Tree nut introduction in a peanut-allergic child: To eat,to screen,or to avoid?

There is no defined standard of care around tree nut introduction in a peanut-allergic child, and the role of screening prior to tree nut introduction is controversial. There is some evidence that peanut-allergic children are at increased risk of tree nut allergy, with approximately 23–68% of children with co-existent peanut/tree nut allergy. In some studies, it has been shown that tree nut allergy in children has the potential to be a severe allergy. However, this appears to be age-specific as infant anaphylaxis in general tends to be milder, and there has been no fatality reported on the first ingestion of an allergen in infancy. Familial hesitancy has been identified as a possible condition for undertaking screening tests prior to allergen introduction. Indeed, there has been limited evidence that caregiver hesitancy may exist in peanut-allergic families with tree nut introduction. However, pre-emptive screening has the potential to overdiagnose tree nut allergy and delay introduction (which could paradoxically increase risk). As a result, the decision is best made in the context of shared decision-making and patient preference-sensitive care.     

The spectrum of cow''s milk allergy

Childhood cow's milk allergy is a diagnosis encompassing various syndromes. Antigen-immunoglobulin E (IgE) antibody interaction is classically involved in mast cell degranulation in IgE-mediated food allergy, while non-IgE mediated cow's milk allergy is mostly mediated by cellular mechanisms. The diagnosis of cow's milk allergy largely relies on a good knowledge of the clinical expression of the disease. In this educational review series, we describe three cases of cow's milk allergy, first a 7-yr-old girl with persisting IgE-mediated cow's milk allergy, second a 8-month-old boy with cow's milk induced flares of atopic dermatitis, and third a 6-yr-old boy with sheep and goat milk allergy, in the absence of cow's milk allergy. The cases are discussed and summarized with more general recommendations for the clinical management of cow's milk allergy.     

Food allergy therapy: is a cure within reach?

There is an unmet medical need for an effective food allergy therapy; thus, development of therapeutic interventions for food allergy is a top research priority. The food allergen-nonspecific therapies for food-induced anaphylaxis include monoclonal anti-IgE antibodies and Chinese herbs. The food allergen-specific therapies include oral, sublingual, and epicutaneous immunotherapy with native food allergens and mutated recombinant proteins. Diet containing heated milk and egg may represent an alternative approach to oral immunomodulation. Oral food immunotherapy remains an investigational treatment to be further studied before advancing into clinical practice.     

Frequency of food allergy in a pediatric population from Spain

We evaluated the prevalence and characteristics of the principal foods implicated in 355 children diagnosed with IgE-mediated food allergy. Diagnosis was established on the basis of positive clinical history for the offending food, positive specific IgE by skin prick test and RAST, and open food challenge. Our results showed the principal foods involved in allergic reactions are: eggs, fish, and cow's milk. These are followed in frequency by fruits (peaches, hazelnuts and walnuts), legumes (lentils, peanuts and chick peas) and other vegetables (mainly sunflower seeds). The legumes demonstrated the highest degree of clinical cross-reactivity. Most patients with food allergy reacted to one or two foods (86.7%). Only 13.3% of patients reacted to 3 or more foods, mostly to legumes and fruits. We found that food allergy begins most frequently in the first (48.8%) and second (20.4%) years of life. Allergy to proteins of cow's milk, egg, and fish begins predominantly before the second year, demonstrating a clear relationship with the introduction of these foods into the child's diet. Allergy to foods of vegetable origin (fruits, legumes and other vegetables) begins predominantly after the second year.;     

Latex allergy in a child with banana anaphylaxis

Allergy to latex and to banana is probably uncommon. Cross-reactivity between these two antigens has been recently demonstrated, but the clinical association of allergic reactions to latex contact and banana ingestion is extremely rare. We report a 3-year-old boy who developed an anaphylactic reaction following banana ingestion and who presented an associated immediate hypersensitivity to latex.     

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??Oral allergy syndrome??OAS?? is an IgE-mediated acute oropharyngeal hypersensitivity to food??which is caused by cross-reactivity between proteins in fresh fruits or vegetables and pollens??with a prevalence of 5% to 24 % in children. A variety of food protein antigens have been implicated in OAS. The most classic of these cross-reactive antigens include birch antigen Betv1??profilin and lipid transfer proteins??LTPs??. Symptoms are usually manifested as numbness??itching or swelling of the lips or mouth??itching or oedema of the lips?? throat??palate or gingiva??erythema of the face and tightness of the throat. OAS can be diagnosed based on clinical history??antigen-specific immunoglobulin E testing??skin prick testing and oral food challenge. If the diagnosis is established??patients should be instructed to avoid the fresh fruits and vegetables that cause symptoms??and emergency administration of epinephrine should be given for severe??generalized reactions.     

Latex allergy in children with no known risk factor for latex sensitization

We describe latex allergy in 11 atopic children, aged 0.7-11.1 years, without any known risk factor. A skin prick-test (SPT) for latex was positive in 8/11, and latex specific IgE was found in all. Latex glove challenge was positive in 9 assessed. These patients demonstrate that latex allergy should be looked for not only in children who have had several operations or those children reporting symptoms from rubber, but also in children with severe atopic eczema, banana allergy, or urticaria or anaphylaxis for which the cause is unknown.;     

Dermatite atopique et allergie : quels liens ?

