Glucose kinetics in glucose-infused small for gestational age infants

To evaluate the maturation of glucose homeostasis in the small for gestational age (SGA) neonate, glucose kinetics were measured with 78% enriched D-[U-13C]glucose by the prime plus constant infusion technique in nine SGA infants and compared with the rate obtained in seven term appropriate for gestational age infants and 13 preterm appropriate for gestational age infants. All of the infants had received glucose intravenously from birth and continued to receive the glucose infusion throughout the study. Fasting plasma glucose and plasma insulin concentrations and plasma [13/12C]ratios were measured during the steady state turnover period. From this data, the glucose production rate was derived. During the turnover period, the SGA and both groups of appropriate for gestational age infants had similar average plasma glucose, plasma insulin, plasma glucagon concentrations, and similar persistent rates of glucose production during glucose infusion. We conclude that under stimulation of glucose infusion, the SGA infant and his AGA counterpart have similar hormonal regulatory responses as well as functional integrity in handling glucose during the second day after birth.     

Leitlinie zur Betreuung von Neugeborenen diabetischer M��tter

All diabetic women are advised to give birth in a hospital with a pediatric service that allows for continuous intravenous glucose administration, precluding the need for out-of-house transfer of the infant. Women with pre-pregnancy diabetes or on insulin treatment during pregnancy should give birth in a hospital offering round-the-clock neonatal care. Early (breast) feeding is of paramount importance and should be started 30?min after birth, subsequently every 2?C3?h. A mandatory preprandial blood glucose measurement should be taken 2?C3?h after birth and again immediately before the infant is transferred out of the delivery room; subsequent preprandial measurements at 6, 12, and possibly 24?h of age. In the event of three consecutive values of >2.5?mmol/l (45?mg/dl), further controls may be dispensed with. Simultaneously, infants should be checked for symptoms of hypoglycemia by a midwife or nurse on the maternity unit. Clinical findings suspicious for hypoglycemia should prompt immediate blood glucose determinations. Blood glucose concentrations below 2?mmol/l (36?mg/dl; in infants without symptoms) or 2.5?mmol/l (45?mg/dl; in infants with hypoglycemia-related symptoms, prior hypoglycemia, or following asphyxia) require immediate intervention in the form of feeding (preferably breast milk, otherwise hydrolyzed formula, or hydrolyzed starch solution only temporarily), by gavage if necessary. Intravenous glucose administration if blood glucose falls below 1.7?mmol/l (30?mg/dl). Routine echocardiography or laboratory tests (Ca2+, Mg2+, hematocrit, bilirubin) are not necessary unless otherwise indicated. Breast feeding should be consistently encouraged before and after delivery.     

Urinary cyclic AMP in infants admitted to a neonatal intensive care unit.

The urinary excretion of cyclic AMP was studied during the first 3 days of life in 46 randomly selected infants admitted to a neonatal intensive care unit. The data were compared with those of normal newborn infants. Urinary cyclic AMP concentrations were significantly correlated with gestational age (all patients), and with birth weight (all patients except infants of diabetic mothers (IDMs)). The urinary cyclic AMP/creatine ratio increased from day 1 to day 3 in normal newborns and in IDMs, and tended to increase also in small-for-gestational age (SGA), low birth weight (LBW), and sick, term infants, although the changes in the latter groups were not statistically significant. Four infants studied with parallel determinations showed increased cyclic AMP/creatinine ratio from day 1 to day 3 both in plasma and urine. All urinary cyclic AMP/creatine ratios were lower than the corresponding ratios found in plasma. In LBW infants, there was an inverse relationship between urinary cyclic AMP and serum calcium. In IDMs a positive correlation was observed between urinary cyclic AMP and blood glucose concentration. In conclusion, the excretion of cyclic AMP in sick newborn infants is influenced by the following factors: gestational age, postnatal age, birth weight, and derangements of serum calcium and blood glucose concentrations.     

