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Possible relations between neonatal circulatory function and maternal diabetic control were investigated in 22 infants of strictly controlled diabetic mothers during the first 2 days after birth. Eleven infants were delivered vaginally (V) and 11 infants by elective cesarean section (S). Maternal diabetes was more severe in the latter group. Half of the infants had one or more episodes of neonatal morbidity although none presented symptomatic hypoglycemia. Plasma glucose FFA and C-peptide were measured at birth and 3-6 hours later together with skinfold thickness; heart size was determined by X-ray at 24-28 hours; stroke volume and cardiac output were repeatedly determined by transthoracic impedance and ECG. C-peptide at birth was higher in group S than in V. C-peptide in both groups were neither related to glucose or FFA nor to birthweight or skinfold thickness. Infants with neonatal complications including cardiomegaly had the highest C-peptide values. Skinfold was positively correlated to maternal pregnancy glucose level, birthweight percentile and infant heart volume. Mean values for stroke volume and cardiac output were similar in both groups and not different from normal controls when related to body weight. Heart volume and stroke volume were significantly related. ECG abnormalities were seen in 6 infants who showed cardiomegaly on X-ray. We suggest that the present finding of an association between elevated C-peptide concentration at birth and the occurrence of neonatal complications including cardiomegaly and ECG abnormalities could be the consequence of functional hyperinsulinism and that the cardiomegaly is of adaptive type.
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PMID:Circulatory adaptation in newborn infants of strictly controlled diabetic mothers. 713 29

We studied the prevalence of mitochondrial gene mutations in subjects with insulin-dependent diabetes mellitus (IDDM) in a Chinese population living in Taiwan. Eighty-four subjects with insulin-dependent diabetes mellitus and 105 unrelated normal controls were recruited in the present study. Both an A-to-G mutation at position 3243 and a mutation at position 8,344 of the mitochondrial DNA were screened by polymerase chain reaction-restriction fragment length polymorphism methods and confirmed by direct DNA sequence analysis. The insulin secretory response was assessed by the C-peptide response to glucagon administration. Among 84 IDDM patients, two (2.4%) subjects were found to carry the 3,243 nucleotide pair (np) mutation. There was no np 8,344 mutation in this series. Of the two subjects carrying a mitochondrial gene mutation, case 1 manifested initially as gestational diabetes mellitus. Manifestation of case 2 was consistent with MELAS, a syndrome of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes. The pancreatic beta cell reserve was reduced, as the glucagon-stimulated C-peptide response was very low in these two cases. HLA genotyping studies revealed that case 2 carried DRB1*0301-DQA1*0501-DQB*0201/ DRB1*0405-DQA1*0301-DQB1*0302, which was the most susceptible genotype to IDDM in our population. Anti-GAD65 antibody was also positive in this patient. In addition to the nuclear genes, a defective mitochondrial gene might contribute to some of the clinical cases with IDDM.
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PMID:Mitochondrial gene mutations in patients with insulin-dependent diabetes mellitus in Taiwan. 883 Mar 30

