Here you will find abstracts from medical reports published in medical and science journals. Sometimes it is difficult to understand everything written but in most cases the abstracts will give you an indication of what the final results were.

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Intestinal barrier function and cow's milk sensitization in guinea pigs fed milk or fermented milk.

Evaluation of the usefulness of lymphocyte proliferation assays in the diagnosis of allergy to cow's milk.

The natural history of cow's milk protein allergy/intolerance.

Anaphylaxis to sheep's milk cheese in a child unaffected by cow's milk protein allergy.

Delayed reaction to cow's milk proteins: a case study.

Gastrointestinal allergy to food: a review.

Identification of casein as the major allergenic and antigenic protein of cow's milk.

A case of cow's milk allergy in the neonatal period--evidence for intrauterine sensitization?

Allergenicity of goat's milk in children with cow's milk allergy.

Intestinal barrier function and cow's milk sensitization in guinea pigs fed milk or fermented milk.
Terpend K, Blaton MA, Candalh C, Wal JM, Pochart P, Heyman M; J Pediatr Gastroenterol Nutr 1999 Feb 28:2 191-8

Abstract
BACKGROUND: The respective effect of milk and fermented milks on intestinal barrier capacity and on sensitization to beta-lactoglobulin was studied using a guinea pig model of cow's milk allergy. METHODS: Guinea pigs were fed a control diet or the same diet supplemented with milk, fermented milk (Streptococcus thermophilus and Bifidobacterium breve), or dehydrated fermented milk. Intestinal barrier capacity to macromolecules was assessed in an Ussing chamber, and sensitization to cow's milk proteins was measured by systemic anti-beta-lactoglobulin immunoglobulin G1 titers and by intestinal anaphylaxis, the latter assessed by the beta-lactoglobulin-induced increase in short-circuit current of jejunal fragments (deltaIsc(beta-LG)). RESULTS: The electrical resistance of jejunum was similar in the four groups (approximately 80 omega/cm2) suggesting the same paracellular permeability. The transport of 14C-beta-lactoglobulin from mucosa to serosa was significantly decreased in the animals fed dehydrated fermented milk (403131 ng / hr x cm2) compared with that in control animals or animals fed milk (767250 ng / hr x cm2 and 749475 ng / hr x cm2, respectively; p < 0.05). Milk fermentation did not modify native beta-lactoglobulin concentration but anti-beta-lactoglobulin immunoglobulin G1 titers were higher in fermented milk and dehydrated fermented milk (log10 titer = 2.86 and 2.79, respectively) than in guinea pigs fed milk (log10 titer = 2.5; p < 0.007). However, beta-lactoglobulin-induced intestinal anaphylaxis remained the same in the three groups (deltaIsc(beta-LG), 9.64.1 microA/cm2, 8.54.3 microA/cm2, and 8.53.4 microA/cm2 in milk-fed, fermented milk-fed, and dehydrated fermented milk-fed guinea pigs, respectively). CONCLUSIONS: The intestinal barrier capacity to milk proteins seems to be reinforced by dehydrated fermented milk, but milk and fermented milks are equally efficient in inducing cow's milk allergy in guinea pigs.

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Evaluation of the usefulness of lymphocyte proliferation assays in the diagnosis of allergy to cow's milk.
Hoffman KM, Ho DG, Sampson HA, J Allergy Clin Immunol 1997 Mar 99:3 360-6

Abstract
BACKGROUND: The significance of cell-mediated mechanisms in IgE-mediated milk allergy (IgE-MA) and in milk-induced enterocolitis syndrome (ME) is controversial. Some investigators have claimed that lymphocyte proliferation assays are useful in the diagnosis of food hypersensitivity, despite the great variability in study designs and results reported. This study was undertaken to address many of these variables and to determine whether lymphocyte proliferation assays correlate with clinical diagnoses. METHODS: Lymphocyte proliferative responses to milk antigen were evaluated in two groups of children, 27 with IgE-MA, and nine with ME and in 21 pediatric control subjects. IgE-mediated food allergy was documented by positive double-blind, placebo-controlled food challenges and positive skin prick test results. ME was diagnosed by oral challenge or by a history of repeated episodes of delayed vomiting (>2 hours) after ingestion of milk and by negative skin prick test responses. Peripheral blood mononuclear cells were isolated and cultured. Cultures stimulated with milk (the food antigen of interest), soy antigen (a nonrelevant food antigen), or tetanus antigen (a positive control antigen) and unstimulated controls were performed in quadruplicate. On days 5, 7, and 9, cells were pulsed with tritium-labeled thymidine and incubated for 4 hours. Results were compared as counts per minute (cpm) and as stimulation indices (SIs). RESULTS: Maximal proliferation was generally seen on day 7. The median cpm (20,941) and the median SI (19.2) in response to milk antigen in the 27 children with IgE-MA were significantly greater than those in the control patients (6969 cpm; SI = 14.2; p = 0.001 and p < 0.05, respectively). However, the ranges were large and overlapped extensively (IgE-MA, 5616 to 52,053 cpm; controls, 469 to 39,260 cpm). The non-soy-allergic patients with IgE-MA also had a significantly greater response to soy antigen than did the control subjects when cpm were compared (0.01 < p < 0.05). There were no differences in background or in response to tetanus antigen. The median response to milk in the patients with ME (11,975 cpm) was significantly greater than that in control subjects (6969 cpm; 0.01 < p < 0.05), when cpm were compared but not when SIs were compared. There were no significant differences between the patients with IgE-MA and those with ME. CONCLUSION: Overall, these results indicate that lymphocyte proliferation assays are neither diagnostic nor predictive of clinical reactivity in individual patients with milk allergy. Lymphocytes of many control patients are highly responsive to milk antigens, and lymphocytes of many patients with milk allergy are not. Statistically significant differences are only evident when the patients are compared as groups.