URINARY CYCLIC AMP IN INFANTS ADMITTED TO A NEONATAL INTENSIVE CARE UNIT

ABSTRACT. The urinary excretion of cyclic AMP was studied during the first 3 days of life in 46 randomly selected infants admitted to a neonatal intensive care unit. The data were compared with those of normal newborn infants. Urinary cyclic AMP concentrations were significantly correlated with gestational age (all patients), and with birth weight (all patients except infants of diabetic mothers (IDMs)). The urinary cyclic AMP/creatinine ratio increased from day 1 to day 3 in normal newborns and in IDMs, and tended to increase also in small-for-gestational age (SGA), low birth weight (LBW), and sick, term infants, although the changes in the latter groups were not statistically significant. Four infants studied with parallel determinations showed increased cyclic AMP/creatinine ratio from day 1 to day 3 both in plasma and urine. All urinary cyclic AMP/creatinine ratios were lower than the corresponding ratios found in plasma. In LBW infants, there was an inverse relationship between urinary cyclic AMP and serum calcium. In IDMs a positive correlation was observed between urinary cyclic AMP and blood glucose concentration. In conclusion, the excretion of cyclic AMP in sick newborn infants is influenced by the following factors: gestational age, postnatal age, birth weight, and derangements of serum calcium and blood glucose concentrations.     

Treatment with hypertonic dextrose and insulin in severe hyperkalaemia of immature infants

Over a three-year period, 12 infants received dextrose/insulin infusions for severe hyperkalaemia from a mean age of 24 h. The infants were born after 24 to 26 weeks of gestation and weighed 730 +/- 172 g (mean +/- SD) at birth. Serum potassium concentration ranged from 7.4 to 8.4 mmol/l (7.7 +/- 0.4 mmol/l; mean +/- SD). Four had cardiac arrhythmias. All infants showed an initial response, serum potassium concentration decreased below 6.5 mmol/l in 5 +/- 2 h. In two infants, rebound hyperkalaemia occurred and was resistant to treatment; both infants died, one during an exchange transfusion. In the other 10 infants, infusions were ceased at a mean postnatal age of 53 h. Hyperglycaemia was the major problem during infusion and was resistant to increases in insulin concentrations. Normoglycaemia was achieved in 10 infants. The hypertonic solution consisted of a dextrose/insulin ratio of 2.2 +/- 0.6 g/IU, which delivered glucose at a rate of 0.46 +/- 0.15 g/kg/h, in addition to the pre-existing stable maintenance glucose intake.     

Nesidioblastosis of the pancreas: definition of the syndrome and the management of the severe neonatal hyperinsulinaemic hypoglycaemia.

Three newborn infants are reported who developed severe non-ketotic hypoglycaemia (blood glucose less than 1.1 mmol/l; 19.8 mg/100 ml) within 6 hours of birth. All had inappropriately raised plasma insulin concentrations for the level of glycaemia, and required high rates of glucose infusion (less than 15 mg glucose/kg per minute) to prevent symptoms of hypoglycaemia. Medical treatment (hydrocortisone, diazoxide, chlorothiazide, phenytoin, propranolol, and depot glucagon) was ineffective in preventing hypoglycaemia and all 3 infants were subjected to partial and then total pancreatectomy. The pathological features of nesidioblastosis are reported from quantitative immunohistochemical studies on the pancreata. These results together with those from metabolic and endocrine studies performed on the 3 infants during the investigation of the cause of the hypoglycaemia and during the preoperative and postoperative period are presented in detail in order to define a practical approach to the management of this difficult clinical problem in the neonate.     

Plasma glucagon levels in the term human infant and effect of hypoxia

The mean plasma pancreatic glucagon level at birth in 44 normal infants delivered vaginally was 140 pg/ml. The simultaneous maternal level was 122 pg/ml which was not quite significantly different at the P [unk]0.05 level. 2 hours after birth 30 of these infants had a mean rise in plasma glucagon of 51 pg/ml (P [unk] 0.01), and their mothers had a fall of 38 pg/ml (P [unk] 0.05). The mean plasma pancreatic glucagon level at birth in 12 normal infants delivered by caesarean section was 130 pg/ml which did not differ significantly from the group delivered vaginally. The glucagon level at birth in 20 infants with fetal distress (fetal scalp pH [unk] 7.2 or umbilical artery pH [unk] 7.15) was 244 pg/ml, and this was significantly higher than for normal infants at birth (P [unk] 0.01). Whereas the rise in neonatal glucagon 2 hours after birth might have been caused by a mean fall in blood glucose of 23 mg/100 ml, the infants with fetal distress had normal glucose levels, so that another mechanism must be responsible for their raised glucagon.     

