Feeding a soy formula to children with cow's milk allergy: the development of immunoglobulin E-mediated allergy to soy and peanuts.

Peanut allergy has been associated with the intake of soy milk or a soy formula. We studied the development of immunoglobulin E antibodies specific to soy and peanuts and of allergic reactions caused by peanuts, in children with confirmed cow's milk (CM) allergy fed either a soy formula or an extensively hydrolyzed formula (EHF). One hundred and seventy infants with documented CM allergy (CMA) were randomly assigned to receive either a soy formula or an EHF. The children were followed to the age of 4 yr. Peanut-specific immunoglobulin E was measured at the age of 4. A detailed history of the occurrence of allergic reactions caused by peanuts was recorded by the parents. Soy-specific immunoglobulin E antibodies were measured at the time of diagnosis and at the ages of 1, 2 and 4 yr. Immunoglobulin E antibodies to soy (> or =0.35 kU/l) were found in 22 of 70 children fed the soy formula, and in 14 of 70 of the children fed the EHF (p = 0.082). In an open challenge with soy at the age of 4, no immediate reactions were observed. One of 72 children from the soy group had a delayed reaction. immunoglobulin E antibodies to peanuts (> or =0.35 kU/l) were found in 21 of 70 children fed the soy formula and 17 of 69 infants fed the EHF (p = 0.717). The incidence of reported peanut allergy in the soy group was two of 72 (3%) and four of 76 (5%) in the EHF group (p = 0.68). Development of immunoglobulin E-associated allergy to soy and peanuts was rare in our study group of milk allergic children. The use of a soy formula during the first 2 yr of life did not increase the risk of development of peanut-specific immunoglobulin E antibodies or of clinical peanut allergy.     

Randomized, double-blind comparison of growth in infants receiving goat milk formula versus cow milk infant formula

OBJECTIVE: To compare growth of infants fed goat milk infant formula (GMF) or cow milk infant formula (CMF) and to compare tolerability and safety of the two formulas. METHODS: The study was conducted in Auckland, New Zealand. This was a double-blind randomized controlled trial. Newborn term infants were randomized within 72 h of birth to GMF or CMF. Milk formula powder in single serve sachets were reconstituted and fed to infants from trial commencement until age 168 days. No other formula given from randomization until age 168 days. Infant weight, length and head circumference were measured at birth and age 14, 28, 56, 84, 112, 140 and 168 days. Bowel motion frequency and consistency, sleeping and crying patterns and adverse events were also measured. RESULTS: Seventy-two infants were randomized, 36 each to GMF or CMF, with 62 infants completing the intervention. At enrollment the average weight of infants in the GMF group (mean +/- SD) was 3.33 +/- 0.43 kg and in the CMF group 3.43 +/- 0.47 kg; and at study completion 8.07 +/- 0.90 kg (GMF) and 7.87 +/- 0.99 kg (CMF). The difference in average weight gain over the study period for the GMF group versus the CMF group was not significant (+309 g; 95% CI = -49 to +668, P = 0.09). Median daily bowel motion frequency was greater in the GMF group than the CMF group (2.4 vs 1.7, P = 0.01). There were no group differences in bowel motion consistency, duration of crying, ease of settling, or frequency of adverse events. CONCLUSION: Growth of infants fed GMF is not different to that of infants-fed CMF.     

Markers of inflammation in the feces of infants with cow's milk allergy

Growing evidence exists that exposure to cow's milk elicits inflammation in the gut of infants with cow's milk allergy, irrespective of symptoms. To demonstrate inflammation and increased protein leakage from the gut during a cow's milk elimination‐challenge test in fecal samples of infants presenting with different symptoms suggestive of cow's milk allergy, we measured the concentrations of α₁‐antitrypsin (AT), eosinophil cationic protein (ECP), immunoglobulin (Ig) A, and cow's milk‐specific IgA antibodies, in fecal samples of 208 infants with a mean age of 7 months. Prechallenge samples were collected after a mean 3‐week elimination period, and post‐challenge samples were obtained 4 days after starting the challenge. Fecal levels of prechallenge total IgA (p = 0.02) and post‐challenge AT (p = 0.001) were higher in infants with a positive challenge. Of these infants, pre‐ and post‐challenge levels of ECP were higher in those reacting after 24 h than in those reacting within 1 h (p = 0.006 and p = 0.045). Prechallenge levels of ECP were higher in those showing intestinal symptoms (p = 0.008), and both pre‐ and post‐challenge levels of total IgA were higher in those with an IgE‐mediated reaction to cow's milk (p = 0.04 and p = 0.008). Regardless of the challenge result, total IgA increased during the challenge (p < 0.001 for both challenge‐positive and ‐negative infants) and was higher in those breast‐fed until the challenge than in those fed formula only (p < 0.01). Hence, in infants reacting to the cow's milk challenge, higher prechallenge levels of fecal IgA indicate increased antigenic stimuli in the gut, and higher post‐challenge levels of AT reflect increased protein loss as a result of intestinal inflammation. In infants with slowly evolving gastrointestinal symptoms, increased fecal ECP may help in distinguishing patients from those who tolerate cow's milk. Individual serial follow‐up of fecal IgA and ECP can be used to estimate the degree of inflammation in the gut and an appropriate time for a challenge test, but are not diagnostic tools for cow's milk allergy.     

