gastrins and Birth-Weight

To study serum gastrin levels in response to early minimal feeding in premature infants and evaluate the clinical effect of early minimal feeding.. Premature infants with critical score < or = 90 were randomly assigned into two groups: early minimal feeding group (n = 48), non-early minimal feeding group (n = 47). Other premature infants (n = 30) without any complications (critical score > 90) were assigned as normal control group. The premature infants in normal control group were fed with water at 6 h after birth, 1 - 2 ml/kg every time, after once or twice, they were fed with formula, increasing in the amount of formula gradually, until adequate. The premature infants in early minimal feeding group were fed with formula within 72 h after birth, 0.5 - 1 ml/kg, once every 3 h, the amount of formula was increased gradually, until adequate. The premature infants without early minimal feeding were not fed with formula until the illness was stable, the amount of formula was increased gradually until adequate. Situation of gastrointestinal feeding tolerance, growth and development, and clinical symptoms were observed and recorded for the three groups. Serum gastrin levels were monitored at 1, 3, 7 day after birth by radioimmunoassay.. Serum gastrin concentrations in the three groups elevated from 1 to 7 days. In early minimal feeding group [(82.4 +/- 24.5) ng/L] and non-early minimal feeding group [(87.0 +/- 40.2) ng/L], the concentrations were significantly higher than those in normal control group [(66.4 +/- 19.7) ng/L] at day 1 (F = 3.36, P < 0.05). At day 3 and 7, the concentrations in early minimal feeding group [(96.3 +/- 14.6) ng/L, (113.0 +/- 16.5) ng/L] were significantly higher than those in non-early minimal feeding group [(73.9 +/- 13.5) ng/L, (92.4 +/- 12.2) ng/L] (P < 0.05). There were significant differences among the three groups in infants with feeding intolerance (2/30, 5/48, 14/47), the period reached full enteral feeding [(20.6 +/- 5.7) d, (27.8 +/- 6.1) d, (39.5 +/- 4.7) d], and in number of hospital day [(29.0 +/- 4.6) d, (39.0 +/- 4.8) d, (48.0 +/- 5.6) d] (P < 0.05). There were significant differences between early minimal feeding group and non-early minimal feeding group in the weight gain three and four weeks after birth [(19.1 +/- 2.4) g/d, (11.9 +/- 3.3) g/d], the period reached birthweight [(19.8 +/- 4.2) d, (25.2 +/- 5.1) d] (P < 0.05). There were no significant difference among the three groups in the weight gain in one and two weeks after birth [(5.9 +/- 2.9) g/d vs. (5.0 +/- 2.1) g/d], the numbers of premature infants with infection, anemia, apnea, or hypoglycemia.. Early minimal feeding in premature infants leads to secretion of gastrin, promotes the development of gastrointestine and may not be associated with occurrence of complications.

Topics: Birth Weight; Enteral Nutrition; Female; Gastrins; Gastrointestinal Tract; Humans; Infant Nutritional Physiological Phenomena; Infant, Newborn; Infant, Premature; Infant, Small for Gestational Age; Male

We examined whether plasma gastrin concentration increases during breast-feeding in infants. The peptide concentration was measured cross-sectionally before, during, and after breast-feeding in healthy, 3-day-old infants (n = 72). Somatostatin, a modulator of gastrin release, was also analyzed. Both peptides were measured by radioimmunoassay and were further characterized by high-performance liquid chromatography (HPLC). The (mean +/- SD) concentration of gastrin rose significantly from 63 +/- 24 pmol/L before feeding to 92 +/- 32 pmol/L (p less than 0.01) and 95 +/- 21 pmol/L (p less than 0.01), 5 and 10 min after the initiation of sucking, respectively. The gastrin concentration was 102 +/- 35 pmol/L (p less than 0.01) immediately after feeding. Plasma somatostatin concentration was unaffected by feeding. As assessed by HPLC, circulating gastrin before, during, and after feeding was found to correspond to gastrin-34, whereas circulating somatostatin was found to correspond to somatostatin-14. We conclude that in contrast to earlier studies, plasma gastrin concentration increases during and immediately after breast-feeding in infants.

Topics: Birth Weight; Chromatography, High Pressure Liquid; Cross-Sectional Studies; Female; Gastrins; Humans; Infant, Newborn; Male; Milk, Human; Protein Precursors; Radioimmunoassay; Somatostatin

To investigate extraesophageal anomalies in infants with esophageal atresia, preoperative plasma gastrin was measured in 12 infants. The median plasma gastrin was 32 ng/L (interquartile range, 24 to 44). There was significant correlation with birth weight (rs = .73, P less than .05) and gestational age (rs = .74, P less than .05). Within this group 9 infants of greater than 36 weeks' gestation were matched to a group of 20 control infants without esophageal atresia. Infants with esophageal atresia had a significantly lower median plasma gastrin (38 ng/L v 55 ng/L, P less than .05). This may indicate preexisting vagal abnormalities in esophageal atresia unrelated to surgical intervention.

Topics: Birth Weight; Esophageal Atresia; Gastrins; Gestational Age; Humans; Infant, Low Birth Weight; Infant, Newborn; Reference Values; Tracheoesophageal Fistula

Serum gastrin I (GLU-GLY-PRO-TRYP-LEU(GLU)6-ALA-[formula, see text]-GLY-TRY-MET-ASP-PHE-CO-NH2) concentrations were investigated by radioimmunoassay in 50 mothers and their newborn infants immediately after birth. The mean serum gastrin concentration in maternal blood was 52.80 +/- 13.37 (SD) pg/ml, and in cord blood 84.12 +/- 42.90 (SD) pg/ml. Both values were significantly higher than serum gastrin levels found in normal, healthy, nonpregnant women (Mean +/- SD = 32.34 +/- 18.35 pg/ml). There were no statistically significant differences in the cord serum gastrin concentrations with respect to sex, weight and length of the infant and age and parity of the mother.

Topics: Adolescent; Adult; Birth Weight; Female; Fetal Blood; Gastrins; Humans; Infant, Newborn; Male; Parity; Pregnancy; Sex Factors