Although frequently associated with use of cow’s milk-based infant formulas, CMPA can actually develop in exclusively breastfed infants as well, and when CMP is introduced into the diet of the young child.1,2 It is important to identify CMPA early in order to distinguish symptoms from various other conditions that require a different approach to treatment, and to avoid unnecessary elimination diets.
Mechanisms of CMPACMPA results from an immunological reaction to one or more milk proteins. The proteins most frequently and most intensively recognized by specific IgE are casein and lactoglobulin. However, all milk proteins appear to be potential allergens, even those that are present in milk in trace amounts. It is this immunological reaction that differentiates CMPA from other adverse reactions to CMP, notably lactose intolerance.
CMPA may be IgE or non-IgE associated.2 Symptoms of CMPA: What and when?An infant can experience symptoms either very quickly after feeding (rapid onset) or up to several days or even weeks after first consuming the cow's milk protein (slower onset). The most common symptoms are gastrointestinal (50-60%), skin (50-60%) and respiratory (20-30%). Many infants may experience two or more of these symptoms.
3 IgE-associated cases of CMPA tend to show an early reaction even to a small quantity of CMP, with symptoms including irritability, urticaria, dermatitis, swelling, or vomiting occurring within minutes. Although anaphylaxis is more common in other food allergies, in rare cases, anaphylaxis can occur in conjunction with CMPA. In these cases, CMPA may be the first expression or predictor of future atopy and other food allergies in the infant, and there is frequently a family history of atopy.
1 Common symptoms of cow's milk protein allergy Organ involvement Symptoms GI tract Frequent regurgitation, vomiting, diarrhea, constipation, blood in stool, iron deficiency anemia Skin Atopic dermatitis, urticaria not linked to infections or medication, swelling of lips or eyelids Respiratory tract (not related to RTI) Runny nose, otitis media, chronic cough, wheezing General Persistent distress, irritability or colic, at least 3 days/week for >3 weeks Source: Vandenplas et al.
, 2007.1 In non-IgE-associated cases, the reaction is later – from several days to weeks after initial exposure – and more likely to involve dermatitis or diarrhea. This slower onset reaction is more common. Symptoms may include loose stools (possibly containing blood), vomiting, gagging, refusing food, irritability or colic, and skin rashes. This type of reaction is more difficult to diagnose because the same symptoms may occur with other health conditions.
This form of CMPA is not considered to predict future atopy.1,2,4 Diagnosis of CMPAIn the breastfed infant: To distinguish CMPA from other possible sensitivities derived from breastmilk, the mother should exclude cow's milk, peanuts, and hen's eggs from her diet for 2-4 weeks. If the infant’s symptoms improve over this time, the mother should introduce one food back into her diet per week. If there is no improvement after an elimination diet, a specialist in pediatric allergy should be consulted.
In the formula-fed infant: Where CMPA is suspected, elimination of CMP from the infant’s diet is accomplished by switching to a therapeutic formula that is indicated for allergy prevention; this could be an extensively hydrolyzed formula or an amino acid-based formula. It has been found that up to 10% of infants with CMPA will have an allergic reaction to an extensively hydrolyzed formula. Again, a specialist in pediatric allergy should be consulted if neither of these formula types improves symptoms.
1 Differential diagnoses: Lactose intolerance, food allergies, colic, GERDThe immunological reaction that characterizes CMPA distinguishes it from other non-immunological adverse reactions to CMP such as lactose intolerance. As well, a number of alternative diagnoses not related to CMP are possible, including allergic reactions to other foods or substances, conditions including celiac disease, and GI or UTI infections.
If it is determined that the reaction is non-immunological, it is recommended that the infant be assessed for other conditions such as gastroesophageal reflux disease or colic.1 Delayed diagnosis: Effects of CMPAWhen there is a delay in diagnosis of CMPA, continued exposure to CMP can lead to increasing enteric inflammation resulting in bloody diarrhea, anemia, dehydration, and failure to follow normal patterns of growth and weight gain.