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The natural history of cow's milk protein allergy/intolerance.
Høst A, Jacobsen HP, Halken S, Holmenlund DEur J Clin Nutr 1995 Sep 49 Suppl 1 S13-8

Abstract
In prospective studies th incidence of cow's milk protein allergy and intolerance (CMPA/CMPI) in infancy in western industrialized countries has been estimated to be about 2-3% based on strict diagnostic criteria. A significant association between early neonatal exposure to cow's milk formula feeding and subsequent development of CMPA/CMPI has been documented. The small amounts of 'foreign' protein in human milk may rather induce tolerance than allergic sensitization. The findings of specific IgE to individual cow's milk proteins in cord blood of the majority of infants who later develop CMPA/CMPI suggests a prenatal sensitization may play a role in the pathogenesis of CMPA/CMPI. Perhaps a weak intrauterine education of low IgE-response may need to 'boosted' neonatally in order to cause clinical disease. The prognosis of CMPA/CMPI is good with a recovery of about 45-56% at one year, 60-77% at two years and 71-87% at three years. Associated adverse reactions to other foods, especially egg, soy, peanut and citrus develop in about 41-54%. Allergy to potential environmental inhalant allergens has been reported in up to 28% by three years and up to 80% before the age of puberty. Especially, infants with an early increased IgE response to cow's milk protein have an increased risk of persisting CMPA, development of persistent adverse reactions to other foods and development of allergy against environmental inhalant allergens. Cow's milk protein/intolerance (CMPA/CMPI), meaning reproducible adverse reactions to cow's milk protein(s) may be due to the interaction between one or more milk proteins and one or more immune mechanisms, possible any of the four basic types of hypersensitivity reactions. Immunologically mediated reactions are defined as CMPA. Mostly, CMPA is caused by IgE-mediated (type I) reactions, but evidence for type III (immune complex) reactions and type IV (cell mediated reactions) have been demonstrated as reviewed by Høst (1994) and Ortolani & Vighi (1995). Non immunologically reactions against cow's milk protein(s) are defined as CMPI. However, it should be stressed that many studies on 'cow's milk allergy' have not investigated the immunological basis of the clinical reactions. In most instances of cow's milk protein hypersensitivity only diagnostic investigations such as skin prick test and RAST indicative of IgE-mediated reactions are performed. In fact, CMPA cannot be ruled out unless extensive diagnostic tests for type II-III-IV reactions have proved negative. Thus, the classification of adverse reactions to cow's milk proteins depends on the extent and the quality of performed diagnostic tests for immune mediated reactions. At present, no single laboratory test is diagnostic of CMPA/CMPI, and differentiation between CMPA and CMPI cannot be based solely on clinical symptoms. Therefore the diagnosis has to be based on strict well-defined elimination and milk challenge procedure (Hill & Hosking, 1991), (Høst, 1994). Preferably, double-blind placebo-controlled challenges (DBPCFC) should be carried out in children older than 1-2 years of age. In infants open controlled challenges have been shown to be reliable when performed under professional observation in a hospital setting (Høst & Halken, 1990).

