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Allergy to soy formula and to extensively hydrolysed whey formula in infants with cow?s milk allergy: A?prospective, randomised study with a follow-up to the age of 2 years.
Timo Klemola, MD et al, Dept Pediatrics, Jorvi Hospital, Espoo & the Dept Dermatology, Turku University, Finland
Objectives: We conducted a prospective, randomised study to evaluate the cumulative incidence of allergy or other adverse reactions to soy formula and to extensively hydrolysed formula up to the age of 2 years in infants confirmed with milk allergy.
Study design: Infants (n=170) with documented cow?s milk allergy were randomly assigned to receive either soy formula or extensively hydrolysed formula (ehf). If it was suspected that the formula caused symptoms, a double-blind, placebo-controlled challenge (DBPCFC) with the formula was performed. The children were followed to the age of 2 years, and soy-specific IgE antibodies were measured at the time of diagnosis and at the ages 1 and 2 years.
Results: An adverse reaction to the formula was confirmed by challenge in 8 patients (10%; 95% confidence interval, 4.4%-18.8%) randomly assigned to soy formula and in 2 patients (2.2%; 95% confidence interval, 0.3% to 7.8%) randomly assigned to extensively hydrolysed formula. Adverse reactions to soy were similar in IgE-associated and non-IgE-associated cow?s milk allergy (11% and 9% respectively)> IgE to soy was detected in only 2 infants with an adverse reaction to soy. Adverse reactions to soy were more common in younger (< 6 months) than in older (>6 months) infants (5 of 20 vs 3 of 60, respectively, P = .01)
Conclusions: Soy formula was well tolerated by most infants with IgE-associated and non-IgE-associated cow?s milk allergy. Development of IgE-associated allergy to soy was rare. Soy formula can be recommended as a first-choice alternative for infants > 6 months of age with cow?s milk allergy.
Reference: J Pediatrics 2002; 140:219-24
Is Adrenaline Administration From a Sublingual tablet Feasible for the Out-of-Hospital First Aid Treatment of Anaphylaxis? Absorption studies in an Animal Model.
X Gu, KJ Simons, F Estelle R Simons, Univ. of Manitoba, Winnipeg, Canada
Purpose: Prompt administration of adrenaline, preferably by intramuscular (IM) injection (Simons et al, J Allergy Clin Immunol 1998;101:33-7) is the cornerstone of systemic anaphylaxis treatment. In the out-of-hospital first-aid treatment of anaphylaxis; however, patients may delay adrenaline self-injection due to fear of ?€a needle". It is not feasible to administer adrenaline orally because it is rapidly conjugated and oxidized in the gastrointestinal tract and liver by catechol-O-methyl-transferase and monoamine oxidase. In order to evaluate the rate and extent of sublingual absorption of adrenaline, we performed a prospective, randomised, four-way cross-over study in a rabbit model.
Methods: On 4 study days at least one week apart, 6 New Zealand white rabbits (4.2 +/- 0.1 Kg) received either sublingual adrenaline tablets 2.5mg or 10mg or adrenaline 0.03mg IM (positive control), or 0.1ml 0.9% saline IM (negative control). Blood samples were obtained at 0.5, 10, 15, 20, 30, 40, 60, 90, 120, 150, and 180 minutes after adrenaline administration. Plasma adrenaline concentrations were measured by HPLC with electrochemical detection. The assay was linear over a range of 25-1000 pg with a coefficient of variation of 3%. Pharmacokinetic and statistical analysis was performed using WinNonlin and PCSAS. Differences between plasma adrenaline concentration (Cmax) and time to peak plasma adrenaline concentrations (tmax) were considered to be significant at p
Results: After adrenaline sublingual tablet 2.5 mg administration, the Cmax was (endogenous adrenaline) 10835.8=/-2234.1 pg/ml, reached at a tmax of 15.8=/-4.7 minutes. In the saline control study, the Cmax 9endogenous adrenaline) was 518.3 =/-142.0 pg/ml. The tmax after both doses of adrenaline did not differ significantly from the Tmax after IM adrenaline, and the Cmax after 10mg sublingual adrenaline dose did not differ significantly from the Cmax after IM adrenaline. No adverse effect was noted.
Conclusion: Sublingual tablet administration of adrenaline results in high, rapidly achieved peak adrenaline plasma concentrations similar to those achieved after IM injection of adrenaline. Absorption studies are now underway in humans to determine whether or not sublingual tablet administration of adrenaline will be a feasible alternative to self-injection of adrenaline in the out-of-hospital first-aid treatment of anaphylaxis.
Anaphylaxis to Sesame (Sesamum Indicum) seed and sesame oil.