Randomized double-blind controlled trial on the effects on iron status in the first year between a no added iron and standard infant formula received for three months

Recent research has not only questioned the necessity of iron supplementation in human milk substitutes prior to weaning, but also suggested some potential adverse effects. This study investigated the hypothesis that infant formula need not contain added iron in the first 3 mo. Healthy term infants were recruited into a double-blind controlled trial and randomized to receive either a new no added iron formula (New; <0.1 mg Fe 100 ml(-1)) or a standard formula (Standard; 0.5 mg Fe 100 ml(-1)) for the first 3 mo of life. A breastfed reference group was also studied. Iron status was assessed at 3 and 12 mo from heel-prick capillary blood samples evaluated by full blood-count analysis, including reticulocytes and serum ferritin. In total, 149 infants were entered (51 New, 49 Standard, 49 breastfed) with no differences between the groups in gender distribution, birthweight, gestation or numbers completing the study. There were no significant differences between the principal outcome measures: mean values for haemoglobin, mean cell volume and ferritin, between the two formula-fed groups, and the proportion with a haemoglobin level <11 g dl(-1) or ferritin <10 microg l(-1) did not differ. CONCLUSION: The use of a "no added iron" infant formula in place of an iron-fortified formula during the first 3 mo of life did not clinically affect iron status at 3 and 12 mo of age. The universal supplementation of formulae with iron during this initial period needs further consideration.     

Plasma amino acid and protein concentrations in infants fed human milk or a whey protein hydrolysate formula during the first month of life

The aim of the study was to compare growth parameters, biochemical indices of protein metabolism and plasma amino acid concentrations in infants fed either human milk ( n = 12) or a whey protein hydrolysate formula ( n = 13) during the first month of life. Growth and gain in skin fold thickness were similar in both groups whereas serum protein concentration was significantly decreased (57.4 ± 3.9 versus 61.2 ± 2.9 g/l) in the infants fed the whey hydrolysate formula. The discrepancies between the plasma amino acid pattern of the whey hydrolysate formula group and that of the human milk group lessened during the first month. Nevertheless, at a mean age of 33 days the plasma threonine concentration remained twice as high and the plasma tyrosine, phenylalanine and proline concentrations were Significantly lower in the whey hydrolysate formula group than in the human milk group. Thus, compared with breast-fed infants, growth and most of the biological indices of protein metabolism were satisfactory in infants fed during the first month of life on a whey protein hydrolysate formula. Nevertheless, the decrease in total plasma protein concentration needs to be confirmed in a larger cohort of infants. In addition, further research is necessary to investigate the possible ways of reducing the hyperthreoninemia and preventing other plasma amino acid disturbances since it would be desirable to obtain plasma amino acid levels similar to those of breast-fed infants.     

牛奶蛋白过敏诱发婴儿胃窦息肉形成2 例报告

目的探讨牛奶蛋白过敏与婴儿胃窦息肉的关系。方法回顾分析2例经电子胃镜和病理组织学检查确诊为胃窦增生性息肉导致胃输出道梗阻患儿的临床资料。结果男、女患儿各1例,分别为7月龄、11月龄,均表现为反复呕吐,营养不良。2例患儿的腹部超声检查均疑似先天性肥厚性幽门狭窄,其中女性患儿行幽门环肌切开术。2例患儿经无痛胃镜检查发现,胃窦附近息肉样增生导致胃输出道完全梗阻,术中置入空肠管。2例患儿的牛奶特异性IgE分别为0.43 IU/mL、1.35 IU/mL,均经激发试验确诊为牛奶蛋白过敏。2例患儿经持续空肠管喂养氨基酸配方粉,同时口服激素治疗,2个月后复查胃镜,胃窦息肉均明显缩小,并可自行进食。结论婴儿胃窦息肉少见,2例患儿的胃窦息肉可能与牛奶蛋白过敏相关。     

Low frequency of CD4+, but not CD8+, T cells expressing interferon‐γ is related to cow's milk allergy in infancy

Low interferon‐γ (IFN‐γ) and tumor necrosis factor‐α (TNF‐α) production in peripheral blood mononuclear cells (PBMC) from patients with atopic dermatitis and food allergy have been reported previously. However, it remains unclear whether the weak cytokine production is caused by the imbalance of specific T‐cell subsets or by dysregulation of T‐cell function. In the present study we investigated the intracellular expression of these cytokines at a single‐cell level to clarify the background of the disruption. Twelve of 27 breast‐fed infants (0.1–8.8 months of age) had challenge‐proven cow's milk allergy (CMA), and 15 infants were studied as a healthy control group. PBMC were stimulated with phorbol 12‐myristate 13‐acetate (PMA) and ionomycin. The frequencies of the cells expressing intracellular IL‐4, IFN‐γ, and TNF‐α were assessed using flow cytometry. In addition, at this time‐point leucocyte subsets from the milk of mothers of these infants were evaluated using light microscopy. A lower number of CD8⁺ T cells and the defective capability of CD4⁺ T cells to express IFN‐γ in infant's peripheral blood co‐existed with a lower number of macrophages in their mother's milk.