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Anaphylaxis to sheep's milk cheese in a child unaffected by cow's milk protein allergy.
Calvani M Jr, Alessandri C; Eur J Pediatr 1998 Jan 157:1 17-9

Abstract
A 5-year-old atopic boy unaffected by cow's milk protein allergy experienced several anaphylactic reactions after eating food containing ''pecorino'' cheese made from sheep's milk. Prick-prick tests were strongly positive to sheep's buttermilk curd and 'pecorino' sheep's cheese. Skin prick tests to fresh sheep's milk and to goat's milk were also positive, whereas they were negative to all cow's milk proteins, to whole pasteurized cow's milk and to cheese made from cow's milk. Specific IgE antibodies were negative to all cow's milk proteins. CONCLUSION: Sheep's milk and cheese derived from sheep's milk may cause severe allergic reactions in children affected and, as we report, in children not affected by cow's milk protein allergy.

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Delayed reaction to cow's milk proteins: a case study.
Vila Sexto L, Sánchez López G, Sanz Larruga ML, Diéguez López I; J Investig Allergol Clin Immunol 1998 Jul-Aug 8:4 249-52

Abstract
Allergy to cow's milk proteins has been defined as any adverse reaction mediated by immunological mechanisms to one or several of these proteins. The diagnosis can be made based on clinical manifestations supported by immune activation of in vitro parameters. Reactions to cow's milk have been classified according on their onset as immediate (< 45 min) or delayed-type (from 2 h to days). We describe a patient with late respiratory manifestations after milk intake, probably due to more than one immunological mechanism. He was an 18-year-old male who since infancy had presented serous rhinorrea, sneezing, nasal blockade, oropharyngeal pruritus and occasional dyspnea 12 to 48 h after ingestion of milk and its derivates. We performed skin prick and intradermal tests with whole milk and fractions. Patch tests were also carried out with whole milk purchased at a supermarket and with the extracts described, in their original form and vehiculized in vaseline. Total and serum specific IgE and IgG4 to milk fractions, histamine release test (HRT) to milk fractions, and precipitating antibodies by contraimmunoelectrophoresis against milk fractions were also measured. As a control we repeated this test in a patient with IgE-mediated manifestations to milk proteins and in two healthy controls. We performed a single-blind placebo controlled challenge with whole milk. Skin prick and intradermal tests were negative. Patch test (48 h) was positive for whole milk and whole milk vehiculized in vaseline, and for alpha-lactalbumin. Total IgE was 559 kU/l; serum-specific IgE was negative; IgG4 was positive (9.48% for alpha-lactalbumin; 7.41% for beta-lactoglobulin and 9.85% for casein). HRT was positive for casein (34%). We found precipitating antibodies to the three milk fractions in our patient and in the atopic control. In the challenge test, 10 h after milk intake the patient presented serous rhinorrea, sneezing and nasal blockade. IgG4 was involved as a blocking or anaphylactic antibody and as an immunological epiphenomenon reflecting a permanent antigenic stimulus. We find this last explanation to be the most coherent in this case.

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Gastrointestinal allergy to food: a review.
Ahmed T, Fuchs GJ; J Diarrhoeal Dis Res 1997 Dec 15:4 211-23

Abstract
Gastrointestinal food allergy still poses a challenge to the clinician because of its variable symptomatology and lack of reliable diagnostic tests. Its prevalence is estimated at 2 approximately 5%, higher in children than in older age-groups. Allergy to food usually diminishes with advancing age. Although a wide variety of foods can cause allergic reactions, cow's milk is the most common cause of food allergy in infants and young children. Depending upon the speed of onset of symptoms, immediate and delayed types of food allergy have been described. Gastrointestinal symptoms in food allergy have been explained by alterations in transport across the intestinal wall (increased secretory and/or decreased absorptive functions), increased permeability, and motility of the intestine. The exact pathogenesis of food allergy is still not clear. However, immediate type of food allergy is believed to be mediated by type I hypersensitivity reaction, involving mast cells and food-specific IgE antibodies. The diagnosis of food allergy is based upon a favorable response to an elimination diet and a response to a challenge with the suspected food. The condition is treated by eliminating the allergenic food from diet for as long as 9-12 months in case of cow's milk allergy. While exclusive breast-feeding for the initial four months or more reduces the chances of development of food allergy, the role of diet restrictions in the mother in reducing the incidence of food allergy in the infant is controversial. Data on food allergy from developing countries are limited. This may be due to lack of diagnosis or less attention given to the condition relative to other diseases including infectious diarrheas and acute respiratory infections. The role of cow's milk allergy in the pathogenesis of persistent diarrhoea, a major problem in the developing world, remains speculative. Frequent intestinal infections and reduced secretory IgA, which are associated with malnutrition, alter intestinal permeability and result in an increased uptake of food antigens. The increased antigenic load combined with factors such as an atopic predisposition may initiate an abnormal mucosal immune response resulting in chronic enteropathy.