Gastrointestinal enhanced insulin release in response to glucose in newborn infants

The purpose of this investigation was to determine whether or not gastrointestinal (GI) enhanced insulin response occurs in newborn infants soon after birth. Glucose infusion by intravenous or orogastric routes was given to infants during the first 4 days of life, aiming at achieving similar plasma glucose concentrations. Their plasma insulin responses were then compared. Thirty term, newborn infants (10 appropriate for gestational age, 8 small for gestational age, 6 large for gestational age, and 6 infants of diabetic mothers) were studied. With intravenous glucose infusions of 8 mg/kg/min or orogastric infusion of 16 mg/kg/min, the plasma glucose concentrations achieved were similar and approximated 110 mg/dl. Plasma insulin responses were greater in infants receiving glucose via the GI route. The finding was in contrast to our previous data, in which no GI enhancement of insulin response was demonstrated. The present data suggest that in the term newborn infant, GI enhanced insulin release occurs only when a threshold of plasma glucose concentration has been exceeded. It appears that the enteroinsular axis is functional in newborns soon after birth.     

Metabolic events in infants of diabetic mothers during first 24 hours after birth. I. Changes in plasma glucose, insulin and glucagon

Changes in plasma glucose, nonantibody-bound insulin and glucagon concentrations were studied in 32 newborn infants of diabetic mothers (IDM) during the first 24 hours after birth. Ten infants were born to White class A mothers and 22 to class B-F mothers. The infants were kept fasting during the investigative period and blood was sampled from an umbilical artery catheter. At birth, plasma glucose and glucagon levels were similar in the class A and B-F infants, whereas nonantibody-bound insulin levels were approximately 15-fold higher in the class B-F infants than in the class A infants (p less than 0.001). After birth, plasma glucose fell in all infants, the nadir being reached at two hours (p less than 0.01). Plasma glucose fell by approximately 35% in the class A infants and 63% in the class B-F infants (p less than 0.01). Eight IDM had asymptomatic hypoglycemia (plasma glucose less than 1.9 mmol/l) and four of these infants had glucose levels below 1.7 mmol/l and were withdrawn from further study. In the remaining four hypoglycemic IDM, plasma glucose was about 1.6-fold higher (p less than 0.01) and insulin about 11-fold higher (p less than 0.001) at birth compared to the 24 normoglycemic IDM. The hypoglycemia was attended by unchanged insulin levels in the class A infants, whereas insulin fell in the class B-F infants (p less than 0.01). However, during the whole investigative period, plasma insulin of the class B-F infants was higher than that of the class A infants (p less than 0.01). After birth, plasma glucagon increased slowly in all IDM and peak values were reached after 12 hours in the class A infants (p less than 0.05) and 24 hours in the class B-F infants (p less than 0.01). Only those infants who became hypoglycemic after birth exhibited a significant increment in plasma glucagon from 0.2 hours (p less than 0.05). These results suggest that neonatal hypoglycemia of IDM results from high plasma levels of nonantibody-bound insulin together with a very retarded increment in plasma glucagon levels. The degree of neonatal hypoglycemia and hyperinsulinemia of an individual IDM seems to be positively correlated to the severity of the diabetes of the mother.     

Glucose Tolerance in Very Low Birthweight Infants

Yu, V. Y. H., James, B. E., Hendry, P. G. and MacMahon, R. A. (1979). Aust. Paediatr. J. , 15, 147–151 Glucose tolerance in very low birthweight infants. The carbohydrate intake and incidence of hyperglycaemia were reviewed in 40 very low birthweight infants with a birthweight of less than 1200g who were randomly assigned to total parenteral nutrition (TPN) or oral (MILK) feeding regimens during the first two weeks after birth. With increasing glucose tolerance after birth, the carbohydrate intake was increased from a mean intake of 8g/kg.d on Day 1 to 17g/kg.d in the TPN group and 12g/kg.d in the MILK group by the second week; the lower intake in the latter group was due to a restricted intake rather than decreased glucose tolerance. Twenty-seven per cent of the infants had moderate or severe hyperglycaemia in the first week compared with 13% in the second week, in spite of the higher carbohydrate intake in the latter period. All hyperglycaemic episodes were corrected promptly without obvious serious sequelae by decreasing the rate of carbohydrate intake. The rational approach to carbohydrate administration in the very low birthweight infant includes the calculation of carbohydrate intake in terms of g/kg.d (rather than arbitrary concentrations given at variable rates based on fluid requirement), a constant infusion at a steady rate, and the close monitoring of blood glucose to establish glucose tolerance limits which increase with postnatal age.     

