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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes is known to be associated with delayed lung development in humans and in experimental animals. This includes delayed expression of surfactant apoproteins. An important component of the metabolic abnormalities in diabetes is elevated levels of analogs of butyric acid, and the effects of diabetes on surfactant apoproteins can be reproduced by exposure of fetal rat lung explants to butyrate. Dexamethasone has the opposite effects on lung development. In humans, antenatal exposure to dexamethasone results in a lower incidence of RDS, whereas in experimental animals, dexamethasone increases the expression of surfactant apoproteins. A subset of Hox genes are expressed in developing lung, and their level of expression decreases with advancing gestation. We hypothesized that: 1) lungs of fetuses of rats with streptozotocin-induced diabetes would have altered levels of expression of Hox genes, 2) the effect would be mediated in part through elevated levels of butyrate, and 3) dexamethasone would reverse the effect. We tested our hypotheses in vivo using fetuses from streptozotocin-treated rats and in vitro by treating lung explants from normal rats with sodium butyrate. Streptozotocin treatment increased expression of Hoxb-5 at 18 d of gestation, but did not affect Hoxa-5 expression. This was associated with a 20-fold increase in alpha-aminobutyrate levels. Dexamethasone tended to reverse this effect. In contrast, butyrate treatment of explants decreased the expression of Hoxa-5 and Hoxb-5. We conclude that diabetes alters expression of Hox genes, but that the effect of butyrate on lung development, and in particular on surfactant apoprotein expression, is independent of its effects on Hox genes.
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PMID:Fetal lung mRNA levels of Hox genes are differentially altered by maternal diabetes and butyrate in rats. 966 78

The Diabetes Mellitus is the pathology that frequently is associated to the pregnancy and it is responsible for perinatal mobility specially by the respiratory distress syndrome since exists delay in the conversion of myoinositol-phosphatidyl inositol-phosphatidyl glycerol. To demonstrate the reliability of the DO tho 650 nm with standard of 20 in the determination of fetal lung maturity of the infant of diabetic mother. There were included 143 patient with pregnancy > or = 37 weeks with amenorrhea reliable and gestational age confirmed by ultrasound, of those 94 corresponded to gestational Diabetes Mellitus, 49 to pregestational (46 non insulin-dependent and 3 insulin-dependent). In all of them amniotic fluid studies was perform at 37 week and the resolution of the pregnancy was when DO to 650 nm showed fetal lung maturity. It was found a correlation among the DO to 650 nm of 20 and absence of RDS in 130 cases (true positive); there were seven cases with immaturity results by DO that they did not express RDS (false negative) and six cases with results that showed immaturity by DO and there were manifestations of RDS (true negative). We did not find results of false positive. The frequency of RDS was of 4.9% with a positive predictive value of the 100% an negative predictive value of 46%, a specificity of 100% and a sensitivity of 94%. An interesting finding was the fact that six cases true negative cases had poor maternal metabolic control of different degrees. For our results can be deduced that DO to 650 nm with standard of .20 it is reliable for the diagnosis of fetal lung maturity in the pregnancies complicated with Diabetes Mellitus, in addition to be an easy elaboration test and low cost.
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PMID:[Reliability of optic density at 650 nm in determining lung maturity in children of diabetic mothers]. 982 5

The aim of this study was to evaluate RDS risk factors in newborns of mothers with define pregnancy complications. The study group included mothers with imminent preterm delivery, intrauterine growth retardation, gestation cholestasis, serological collision, oligo- and polyhydramnios and foetus life threatens risk factors. RDS appeared in newborns born up till 35 weeks of gestation, for the risk factors analysis only preterm delivery, which were ended until 36 weeks of gestation were taken into consideration. Hypertension appeared to be a significant risk factor increasing the risk of RDS evidence 5 times and asphyxia, which increased by 4. In the logistic regression analysis model hypertension showed to increase the risk of RDS evidence 6 times, even when the time of delivery was considered. A, when the time of gestation was prolonged even one week the risk of RDS was decreased by 30%. The was no significant increase in RDS evidence in offspring of mothers with diabetes mellitus, cholestasis gravidarum, hypotrophia foetus or oligo and polyhydramnios.
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PMID:[The evaluation of respiratory distress syndrome (RDS) risk factor evidence in newborns]. 1086 Feb 69