Intestinal inflammation may be limited to mild proctitis or true enterocolitis with esophagitis, gastritis and colitis.4 There is higher risk of growth restriction when CMPA develops in the very young infant, therefore early diagnosis and treatment via a change to the infant’s diet can decrease risks associated with CMPA, including impaired growth.1 Management of CMPAInfants at high risk of atopy: For infants at high risk of developing atopy, evidence has shown that exclusive breastfeeding for at least 4 months or supplementing breastfeeding with an infant formula containing partially hydrolyzed or extensively hydrolyzed protein decreases the risk of atopic dermatitis compared with breastfeeding supplemented with standard cow’s milk protein infant formula.
5 For infants who are exclusively formula-fed, the German Infant Nutritional Intervention (GINI) Study, which compared 3 hydrolyzed formulas (partially hydrolyzed whey, extensively hydrolyzed whey and extensively hydrolyzed casein), reported reduced incidence of atopic dermatitis with the partially hydrolyzed whey formula and the extensively hydrolyzed casein formula compared with standard cow’s milk formula or extensively hydrolyzed whey formula.
5,6 Infants with confirmed CMPA: For exclusively breastfed infants with confirmed CMPA, it has traditionally been recommended that the mother avoid cow’s milk for the duration of breastfeeding; a clinical report released by the AAP in January 2008 now points to a lack of evidence for dietary restrictions during breastfeeding to prevent atopic disease with the possible exception of atopic eczema.
5 For formula-fed infants, whether exclusive or in combination with some breastfeeding, formula options include those with specific indication for allergic infants. Extensively hydrolyzed casein formulas are well tolerated by most infants with CMPA, but in some cases, they may still cause an allergic reaction. Amino acid-based formulas contain protein in its simplest form, and may be recommended if the infant’s condition doesn't improve with a hydrolyzed formula.
Soy protein-based formulas are frequently recommended as an alternative formula. However, soybean protein ranks second as an antigen in the first months of life, particularly in infants with primary cow's milk intolerance who are placed on a soy formula.5 The recent AAP report states that there is no conclusive evidence for allergy prevention with soy-based formula.5 It is important to note that only extensively hydrolyzed casein or amino acid-based formulas have official indication for the treatment of known allergic disorders.
Partially hydrolyzed formula is not recommended for the treatment of allergy.8 Long-term prognosis: what is the likelihood of becoming tolerant to CMP?The majority of children with early CMPA will eventually become tolerant to CMP. It is usually assumed that the child will become tolerant of CMP by the age of 5 years when their mucosal immune system matures and they become immunologically tolerant of milk proteins.
In most children with non-IgE-associated CMPA, symptoms are likely to resolve by the time the child is 1 to 2 years of age.1,2 Children with a history of IgE-positive CMPA are at increased risk of developing further atopic conditions including atopic dermatitis and asthma as well as food allergies and allergy to environmental allergens. On the other hand, children who are IgE-negative will become tolerant to CMP earlier and are at lower risk to develop other allergies.
1,9 CMPA: Is there potential for primary prevention?The increasing incidence of pediatric allergies including CMPA calls for new primary prevention strategies. It is well understood that exclusive breastfeeding provides early and extensive immune support. For formula-fed infants, a growing body of evidence suggests that primary prevention of CMPA in the form of a nutritional strategy may be possible.
This may be of particular interest in families with a history of atopy. Protein composition: A 2003 meta-analysis conducted by the Cochrane Collaboration indicated that reducing the risk of common allergic manifestations in infancy is possible by feeding either 100% whey protein, partially hydrolyzed formula or extensively hydrolyzed casein formula instead of intact cow's milk protein formula.8 As noted earlier in this article, the GINI study found that feeding a hydrolyzed formula – partially hydrolyzed whey or extensively hydrolyzed casein – vs.
intact cow's milk formula or extensively hydrolyzed whey formula during the first 4 months of life reduced the risk of allergic manifestations during the first year of life.5,6 Timing for introduction of solids: In contrast to long-held beliefs regarding introduction of solids, in the recent clinical report, the AAP reversed its stance on delaying the introduction of common allergens including dairy, eggs, and nuts, citing a lack of evidence that delaying introduction beyond age 4-6 months has a significant protective effect on the development of atopic disease.