Five thousand five hundred seventy-two newly diagnosed non-insulin-dependent diabetes mellitus (NIDDM) patients (3,225 men and 2,347 women; mean age, 58.5 years) were recruited through the General Practitioners (GPs) network in France. All had persistent hyperglycemia after a preliminary 3-month period with dietary and life-style modification. Gliclazide (80 to 320 mg/d) was then prescribed as diabetic pharmacotherapy for 2 years. Additional therapy for hypertension and dyslipidemia was started if necessary. The aim of the study was mainly to determine the feasibility of a GP-directed protocol for the monitoring and treatment of newly diagnosed NIDDM patients, and to assess the effectiveness of diabetic therapy in this cohort. Diabetes was diagnosed in 78% of the cohort during routine screening. Among the women, 6.5% had a history of gestational diabetes. Eighteen percent of the patients had a parental history of diabetes, and the dominant maternal role in the genesis of NIDDM was confirmed. High blood pressure (Joint National Committee V criteria) was found at inclusion in 38.8% of the whole cohort. Hyperlipidemia was known in 44.6%. A history of stroke was present in 1.6% of the patients, and coronary heart disease (CHD) in 6.3%. These data support the relationship between the atherogenic state and development of NIDDM. Microalbuminuria defined as urinary albumin excretion (UAE) of at least 20 mg/L was found in 29.6% of the patients, and retinopathy in 9.8%. Among the included patients, 23% did not complete the study and were excluded from the efficacy analysis. Of these, 14% (808 patients) had only baseline evaluation data and 9% (499 patients) withdrew later. Comparison of mean baseline and final results in study completers uncovered a significant improvement in fasting blood glucose ([FBG] 182 +/- 48 v 137 +/- 40 mg/dL), post prandial blood glucose ([PPBG] 209 +/- 68 v 162 +/- 52 mg/dL), and hemoglobin A1c ([HbA1c] 8.7% +/- 2.5% v 7.3% +/- 2.0%). A slight improvement in total cholesterol (228 +/- 44 v 222 +/- 41 mg/dL), body mass index ([BMI] 28.5 +/- 4.7 v 27.9 +/- 4.5 kg/m2), and waist to hip ratio (0.99 +/- 0.1 v 0.98 +/- 0.1) was observed. There was a decrease in the percentage of patients with high blood pressure (38.5% v 30.7%). A mild increase in the prevalence of retinopathy (10.2% v 11.8%) was noted during the study, while the incidence of microalbuminuria remained unchanged (30.2% v 29.5%). In conclusion, the data indicate that the GPs involved in this study were able to successfully monitor and manage NIDDM patients in accordance with a standardized protocol. Gliclazide appeared to be an effective and well-tolerated treatment. The high prevalence of chronic diabetic complications at diagnosis emphasizes the delay encountered in reaching the diagnosis of NIDDM and the problems associated with this delay. In addition to the classic risk factors for NIDDM exhibited in this patient cohort, we have identified CHD and a maternal genetic component as further potential predicting factors.
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PMID:Management of newly diagnosed non-insulin-dependent diabetes mellitus in the primary care setting: effects of 2 years of gliclazide treatment--the Diadem Study. 943 56

Insulin resistance appears to be a causative mechanism for the development of essential hypertension. Insulin resistance syndrome consists of a cluster of abnormalities that aggravate preexisting tendencies to develop hypertension, resulting in a cascade of physiologic alterations and ultimately leading to increased rates of heart attack, stroke, and peripheral vascular disease. Like hypertension, NIDD is mediated by insulin resistance and is expressed in individuals with limited beta-cell reserve. Episodes of increased insulin resistance, such as aging, weight gain, and pregnancy, cannot be compensated for in these states, and glucose intolerance results. In the case of pregnancy, the temporary state of insulin resistance unmasks individuals with an early beta-cell defect and allows for identification of high-risk groups at a time when therapeutic interventions could result in primary prevention of disease. Evidence is beginning to accumulate that preeclampsia is at least partially mediated by insulin resistance as well, and that individuals with preeclampsia may have clinically silent but persistent alterations in insulin resistance. If this condition proves a corollary to gestational diabetes, there may be an opportunity to intervene for primary prevention of some forms of essential hypertension as well. The availability of new pharmacologic agents to enhance insulin sensitivity represents a true opportunity effectively to prevent the long-term complications associated with insulin resistance and hyperinsulinemia. To achieve this goal, early and accurate identification of populations at risk is essential. A complete understanding of the role of insulin resistance in the generation of preeclampsia will aid significantly in the discovery of the genetic polymorphisms and intracellular pathways by which insulin resistance is translated into cardiovascular disease, stroke, and nephropathy.
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PMID:Insulin resistance and preeclampsia. 989 20

Mitochondrial DNA (mtDNA) defects are associated with a number of human disorders. Although many occur sporadically, maternal transmission is the hallmark of diseases due to mtDNA point mutations. The same mutation may manifest strikingly different phenotypes; for example, the A to G substitution at np 3243 was first reported in patients with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (the MELAS syndrome), but is also found in patients with diabetes and deafness. Here we present a case of gestational diabetes, deafness, premature greying, placenta accreta and Wolff-Parkinson-White (WPW) syndrome associated with a mtDNA mutation. Although this is the first report of such an association, study of 27 other patients with WPW syndrome failed to confirm that this mtDNA mutation is a common cause of such pre-excitation disorders.
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PMID:Identification of mtDNA mutation in a pedigree with gestational diabetes, deafness, Wolff-Parkinson-White syndrome and placenta accreta. 1109 78