The use of perinatal steroid therapy, first introduced in 1972 is effective in precocious maturation of human lungs. Antenatal corticosteroid therapy results in reduction of fetal mortality, respiratory distress syndrome, intraventricular hemorrhage in preterm babies. These benefits extend to a broad range of gestational age. They comprise the interval between 24 and 34 weeks of human pregnancy and are not limited by the infant's gender or race. The beneficial effects of corticosteroids are the best pronounced after more than 24 hours from the beginning of the treatment. Noteworthy is that therapy less than 24 hours of duration may also improve outcomes. In the presence of premature rupture of membranes, or better with intact membranes, antenatal corticosteroids reduce frequency of RDS, IVH and finally mortality and morbidity. Review of meta-analyses based on randomized trials supports general option that premature infants whose mothers received corticosteroids before delivery are less likely to develop RDS and its complications. Recent data showed that benefits derived from ANS are additive to those of surfactant therapy, rendering the latter more effective. Followup of children up to 12 years of age indicate that ANS do not impair physical growth or psychomotor development. Short-term adverse effects including maternal infection, maternal pulmonary edema were not clearly demonstrated. Pulmonary edema has not been reported when ANS were used alone (i.e. not in combination with betamimetic tocolytics). No long-term unwanted effects on maternal adrenal function have been observed. There is no serious maternal risk resulting from immunosuppressive effect of corticosteroid therapy on maternal immune system. Although glucocorticoid therapy is likely to provoke insulin resistance, and thereby deterioration in diabetic control, and potentially causes cortisol resistance in the fetal lung, the results of scarce randomized trials are not conclusive. In any rate strict control of maternal diabetes mellitus reduces incidence of RDS. Current available data are not indicative of higher risk of fetal mortality in association with maternal hypertensive disease and ANS. In conclusion, most randomized trials of ANS has provided a positive evidence of efficacy and safety of this highly cost effective therapy in most common clinical situations. However, further trials and more precise estimates are justified on ANS treatment specifically related to blood glucose control and evidence concerning the promotion of fetal lung maturity in babies of women with diabetes mellitus. Although benefits of the corticosteroid therapy are beyond any doubts, more experience is needed to assess the effect of ANS on maternal and/or fetal infection in presence of premature rupture of membranes. And finally, further assessments are required on antenatal corticosteroids with dose regimens in patients with multifetal gestation, more common after wide use of techniques of the assisted human reproduction.
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PMID:[Intrauterine stimulation for fetal respiratory system maturation; benefits and risks]. 1114 22

Prematurity is a major cause of perinatal morbidity and mortality. Antenatal administration of glucocorticoids improves the neonatal outcome of preterm born infants. 1994 the NIH published recommendations for the use of glucocorticoids for women at risk of preterm delivery. A recent evaluation by the Cochrane Collaboration in 1999 showed that antenatal administration of glucocorticoids significantly reduced the rate of RDS and IVH in the gestational age between 24 and 34 weeks. Consequences of repeated courses of antenatal glucocorticoids are not sufficiently studied. The effectivity and safety regarding birth weights, infectious diseases, and the best timing remains unknown. Administration of glucocorticoids lowers fetal activity and heart rate variability. Effects on fetal growth, maternal and fetal immunosystem, and the development of atopic diseases are controversely discussed. Thus preterm labour not leading to a cervical ripening is not necessarily a reason for antenatal glucocorticoids. Antenatal glucocorticoids with PROM do not lower the rate of RDS but of IVH. No prospective randomized trial evaluated the effectivity of antenatal glucocorticoids in diabetes mellitus and IUGR. In preeclampsia beta-methason could improve the rate of RDS and the neonatal outcome. Still our knowledge of antenatal glucocorticoid administration is not sufficient. But despite possible (longtime-) risks for mother and child the administration of glucocorticoids according to the guidelines of the NIH is a major part in the treatment of prematurity and improves the outcome of premature infants. The indication for multiple courses of glucocorticoids should be considered carefully.
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PMID:[Lung maturation therapy with glucocorticoids in threatened premature labor. Considerations of risk-benefit in evidence-based medicine]. 1119 48