5 Probiotic supplementation: Evidence shows that the intestinal flora in formula-fed infants is influenced by the protein composition of the formula used. A higher proportion of bifidobacteria and lactobacilli has been found in infants fed with whey formula vs. casein formula. Since it is known that oral probiotic supplementation can reduce the prevalence of atopic disease by stabilizing intestinal integrity, increasing numbers of specific intestinal flora and reducing intestinal inflammation, a formula that increases the number of these bacteria could offer benefits in reducing the risk of allergy in infants.
9,10 References: Vandenplas Y et al. Guidelines for the diagnosis and management of cow’s milk protein allergy in infants. Arch Dis Child 2007;92:902–8. Nocerino A. Protein Intolerance. http://www.emedicine.com/ped/topic1908.htm Høst A. Frequency of cow’s milk allergy in childhood. Ann Allergy Immunol2002;89(Suppl 1):33–7. Lake AM. Dietary protein enterocolitis. Curr Allergy Rep 2001;1(1):76–9.
Greer FR et al. and the American Academy of Pediatrics Committee on Nutrition and Section on Allergy and Immunology. Effects of Early Nutritional Interventions on the Development of Atopic Disease in Infants and Children: The Role of Maternal Dietary Restriction, Breastfeeding, Timing of Introduction of Complementary Foods, and Hydrolyzed Formulas. Pediatrics 2008;121(1):183-91. von Berg A et al.
The effect of hydrolyzed cow’s milk formula for allergy prevention in the first year of life: The German Infant Nutritional Intervention Study, a randomized double-blind trial. J Allergy Clin Immunol 2003;111(3):533–40. Osborn DA, Sinn J. Soy formula for prevention of allergy and food intolerance in infants. Cochrane Database of Systematic Reviews 2006, Issue 4. Art. No.: CD003741. DOI: 10.
1002/14651858.CD003741.pub4. http://mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD003741/frame.html Osborn DA, Sinn J. Formulas containing hydrolysed protein for prevention of allergy and food intolerance in infants. Cochrane Database of Systematic Reviews 2006, Issue 4. Art. No.: CD003664. DOI: 10.1002/14651858.CD003664.pub3. http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD003664/frame.
html Høst A et al. The natural history of cow’s milk protein allergy/intolerance. Eur J Clin Nutr 1995;49(Suppl 1):S13–8. Lara-Villoslada F et al. The Balance Between Caseins and Whey Proteins in Cow’s Milk Determines its Allergenicity. J Dairy Sci 2005 88:1654–60. Kalliomaki M et al. Probiotics in primary prevention of atopic disease: A randomized placebo-controlled trial. Lancet 357:1076–79.
See Also: When Does A Cow Give Milk
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Can Fam Physician. 2008 Sep; 54(9): 1258–1264. PMCID: PMC2553152 Language: English | French This article has been cited by other articles in PMC. ABSTRACT OBJECTIVE To provide a practical, evidence-based approach to the diagnosis and management of milk protein allergy in infants. SOURCES OF INFORMATION MEDLINE was searched from 1950 to March 2008 using the MeSH heading milk-hypersensitivity.
Additional sources were derived from reviews found with the initial search strategy. Evidence was levels I, II, and III. MAIN MESSAGE Milk protein allergy is a recognized problem in the first year of life; cow’s milk protein allergy is the most common such allergy. Diagnosis is suspected on history alone, with laboratory evaluations playing a supporting role. Confirmation requires elimination and reintroduction of the suspected allergen.
