Pre-pregnancy clinics for diabetic women.
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Biomedical subjects
Publications and source records attributed to J L Kitzmiller.
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OBJECTIVE: Macrosomia occurs in infants of diabetic mothers in spite of "nearly normal maternal blood glucose levels" with insulin treatment. Insulin antibodies may carry bound insulin into the fetal blood and thus may be associated with fetal hyperinsulinemia and macrosomia in these infants. Our objective was to test the hypothesis that human insulin is associated with lower insulin antibody levels and less macrosomia than is animal species insulin. STUDY DESIGN: Forty-three insulin-requiring pregnant (< 20 weeks' gestation) women, previously treated with animal insulin, were randomized to human and animal insulins and studied at weeks 10 through 20, 24, 28, 32, 36, and 38, at delivery, and at 3 months post partum. Infant blood was drawn at delivery (cord) and at 1 day and 3 months post partum 1 hour after a glucose-amino acid challenge. RESULTS: Women receiving human insulin required significantly less insulin per kilogram of body weight and showed significant dampening of glucose excursions (p < 0.05 for each comparison). Infants born to mothers receiving human insulin weighed 2880 +/- 877 gm compared with 3340 +/- 598 gm for infants of women treated with animal insulin (p < 0.05). There was no difference in insulin antibody levels between groups for either mothers or infants. Infants born to mothers receiving human insulin had a 1 hour C-peptide level after the glucose-amino acid challenge at 3 months of age of 0.21 +/- 0.13 pmol/ml compared with 0.32 +/- 0.13 pmol/ml (p = 0.01). CONCLUSION: Administration of human insulin to pregnant diabetic women has a therapeutic advantage over animal insulin, with less maternal hyperglycemia or hypoglycemia, fewer larger-for-gestational-age infants, and less neonatal hyperinsulinemia. Our data do not support the hypothesis that maternal antibodies to insulin influence infant birth weight.
This article examines the financial implications of implementing standards of care for pregnancy among women with diabetes, including both the costs of enhanced treatment and the savings of avoided adverse outcomes. Numerous studies have demonstrated the harmful effects of poor blood glucose control for both mother and fetus. Standards set forth by the American Diabetes Association aim to reduce maternal complications and fetal adverse outcomes, such as congenital malformations. Because the precise configuration of resources required to meet these standards was not outlined in the American Diabetes Association statement, a panel of physicians (all specialists in pregnancy care for women with diabetes) was convened to develop a model program. Implementing such a program during the preconception and prenatal periods will represent an intensification of resource use in the outpatient setting. However, through these preventive measures, medical care costs for maternal and fetal complications can be avoided.
OBJECTIVE: To determine the gestational ages at which maternal hyperglycemia is most closely related to fetal macrosomia; to determine whether macrosomia is related to elevations of fasting glucose, postprandial glucose, or both; and to assess the relationship of macrosomia to maternal insulin dose and caloric intake. RESEARCH DESIGN AND METHODS: One hundred eleven consecutive pregnant women with Class B through RF diabetes were studied longitudinally from 13 to 36 wk gestation. Macrosomia was defined by birthweight greater than 90th percentile for gestational age based on California norms. Women who delivered macrosomic infants were compared with those without macrosomic infants on pre- and postprandial blood glucose, GHb, insulin dose, macronutrient intake, and several other maternal variables. RESULTS: Macrosomia occurred in 32 (29%) cases, although several measures indicated reasonable glycemic control throughout pregnancy. Women delivering macrosomic infants did not differ from those without macrosomic infants in maternal age, prepregnant weight, duration of diabetes, White class, macronutrient intake, GHb, or fasting glucose. Macrosomia was associated with higher postprandial glucose levels up to 32 wk gestation and lower insulin doses from 29 to 36 wk gestation. In multiple logistic regression, macrosomia was significantly associated with postprandial glucose only between 29 and 32 wk gestation. Postprandial glucose values less than 7.3 mM (less than 130 mg/dl) were associated with a higher risk of small-for-gestational-age infants (18%) compared with values above this level (1%). CONCLUSIONS: Because macrosomia was related to postprandial glucose but not fasting glucose, we conclude that postprandial glucose measurement should be a part of routine care for diabetes in pregnancy. A target 1-h postprandial glucose value of 7.3 mM (130 mg/dl) may be the level that optimally reduces the incidence of macrosomia without increasing the incidence of small-for-gestational-age infants.