The 1989 St Vincents Declaration stated, as a 5-year goal, ".that the outcome of the diabetic pregnancy should approach that of non-diabetic pregnancies" and indeed, over the last 20 years, significant reductions in spontaneous abortions, stillbirths, congenital malformations and perinatal mortality have been achieved. However, recent reports have shown that even in western countries, spontaneous abortions may be as high as 17%, stillbirths rate to be 5-times greater, congenital malformations to range from 4 to l0 times the usual rate, perinatal mortality to be 5-fold, neonatal mortality 15 times greater and that infant mortality might be trebled as the result of diabetic pregnancies. It can be argued that these bad results are the consequences of poor medical and social care, from prior to conception to perineonatal services and they most probably are. Nevertheless, even in the best series, corrected rates for diabetes-related malformations are considerably higher than the rest of the population and macrosomia poses a major problem, ranging from 20% in gestational diabetes to 35% or more in pre-existing diabetes. Again, it can be argued that good metabolic control has not been achieved or that good is not necessarily optimal. Alternatively, it can be put forward that there might be an abnormal genetic background contribution (and the evidence is pretty scanty) or that there might be other metabolic fuels besides glucose operating at different developmental stages of pregnancy and accounting for the aetiopathogenesis of the whole syndrome of the infant of the diabetic mother from congenital malformations to macrosomia, hypoglycaemia, RDS, polycythaemia, hyperbilirrubinaemia and so forth. Over the last 10 years there has been increasing evidence from animal and human studies to support the theory that in addition to sugars, other metabolic fuels, from ketones to deranged lipid peroxidation, may be responsible for the pathomechanisms of congenital malformations providing that they are present at certain (high) levels for a reasonable amount of time and especially at crucial developmental windows. Similarly, the same general principles of multifactorial influences at critical gestational ages have been postulated to explain the macrosomia, respiratory complications, the hypoglycaemia and the whole metabolic disturbances of the infant of the diabetic mother. It is quite possible that some, or all of these metabolic fuels may per se or in synergy, play a significant role and it is quite conceivable that besides the classical approach to strict glucose control, other dietary manipulations with supplementation or replacement of deficient substracts, free oxygen radical scavengers and antioxidants, might hold a promise for the near future. Whether the unfavourable intra-uterine diabetic millieu will also condition the later appearance of adult diseases from cardiovascular disorders to insulin resistant syndromes, remains to be confirmed, or conversely, disproved. For the moment, although priority should focus on pre-conceptional planning and strict metabolic control throughout pregnancy, special attention should nevertheless be paid to the various, but critical, developmental stages of the diabetic pregnancy.
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PMID:The infant of the diabetic mother: The critical developmental windows. 1175 15

Premature infants born with IUGR are at a several-fold increased risk for mortality and major neonatal morbidities, including RDS, BPD, ROP, and NEC. These severe complications of prematurity are intensified by the effect of suboptimal fetal growth. The possible pathophysiologic processes initiated in utero and continuing after birth have been discussed. Recently reported data suggest that IUGR is a risk factor in programming for the later development of cardiovascular diseases, hypertension, and diabetes mellitus in adult life. Experimental research related to the pathophysiology and etiology of these conditions may enable appropriate intervention directed at reducing the excess risk associated with the short- and long-term mortality and morbidity among premature SGA infants.
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PMID:Prematurity and intrauterine growth retardation--double jeopardy? 1532 32