Management includes diet modification for nursing mothers and hydrolyzed formulas for formula-fed infants. Assessing the underlying immunopathology can aid in determining prognosis. CONCLUSION The therapeutic model presented allows rapid assessment of the presence of allergy, timely management, and surveillance for recurrence of symptoms. Breastfeeding can be continued with attentive diet modification by motivated mothers.
RÉSUMÉ OBJECTIF Proposer une méthode pratique fondée sur des données probantes pour diagnostiquer et traiter l’allergie aux protéines du lait chez le nourrisson. SOURCE DE L’INFORMATION On a consulté MEDLINE entre 1950 et 2008 à l’aide de la rubrique MeSH milk-hypersensitivity. D’autres sources d’information ont été tirées des revues repérées par la stratégie initiale.
Les preuves obtenues étaient de niveaux I, II et III. PRINCIPAL MESSAGE L’allergie aux protéines du lait est un problème connu chez l’enfant de moins d’un an; l’allergie aux protéines du lait de vache est la forme la plus fréquente. L’historique est suffisant pour suggérer ce diagnostic, les tests de laboratoire jouant un rôle de support. La confirmation exige le retrait et la réintroduction de l’allergène présumé.
Le traitement comprend une modification du régime pour la mère allaitant et des préparations hydrolysées pour les bébés au biberon. L’évaluation de l’immunopathologie sous-jacente peut aider à établir le pronostic. CONCLUSION Le modèle thérapeutique proposé permet la détection rapide de l’allergie, un traitement opportun et la surveillance d’une réapparition des symptômes.
Les mères motivées peuvent continuer d’allaiter si elles modifient correctement leur alimentation. Milk protein allergy (MPA) is a recognized problem in infancy and might affect up to 15% of infants.1 Most cases of MPA can be managed successfully in the outpatient setting. This article summarizes the current evidence for diagnosis and management of MPA. Case description Baby M. is a full-term, 4-kg infant girl delivered vaginally of a 22-year-old primiparous mother after an uneventful pregnancy.
At the 2-week follow-up visit, Baby M. has regained her birth weight. Her mother reports frequent episodes of regurgitation after breastfeeding, which do not distress her. Family history is significant for environmental allergies in both parents and a paternal uncle with eczema and severe asthma. At the 4-week follow-up visit, the mother reports ongoing regurgitation followed occasionally by crying.
Stools have become more frequent and appear watery. The baby’s weight is 4150 g, a gain of 10 g/d since the last visit. Sources of information A MEDLINE search was conducted using the MeSH heading milk-hypersensitivity. English-language articles studying subjects younger than 1 year of age were selected. Additional articles were derived from review articles found with the initial search strategy, yielding a total of 36 publications.
Evidence was levels I, II, and III. Epidemiology Cow’s milk protein allergy (CMPA) appears to be the most common MPA, with controlled challenge trials demonstrating an incidence of 2% to 5% among formulafed infants (level I evidence).1 The incidence in breastfed infants is 0.4% to 0.5% according to 2 trials (level I evidence), 2,3 but might be as high as 2.1% (level II evidence).4 Determining the incidence of allergy to milk proteins from other sources is complicated by the widespread use of bovine milk.
A population-based cohort study found the incidence of soy allergy to be 0.25% (level II evidence).5 Among high-risk infants, CMPA appears to outweigh soy milk protein allergy (SMPA) by a factor of 6 to 1 (level I evidence).6 A study by Klemola et al found the incidence of SMPA to be 10% among children with CMPA.7 Interestingly, qualitative observation alone suggested a cross-reactivity as high as 30%, but only a 10% rate was observed using rigorous quantitative measures.
This underscores the importance of appropriately testing diagnostic suspicions. Cross-reactivity between milk protein from ewe, goat, or buffalo and bovine milk protein has been demonstrated in vitro.8 Unfortunately, Canadian data are lacking. Pathophysiology Milk protein allergy can manifest via IgE-mediated and non–IgE-mediated pathways.9 An IgE-mediated allergy (also known as type I hypersensitivity reaction) occurs when antigens bind to IgE antibodies bound to mast cells.