METABOLIC EVENTS IN INFANTS OF DIABETIC MOTHERS DURING FIRST 24 HOURS AFTER BIRTH I.

ABSTRACT. Changes in plasma glucose, nonantibody-bound insulin and glucagon concentrations were studied in 32 newborn infants of diabetic mothers (IDM) during the first 24 hours after birth. Ten infants were born to White class A mothers and 22 to class B-F mothers. The infants were kept fasting during the investigative period and blood was sampled from an umbilical artery catheter. At birth, plasma glucose and glucagon levels were similar in the class A and B-F infants, whereas nonantibody-bound insulin levels were approximately 15-fold higher in the class B-F infants than in the class A infants (p<0.001). After birth, plasma glucose fell in all infants, the nadir being reached at two hours (p<0.01). Plasma glucose fell by approximately 35 % in the class A infants and 63 % in the class B-F infants (p<0.01). Eight IDM had asymptomatic hypoglycemia (plasma glucose <1.9 mmol/l) and four of these infants had glucose levels below 1.7 mmol/l and were withdrawn from further study. In the remaining four hypoglycemic IDM, plasma glucose was about 1.6-fold higher (p<0.01) and insulin about 11-fold higher (p<0.001) at birth compared to the 24 normoglycemic IDM. The hypoglycemia was attended by unchanged insulin levels in the class A infants, whereas insulin fell in the class B-F infant (p<0.01). However, during the whole investigative period, plasma insulin of the class B-F infants was higher than that of the class A infants (p<0.01). After birth, plasma glucagon increased slowly in all IDM and peak values were reached after 12 hours in the class A infants (p<0.05) and 24 hours in the class B-F infants (p<0.01). Only those infants who became hypoglycemic after birth exhibited a significant increment in plasma glucagon from 0-2 hours (p<0.05). These results suggest that neonatal hypoglycemia of IDM results from high plasma levels of nonantibody-bound insulin together with a very retarded increment in plasma glucagon levels. The degree of neonatal hypoglycemia and hyperinsulinemia of an individual IDM seems to be positively correlated to the severity of the diabetes of the mother.     

Insulin infusion with parenteral nutrition in extremely low birth weight infants with hyperglycemia

From Nov. 7, 1983, to Nov. 6, 1986, all infants with birth weight less than or equal to 1000 gm admitted to Oregon Health Sciences University who had persistent hyperglycemia and glycosuria were treated with graded insulin infusion while energy intake was increased to at least 100 kcal/kg/day (419 kilojoules/kg/day). The records of these infants were reviewed to define the clinical characteristics of infants likely to develop hyperglycemia and to see whether insulin administration would allow goals for energy intake to be met. There were 76 surviving infants; 34 received insulin and 42 did not. Treated infants were smaller (767 +/- 161 vs 872 +/- 98 gm; p = 0.0004), were more immature (26.8 +/- 1.4 vs 27.7 +/- 2.0 weeks; p = 0.0115), and required mechanical ventilation longer (28 +/- 19 vs 17 +/- 15 days; p = 0.0196). There were no significant differences between the groups at 3, 7, 10, or 14 days for intravenously administered glucose or for total nonprotein energy intake at 3, 7, 10, 14, 28, or 56 days. Treated infants achieved an intake of 100 kcal/kg/day (419 kilojoules/kg/day) at 15 +/- 8 vs 17 +/- 11 days and regained birth weight at 12 +/- 6 vs 13 +/- 6 days (NS). There was no difference in percent change from birth weight at 7, 14, 28, or 56 days. Treated infants had a glucose concentration of 195 +/- 60 mg/dl (10.8 +/- 3.3 mmol/L) while receiving 7.9 +/- 3.0 mg/kg/min (43 +/- 17 mumol/kg/min) of glucose at the start of insulin infusion on days 1 to 14. Insulin was given for 1 to 58 days. The initial dose was 40 to 100 mU/gm of dextrose infused (57 to 142 nmol/mol) and then gradually decreased. Less than 0.5% of blood glucose values were 25 to 40 mg/dl (1.4 to 2.2 mmol/L). We conclude that insulin infusion improves glucose tolerance in extremely low birth weight infants and allows hyperglycemic infants to achieve adequate energy intake similar to that of infants who do not become hyperglycemic.     