The increased burden of type 2 diabetes (T2D) necessitates the need for effective and safe novel drugs to treat this epidemic disease and its complications. By compiling this RDS Special Issue, our aim was to provide a comprehensive and critical overview on recent, ongoing, and future developments in this field. In collaboration with distinguished and renowned experts, we analyzed and discussed the most important advances in the field of incretin-based therapies, their extraglycemic effects, cardiovascular actions, and specific properties of the central nervous system. Another important drug class currently in development, the SGLT-2 inhibitors, and the role of the kidney in T2D are topics also covered by this issue. In addition to drug developments, new physiological insights into the understanding of the organ pathophysiology in T2D are presented that may eventually lead to additional therapeutic targets for obesity, T2D, and chronic inflammation acting on the brain, cardiovascular system, and pancreatic islets. The outcome of this Special Issue is a comprehensive reference work including bundled knowledge and expert opinions on the various aspects of the disease and its possible therapy strategies available now and in the near future. However, despite the advances delivered by modern incretin-based therapies today, there are still many limitations associated with efficacy data, application routes, and safety issues, which prevent the decline in diabetes complication rates. We conclude that further drug development and clinical trials are required to overcome these limitations, and to counteract the movement towards higher incidence rates of T2D and its complications.
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PMID:The continuing need for drug development and clinical trials in type 2 diabetes and its complications: introduction to the RDS special issue. 2226 67

Newborns from diabetic mothers are more frequently born prematurely, large for the gestational age, with difficult respiratory adaptation and risk of RDS (respiratory distress syndrome) and, subsequently, exposed to a higher risk of perinatal distress, hypoxia, metabolic stress and hematologic alterations. Comparing the status at birth of 120 newborns from mothers with diabetes, with 120 controls from uncomplicated pregnancies, over a period of 4 years, in a specialized tertiary center, no significant differences in the immediate outcome of such newborns and similar incidence of hypoxia at birth were shown, as illustrated by the parameters of the acid-base balance (cord pH, BE and HCO3). However, there are significant differences in the route of delivery, with a predominance of C-section deliveries in the diabetic group (4 out of every 5 cases), which might be an important contribution to the relative good status of these newborns at birth. Although balanced at birth, the newborns from diabetic mothers need intensive monitoring and care in the subsequent hours after birth, for important risks such as hypoglycemic episodes.
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PMID:Assessment of acid-base balance at birth in newborns from diabetic mothers. 2587 Jul 3

Obstetric outcome in early onset and late onset GDM was compared in a prospective study conducted at the Department of Obstetrics & Gynecology in BIRDEM, Dhaka, Bangladesh. A total 120 pregnant women were recruited purposively for the study in which 60 were early onset GDM and 60 were late onset GDM during study period of January 2008 to December 2009. Patients were followed up in different periods of gestation, during delivery and early postpartum period & findings were compared between two groups. BMI & family history of diabetes were significantly higher in early GDM group (p<0.05). Evidence of increased glycaemia was observed in early GDM group & difference of glycaemic status was statistically significant (p<0.05). Insulin was needed in 85% of early onset GDM and 55% in late onset GDM. There was also significant difference (p<0.05). In this study, 23.3% of early onset GDM group developed pre-eclampsia while in late onset GDM it was 10% and was statistically significant (p<0.05). Regarding intrapartum & postpartum complications - perineal tear, PPH wound infection, puerperal sepsis were more in early onset than late onset GDM group with no significant difference. Regarding foetal outcome, 8.3% early GDM group delivered asphyxiated baby in comparison to 3.3% in late GDM group. Twenty percent (20%) of early onset GDM group had to admit their babies in neonatal unit while in late onset group it was 5%. There was significant difference between two groups (p<0.05). Neonatal hypoglycaemia was also statistically significantly (p<0.05) higher in early GDM group. Neonatal hyper-bilirubinaemia, RDS, perinatal death was more in early onset GDM subjects. Early onset GDM subjects are high risk subgroup & have significant deleterious effect on maternal and perinatal outcome than late GDM groups.
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PMID:Obstetric Outcome in Early and Late Onset Gestational Diabetes Mellitus. 2632 38


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