Yael Levy

Food protein-induced enterocolitis syndrome: not only due to cow's milk and soy

Over a of 7‐year period, six patients (four males, two females aged 3–12 months) were diagnosed with food protein‐induced enterocolitis syndrome (FPIES) triggered by foods other than cows milk and soy: chicken in four, turkey in two, peas in one, and lentils in one (five patients reacted to more than one food type). All reactions developed within 2 h of ingestion of the allergenic food. To exclude other conditions with similar clinical symptoms, three infants underwent work‐up for sepsis, one infant underwent work‐up to exclude metabolic defects, and one underwent a barium enema to rule out intussusception. All were negative. Pediatricians should be aware that FPIES may be caused by foods other than cows milk and soy, mainly chicken, turkey and foods from the legume family, and that it may present also in infants older than 6 months.

New-onset post-transplantation food allergy in children--is it attributable only to the immunosuppressive protocol?

Abstract:  New‐onset post‐transplantation food allergy has been described mainly after liver transplantation, and its pathogenesis was attributed to the immunomodulatory effects of tacrolimus therapy. The aim of the present study was to evaluate the association of food allergy with solid organ transplantation in our center. The medical records of children who underwent kidney transplantation and children who underwent liver or liver and kidney transplantation from 1986 to 2005 were reviewed. A total of 189 children (124 after kidney transplantation, 65 after liver or liver and kidney transplantation) received tacrolimus as part of the immunosuppressive regimen. New‐onset post‐transplantation food allergy was documented in four of them: two with liver transplants and two with combined kidney and liver transplants. The absence of new‐onset food allergy in the children with isolated kidney transplants is compatible with other reports in the literature. This study supports the concept that the functioning liver itself, and not only tacrolimus immunosuppression, is a main contributor to food allergy in this patient population.

Calcium-deficiency rickets in a four-year-old boywith milk allergy

A 4-year-old boy was found to have rickets associated with normal serum levels of 25-hydroxyvitamin D and high serum levels of 1,25-dihydroxyvitamin D. These findings were thought to be the result of dietary calcium deficiency caused by the prolonged elimination from his diet of cow milk and milk products because of allergy. Adequate intake of calcium resulted in rapid improvement.

Lessons from the clinical course of IgE-mediated cow milk allergy in Israel

Cow milk and milk products are the most common food products consumed in Israel; rates of allergy to cow milk exceed those of peanuts in infants and children. The aim of the present study was to evaluate retrospectively the clinical features and natural course of immunoglobulin (Ig) E‐mediated cow milk allergy (CMA) in Israel. Data of children diagnosed with CMA from 1995 to 2003, were collected regarding age at first and most recent reactions, symptoms and signs, family history of atopy, other allergic diseases, emergency department visits, hospitalizations, and treatment. Patients with transient CMA were compared to those with persistent CMA (≥3 yr old). The study group consisted of 105 patients, 43 with transient CMA (age range: 0.48–11 yr). The remaining 62 patients (age range: 3–16.5 yr) did not achieve tolerance to cow milk during the follow‐up period. No differences were found between the groups in mean age and symptoms and signs at the first allergic reaction and family history of atopy. Patients with persistent CMA had a higher rate of asthma than patients with transient CMA (61.2% vs. 18.6%, p < 0.001). Fifty patients with persistent CMA had 137 subsequent allergic reactions after diagnosis, 25% of the reactions were due to oral milk challenge at the clinic and 75% due to accidental exposure, of which 13% required an emergency department visit and 8%, hospitalization. Only 19% of the reactions were treated with epinephrine injection. In conclusion, in our experience, less than half of the children diagnosed with IgE‐mediated CMA during 9 yr, outgrew it. The patients with persistent CMA have a higher prevalence of asthma compared with the general population or to children with transient CMA. The high number of recurrent allergic reactions due to accidental exposure and the low rate of epinephrine usage in these patients point to a need for better education of patients and their families.

Anaphylaxis in Israel: Experience with 92 hospitalized children

To cite this article: Hoffer V, Scheuerman O, Marcus N, Levy Y, Segal N, Lagovsky I, Monselise Y, Garty BZ. Anaphylaxis in Israel: Experience with 92 hospitalized children. Pediatr Allergy Immunol 2011; 22:172–177.

