diagnosis of GDM have an increased risk for fetal obesity, hyperinsulinism, postpartum hypoglycemia and placental immaturity. These findings indicate the continuum of risk for fetal morbidity associated with increasing maternal glucose intolerance in pregnancy.
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PMID:Hyperinsulinism, neonatal obesity and placental immaturity in infants born to women with one abnormal glucose tolerance test value. 959 64

So far, gestational diabetes treated with tolbutamide has never been associated with severe hypoglycaemia in the newborn when the mother's diabetes was well controlled. We report a case of a premature neonate, gestational age 34 weeks, with severe and long-standing hypoglycaemia from birth. The mother had well-controlled gestational diabetes, treated with tolbutamide from the 24th week of gestation until delivery. The neonate had inappropriately high levels of serum proinsulin, insulin and C-peptide relative to blood glucose concentrations. From day 19 after birth, the levels were normalized. Serum tolbutamide was 140.6 micromol/l (38 microg/ml) at 3 h after birth. Zero-order kinetics were seen during the first 90 postnatal hours. The half-life of serum tolbutamide decreased from 46 to 6 h. It is suggested that tolbutamide, when given to the mother until delivery, may cause severe and prolonged hyperinsulinaemic hypoglycaemia in premature neonates. The initially prolonged tolbutamide half-lives and zero-order kinetics suggest immaturity of hepatic elimination during the first 2 days of postnatal life.
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PMID:Prolonged elimination of tolbutamide in a premature newborn with hyperinsulinaemic hypoglycaemia. 967 39

Young maternal age has been associated with an increased risk of gastroschisis, while high maternal weight status has been associated with a decreased risk. We were interested in investigating the joint effect of these two risk factors to identify thresholds in risk associated with body mass index (BMI) for a given age. Data from the National Birth Defects Prevention Study included 464 case infants with gastroschisis and 4842 healthy controls. A generalised additive model with a bivariate spline for continuous maternal age and prepregnancy BMI was used to model the probability of gastroschisis. The bivariate spline in BMI and maternal age was significantly associated with gastroschisis (P = 0.0001) after adjustment for study centre, maternal race/ethnicity, education, income and number of persons supported by income, smoking, alcohol use, vitamin use, vasoconstrictor medication use and gestational diabetes. The data indicate that women who are younger and who have lower BMI are at the greatest risk; a woman with a BMI of 17 who gives birth at age 15 has 7 times the odds (adjusted odds ratio = 7.0 [95% CI 4.2, 11.5]) of having an offspring with gastroschisis compared with a woman of age 24 with a BMI of 23. Furthermore, there was an interaction between maternal age and BMI for this risk. The increased risk of low maternal age and prepregnancy BMI associated with gastroschisis appears to suggest an aetiological role related to biological immaturity for this particular birth defect.
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PMID:The joint effects of maternal prepregnancy body mass index and age on the risk of gastroschisis. 1922 14

Normal human pregnancy is considered a state of enhanced oxidative stress. In pregnancy, it plays important roles in embryo development, implantation, placental development and function, fetal development, and labor. However, pathologic pregnancies, including gestational diabetes mellitus (GDM), are associated with a heightened level of oxidative stress, owing to both overproduction of free radicals and/or a defect in the antioxidant defenses. This has important implications on the mother, placental function, and fetal well-being. Animal models of diabetes have confirmed the important role of oxidative stress in the etiology of congenital malformations; the relative immaturity of the antioxidant system facilitates the exposure of embryos and fetuses to the damaging effects of oxidative stress. Of note, there are only a few clinical studies evaluating the potential beneficial effects of antioxidants in GDM. Thus, whether or not increased antioxidant intake can reduce the complications of GDM in both mother and fetus needs to be explored. This review provides an overview and updated data on our current understanding of the complications associated with oxidative changes in GDM.
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PMID:The role of oxidative stress in the pathophysiology of gestational diabetes mellitus. 2167 77

Renal glycosuria is defined as the excretion of glucose in urine in a normoglycemic state. It results from renal tubular dysfunction or immaturity of tubular function in the newborn. Etiologically, renal glycosuria is of 3 types-benign renal glycosuria, glycosuria with diabetes mellitus (including gestational diabetes) and tubular defects (Fanconi syndrome). Prognosis of benign renal glycosuria is excellent and reversible. Acute interstitial nephritis (AIN) is one of the main causes of acute renal failure and may often result in tubular dysfunction. In this study, the authors report the occurrence of AIN with acute renal failure that contributed to reversible renal glycosuria. The glycosuria observed in the patient of this study was an isolated tubular defect, with no phosphaturia, aminoaciduria or bicarbonaturia. Such a presentation is very rare in adults and has not been previously reported. These findings confirm that AIN with acute renal failure can cause an isolated tubular defect with benign reversible glycosuria in an adult.
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PMID:Reversible renal glycosuria in acute interstitial nephritis. 2292 13

Gestational diabetes mellitus (GDM)-associated fetal and neonatal adverse outcome results from the metabolic milieu projected on the fetus via the placental interface. Therefore, it can be considered to be one of the great obstetrical syndromes. Placentas from GDM pregnancies differ from nondiabetic pregnancies by an increased placental to fetal ratio and by histological findings such as villous fibrinoid necrosis, villous immaturity, chorangiosis, and ischemic changes. While early onset diabetes is more associated with marked structural changes of the placenta, GDM that rises at late gestation is associated more with placental functional changes. These placental changes, causing increased intervillous diffusion distance of immature villi and placental size to perfusion mismatch, may predispose the fetus to chronic and acute changes in gas and nutrient exchange thus turning the placenta from being a "fetus protector" to a potential source of adverse outcome. Understanding placental changes and how they affect outcome is necessary in order to develop effective screening, prevention, and management approaches.
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PMID:Gestational diabetes as one of the "great obstetrical syndromes"--the maternal, placental, and fetal dialog. 2522 57

Nowadays, the continuous rise of maternal obesity is followed by increased gestational diabetes mellitus incidence. GDM is associated with adverse fetal and neonatal outcome that often presents with macrosomia, birth trauma, neonatal hypoglycemia, and respiratory distress syndrome. Inclusion of GDM into 'the great obstetrical syndromes' emphasizes the role of the placenta in interactions of the maternal and fetal unit. The placenta acts as a natural selective barrier between maternal and fetal blood circulations. Placenta is sensitive to the hyperglycemic milieu and responses with adaptive changes of the structure and function. Alteration of the placental development and subsequent vascular dysfunction are presented in 6 out of 7 women with all ranges of diabetic severity. Most placentas from GDM pregnancies present typical histological findings such as villous immaturity, villous fibrinoid necrosis, chorangiosis, and increased angiogenesis. The type of dysfunction depends on how early in pregnancy glycaemia disorders occurred. Generally, if impaired glucose metabolism is diagnosed in the early pregnancy, mainly structural dysfunctions are observed. GDM that is detected in late gestation affects placental function to a greater extent. Moreover many studies suggest that diabetic placental changes are associated with inflammation and oxidative stress that can lead to the chronic fetal hypoxia. This article aims to review particular changes of the development, anatomy and function of the placenta in the environment of abnormal glucose metabolism which can establish the maternal-placental-fetal interface dysfunction as a potential source of adverse pregnancy outcomes. A detailed sequence of events that leads from hyperglycemia to placental dysfunction and subsequent pregnancy complications may become an important issue for further studies.
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PMID:Placental pathologic changes in gestational diabetes mellitus. 2607 74


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