Gastric Acidity in the First Ten Days of Life of the Prematurely Born Baby

Ames, Mary D.

doi:10.1001/archpedi.1960.04020040254015

Cited by 23 publications

(13 citation statements)

References 4 publications

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“…It might be argued that free acid is not always present in the stomach of the newborn infant, but Miller (1941) has shown that there can be a degree of acidity equivalent to that of an adult. That this is not dependent on birth weight or maturity was demonstrated by Ames (1960): she found that only 5% of premature babies had no free acid at any time during the first 10 days of life. As it is well recognized that adults with intracerebral disease are liable to aspirate gastric contents (Irons and Apfelbach, 1940;Gardner, 1958), it is reasonable to suggest that pulmonary haemorrhage associated with intracranial haemorrhage in infants has a similar pathogenesis.…”

Section: Resultsmentioning

confidence: 91%

Neonatal Death and Massive Pulmonary Haemorrhage in Jamaica

Thorburn¹

1963

Archives of Disease in Childhood

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Massive pulmonary haemorrhage in the newborn is a well-recognized but little understood condition, characterized by the presence in the alveoli and alveolar ducts, and sometimes in the interstitial spaces, of large numbers of erythrocytes. The distribution of haemorrhage may be patchy or confluent causing consolidation, as distinct from the petechial haemorrhages seen in infants dying after premature separation of the placenta, or the septal haemorrhages seen in stillbirths. The condition was probably first described by Browne (1922a) Indies, of which 336 were neonatal deaths and 231 were stillbirths. In this period there were 14,013 births in the obstetric unit and domiciliary service, of which 304 were stillborn and 301 died in the neonatal period. The additional autopsies on newborns were performed on infants from other hospitals in Kingston. The population served by the hospital is multiracial: there is some selection, as the majority of patients come from the poorer classes. The racial constitution of the autopsy population (Bras, Brooks and Watler, 1961) is Negro or mixed-97-2%, White-1-2%, Chinese-08% and East Indian-0 8%.Method of Examination. The autopsy records of all the perinatal deaths were examined and all cases mentioning the presence of pulmonary haemorrhage of any type were scrutinized. The clinical records, gross autopsy findings and microscopic sections were examined. Lung sections were available from all autopsies. Blocks of lung tissue had been fixed in 10% neutral buffered formalin and embedded in paraffin wax. Sections were stained with haematoxylin and eosin.Conditions of Study. Criteria for selection were as follows:1. Death occurred in the first or second week of life; stillbirths were excluded.

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Section: Resultsmentioning

confidence: 91%

Neonatal Death and Massive Pulmonary Haemorrhage in Jamaica

Thorburn¹

1963

Archives of Disease in Childhood

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“…[11][12][13] These studies resulted in the misconception that neonates are incapable of secreting gastric acid. By the early 1960s, reports of low gastric pH in neonates were published 14,15 and seemed to contradict the other studies but failed to change opinions.…”

Section: Gastric Acid Secretionmentioning

confidence: 99%

“…16,17 By age 4 hours gastric pH decreases to below 4 in most term and preterm neonates, and the lower pH can continue through the first 24 hours. [16][17][18] During the first months of life, gastric pH is variable but often is below 4 before feeding in healthy 14,15 and critically ill neonates. [19][20][21][22] With increasing age, the average gastric pH decreases from about 3-4 in neonates, to 1.5-3 in infants, 1-3 in preschool children, 1-2 in school-age children, and 0.5-2 in adolescents.…”

Section: Gastric Acid Secretionmentioning

confidence: 99%

“…[19][20][21][22] With increasing age, the average gastric pH decreases from about 3-4 in neonates, to 1.5-3 in infants, 1-3 in preschool children, 1-2 in school-age children, and 0.5-2 in adolescents. [14][15][16][17][18][19][20][21][22] Gastrin serum concentrations are increased during the first 4 months of life and hypergastrinemia does not result in an increase in gastric secretions. 12,21 Based on this finding, it is not surprising that pentagastrin and histamine have a minimal effect on acid secretion for the first 2 days of life.…”

