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Biomedical subjects

J L Kitzmiller

Publications and source records attributed to J L Kitzmiller.

At least 19 recordsLinked to original sources
PubMed1998

Assessment of costs and benefits of management of gestational diabetes mellitus.

The purpose of this pilot study was to perform a cost-identification analysis of care for gestational diabetes mellitus (GDM) by determining the direct costs of the diagnostic procedures and treatment used for the outpatient management of GDM (program input costs) and the direct costs of maternal hospitalization after diagnosis of GDM, delivery of the baby, and newborn care (outcome costs). Reimbursed average charges in the Northern California (NoCal) managed care market in 1996 were used to establish the direct costs, and the direct costs were then applied to the elements of care and pregnancy outcomes of three GDM management programs in NoCal, Southern California (SoCal), and New England (NewEng), using prospectively collected data. Reimbursed amounts for the detailed elements of GDM management (program input costs) are presented in the categories of diagnosis of GDM, diabetes treatment supplies, doctor's office visits, office visits to ancillary providers, and fetal surveillance. Program input costs per patient were $817 for diet-treated and $1,838 for insulin-treated women in NoCal, and were estimated to be $882 for diet-treated and $1,425 for insulin-treated women in NewEng. Program input costs for women requiring insulin treatment who were randomized to premeal or postprandial blood glucose testing (N Engl J Med 333:1237, 1995) in SoCal were estimated to be $3,596 per patient for the premeal group and $3,770 per patient for the postprandial group. Reimbursed amounts for health care expenditures related to pregnancy outcomes are detailed in the categories of hospital and physician charges for maternal antepartum hospitalization ($1,864 for 2 days), vaginal delivery with 50% use of epidural anesthesia ($4,050), cesarean section ($5,932), and neonatal intensive care ($9,130 for 4 days). Outcome costs per patient were $5,792 for diet-treated and $6,462 for insulin-treated women in NoCal. Outcome costs per patient were estimated to be $6,096 for diet-treated and $11,216 for insulin-treated women in NewEng, and $8,013 for the premeal blood glucose group and $7,495 for the postprandial blood glucose group in SoCal (both groups required insulin treatment). Incremental cost-effectiveness of postprandial monitoring in the SoCal controlled trial was $35 per patient in input costs per cesarean section averted and $25 per patient in input costs per neonatal intensive care unit day prevented. The benefit-to-cost ratio of the difference in input and outcome costs was 2.98 in favor of postprandial monitoring in the SoCal study. Cost analysis should be included in clinical trials of the management of GDM.

Cesarean Section↗
PubMed1996

Diabetic nephropathy and pregnancy.

Knowledge of the pathogenic mechanisms of diabetic nephropathy (by which hyperglycemia, hyperfiltration, and hypertension cause the gradual development of microproteinuria, mesangial expansion, and eventual glomerular closure) provides the basis for effective treatment. Intensified glycemic control and antihypertensive therapy that is safe for the fetus are crucial for success during pregnancy. Considered outcome measures include perinatal survival, size at birth, child development, and long-term maternal renal function.

Antihypertensive Agents↗
PubMed1994

Metabolic interactions of diabetes and pregnancy.

Many of the embryonic and fetal abnormalities that occur in pregnancies complicated by maternal diabetes are the result of development in a metabolically abnormal environment. Diabetic embryopathy (birth defects and spontaneous abortions) results from maternal metabolic abnormalities during the first 6-7 weeks of gestation. The embryopathy appears to be multifactorial in origin, and the resulting defects remain important causes of morbidity and mortality in diabetic pregnancies. Diabetic fetopathy (predominantly macrosomia and neonatal hypoglycemia) results from fetal overnutrition and hyperinsulinemia during the second and third trimesters. Fetopathy may cause significant morbidity not only in the perinatal period, but also in later life as overweight infants grow up to be overweight children and young adults. Careful regulation of maternal metabolism from the preconceptional period onward can reduce greatly or even eliminate the excess risks that have been incurred by infants of diabetic mothers in the past. Successful management of maternal diabetes requires knowledge of the alterations in intermediary metabolism that normally occur during pregnancy, as discussed in this chapter.

Congenital Abnormalities↗
PubMed1993

Experimental preeclampsia produced by chronic constriction of the lower aorta: validation with longitudinal blood pressure measurements in conscious rhesus monkeys.

OBJECTIVES: Our goals were (1) to determine whether hypertension, proteinuria, and glomerular endotheliosis can be produced by chronic reduction of lower aortic pressure in pregnant rhesus monkeys and (2) to study the time course of the development of hypertension by means of longitudinal arterial blood pressure measurements in conscious, unrestrained pregnant rhesus monkeys. STUDY DESIGN: Indwelling arterial catheters were placed at 103 +/- 4 days of gestation (term 160 days) for measurement of arterial pressure before and after reduction of lower aortic pressure. At 116 +/- 7 days lower aortic pressure was reduced by 24 +/- 11 mm Hg in 11 monkeys (experimental group) by a stricture on the aorta just below the renal arteries; six monkeys (controls) underwent a sham operation. Resting on the aorta just below the renal arteries; six monkeys (controls) underwent a sham operation. Resting pressures were measured three to five times per week by a tether-and-swivel system. RESULTS: Baseline arterial pressure averaged 81 +/- 6 mm Hg. In the experimental group four monkeys had adverse outcomes (one maternal death with severe hypertension, one abruptio placentae with stillbirth, and two spontaneous preterm deliveries with hypertension). There was one preterm delivery in the control group. Of the seven monkeys with aortic stricture who continued to term, four developed sustained hypertension (mean pressure 18 +/- 6 mm Hg above baseline), proteinuria, and moderate-to-severe glomerular endotheliosis. None of the controls had hypertension or proteinuria, but two had endotheliosis. CONCLUSION: These observations confirm that a syndrome resembling preeclampsia can be produced by a reduction of lower aortic pressure, and they demonstrate that the associated hypertension is not an artifact of anesthesia. This model may prove useful in studying the pathophysiologic mechanisms of preeclampsia.

