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Query: UMLS:C0011849 (diabetes)
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The recurrence rate of gestational diabetes in 58 patients who had had the foregoing pregnancy complicated by diabetes was estimated to be 30% if our former criteria for abnormal glucose tolerance were strictly applied and 25% if our new, more stringent criteria were used. The recurrence rate is not influenced by prophylactic administration of pyridoxine. The perinatal morbidity complicating the 'second' pregnancy of former gestational diabetics was not increased in those patients who were not treated again, as compared with those who were. Recurrent gestational diabetes is associated with a degree of overdiagnosis in an attempt to detect all gestational diabetics. It is suggested that recurrent gestational diabetes occurs mainly in prediabetic patients.
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PMID:Recurrence of gestational diabetes. 26 62

One hundred and ninety-six pregnancies complicated by gestational diabetes in a referred private practice over an 18-year period have been reviewed. Initially they were managed as true diabetics and the pregnancies terminated before the 38th week. More recently, pregnancies have been managed on an outpatient basis and allowed to proceed to term, with a higher percentage of vaginal deliveries and no increase in perinatal mortality or morbidity. A high incidence of neonatal jaundice was noted, but no explanation emerged. Differences between true diabetes and gestational diabetes, with particular reference to perinatal mortality are discussed and the good prognosis for the gestational form emphasised. Follow-up suggests that a continuation of the rapport established between physician, obstetrician and patient during pregnancy may be important in delaying or preventing the subsequent onset of diabetes.
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PMID:A review of the significance of gestational diabetes. 27 83

Intrvenous injection of 30 mg of streptozotocin per kg body weight induces a mild diabetes in pregnant rats (first generation); the non-fasting blood glucose is increased and the percentage of endocrine tissue and also the percentage of granulated beta cells do not increase. The fetuses of these mildly diabetic pregnant rats have an increased percentage of pancreatic endocrine tissue and there is beta-cell degranulation. The modifications in the endocrine pancreas during intrauterine life causes persistent changes in later adult life (second generation), which are not perceptible in basal conditions, but become apparent in situations stressing the beta-cell activity, such as an intravenous glucose load or pregnancy. During pregnancy in the second generation rats an increased non-fasting blood glucose and no adaptation of the beta cells is seen. This inadequate adaptation to pregnancy causes changes in the fetal endocrine pancreas of the fetuses of the third generation. From these experiments it may be concluded that gestational diabetes is an acquired condition.
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PMID:Is gestational diabetes an acquired condition? 39 56

Fasting plasma glucose determination is the test of choice for diagnosis of diabetes. Glucose tolerance testing should be reserved for patients with borderline fasting values or possible diabetic complications and those suspected of having gestational diabetes. Strict attention to patient variables is essential if glucose tolerance testing is to be of value. The diagnosis of diabetes should be reserved for those patients with symptoms and unequivocal hyperglycemia, those with fasting plasma glucose values of 140 mg/dl or more repeatedly, and those with glucose tolerance test values of 200 mg/dl or more at two hours and at least one other time.
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PMID:Diabetes mellitus: test strategies for diagnosis and management. 49 89

To characterize the defect of insulin secretion in diabetes, the response to different iv glucose loads has been studied in women who have had gestational diabetes and are, by definition, latent diabetic (LD). Women who have produced a large-for-dates baby, but who were not known to have been diabetic (LFD), have been investigated to determine if they have abnormal metabolism. Both groups were found to have raised fasting plasma glucose concentrations. Only the LD had glucose intolerance, which was associated with a reduced first phase insulin response to all glucose loads with a decreased maximal secretory capacity (low V max). The LFD women appeared to include a distinct abnormality in which the beta cells had decreased sensitivity to glucose (high Km), with diminished secretory response to small but normal response to large loads. Whereas the LD probably have disordered beta cell function, some of the LFD women may represent the upper end of the normal range of the glucose "set" of beta cell function. Neither group had insulin resistance, as measured by the hypoglycaemic response to an iv insulin bolus. A woman who has produced a LFD, but who was not known to be diabetic, does not necessarily have a diabetic tendency.
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PMID:Two abnormalities of glucose-induced insulin secretion: dose-response characteristics and insulin sensitivity. 49 84

The indications for and results of all glucose tolerance tests (GTTs) performed at the Antenatal Clinic, Groote Schuur Hospital, Cape Town, over a period of 1 year, and the indications for a GTT in the first 80 newly diagnosed diabetics over a 4-year period are analysed. Out of 558 GTTs, only 17 tentative diagnoses of 'gestational diabetes' were made. The most rewarding single indication for a GTT was repeated glycosuria, which was an indication in 61 out of the 80 newly diagnosed diabetics. A combination of two indications in the same patient was related to twice as many abnormal GTTs as a single indication, while reported previous diabetes or hyperglycaemia certainly merited confirmation. Reasons for repeating GTTs are discussed, as well as the management of 'borderline' and 'potential' diabetics. It is emphasized that 'diabetes' or 'hyperglycaemia' diagnosed during pregnancy is not equivalent to a definite diagnosis of diabetes in the non-pregnant state.
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PMID:Gycosuria as an indication for glucose tolerance testing during pregnancy. 51 73

