Milk bolus obstruction secondary to the early introduction of premature baby milk formula: an old syndrome re-emerging in a new population

1989 ◽  
Vol 148 (7) ◽  
pp. 676-678 ◽  
Author(s):  
J. K. H. Wales ◽  
D. Milford ◽  
N. M. Okorie
2006 ◽  
Vol 95 (3) ◽  
pp. 603-608 ◽  
Author(s):  
Jeanette Wahlberg ◽  
Outi Vaarala ◽  
Johnny Ludvigsson ◽  

We studied dietary risk factors by analysing a questionnaire administered at birth, 1 year and 2½ years of age, as well as the level of glutamic acid decarboxylase autoantibodies (GADA) and tyrosine phosphatase autoantibodies (IA-2A), in 7208 2½-year-old children from the All Babies in Southeast Sweden cohort, using the 95th percentile cut-off for autoantibodies to identify children at risk of type 1 diabetes. A total of 657 children had either IA-2A (n 360) or GADA (n 335), and thirty-eight children had both GADA and IA-2A. In univariate analysis, male gender and maternal coeliac disease implied a risk of possessing IA-2A. Maternal type 2 diabetes, a high consumption of fresh cows milk at the age of 1 year and a late introduction of gluten were associated with a risk of GADA. Early cessation of breast-feeding (≤2 months of age) was associated with a risk of the simultaneous occurrence of both IA-2A and GADA. In logistic regression analysis, a high consumption of milk at the age of 1 year (odds ratio 2·6) represented a risk for GADA, and maternal coeliac disease (odds ratio 2·9) represented a risk for IA-2A. The combination of an early introduction of cows milk formula and a late introduction of gluten-containing food gave an odds ratio of 6·0 for positivity for at least one autoantibody at 1 and 2½ years of age. The induction of autoantibodies by the age of 2½ years has a male preponderance and is more common in children with maternal type 2 diabetes or maternal coeliac disease. Dietary risk factors for the induction of β-cell autoantibodies in 2½-year-old children are a short duration of breast-feeding, an early introduction of cows milk formula and a late introduction of gluten, as well as a high consumption of milk at the age of 1 year.


2003 ◽  
Vol 92 (0) ◽  
pp. 86-90 ◽  
Author(s):  
Savino F ◽  
Cresi F ◽  
Maccario S ◽  
Cavallo F ◽  
Dalmasso P ◽  
...  

2009 ◽  
pp. 83-89 ◽  
Author(s):  
T. Okubo ◽  
Y. Nakano ◽  
S. Uchikawa ◽  
Y. Fukaya
Keyword(s):  

2017 ◽  
pp. 91-94
Author(s):  
T.M. Klymenko ◽  
◽  
O.A. Serdtseva ◽  
O.S. Karatai ◽  
O.P. Melnychuk ◽  
...  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 159-LB
Author(s):  
ANANTA ADDALA ◽  
SARAH HANES ◽  
DESSI ZAHARIEVA ◽  
CHRISTIN NEW ◽  
PRIYA PRAHALAD ◽  
...  

2019 ◽  
Vol 40 (6) ◽  
pp. 450-452 ◽  
Author(s):  
Ashley L. Devonshire ◽  
Rachel Glick Robison

Primary prevention and secondary prevention in the context of food allergy refer to prevention of the development of sensitization (i.e., the presence of food-specific immunoglobulin E (IgE) as measured by skin-prick testing and/or laboratory testing) and sensitization plus the clinical manifestations of food allergy, respectively. Until recently, interventions that target the prevention of food allergy have been limited. Although exclusive breast-feeding for the first 6 months of life has been a long-standing recommendation due to associated health benefits, recommendations regarding complementary feeding in infancy have significantly changed over the past 20 years. There now is evidence to support early introduction of peanut into the diet of infants with egg allergy, severe atopic dermatitis, or both diagnoses, defined as high risk for peanut allergy, to try to prevent development of peanut allergy. Although guideline-based recommendations are not available for early introduction of additional allergenic foods, this topic is being actively studied. There is no evidence to support additional dietary modification of the maternal or infant diet for the prevention of food allergy. Similarly, there is no conclusive evidence to support maternal avoidance diets for the prevention of food allergy.


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