Atopic dermatitis (AD) is a very common chronic inflammatory skin disease in childhood, often the first step in the atopic march. It seems justified to look for a food or a respiratory allergy, being worsening or responsible for the AD. At infant age, some clinical features are consistent with a food allergy: a severe AD, with an early onset, uncontrolled by topical corticosteroids, and a history of immediate-type reactions. As sensitization to food allergens is very common (positive skin prick-test, atopy patch-test or specific IgE), the role of food allergens in worsening AD is difficult to affirm. So, it could be necessary to ask the advice of an allergist, to avoid unnecessary elimination diets. At older age, exposure to aeroallergens cans worsen AD. Looking for an aeroallergen allergy can help to choose the specific immunotherapy, which clinical efficacy on AD seems interesting.     

Fish and shellfish allergy in children: Review of a persistent food allergy

The increased consumption of fish and shellfish has resulted in more frequent reports of adverse reactions to seafood, emphasizing the need for more specific diagnosis and treatment of this condition and exploring reasons for the persistence of this allergy. This review discusses interesting and new findings in the area of fish and shellfish allergy. New allergens and important potential cross‐reacting allergens have been identified within the fish family and between shellfish, arachnids, and insects. The diagnostic approach may require prick to‐prick tests using crude extracts of both raw and cooked forms of seafood for screening seafood sensitization before a food challenge or where food challenge is not feasible. Allergen‐specific immunotherapy can be important; mutated less allergenic seafood proteins have been developed for this purpose. The persistence of allergy because of seafood proteins’ resistance after rigorous treatment like cooking and extreme pH is well documented. Additionally, IgE antibodies from individuals with persistent allergy may be directed against different epitopes than those in patients with transient allergy. For a topic as important as this one, new areas of technological developments will likely have a significant impact, to provide more accurate methods of diagnosing useful information to patients about the likely course of their seafood allergy over the course of their childhood and beyond.     

Fish allergy in childhood

Fish and its derived products play an important role in human nutrition, but they may also be a potent food allergen. Fish can be an ingested, contact, and inhalant allergen. Gad c I, a Parvalbumin, the major allergen in codfish, is considered as fish and amphibian pan‐allergen. Prevalence of fish allergy appears to depend on the amount of fish eaten in the local diet. In Europe, the highest consumption occurs in Scandinavian countries, Spain and Portugal. In Spain, fish is the third most frequent allergen in children under 2 yr of age after egg and cow’s milk. An adverse reaction to fish may be of non‐allergic origin, due to food contamination or newly formed toxic products, but the most frequent type of adverse reactions to fish are immunologic‐mediated reactions (allergic reactions). Such allergic reactions may be both IgE‐mediated and non‐IgE‐mediated. Most cases are IgE‐mediated, due to ingestion or contact with fish or as a result of inhalation of cooking vapors. Some children develop non‐IgE‐mediated type allergies such as food protein induced enterocolitis syndrome. The clinical symptoms related to IgE‐mediated fish allergy are most frequently acute urticaria and angioedema as well as mild oral symptoms, worsening of atopic dermatitis, respiratory symptoms such as rhinitis or asthma, and gastrointestinal symptoms such as nausea and vomiting. Anaphylaxis may also occur. Among all the species studied, those from the Tunidae and Xiphiidae families appear to be the least allergenic.     

Altered T-cell immunity in patients with adverse reactions to phenobarbital

Twenty-five patients with hypersensitivity reactions to phenobarbital and/or phenytoin are described. Clinical manifestations uniformly consisted of fever and a pruritic skin rash, and were often accompanied by conjunctivitis and lymphadenopathy. Less frequent complications included exfoliative dermatitis and protein-losing enteropathy. Histologic examination of skin in 4 patients and jejunal biopsies in 2 patients demonstrated a prominent inflammatory response consisting predominantly of mononuclear cells. Immunoperoxidase studies identified these cells as mainly activated T cells in the skin and activated T-suppressor/cytotoxic cells in the gastrointestinal tract. In vitro lymphoproliferative responses by patients' peripheral blood mononuclear cells demonstrated increased blastogenesis to phenobarbital stimulation, 1237 versus 74 cpm (p<0.01), and in some patients to phenytoin, 848 versus 87 cpm (p<0.01), suggesting some cross-reactivity with phenytoin. Five patients subsequently treated with phenytoin also developed an allergic reaction to this medication. The clinical findings and laboratory studies suggest that adverse drug reactions to phenobarbital and/or phenytoin are probably mediated by a T-cell immune hypersensitivity response.     

A FOLLOW-UP STUDY OF INFANTS WITH ADVERSE REACTIONS TO COW'S MILK I. Serum IgE, Skin Test Reactions and RAST in Relation to Clinical Course

Abstract. 47 infants with cow's milk sensitivity were followed for a period varying between 6 months to 4 years (mean 28 months). The age at onset of symptoms varied between 14 days to 20 months. The clinical course was studied in relation to reaginic allergy by use of serum IgE, skin prick test and RAST. Infants with an immediate onset of symptoms from the gastrointestinal tract and the skin after cow's milk intake were discerned as a distinct entity having a high frequency of atopy in the family, positive skin tests and positive RASTs to milk (71%). Cases with delayed reactions to cow's milk seldom had a positive RAST or skin test. Most infants of both groups showed an increasing tolerance to milk. In RAST positive infants the RAST-titers increased significantly after onset of symptoms. After having reached a peak the titers subclined in several cases. The titers did not reflect the degree of milk sensitivity during the follow-up period. However, infants who developed high titers seemed to develop tolerance more slowly than infants with low titers.