Cross-linking of 2 IgE antibodies by an antigen causes the mast cell to release histamine, a potent inflammatory mediator, resulting in an immediate allergic reaction. Non–IgE-mediated MPA is likely multifactorial and includes immune complexes of IgA or IgG antibodies bound to milk antigens (type III hypersensitivity reaction) and direct stimulation of T cells by milk protein antigens (type IV hypersensitivity reaction).
The interactions result in cytokine release and increased production of antibodies that recognize the offending milk proteins, contributing to an inflammatory cascade. These more complex immune interactions result in delayed onset of clinical symptoms. While there is overlap of clinical symptoms in the 2 groups of immune reactions,9 a non–IgE-mediated allergy is certain with isolated bloodstreaked stools (level III evidence).
With the other symptoms, while a distinction might be suspected it cannot be confirmed by clinical history alone (10–12). Making the distinction is important, as IgE-mediated MPA is associated with a higher risk of multiple food allergies and atopic conditions such as asthma later in life (level I and II evidence).10,13 Symptoms of milk protein allergy and their differential diagnoses Cross-sensitization between protein sources is well established.
Among infants with CMPA, 13% to 20% have allergies to beef (level II evidence).14 Restani et al demonstrated that antibodies harvested from children with CMPA recognize milk proteins from ewe, goat, and buffalo species, but not from camels (level II evidence).8 Completely different organisms produce soy and bovine proteins. Rozenfeld et al demonstrated that a monoclonal antibody specific to casein (a bovine milk protein) displayed affinity to a component of glycinin, an ingredient in soy-based formulas.
15 Clinical presentation Infants with MPA usually present with symptoms similar to allergic reactions in older individuals. These include cutaneous symptoms such as urticaria, rash, and pruritus, as well as respiratory symptoms such as wheeze and cough (level I evidence).11 These symptoms are usually indicative of IgE-mediated MPA.9 Milk protein allergy can also present with gastrointestinal and nutritional manifestations.
These include gastroesophageal reflux, esophagitis, gastritis, delayed gastric emptying, enteropathy, colitis, constipation, and failure to thrive (level I to II evidence).12 These symptoms might be the cause of behaviour such as crying inconsolably and refusing feeding. The symptoms are the same among breastfed and formula-fed infants. Gastrointestinal symptoms are particularly challenging owing to their nonspecificity and wide differential diagnosis, but MPA should always be suspected.
One study administered a cow's milk—free diet to 10 infants with refractory gastroesophageal reflux that had not improved with pharmacologic therapy and reported that 2 of the infants' symptoms improved (level II evidence).16 Jakobsson et al administered hydrolyzed formula to 15 infants with severe colic and demonstrated a 60% to 70% reduction in daily crying time (level II evidence),17 but caution should be used in generalizing these results to all infants with colic.
Levels of evidence Level I: At least one properly conducted randomized controlled trial, systematic review, or meta-analysis Level II: Other comparison trials, non-randomized, cohort, case-control, or epidemiologic studies, and preferably more than one study Level III: Expert opinion or consensus statements Diagnosis Confirming the diagnosis of MPA is important owing to the discrepancy between parental description of symptoms and scientific confirmation.
7,9 Double-blind, placebo-controlled food challenge has long been regarded as the criterion standard (level I evidence),18 however, owing to the risk of substantial allergy during food challenge, an alternative test with equal efficacy is preferred. Other investigational options include skinprick testing (SPT), serum measurement of IgE antibodies to the specific allergen, and patch testing. A recent study suggests that a combination SPT and measuring IgE antibodies results in a positive predictive value of 95% for diagnosing IgE-mediated CMPA, obviating the need for the food challenge if an IgE-mediated CMPA is suspected (level I evidence).