Copper deficiency in infants fed cow milk

NUTRITIONAL COPPER DEFICIENCY in infancy has been observed by Tanaka et al. ~ in a premature baby fed milk formula low in copper. Copper deficiency has also been reported in infants given total parenteral nutrition w i thou t copper supplementation in cases of severe diarrhea, malabsorption, protein loss, or the use of chelating agents. 2-5 Copper deficiency may cause anemia and other subtle symptoms that may go undiagnosed but resolve with diet enrichment. We describe two infants with copper deficiency, and draw attention to the similarities between our patients and those of Tanaka.

Acute Dystonic Reaction to Bethanechol—a Direct Acetylcholine Receptor Agonist

Bethanechol is a direct agonist of the acetylcholine receptor that was recently introduced in the therapy of gastro‐oesophageal reflux. Acute dystonic reactions to bethanechol were observed in a 10‐month‐old infant who also demonstrated similar dystonic reactions to dopamine receptor blocking agents of two different classes. This first report of acute dystonic reaction to cholinergic agonists in humans is in accord with the current theories of the röle of acetylcholine and dopamine in the pathogenesis of acute dystonic reactions.

Exserohilum sinusitis presenting as proptosis in a healthy adolescent male

Allergic fungal sinusitis, first described by Katzenstein et al. [1] in 1983, usually occurs in immunocompetent patients with a history of chronic sinusitis. Early reports cited Aspergillus as the causative organism, based on the histologic appearance and similarity of the disorder to allergic bronchopulmonary aspergillosis. However, more recently, changes in the identification and classification of certain fungi have yielded cultures positive for dematiaceous fungi when the histologic diagnosis was that of Aspergillus sinusitis [2]. Of the dematiaceous fungi, only a few cases of Exserohilum have been reported [3,4]. We hereby describe a case of Exserohilum sinusitis in a 15-year-old boy.

Severe allergic bronchopulmonary aspergillosis in an infant with cystic fibrosis and her asthmatic father

An infant with cystic fibrosis and her asthmatic father were diagnosed as suffering from allergic bronchopulmonary aspergillosis (ABPA). Cystic fibrosis was diagnosed in the infant at 6 weeks of age, and gene mutations were W1282X/G542X. She was diagnosed definitively as suffering from ABPA at age 3.5 years, but had suggestive symptoms from age 11 months. This may be the youngest age described to date for ABPA. The child responded well to systemic steroid therapy, but remained steroid‐dependent over the next 4 years. Treatment with itraconazole enabled a marked reduction in steroid dosage. The father was an asthmatic, and a heterozygote for the cystic fibrosis transmembrane regulator (CFTR) mutation W1282X. He had a normal sweat test, atopy, and moderate reversible airway obstruction. There was no proven exposure to Aspergillus in the home environment. The importance of considering the diagnosis of ABPA even in infancy, the therapeutic dilemmas, and the possible role of abnormal CFTR function in the development of ABPA are discussed. Pediatr Pulmonol. 2000; 29:155–159.

Molecular assessment of thymic capacities in patients with Schimke immuno-osseous dysplasia

Schimke immuno-osseous dysplasia (SIOD) is caused by SMARCAL1 deficiency and characterized by defective T-cell immunity. The immunodeficiency and the role of thymic function in SIOD patients are not clearly understood. We performed thymic evaluations by assessing T-cell receptor (TCR) diversity, rearrangement, and excision circles in family members with different disease severity carrying the same bi-allelic mutation and in a heterozygous carrier. The expression of SMARCAL1 mRNA in a normal thymic sample was measured using real-time quantitative polymerase chain reaction. Thymus functions were significantly reduced in SIOD patients, and these findings were highly correlated with the clinical phenotype. Quantification of SMARCAL1 mRNA transcript was 3.86-fold higher than normal values for adult kidneys. Genotype alone apparently does not define phenotype, and analysis of TCR diversity, rearrangement, and thymus output can quantify the extent of T-cell immunodeficiency. High thymic expression of SMARCAL1 mRNA raises the possibility of its importance in thymus maintenance and function.