Many studies show that low-dose OCs have little adverse effect on carbohydrate metabolism and are safe for healthy women, women with a history of gestational diabetes, and women with insulin-dependent diabetes to use. In fact, large epidemiologic studies indicate that OCs, even the high-dose OCs (=or 50 mcg) for long periods, do not increase the risk of diabetes. There is some evidence indicating that OC use does not heighten the progression of diabetic retinopathy, nephropathy, or cardiovascular complications among women with insulin-dependent diabetes. There is no significant difference in carbohydrate metabolism among the different OC formulations. One must carefully consider the risk:benefit ratio of OC use in diabetic women since pregnancy has serious consequences for both mother and fetus. Cardiovascular complications in OC users do not originate from atherogenesis. The androgenic properties of the progestin in low-dose OCs and their effect on lipids are inconsequential for later development of coronary atherogenesis. The estrogen in OCs may protect against atherosclerosis, particularly among women at high risk of atherosclerosis. Former OC users are not at an increased risk of coronary heart disease, stroke, or other heart disease. Lipid changes in OC users tend to remain within the normal range and return to pretreatment values during the pill-free week. All OCs suppress gonadotropins and subsequent ovarian androgen production. They partially suppress androgen production by the adrenals as well. This suppression from two fronts outweighs any androgenic action of the progestin alone. Further, androgenic action probably cannot overpower the estrogen effect. The dose of levonorgestrel used in OCs is too low to express androgenic effects. Since OCs suppress androgen production, all OCs tend to improve acne. OCs reduce free testosterone and increase sex hormone binding globulin levels.
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PMID:Metabolic effects of oral contraceptives: fact vs. fiction. 1232 11

This review summarizes the published information on diabetes mellitus and gestational diabetes among Alaska Natives. The most recently published age-adjusted prevalence was 28.3/1000 in 1998. There is evidence of a steadily increasing prevalence, documented both by cross sectional screening studies and patient registry methods. The overall incidence rates in 1986-1998 of lower extremity amputation (6.1/1000) and renal replacement therapy (2.1/1000) appear to be lower than those in other Native American populations in the United States. Incidence of stroke and MI in 1986-1998 varied widely by ethnic group and gender with Eskimo women having the highest rate of stroke (19.6/1000), and Aleut men the highest rate of MI (14/1000). The overall mortality among diabetic Alaska Native people in 1986-1993 (43.2/1000) was somewhat lower than that in other US diabetic populations, with heart disease being the most common cause of death. A high rate of gestational diabetes (6.7%) was reported in one region in 1987-88, but this appeared to decline following nutritional education intervention. In screening studies, the prevalence of abnormal glucose tolerance has been found to be positively associated with body mass index and negatively associated with daily seal oil or salmon consumption and higher levels of physical activity. Observations on the prevalence and relationships among other factors in the insulin resistance syndrome are summarized. Suggestions for prevention of diabetes and further studies are presented.
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PMID:Diabetes among Alaska Natives: a review. 1496 64

Pregnancy in acromegaly is a rather rare event since the fertility is reduced in acromegalic women. Besides, metabolic complications of acromegaly are harmful to both mother and fetus. Little is known about the outcome of pregnancy in acromegalic women. Here, we report seven cases of pregnancy out of 48 acromegalic women followed for 16 years. At diagnosis, five patients had macroadenoma, one patient had microadenoma and the size of the tumor was not documented in one patient. In one patient, acromegaly was initially diagnosed during pregnancy at 29 weeks. When she was 33 weeks, she developed pituitary apoplexy and had an emergency transsphenoidal resection of her macroadenoma during which she also had a cesarian section and delivered a healthy baby girl. In the remaining six patients, pregnancy occurred 6 to 64.5 months after the adenoma resection. Three patients received radiotherapy before getting pregnant. In three patients, pregnancy occurred during bromocriptine treatment and the drug was withdrawn. In one patient, pregnancy occurred during chronic octreotide treatment and therapeutic abortion was performed. In another patient, therapeutic abortion was performed because of uncontrolled disease. In the remaining four patients, there were neither worsening of symptoms nor tumor growth. All four patients gave birth to full-term healthy infants. Out of our seven patients, two developed gestational diabetes mellitus which was controlled with diet. None of the patients had coronary artery disease, hypertension or dyslipidemia. These cases show that pregnancy might be uneventful in acromegalic women when the disease is controlled with prior surgery and radiotherapy.
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PMID:Follow-up of pregnancy in acromegalic women: different presentations and outcomes. 1663 80