BACKGROUND: Recombinant human erythropoietin has been approved for treatment of the anemia of renal failure since 1989, yet data regarding the safety and efficacy of this drug in pregnancy are limited. We used recombinant human erythropoietin to treat the anemia of renal disease in three pregnant women. CASES: Nadir hematocrit values before initiation of erythropoietin were 19-23%. Erythropoietin, 50-160 U/kg/week subcutaneously, was begun at 14-26 weeks' gestation. Initially, the rise in hematocrit averaged 0.6-2% each week, with peak values of 26.7-32%. Iron supplementation was given simultaneously. Maternal and neonatal outcomes were favorable despite the development of preeclampsia or worsening renal function requiring early delivery. CONCLUSION: In this small series, erythropoietin begun during the second trimester in a dose of about 100 U/kg/week, in conjunction with orally administered iron, appeared to be effective in treating the anemia of renal failure during pregnancy. Additional experience is needed to evaluate the safety of this medication during pregnancy.
C peptide is secreted by pancreatic beta cells in amounts equimolar with insulin, and its levels provide a direct indication of endogenous fetal levels of insulin despite the presence of maternal insulin antibodies. To determine the presence of hyperinsulinemia and its relation to the development of complications in infants of diabetic mothers, we measured cord serum levels of C peptide in 79 infants of diabetic mothers and 62 infants of nondiabetic mothers. Infants of diabetic mothers had higher cord levels of C peptide, which were significantly associated with neonatal hypoglycemia and macrosomia (P less than 0.001) but not with hyaline-membrane disease. Cord levels of C peptide in infants of diabetic mothers were elevated at the earliest gestational age studied (less than 34 weeks) and were directly related to the severity of maternal diabetes, as assessed by the White classification. We conclude that hyperinsulinemia is present in infants of diabetic mothers and that it is related to some major complications in such infants.
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Propranolol is a beta-adrenergic blocking drug with a wide spectrum of use and may diverse pharmacologic effects. This case report is an example of a parturient who was on a large dose of propranolol for idiopathic hypertrophic subaortic stenosis. The effects of this drug on pregnancy, labor, and above all, the fetus are discussed.
In this study, an attempt was made to elucidate further the role of intravascular fibrin formation in the pathogenesis of sepsis in the primate. It was found that injected live Escherichia coli caused death in primates within four to 11 hours as a result of microcirculatory failure and acidosis. Pretreatment with Arvin did not prolong the survival rate, probably because of an overloading of the reticuloendothelial system with fibrin degradation products. This study does not support an obligatory role for intravascular coagulation or fibrin formation in primate sepsis and coincides with an earlier report (6) from this laboratory on cats. Vascular damage and malfunction, secondary to mediators released by platelets, leukocytes, red cells or Hageman factor, are not ruled out.
We report here six pregnancies in 5 women with juvenile diabetes and Graves disease. The diabetes was managed in a standard fashion. The Graves disease was managed with propylthiouracil when required. The course of neither the diabetes nor Graves disease was different than expected. When established guidelines for therapy are followed the two have no interaction with one another. One infant was mildly hypothyroid. None developed neonatal Graves disease. Four of the infants had hyperbilirubinemia.
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We investigated an immunologic mechanism that might explain the apparent "tolerant" state of the mother during pregnancy. Cellular-immune reactivity in vitro to paternal alloantigens was demonstrated in multigravid women by production of lymphocyte migration inhibitory factor. Serum from normal multigravid women contained a factor that blocked production of migration inhibitory factor by maternal lymphocytes to paternal antigens in a specific manner. The blocking factor was an IgG antibody whose activity was removed by absorption with paternal lymphocytes but not with pooled human platelets. We tested the biologic importance of this blocking factor in women who have difficulty maintaining a normal term pregnancy. Our observations indicate that women who experience idiopathic spontaneous abortions produce lymphocyte migration inhibitory factor to paternal alloantigens, but their serums lack the blocking factor. The presence of the serum blocking factor during pregnancy may contribute to the success of the fetus as an allograft.