RESUMO
OBJECTIVE: To assess the ability to de-label pediatric patients of their beta-lactam allergy by using a newly implemented institutional protocol and to identify potential barriers to the de-labeling process. METHODS: All patients with reported allergies to prespecified beta-lactam antibiotics were eligible for a -beta-lactam allergy interview. Following the interview, patients were grouped into 4 risk categories-no risk, low risk, moderate risk, and high risk-and assessed for intervention eligibility. Potential interventions included de-labeling based on the interview alone or proceeding to an oral amoxicillin challenge with or without penicillin allergy skin testing. RESULTS: Of the 62 patients eligible for beta-lactam allergy interviews, 40% (n = 25) were de-labeled. Among de-labeled patients, 60% (n = 15) were de-labeled on the basis of the interview alone. Additionally, no failures were documented in patients who underwent an oral amoxicillin challenge or penicillin skin testing. Barriers to performing oral amoxicillin challenges or penicillin skin testing included concomitant systemic steroid or antihistamine use, refusal of intervention, and insufficient resources to perform penicillin skin testing. CONCLUSIONS: There was a high frequency of patients de-labeled of their beta-lactam allergies in this study. Increased education to patients, parents, and providers on the de-labeling process, as well as increased personnel available to coordinate and perform de-labeling interventions, may result in more beta-lactam allergy de-labeling.
RESUMO
A cellular proliferation to milk allergens has been found in the cord blood cells of neonates. While this reflects a sensitivity during the fetal life, its clinical significance and disease, particularly its unconventional presentations, have remained largely unrecognized by care providers. Here, we report three cases of infants whose mothers consumed dairy products during pregnancy, who developed a severely constipated pre- and postnatal bowel. The passage of meconium was significantly delayed with subsequent early-onset infant constipation that was intractable to conventional therapies but remitted when milk proteins were withheld, recurred when milk proteins were reintroduced, and resolved again when switched to an extensively hydrolyzed or amino acid-based infant formula. Based on this and other observations, it is believed that these infants must have initiated and/or developed cow's milk protein allergy prenatally during fetal life. We suggest that a 2-week trial of cow's milk protein avoidance be applied to these neonate infants with early-onset constipation before an unnecessary invasive work-up for Hirschsprung disease and others is initiated per the current guidelines.