The complexity of the several pathogenic pathways that cause hypertension and vascular disease and the prolonged interval that appears to predate clinical morbidity have hindered inquiry into the association between GDM and vascular disorders. As a forme fruste of later type 2 diabetes, GDM-affected gravidas are identified as at risk of diabetes-related atherosclerosis, glomerular disruption, and pathogenic retinal angio-genesis. That GDM is evidence for underlying chronic conditions such as dysregulation of innate immune response that, independent of the diabetic state, produces vascular disease is difficult state, produces vascular disease is difficult to assert with the present published literature. Cross-sectional studies of patients with established gestational hypertension or preeclampsia are ambiguous as to the possible pathogenic effect of insulin resistance. Cohort studies initiated in early and mid-pregnancy show evidence that both gestational hypertension and preeclampsia may be more prevalent in gravidas with greater insulin resistance. The association of gestational glucose intolerance with gestational hypertension appears to be independent of obesity and ambient glycemia but explained in part by insulin resistance. Late pregnancy preeclampsia is associated with elevated mid-pregnancy BMI, blood pressure, fasting glucose and insulin, urate, and C-reactive protein, suggestive of metabolic and immune dysregulation. GDM appears to be associated with overexpressed innate immune response, which, in turn, is associated with vascular dysfunction and vascular disease. Among women with GDM, markers of insulin resistance do not appear to correlate with hypertension in short-term cohort studies. However, when non-GDM subjects are compared with subjects with GDM, postpregnancy studies do show an associated with vascular dysfunction and vascular disease. Among women with GDM, markers of insulin resistance do not appear to correlate with hypertension in short-term cohort studies. However, when non-GDM subjects are compared with subjects with GDM, postpregnancy studies do show an association of insulin resistance with both inflammatory dysregulation and vascular dysfunction. Cohort studies that have used population-based pregnancy databases consistently identify a clinically significant association of both gestational hypertension and preeclampsia with later hypertensive disorders. Associations with coronary artery disease or stroke are less consistent, requiring further investigation. Preventing the evolution of diabetes and lipid and immune dysregulation of the metabolic syndrome has become a silent public health issue because of the epidemic of childhood and early adulthood obesity and the opportunity at hand to treat insulin resistance by behavioral and pharmacological interventions. However, limited available literature highlights the need for long-term cohort studies of women with well-characterized metabolic and vascular profiles during pregnancy and decades later. Our present knowledge suggests that screening for GDM provides an opportunity of pregnancy outcome improvement. Limited studies of diabetes prevention in at-risk patient groups suggest that we may have the opportunity to reduce the risk of later diabetes. Additional investigation is required to determine if interventions that prevent or postpone diabetes also delay the onset of vascular disease.
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PMID:Gestational diabetes, pregnancy hypertension, and late vascular disease. 1759 80

Successful pregnancy is one of the better indicators of quality of life for women who are of child-bearing age with restored fertility after kidney transplantation. Our objective was to evaluate whether pregnancy represented a risk factor for worsening of renal function or for cardiovascular disease among renal transplant recipients. From 1976 to 2007, we followed 30 successful pregnancies in 27 renal recipients in our hospital; three women had two twin gestations. We compared this population with 27 women with renal transplants who were not pregnant. They were of similar ages at transplantation (pregnant 31.1 +/- 5.4 years vs not pregnant 31.3 +/- 5.4 years, P = NS) and similar evolution time between kidney transplantation and pregnancy (51.5 +/- 36 months vs 47.2 +/- 41 months respective; P = NS). There were no acute rejection episodes or graft losses. Renal function measured by serum creatinine and MDRD4 at the end of pregnancy was lower among the pregnant compared with the control group: mainly, 1.1 +/- 0.2 mg/dL versus 0.9 +/- 0.2 mg/dL (P = .05), and 66 +/- 20 mL/min/1.73 m(2) versus 80 +/- 26 mL/min/1.73 m(2) (P = .03). At 1 and 10 years, renal function was similar among the groups. Ten pregnant women developed preeclampsia (37%) and three, gestational diabetes mellitus (11%). There was one major cardiovascular event (4%; acute myocardial infarction) among the pregnant group, whereas there were two in the control group (7.4%; stroke and severe hypertensive retinopathy). One death occurred in each group secondary to cardiovascular complications. Our results showed that successful pregnancy after renal transplantation did not represent a long-term risk factor to worsen renal function and or produce severe cardiovascular complications. Therefore, pregnancy should be promoted. for young women with renal transplants that show excellent function.
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PMID:Renal allograft function and cardiovascular risk in recipients of kidney transplantation after successful pregnancy. 1971 32


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