19 A similar study, however, failed to reproduce these results (level II evidence).20 Skin-prick testing and specific IgE levels are not useful for the diagnosis of non–IgE-mediated MPA,9 but patch testing shows promise.21 Laboratory investigations are not diagnostic but can support a diagnosis made on clinical grounds. A decreased albumin level is suggestive of enteropathy (level III evidence). Increased platelets, erythrocyte sedimentation rate, C-reactive protein, and fecal leukocytes are all evidence of inflammation but are nonspecific; normal values do not rule out MPA (level III evidence).
Eosinophilic leukocytosis might be present in both types of MPA.20 Management The main principle in management of MPA is to avoid allergens while maintaining a balanced, nutritious diet for infants and mothers. Although it is difficult, breastfeeding can be continued if allergens are avoided. For CMPA, a breastfeeding mother must sequentially eliminate all cow’s milk protein, then all bovine protein (milk and meat), and occasionally other protein sources such as soy (level II evidence).
22,23 A similar broad restriction is recommended for other MPAs given their low incidence and association with CMPA (level III evidence). Consultation with a dietitian is essential for a mother who continues breastfeeding; particular attention must be paid to adequate calcium intake. A list of foods containing cow’s milk and soy proteins is found in .24,25 Sources of cow’s milk protein and soy protein For formula-fed infants, current options include specific allergen avoidance, extensively hydrolyzed protein formulas (EHFs), and amino acid–based formulas (AAFs) ().
Extensively hydrolyzed protein formulas incorporate hydrolysates of casein or whey derived from cow’s milk. Their efficacy among those with CMPA is approximately 90% (level I to II evidence),23,26–29 though their efficacy among those with other forms of MPA is less well demonstrated. These formulas do have potentially allergenic material,30 and allergic reactions have been reported.31,32 A rice-based EHF shows promise in young children,33 but is not commercially available.
Amino acid–based formulas are created from constituent amino acids and have demonstrated efficacy of approximately 99% (level I evidence)28,34; they can be considered as an immediate or secondary alternative to EHFs. However, even AAFs contain potentially allergenic material, such as soy lecithin, so their use must be monitored. The taste of the formula might be an issue for compliance; as a rule of thumb, the more hydrolyzed a formula, the worse the taste.
Hydrolyzed formulas available in Canada Specific allergen avoidance, such as substituting soy-based formulas for milk-based in CMPA, is not recommended. The concomitant presence of multiple MPAs reduces the likelihood of success of milk protein substitution.7,8 Additionally, cross-sensitization of milk proteins correlates with increased intestinal permeability (level II evidence).35 Thus, allergy-induced enteropathy might increase the risk of cross-sensitization if specific allergen avoidance is pursued during the acute phase (level III evidence).
If the expense of EHFs or AAFs is a concern, in order to avoid the risk of cross-sensitization, have patients avoid alternate protein sources for at least 1 month to give the intestinal mucosa time to heal, then challenge with a protein alternative (level III evidence). Introduction of solid food can occur at the usual age barring complications such as feeding aversion. Education regarding diet restriction is essential and is best achieved with the help of a dietitian (level III evidence).
36 The importance of a dietitian referral is underscored by a study demonstrating a high rate of parental error in avoiding milk protein–laced foods at the grocery store (level II evidence).37 Parents might also worry about lactose intolerance, and they should be reassured of the extreme rarity of lactase deficiency in infants younger than 1 year of age.38 Prognosis The timing of reintroducing milk protein is of great concern to parents.
Traditionally, it was thought that MPA resolved by 1 to 2 years of age (level III evidence).9,39 Two recent studies, however, suggest a more complex answer. Carroccio et al40 found the proportions of Italian infants with CMPA who had milk tolerance at 1, 2, and 3 years after initiation of milk-free diets were 30%, 54%, and 70%, respectively. Vanto et al41 demonstrated a difference in tolerance when considering the type of CMPA among Finnish infants (level II evidence).