The obstetric performance and pregnancy outcome in 208 massively obese patients who were delivered over an eight-year period were compared with those of nonobese control subjects. The incidence of obesity in their infants was also compared. No significant increase in the incidence of urinary tract infection, diabetes, breech presentation, cesarean section, forceps delivery, or maternal and infant morbidity was noted in the obese women. Significantly increased incidences of hypertensive disorders of pregnancy (p less than 0.01), gestational diabetes (p less than 0.01), inadequate weight gain (p less than 0.001), and wound or episiotomy infection (p less than 0.05) were observed in the study group. The mean birth weight of the infants of obese women was 209 grams greater than that of the control subjects. A significantly increased number of the obese patients were delivered of excessive-sized infants. Despite this, the incidence of obesity in infants of obese women was not significantly increased at birth or six months of age. By 12 months of age, however, these infants were significantly more obese than the control infants.
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PMID:Pregnancy in the massively obese: course, outcome, and obesity prognosis of the infant. 67 88

Based on the glucose infusion test, we find with 17.9 per cent of a group of anamnestically tainted pregnant women gestational diabetes, and with 5.7 per cent of this group a carbohydrate tolerance with disturbed boundaries. With probands having a carbohydrate tolerance with disturbed boundaries we find a significantly more frequent IRI-high-response. This coincidence of a carbohydrate tolerance in the border range and of an IRI-high-response might correspond to the early asymptomatic stage of diabetes. In the following stages, there will take place a depression of the early insulin phase with a pathological carbohydrate tolerance of the pregnant women in the sense of a gestational diabetes. With probands exhibiting a disturbed carbohydrate tolerance, a diminished depression of free fatty acids is found. The total lipid content and cholesterol are not essentially changed. With women suffering from gestational diabetes urinary sugar excretion is significantly higher than with probands showing a normal carbohydrate tolerance.
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PMID:[Incidence of gestational diabetes as well as changes in insulin secretion during pregnancy. 1. Studies on pregnant women suspected of diabetes using the glucose infusion test (GIT)]. 74 51

The effect of maternal diabetes on the risk of congenital malformations was investigated in 23,695 pregnancies of white mothers, inclucing 339 patients of the Joslin Clinic, and in 24,742 pregnancies of Negro mothers, drawn from the prospective Collaborative Perinatal Project. Of these, 372 mothers had gestational diabetes and 567 had overt diabetes (before and during pregnancy). Pregnancy outcomes studied included stillbirths and live births. Among core women (excluding the Joslin Clinic cases), the frequencies of diabetic pregnancies were 1.31% and 1.18% for white and Negro mothers, respectively; in both groups, approximately two thirds of these pregnancies had gestational diabetes. There was no increase in malformation risk in the pregnancies of mothers with gestational diabetes over that of nondiabetic mothers in either racial group. However, the risk of malformation for white mothers with overt diabetes was double that of nondiabetic mothers for both major and minor categories of malformations. The incidences of major and minor types of malformations in the pregnancies of white mothers with overt diabetes were 17.94% and 10.94%, respectively, compared to the corresponding incidences of 8.34% and 6.25% for the white nondiabetic group. In Negro mothers with overt diabetes, a smaller increase of risk was seen only in major malformations; the incidences were 13.64% and 8.45% for the diabetic and nondiabetic groups, respectively. The increased risks for malformations were distributed generally throughout the organ systems. Multiple malformations occurred more frequently in the overt diabetic than in the nondiabetic group, suggesting that maternal diabetes must act adversely an an early stage of fetal development. Two cases with the caudal regression syndrome were observed in children of diabetic mothers, whereas none was found among births from nondiabetic mothers. Insulin (or analog) therapy of diabetes neither decreased nor increased the risk of malformation in the fetus. However, duration of diabetes had a significant effect on the malformation risk: the longer the mother had the disease, the higher was the incidence of malformations in the fetus. Paternal diabetes did not contribute to increase in risk. These observations suggest that maternal diabetes per se, through its adverse effects on maternal metabolism, is the responsible factor for the increase of malformations in the offspring.
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PMID:Factors affecting risks of congenital malformations. II. Effect of maternal diabetes on congenital malformations. 76 59

A light microscopic, an electron microscopic, and a ultrahistochemical study have been made of seven placentas from women with mild and excellently controlled chemical gestational diabetes. Only one placenta showed no significant abnormality; the remainder showed, to a varying degree, changes in the syncytiotrophoblast, cytotrophoblast, trophoblastic basement membrane, and fetal vessels. These abnormalities were identical to and in some cases as severe as those found in placentas from women with longstanding, moderately controlled, overt diabetes mellitus. These findings indicate that control of hyperglycemia only partially prevents the development of placental abnormalities which must be due to some other constituent factor of the diabetic state.
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PMID:Placental changes in gestational diabetes. An ultrastructural study. 94 70


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