Ontogeny of glucose homeostasis in low birth weight infants

Suppression of the endogenous glucose production rate (Ra) is the adult response to glucose infusion. Persistent Ra (greater than or equal to 1 mg.kg-1min-1 or less than 80% decrease in basal Ra) in response to glucose infusion is evidence of a transitional homeostatic state in the neonate during the first days after birth. To determine whether postnatal development produces an adultlike response, Ra was measured in 11 infants (birth weight 1716 +/- 48 g, gestational age 33 +/- 0.3 weeks) at 2 to 5 weeks of age. In these paired studies, 4 micrograms.kg-1min-1 D-(U-13C)glucose tracer was infused by prime constant infusion to determine Ra, during infusion of either saline solution or glucose, the latter at a rate of 5.3 +/- 0.2 mg.kg-1min-1 (mean +/- SEM). When the results of the saline infusion turnover period were compared with those of the glucose infusion turnover period, plasma glucose concentration increased significantly, from 88 +/- 3 mg/dL to 101 +/- 4 mg/dL (P less than 0.001). Plasma insulin concentration remained unchanged (12 +/- 5 microU/mL vs 8 +/- 3 microU/mL). Ra was heterogenous during glucose infusion, and persistent Ra was present in six of 11 infants. Of the five infants who had decreased Ra during glucose infusion, three received glucose at a rate exceeding basal Ra. Of the remaining six infants who evidenced persistent Ra during glucose infusion, three received glucose at a rate equal to or in excess of basal Ra. We conclude that glucose homeostasis in low birth weight infants is transitional throughout the neonatal period.     

METABOLIC EFFECTS OF OBSTETRIC REGIONAL ANALGESIA AND OF ASPHYXIA IN THE NEWBORN INFANT DURING THE FIRST TWO HOURS AFTER BIRTH: I. Arterial Blood Glucose Concentrations

Abstract. Swanstrom, S. and Bratteby, L.-E. (Perinatal Research Unit of the Department of Paediatrics and the Unit of Paediatric Physiology of the Department of Clinical Physiology, University Hospital, Uppsala, Sweden). Metabolic effects of regional analgesia and of asphyxia in the newborn infant during the first two hours after birth. I. Arterial blood glucose concentration. Acta Paediatr Scand, 70: 791, 1981. Effects of obstetric regional analgesia and of asphyxia on the arterial blood glucose concentrations were inestigated in 83 newborn infants divided into a control group, an asphyxia group, a continuous epidural, and a paracervical + pudendal block group. Lidocaine was used in the analgesia groups. All infants except those of the asphyxia group had 1-minute Apgar scores ≥7. 1) In the asphyxiated infants high blood glucose values and strong correlations between blood glucose concentrations and different signs of asphyxia (Apgar score, base deficit and lactate) were found. 2) In infants whose mothers were given regional analgesia the results were: (a) high glucose values in 20 % of the infants and an association between increased glucose concentrations in these infants and signs of fetal distress, (b) low blood glucose values (< 1.67 mmol/1) in 27 % of the infants. It is recommended that the blood glucose is checked in the newborns after obstetric regional analgesia.     