Identification of casein as the major allergenic and antigenic protein of cow's milk.
Docena GH, Fernandez R, Chirdo FG, Fossati CAAllergy 1996 Jun 51:6 412-6

Abstract
The objective of this study was to analyze both the allergenicity and immunogenicity of cow's milk proteins. To this end, 80 milk-atopic patients were selected on the basis of the presence of cow's milk-specific IgE antibodies in serum and compatible clinical history. Fifteen patients allergic to other allergens and 10 nonatopic subjects were studied as controls. The specificity of serum IgG and IgE antibodies was determined by immunoblotting, employing both cow's milk and milk components, i.e., alpha- and beta-casein, beta-lactoglobulin, and alpha-lactalbumin separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The experiments showed that casein-specific IgE antibodies were present in all (80/80) sera examined; 10/80 showed reactivity to beta-lactoglobulin, and 5/80 showed reactivity to alpha-lactalbumin. None of the 25 negative control sera analyzed showed the presence of specific IgE antibodies against milk proteins. These results were similar to those corresponding to the detection, by the radioallergosorbent test, of IgE antibodies against the milk components coupled to paper disks. All sera from milk-atopic patients also showed IgE reactivity against a high-molecular-mass fraction that hardly enters the gel. This fraction, after separation by gel filtration and treatment with beta-mercaptoethanol and urea, was shown by SDS-PAGE analysis to be formed by casein monomers. All sera analyzed by immunoblotting reacted against the components corresponding to casein monomers. Inhibition of immunoblotting by adsorption with different milk components confirmed that those high-molecular-mass aggregates are formed by casein components. The results presented here strongly suggest that casein is the major allergenic component of cow's milk.

A case of cow's milk allergy in the neonatal period--evidence for intrauterine sensitization?
Feiterna-Sperling C, Rammes S, Kewitz G, Versmold H, Niggemann B; Pediatr Allergy Immunol 1997 Aug 8:3 153-5

Abstract
Clinical manifestations of cow's milk allergy rarely occur in the first days after birth. We report on a newborn presenting with hemorrhagic meconium in the first hour of life followed by bloody diarrhea in the next few days. At day 14, an elevated total IgE, specific IgE to cow's milk and an eosinophilia in peripheral blood were found. Symptoms disappeared when the milk feed was changed to an extensively hydrolyzed casein-formula. Two challenges with cow's milk formula (on day 30 and at 7 months of age) were followed by recurrence of vomiting, watery diarrhea and failure to thrive. At the age of 17 months cow's milk was tolerated well. Although other pathogenetic mechanisms cannot completely be ruled out, there is strong evidence that cow's milk allergy--induced by intra-uterine sensitization--explains the symptoms in our patient. In conclusion, cow's milk allergy can occur even in the first days of life, and our clinical observation supports the concept of intra-uterine sensitization to allergens.

Allergenicity of goat's milk in children with cow's milk allergy.
Bellioni-Businco B. Paganelli R. Lucenti P. Giampietro PG. Perborn H. Businco L.; Journal of Allergy & Clinical Immunology. 103(6): 1191-4, 1999 Jun.

Abstract
BACKGROUND:Cow's milk allergy (CMA) is a common disease of infancy and childhood. An appropriate cow's milk (CM) substitute is necessary for feeding babies with CMA. CM substitutes are soy formulas and casein- or whey-based extensively hydrolyzed formulas. In several countries, including Italy, goat's milk (GM) formulas are available, and some physicians recommend them for feeding babies with CMA. OBJECTIVE: We sought to investigate, in vitro and in vivo, the allergenicity of GM in 26 children with proven I~-mediated CMA. METHODS: All the children underwent skin tests with CM and GM; detection of specific serum I~ to CM and GM; and double-blind, placebo-controlled, oral food challenges (DBPCOFCs) with fresh CM, GM, and, as placebo, a soy formula (Isomil, Abbott, Italy). CAP inhibition and immunoblotting inhibition assays were also carried out in 1 of 26 and 4 of 26 children with positive RAST results to both CM and GM, respectively. RESULTS: All the children had positive skin test responses and CAP results to both CM and GM, all had positive DBPCOFC results to CM, and 24 of 26 had positive DBPCOFCs to GM. In CAP inhibition tests, preincubation of serum with CM or GM strongly inhibited I~ either to CM or to GM. In immunoblotting inhibition assays, preincubation with CM completely extinguished reactivity to GM, whereas GM partially inhibited reactivity to CM. CONCLUSIONS: These data strongly indicate that GM is not an appropriate CM substitute for children with I~-mediated CMA. A warning on the lack of safety of GM for children with CMA should be on the label of GM formulas to prevent severe allergic reactions in babies with CMA.