At 2, 3, and 4 years of age, children with non–IgE-mediated CMPA had milk tolerance at rates of 64%, 92%, and 96%, respectively, while children with IgE-mediated allergy were milk tolerant at rates of 31%, 53%, and 63% (level II evidence). Furthermore, children with less reactive SPT results and fewer specific IgE antibodies were milk tolerant sooner than children with more dramatic findings. Taken together, these results suggest that cow’s milk protein can be reintroduced in trial fashion at 1 year of age in children deemed to have non–IgE-mediated allergy, while children suspected of IgE-mediated allergy should not be exposed to cow’s milk for longer time periods, with the length of time guided by allergy testing.
Data regarding resolution of other types of MPA are lacking, though children with multiple food allergies are more likely to remain allergic. When to refer There are no published guidelines on when to refer infants with MPA to specialist care. A list of potential situations in which it is prudent to refer infants for specialized care can be found in 10 (level III evidence). When and to whom to refer infants with milk protein allergy Summary of a practical approach A diagnostic and treatment algorithm is provided in .
Algorithm for diagnosis and treatment of milk protein allergy (MPA) Weight should be followed closely (42). Appropriate weight gain in infancy The timing of clinical response to protein elimination depends on the symptoms observed and the manner of infant feeding. - In formula-fed infants, esophagitis and behavioural symptoms should respond within 72 hours. - Other non–IgE-mediated symptoms should start to improve within 7 days.
- Colitis can take up to 3 weeks to heal; ongoing bloody stools can persist even when patients are improving generally. - Advise breastfeeding mothers that a 7-day washout of milk proteins is required when instituting a restricted diet, delaying the expected clinical response. Milk protein allergy can be successfully managed in primary care with the support of a dietitian; consultation with other specialists should be reserved for severe allergies, failure to respond to standard management, and specific allergy testing if indicated.
Case resolution Baby M.’s bloodwork results revealed the following: platelet count 474 × 109/mL; albumin 34 g/L; and no eosinophilic leukocytosis. Stool microscopy results revealed many fecal leukocytes per high-powered field. The mother was advised to remove all bovine milk products from her diet. She returned for a followup visit 2 weeks later and reported normalization of stools and resolution of crying with regurgitation.
She was advised to resume consumption of cow’s milk products. She called the office 3 days later and reported a recurrence of the looser, more frequent stools. Upon removing cow’s milk from the diet, the stool pattern improved. A diagnosis of CMPA was made. A dietitian saw mother and infant when Baby M. was 5 months of age and provided advice regarding introduction of solid foods. Cow’s milk was reintroduced at 11.
5 months of age without a relapse of symptoms, and Baby M. ate cake at her first birthday party. Acknowledgments I thank Dr Deanna Telner for her assistance with this manuscript. Notes EDITOR’S KEY POINTS Milk protein allergy can occur in both formula-fed and breastfed infants, usually in the first year of life. The presentation can be cutaneous (eg, rashes, pruritus), but can also include respiratory, gastrointestinal, and nutritional manifestations.
Some might present with behaviours such as crying inconsolably and refusing feeding. Milk protein allergy is suspected based on history. Investigational options include food challenge, skinprick testing, serum measurement of specific IgE antibodies, and patch testing. The main principle in management is to avoid allergens while maintaining a balanced, nutritious diet for infants and mothers; breastfeeding can be continued if allergens are avoided by the mother.
Infants’ weight should be followed closely. Milk protein allergy can be successfully managed in primary care with the support of a dietitian; consultation with other specialists should be reserved for severe allergies, failure to respond to standard management, and specific allergy testing if indicated. POINTS DE REPÈRE DU RÉDACTEUR L’allergie aux protéines du lait peur survenir durant l’allaitement au biberon ou durant l’allaitement maternel, habituellement avant l’âge d’un an.
Les manifestations initiales peuvent être cutanées (p.ex. rash, prurit), mais elles peuvent aussi être d’ordre respiratoire, digestif ou nutritionnel. Certains nourrissons présentent d’abord des pleurs irréductibles et refusent toute nourriture. L’historique permet de soupçonner une allergie aux protéines du lait. Les investigations possibles incluent la provocation alimentaire, le prick-test, la mesure du taux sérique des anticorps IgE spécifiques et l’épidermoréaction.