Neonatal blood glucose concentrations in caesarean and vaginally delivered term infants

Background: Little is known about the glucose concentrations at and after birth of infants delivered by caesarean section (CS), when compared with infants born vaginally (VD). Aim: To compare venous cord blood glucose concentrations of term infants born after elective CS to infants born by VD. We studied the null hypothesis that mode of delivery does not affect neonatal blood glucose values. Methods: We compared cord blood glucose concentrations in healthy term infants born after VD (n = 16) or by elective CS (n = 21). Glucose concentrations were obtained immediately at birth from the umbilical cord. Kruskal–Wallis was used to compare glucose concentrations and demographic variables between the groups. Results: Gestational age was 39.6 ± 0.8 weeks in VD group vs. 38.7 ± 0.9 weeks in CS group, and birthweight was 3359 ± 494 vs. 3500 ± 528 g. Cord blood glucose concentration was higher in VD (81.3 ± 16.9 mg/dL) than CS infants (70.3 ± 9.7 mg/dL, p = 0.039). The change in blood glucose concentration over the first 2‐h of life differed significantly between the two groups, being an increase in CS versus a decrease in VD infants (?3.5 ± 15.2 vs. ?15.4 ± 24.6 mg/dL, p = 0.013). Conclusions: Glucose concentrations in VD infants are higher than in infants born by elective CS without labour.     

Decreased plasma glucose following indomethacin therapy in premature infants with patent ductus arteriosus

The effect of indomethacin on carbohydrate metabolism was studied in six premature infants with significant patent ductus arteriosus (mean +/- S.D., birth weight 1,066 +/- 244 gm, gestational age 30 +/- 1.6 weeks). All infants were in a glucose steady state between 50 and 100 mg/dl over a 2-hour period before indomethacin administration. There was a significant fall in plasma glucose at 1, 6, 12, and 24 hours following intravenous indomethacin infusion. Since there was no significant change in insulin levels from the baseline, the mechanism of indomethacin-mediated lack of prostaglandin inhibition of insulin release was not substantiated. Based on this study, plasma glucose levels should be followed closely in the first 24 hours following intravenous indomethacin administration.     

Hyperglycemia and glucosuria in preterm infants receiving parenteral glucose: influence of birth weight, gestational age and infusion rate

OBJECTIVE: Morbidity and mortality of premature infants have decreased considerably over the last decades, therefore, adequate nutrition of the premature is a major concern. Enteral feeding is the route of choice, but when it is not possible the parenteral route, which contains glucose as one of its main components, is used. Glucose infusions are not devoid of risk as they facilitate the development of hyperglycemia leading to intracranial hemorrhage, glucosuria and dehydration. The aim of this paper is to relate hyperglycemia and glucosuria to birth weight, gestational age and glucose infusion rate.METHODS: The study was developed at the Nursery of Santa Catarina Hospital (S?o Paulo). The authors developed a prospective study; 511 concurrent determinations of glycemia and qualitative glucosuria were performed in 40 preterm newborn infants receiving parenteral glucose (mean of 12.8 dosages per newborn).RESULTS: Fifty-nine (11.5%) episodes of hyperglycemia were detected, and their frequency was higher at lower gestational ages (/= 6 mg/kg/min). Thirty-one (6.1%) episodes of glucosuria were detected, and were more frequent in lower gestational ages (/= 6 mg/kg/min).CONCLUSIONS: The frequency of hyperglycemia and glucosuria in preterm newborn infants receiving glucose infusion was higher in lower gestational ages, lower birth weights and higher glucose infusion rates. In preterm newborn infants it is necessary to observe the glucose infusion rate and its respective glycemia, in order to avoid the complications of hyperglycemia.     

Hyperammonemia in hypoglycemic preterm neonates

Plasma glucose, blood urea nitrogen, and ammonia were measured simultaneously in 44 newborns a few hours after birth. When the concentration of plasma glucose was below 30 mg/dl, plasma ammonia concentration was significantly higher (129 +/- 67 mumol/l) than in normoglycemic infants (74 +/- 33 mumol/l; p less than 0.01). Blood urea nitrogen was slightly lower in hypoglycemic infants (3.65 +/- 0.7 mmol/l) than in the control group (4.5 +/- 1 mmol/l) but the difference was not significant. These data show that hyperammonemia can be associated to hypoglycemia in low birth weight infants. Therefore, further investigations are required to determine the link between urea and glucose production rates in hypoglycemic newborns and whether hyperammonemia participates in the deleterious effects of hypoglycemia on the neonatal brain.     