Section: Gastric Acid Secretionmentioning

confidence: 99%

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Upper Gastrointestinal Tract Bleeding in Critically Ill Pediatric Patients

Crill

Hak

1999

Pharmacotherapy

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Similar to adults, children under physiologic stress can develop an imbalance in defensive (mucosal layer, motility) and aggressive (gastric acid, bile salts, enzymes) factors responsible for maintaining a healthy gastrointestinal tract. Hypoxia in the gastrointestinal tract likely disrupts the defensive factors, thereby permitting damage by aggressive factors to upper gastrointestinal epithelium that may progress to stress ulceration and acute upper gastrointestinal tract bleeding (UGIB). The basic pathophysiology may be similar in children and adults; however, differences in the time to developing ulceration, ulcer location, and number of ulcers have been reported. Functional development of the gastrointestinal tract is influenced by disease, gestational and postnatal age, and exposure to and type of enteral feedings, thereby confounding the development and prophylaxis of UGIB in neonates and infants. In addition, pharmacotherapy decisions are often complicated by drug administration issues and adverse effects.

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“…Unlike the situation in adult subjects, "preactivation" of milk-borne TGF-␤ may be particularly important in premature infants, because gastrointestinal mechanisms for in situ activation of orally ingested TGF-␤, such as gastric acidity and intestinal gelatinases, are relatively deficient (2,23,27,33,45). In this context, we hypothesized that 1) premature infants remain at higher risk of NEC than full-term infants, even when they receive their own mother's milk, because preterm human milk contains less bioactive TGF-␤ than full-term milk; 2) lower TGF-␤ bioactivity in preterm milk reflects the deficiency of one or more activators of TGF-␤ in preterm milk; and 3) TGF-␤ bioactivity in preterm milk can be increased to levels comparable to full-term milk by addition of TGF-␤ activator(s) that are expressed at lower levels in preterm than full-term milk.…”

mentioning

confidence: 99%

Preterm human milk contains a large pool of latent TGF-β, which can be activated by exogenous neuraminidase

Namachivayam

Blanco

Frost

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Human milk contains substantial amounts of transforming growth factor (TGF)-β, particularly the isoform TGF-β2. We previously showed in preclinical models that enterally administered TGF-β2 can protect against necrotizing enterocolitis (NEC), an inflammatory bowel necrosis of premature infants. In this study we hypothesized that premature infants remain at higher risk of NEC than full-term infants, even when they receive their own mother's milk, because preterm human milk contains less bioactive TGF-β than full-term milk. Our objective was to compare TGF-β bioactivity in preterm vs. full-term milk and identify factors that activate milk-borne TGF-β. Mothers who delivered between 23 0/7 and 31 6/7 wk or at ≥37 wk of gestation provided milk samples at serial time points. TGF-β bioactivity and NF-κB signaling were measured using specific reporter cells and in murine intestinal tissue explants. TGF-β1, TGF-β2, TGF-β3, and various TGF-β activators were measured by real-time PCR, enzyme immunoassays, or established enzymatic activity assays. Preterm human milk showed minimal TGF-β bioactivity in the native state but contained a large pool of latent TGF-β. TGF-β2 was the predominant isoform of TGF-β in preterm milk. Using a combination of several in vitro and ex vivo models, we show that neuraminidase is a key regulator of TGF-β bioactivity in human milk. Finally, we show that addition of bacterial neuraminidase to preterm human milk increased TGF-β bioactivity. Preterm milk contains large quantities of TGF-β, but most of it is in an inactive state. Addition of neuraminidase can increase TGF-β bioactivity in preterm milk and enhance its anti-inflammatory effects.

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Gastric Acidity in the First Ten Days of Life of the Prematurely Born Baby

Cited by 23 publications

References 4 publications

Neonatal Death and Massive Pulmonary Haemorrhage in Jamaica

Neonatal Death and Massive Pulmonary Haemorrhage in Jamaica

Upper Gastrointestinal Tract Bleeding in Critically Ill Pediatric Patients

Preterm human milk contains a large pool of latent TGF-β, which can be activated by exogenous neuraminidase

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