W, J Stevens et al, University of Antwerp, Antwerp, Belgium
A 42-year old man with house dust mite and pollen allergy was referred to our department because of several allergic reactions within minutes after consumption of sesame seed containing food such as bread and pancakes. Initially he suffered from urticaria but progressively more sever reactions with angioedema, bronchospasm, hypotension and shock had occurred. The last episode had occurred in connection with consumption of meat and vegetables without sesame seeds but the food was baked in sesame oil (Chinese wok).
After invitro allergen-specific stimulation basophils became activated and expressed the membrane activation marker CD63. This up-regulated expression of CD63 on the plasma membrane can be detected by flow cytometry using monoclonal antibodies like anti-CD63-PE. Calculating the net percentage of basophils that express CD63 relative to buffer control allows assessing basophil activation.
Sesame and its derivative are widely employed in food industry and in the cosmetic and pharmaceutical industry as vehicles for parenteral and topical therapeutics because of their presumed low allergenicity. Anaphylaxis due to ingestion of sesame seed containing food has been increasingly reported. Reactions occurred in connection with a broad variety of foods in which the presence of sesame is not always apparent. Symptomatology included pruritus, erythematous rashes, urticaria, angioedema, nausea, vomiting, dyspnea, bronchospasm, hypotension and shock. Anaphylaxis from sesame oil is considered to be anecdotal,. This case report confirms that anaphylaxis due to sesame oil can occur and that the basophil activation test can be safe and reliable method for in vitro diagnosis of food allergy.
Wheat Anaphylaxis in Thailand
Tassalapa Daengsuwan, Nualanong Visitsunthorn, Mahidol University, Bangkok, Thailand
Although allergy to wheat is not an uncommon condition, anaphylaxis from wheat consumption is rarely observed in Thailand. Wheat is not a common food consumed in Thailand. Nonetheless, wheat anaphylaxis has been increasingly observed at our institution over the past 10 years.
We, herein, report 8 cases of wheat-induced anaphylaxis from Thailand. Seven children (3 girls and 4 boys, age range 2-14 years, mean 9 years) presented with wheat-induced anaphylaxis. Their symptoms occurred at various ages, ranging from 7 months to 14 years old.
Type of wheat containing foods causing anaphylaxis were cakes, bread, Kentucky fried chicken, pizza, crisps, doughnut, and noodle. Amount of wheat inducing symptoms ranged from a bite of cake to 2 rolls of noodle.
Symptoms were a combination of angioedema of mouth and eyelids, urticaria, with or without hypotension in 6 patients. Gastrointestinal symptoms together with skin manifestations (angioedema of mouth and eyelids) were presented in one case. Most symptoms occurred within 30 minutes after the ingestion. Our last patient was a 40-year-old male who presented with wheat-dependent, exercise-induced anaphylaxis (after ingestion of bread).
Wheat was the only allergen sensitising 4 of the patients, whereas, the other patients were sensitised to other allergens as well.
Treatment involved avoidance & prescription of injectable adrenaline for emergency use.
No fatality was observed in the follow-up period.
Anaphylaxis from wheat has become one of the most common causes of anaphylaxis in Thailand. Systematic study of anaphylaxis including epidemiology and basic research will need to be done in Thailand.
Urticaria caused by Coca-Cola
MJ Gavilan, M Fernandez-Nieto, Santiago Quirce, Madrid Spain
We report a patient who developed urticaria after ingestion of coca-cola. A 16-year-old woman, with personal and family history of atopy (hay fever), had suffered from recurrent episodes of generalized urticaria after ingestion of cola-drinks (coca-cola) in the last 8 years. She noticed that the larger the amount she drank, the more severe the skin rash. On one occasion, she needed emergency treatment because of her symptoms. She had no history of any adverse drug reactions. Skin prick tests with coca-cola (as is) were all negative. A double-blind, oral challenge test was performed with plain coca-cola and decaffeinated coca-cola. Oral challenge with plain coca-cola provoked itching and urticaria on her trunk and legs within 10 minutes after administration of 630 mls. Oral challenge with caffeine-free coca-cola elicited no adverse reactions.
We suspected that caffeine might be the agent responsible for allergic symptoms. Skin prick test with caffeine (10mg/ml) was negative. However a positive intradermal test (10mm wheal with ertythema0 was obtained with caffeine at 10mg/ml. The same test performed in 5 atopic patients elicited no response. A double-blind, placebo-controlled oral challenge with caffeine (50mg) administered in green opaque, tartrazine-free capsules produced itching and urticaria on the face, neck and trunk. The patient required treatment with oral antihistamine, corticosteroids and subcutaneous adrenaline to control her symptoms. Caffeine is an amine present in beverages such as coffee, tea, cola drinks and chocolate. It is a methylxanthine closely related to theophylline and theobromine. Allergic reactions caused by caffeine are extremely rare. However, the oral challenge tests performed in this patient confirm that caffeine was the substance responsible for the development of urticaria after drinking coca-cola.