妊娠期合并糖代谢异常对新生儿胰岛素敏感性的影响

目的探讨妊娠期合并糖代谢异常对子代新生儿期胰岛素敏感性的影响。方法选择2009年12月至2010年11月本院产科出生的新生儿,根据母亲妊娠期是否合并糖代谢异常分为糖代谢异常母亲的新生儿和糖代谢正常母亲的新生儿。所有研究对象均进行出生体格测量,并于生后 3 天内测定空腹血糖( FPG) 和空腹血清胰岛素( FINS) ,计算胰岛素敏感指数( ISI) ,采用胰岛素稳态模型( HOMA) 计算胰岛素抵抗指数( IR) ,即 HOMA-IR,其中 FINS、ISI 和 HOMA-IR 值为胰岛素敏感性的评价指标。以性别、胎龄、出生体重为协变量,分别在早产儿和足月儿中进行胰岛素敏感性的协方差分析。结果 89 例早产新生儿和 96 例足月新生儿纳入分析。糖代谢异常母亲新生儿的出生体重、出生身长和重量指数( PI) 与糖代谢正常母亲的新生儿相比,差异无统计学意义( P >0. 05) 。与糖代谢正常母亲的早产儿相比,糖代谢异常母亲的早产儿 FPG 降低、FINS 升高,差异有统计学意义[FPG( mmol/L) : ( 4. 00 ±0. 25) 比( 4. 82 ±0. 18) ,FINS( 经对数 Lg 转换) : ( 0. 69± 0. 06) 比( 0. 54 ± 0. 04) ,P < 0. 05],ISI 值降低、HOMA-IR 值升高,但差异无统计学意义[ISI( 经对数 Ln 转换) : ( -2. 89 ±0. 15) 比( -2. 78 ±0. 11) ,HOMA-IR 值( 经对数 Lg 转换) : ( -0. 10 ±0. 06)比( -0. 15 ±0. 05) ,P >0. 05]; 足月儿中糖代谢异常母亲的新生儿 FPG、FINS 和 HOMA-IR 值低,ISI 值高,但差异均无统计学意义[FPG( mmol / L) : ( 4. 68 ± 0. 23) 比( 5. 17 ± 0. 13) ,FINS( 经对数 Lg转换) : ( 0. 56 ±0. 06) 比( 0. 61 ±0. 03) ,HOMA-IR 值( 经对数 Lg 转换) : ( -0. 14 ±0. 06) 比( -0. 03± 0. 03) ,ISI( 经对数 Ln 转换) : ( - 2. 79 ± 0. 14) 比( - 3. 04 ± 0. 08) ,P > 0. 05]。结论母亲妊娠期合并糖代谢异常虽然对新生儿的出生体重没有影响,但血糖仍然呈现低水平趋势,且对早产儿胰岛素敏感性可能有一定的影响。     

A controlled trial of insulin infusion and parenteral nutrition in extremely low birth weight infants with glucose intolerance

To determine whether a continuous insulin infusion improves glucose tolerance in extremely low birth weight infants, we conducted a prospective, randomized trial in 24 neonates 4 to 14 days old (mean birth weight 772.9 +/- 128 gm; mean gestational age 26.3 +/- 1.6 weeks). Infants who had glucose intolerance were randomly assigned to receive either intravenous glucose and total parenteral nutrition with insulin through a microliter-sensitive pump or standard intravenous therapy alone. One infant assigned to receive insulin never required it. The groups were similar in birth weight, gestational age, race, gender, medical condition, and energy intake before the study. The mean duration of therapy was 14.6 days (range 7 to 21 days). During the study, the 11 insulin-treated infants tolerated higher glucose infusion rates (20.1 +/- 2.5 vs 13.2 +/- 3.2 mg/kg/min (1.1 +/- 0.1 vs 0.7 +/- 0.2 mmol/L); p less than 0.01), had greater nonprotein energy intake (124.7 +/- 18 vs 86.0 +/- 6 kcal/kg/day; p less than 0.01), and had better weight gain (20.1 +/- 12.1 vs 7.8 +/- 5.1 gm/kg/day; p less than 0.01) than the 12 control infants. The incidence of hypoglycemia, electrolyte imbalance, chronic lung disease, and death did not differ between groups. We conclude that a controlled insulin infusion improves and sustains glucose tolerance, facilitates provision of calories, and enhances weight gain in glucose-intolerant premature infants.