Animals↗
PubMed1993

Increased depth of trophoblast invasion after chronic constriction of the lower aorta in rhesus monkeys.

OBJECTIVE: Our purpose was to investigate whether a reduction in uteroplacental perfusion pressure would produce changes in trophoblast-uterine interactions at the cellular level. STUDY DESIGN: Strictures were placed around the abdominal aortas of rhesus monkeys at 116 +/- 7 days of pregnancy to reduce uteroplacental perfusion pressure. Placental bed biopsy specimens were obtained at cesarean section, and cytotrophoblasts were identified by means of an anticytokeratin antibody. RESULTS: In monkeys without aortic strictures, interstitial trophoblast invasion was restricted to the outer half of the endometrium. Endovascular trophoblast invasion involved the entire endometrial portion of uterine vessels and extended through the subjacent half of their myometrial segments. In seven of nine monkeys with aortic strictures the depth of interstitial trophoblast invasion was substantially increased and extended throughout the entire decidua and at least a portion of the myometrium. In contrast, the pattern of endovascular trophoblast invasion was identical to that observed in the placental beds of control animals. CONCLUSION: These results suggest that uteroplacental perfusion pressure or oxygen content may be important physiologic factors controlling the depth of interstitial cytotrophoblast invasion.

Animals↗
PubMed1993

Cost-benefit analysis of preconception care for women with established diabetes mellitus.

OBJECTIVE: To determine whether the additional costs of preconception care are balanced by the savings from averted complications. Several studies have demonstrated the efficacy of preconception care in reducing congenital anomalies in infants born of mothers with pre-existing diabetes mellitus. RESEARCH DESIGN AND METHODS: This study used literature review, consensus development among an expert panel of physicians, and surveys of medical care personnel to obtain information about the costs and consequences of preconception plus prenatal care compared with prenatal care only for women with established diabetes. Preconception care involves close interaction between the patient and an interdisciplinary health-care team as well as intensified evaluation, follow-up, testing, and monitoring. The outcome measures assessed in this study are the medical costs of preconception care versus prenatal care only and the benefit-cost ratio. RESULTS: The costs of preconception plus prenatal care are $17,519/delivery, whereas the costs of prenatal care only are $13,843/delivery. Taking into account maternal and neonatal adverse outcomes, the net savings of preconception care are $1720/enrollee over prenatal care only and the benefit-cost ratio is 1.86. The preconception care program remained cost saving across a wide range of assumptions regarding incidence of adverse outcomes and program cost components. CONCLUSIONS: Despite significantly higher per delivery costs for participants in a hypothetical preconception care program, intensive medical care before conception resulted in cost savings compared with prenatal care only. Third-party payers can expect to realize cost savings by reimbursing preconception care in this high-risk population.

Blood Glucose↗
PubMed1993

Maternal and perinatal implications of diabetic nephropathy.

Nephropathy is a serious and challenging complication of diabetes with regard to maternal health, fetal well-being, and outcome of infants. This article describes the available information and the controversies regarding clinical course, pregnancy complications, and treatment.

Congenital Abnormalities↗
PubMed1993

Early-pregnancy proteinuria in diabetes related to preeclampsia.

OBJECTIVE: To test the hypothesis that the risk of preeclampsia in diabetic mothers is increased with incipient diabetic nephropathy as well as with overt nephropathy. METHODS: Pregnancy outcome was studied in 311 women with class B-RF diabetes from two institutions. Using 104 women without chronic hypertension followed at the University of California, San Francisco, we constructed a receiver-operating characteristic curve relating 24-hour urinary total protein before 20 weeks' gestation to the subsequent development of preeclampsia. From the curve, a predictive cutoff level of proteinuria was selected and tested in two validation groups not used to construct the curve: 158 women without chronic hypertension followed at the University of Cincinnati and 49 women with chronic hypertension from both institutions. RESULTS: The receiver-operating characteristic curve showed an increased risk of preeclampsia with early-pregnancy proteinuria of 190 mg/day or more. In the Cincinnati validation group, the rate of preeclampsia was 7% in women with early-pregnancy proteinuria of less than 190 mg/day, 31% with proteinuria of 190-499 mg/day, and 38% with proteinuria of 500 mg/day or more. In the chronic-hypertension validation group, the rates were 0, 50, and 58%, respectively. By multiple logistic regression, the increased risk of preeclampsia with proteinuria above 190 mg/day persisted after controlling for the effects of parity, chronic hypertension, retinopathy, and glycemic control. CONCLUSIONS: Diabetic gravidas with early-pregnancy proteinuria of 190-499 mg/day are at increased risk for preeclampsia. The risk is comparable to that in women with overt diabetic nephropathy and is independent of chronic hypertension. We speculate that diabetic women with proteinuria in this range have incipient or subclinical diabetic nephropathy.

Adult↗
PubMed1992

Randomized trial of human versus animal species insulin in diabetic pregnant women: improved glycemic control, not fewer antibodies to insulin, influences birth weight.

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.

Adult↗
PubMed1992

Financial implications of implementing standards of care for diabetes and pregnancy.

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.

Female↗
PubMed1992

Relationship of fetal macrosomia to maternal postprandial glucose control during pregnancy.

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.

Adult↗