Le traitement cherchera principalement à éviter l’allergène tout en maintenant un régime nourrissant et équilibré, pour le nourrisson comme pour la mère; l’allaitement au sein peut être poursuivi si la mère évite les allergènes. Le poids du bébé doit être étroitement surveillé. L’allergie aux protéines du lait peut être traitée avec succès en soins primaires avec le soutien d’une diététicienne; les autres spécialistes ne devraient être consultés qu’en cas d’allergie sévère ou d’échec du traitement standard et quand des tests d’allergie spécifiques sont indiqués.
Footnotes This article has been peer reviewed. Cet article a fait l’objet d’une révision par des pairs. Competing interests None declared References 1. Høst A. Frequency of cow’s milk allergy in childhood. Ann Allergy Asthma Immunol. 2002;89(6 Suppl 1):33–7. [PubMed] 2. Jakobsson O, Lindberg T. A prospective study of cow’s milk protein intolerance in Swedish infants. Acta Paediatr Scand.
1979;68(6):853–9. [PubMed] 3. Høst A, Husby S, Osterballe O. A prospective study of cow’s milk allergy in exclusively breast-fed infants. Incidence, pathogenetic role of early inadvertent exposure to cow’s milk formula, and characterization of bovine milk protein in human milk. Acta Paediatr Scand. 1988;77(5):663–70. [PubMed] 4. Saarinen KM, Juntunen-Backman K, Järvenpää AL, Klemetti P, Kuitunen P, Lope L, et al.
Breast-feeding and the development of cows’ milk protein allergy. Adv Exp Med Biol. 2000;478:121–30. [PubMed] 5. Arshad SH, Tariq SM, Matthews S, Hakim E. Sensitization to common allergens and its association with allergic disorders at age 4 years: a whole population birth cohort study. Pediatrics. 2001;108(2):e33. [PubMed] 6. Cantani A, Lucenti P. Natural history of soy allergy and/or intolerance in children, and clinical use of soy-protein formulas.
Pediatr Allergy Immunol. 1997;8(2):59–74. [PubMed] 7. Klemola T, Vanto T, Juntunen-Backman K, Kalimo K, Korpela R, Varjonen E. Allergy to soy formula and to extensively hydrolyzed whey formula in infants with cow’s milk allergy: a prospective, randomized study with a follow-up to the age of 2 years. J Pediatr. 2002;140(2):219–24. [PubMed] 8. Restani P, Gaiaschi A, Plebani A, Beretta B, Cavagni G, Fiocchi A, et al.
Crossreactivity between milk proteins from different animal species. Clin Exp Allergy. 1999;29(7):997–1004. [PubMed] 9. Baehler P, Chad Z, Gurbindo C, Bonin AP, Bouthillier L, Seidman EG. Distinct patterns of cow’s milk allergy in infancy defined by prolonged, two-stage doubleblind, placebo-controlled food challenges. Clin Exp Allergy. 1996;26(3):254–61. [PubMed] 10. Høst A. Cow’s milk protein allergy and intolerance in infancy.
Some clinical, epidemiological and immunological aspects. Pediatr Allergy Immunol. 1994;5(5 Suppl):1–36. [PubMed] 11. Heine RG, Elsayed S, Hosking CS, Hill DJ. Cow’s milk allergy in infancy. Curr Opin Allergy Clin Immunol. 2002;2(3):217–25. [PubMed] 12. Salvatore S, Vandenplas Y. Gastroesophageal reflux and cow milk allergy: is there a link? Pediatrics. 2002;110(5):972–84. [PubMed] 13. Høst A, Halken S.
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21st ed. New York, NY: McGraw-Hill Professional; 2003. p. 5. Articles from Canadian Family Physician are provided here courtesy of College of Family Physicians of Canada