Recurrence of Peanut Allergy
Paula J Busse, Sally A Noone, Hugh Sampson, et al, Mount Sinai School of Medicine, New York, NY
Knowledge of the clinical course of peanut (PN) allergy (A) is evolving. In our ongoing natural history study, double-blind, placebo-controlled oral food challenges (DBPCFC) are offered to children over the age of 3.5 yrs with a recent CAP_RAST <10kU/L, no reaction within 1 year and no severe reactions within 2 years. Subjects are avoiding PN based on prior reactions or prophylactic avoidance; with evidence of PN-specific IgE antibody skin prick test (SPT) and /or RAST. 44 children have been challenged (mean age 6.8 yrs, range 3.5 ?• 12.8 yrs), of whom 13 were avoiding PN without a history of ingestion. Thus far, 7/13 (54%) without and 19/31 (61%) with a history of reaction passed challenges. The highest PN-IgE levels (0.35 vs. 1.6, p=0.01) and mean diameter SPT wheals (2mm vs. 6.4 mm, p<0.0001). At PN-IgE <2kU/L, 22/32 (69%) passed challenges; 10 subjects who passed had converted to undetectable (wheal=0mm). Follow-up (mean, 15 mo; range 3-30 mo) on 21 children who passed their challenge revealed 10 routinely ate PN, 5 occasionally ate small amounts but disliked it, 1 avoids completely for dislike and 2 never re-introduced it. 3 children re-developed symptoms.
Patient 1 had hives, facial angioedema at age 1.5 yrs, and a similar reaction a few months later. SPT decreased to 1mm at the time of the challenge (age 5) with undetectable PN-IgE (0.35). Following the negative challenge, he ingested only small quantities of peanut but gradually over the ensuing year he complained of oral symptoms. Re-testing revealed SPT wheal increased to 7mm and RAST to 16.6kU/L>
Patient 2 had first reaction at 18 mo with hives, rhinitis and wheezing, but had no reactions and passed a challenge at age 9.5 yrs [SPT wheal 5 mm and PN-IgE undetectable (0.35)]. The year following challenge he ingested small amounts of PN but did not like PN butter and by 2 years, he complained of oral pruritus from small ingestions. Repeat DBPCFC 2.5 years after the negative challenge resulted in oral and throat pruritus at 400 mg dose. PN-IgE had increased to 1.2 kU/L and SPT wheal 12 mm.
Patient 3 [challenged age 4, PN-IgE converted from 0.54 to undetectable]. To tolerated PN several times but developed lip oedema 12 months following challenge (further evaluation pending). In conclusion, the selection criteria presented (with median PN-IgE 0.6kU/L among participant) resulted in a 60% pass-rate for SPT wheal <3 mm). PNA recurred in 14%; further studies must address this possibility and investigate features that predict this eventuality.
Re-Sensitisation to Fish in Allergic Children After a Temporary Tolerance Period: Two case reports
Consolacion De Frutos, et al, Gregorio Maranon Hospital, Madrid, Spain
Introduction: Fish is the third food allergen in young children in Spain. Once acquired, intolerance is usually permanent. We present 2 cases of fish allergy with temporary intolerance.
Material, methods and Results: 2 children (2 and 5 year-old) suffered urticaria-angioedema) after eating sole and codfish respectively) They had positive skin prick tests (SPT) to cod sole, hake, negative to Anisakis simplex, and positive specific IgE to cod (1.31 KU/L, 1.86 KU/L), sole (2.90 KU/L) and hake (9.45 KU/L, 12.8 KU/L). After a fish-free diet of 3 and 4 years respectively, their SPT and specific IgE became negative. Oral challenges were negative to cod in the first child and sole in the second one, so fish was re-introduced in their diet. Children ate fish regularly, twice a week. After an 8-month-period with normal diet (including fish), the first child developed oral allergy syndrome to cod, sole, tuna and salmon. After a 2-month-period with normal diet, the second child developed oral pruritus, lip angioedema and dyspnea with sole. SPT and specific IgE turned positive (cod: 5.3 KU/L, 0.80 KU/L, 0.40 KU/L respectively).
Conclusion: Some fish allergic children may re-sensitize to fish after a short time of tolerance. It can possibly be caused by a short loss of immune memory.
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