ABSTRACT
Peanut allergy has increased substantially in the past few decades, both in developed and developing countries. Peanut allergy has become a major public health concern, affecting up to 1 in 50 children, with repercussions for school and airline policies. Recent research findings have shown that, contrary to the long-standing teaching of "delayed" introduction of allergens, early introduction of peanut protein is of benefit as an allergy prevention strategy, especially in high-risk cases. Ideal dose, frequency and duration of "proactive" peanut therapy for maximum protection remain to be determined in order for it to become acceptable and practical on a large scale. Logistics around widespread screening of high-risk patients remain complex. The correct diagnosis of peanut allergy is crucial and diagnostic tests have been fine-tuned in the past 2 decades in order to help differentiate true allergy from false-positive sensitization through cross-reactivity. Component-resolved diagnostics have become routinely available, and the use of basophil activation tests has increased, although standardization and availability remain issues. Future tests, including epitope testing and histamine-release assays, promise to be even more specific in ruling out false positives and reducing the need for incremental food challenges. Stringent peanut avoidance and prompt treatment of reactions remain the cornerstone of treatment. The concept of exposing the allergic body to small amounts of peanut protein in a cautious, orderly, escalating fashion in the form of desensitization has been widely applied in the past 10-15 years, mainly in the research domain, but of late spilling over into every-day practice. However, desensitization does not equate to a cure, and has significant safety concerns and practical ramifications; probably requiring lifelong-controlled peanut ingestion for ongoing protection. Further strategies to enhance the safety and efficacy of immunotherapy are under exploration, many with a non-specific immune-modifying effect. Despite recent advances in peanut allergy, we still need to go back to basics with accurate diagnosis, nutritional counselling, well-organized allergy action plans and accessible emergency kits.
ABSTRACT
BACKGROUND: Diagnosing peanut allergy based on sensitisation alone leads to an unacceptable rate of overdiagnosis. OBJECTIVE: To define parameters that may help differentiate peanut allergy from asymptomatic sensitisation in a cohort of South African (SA) children with atopic dermatitis (AD). It is the first study in SA to utilise oral food challenge tests and analyse peanut component patterns. METHODS: This was a prospective, observational study at a paediatric university hospital in Cape Town, SA. Children with AD, aged 6 months - 10 years, were recruited randomly. They were assessed for sensitisation and allergy to peanut by questionnaire, skin-prick tests (SPTs), immuno solid-phase allergen chip (ISAC) tests, ImmunoCAP component tests to Ara h 1, 2, 3, 8 and 9, and incremental food challenges. RESULTS: One hundred participants (59 Xhosa (black Africans) and 41 of mixed race, median age 42 months) were enrolled. Overall, 44% of patients were peanut sensitised and 25% had a true peanut allergy. SPTs and ImmunoCAP Ara h 2 produced the highest areas under the receiver operating characteristic curve for predicting peanut allergy in peanut-sensitised patients. The ISAC test was less sensitive, more specific and produced significantly lower median values than ImmunoCAP tests. Ara h 2 was the most useful component in differentiating allergy from tolerance in both ethnic groups, being positive in 92% of allergic and 40% of sensitised but tolerant children (p<0.001). There was little additional contribution from Ara h 1 and 3. Ara h 8 and 9 were associated with tolerance. Commonly used 95% positive predictive values (PPVs) for SPTs, peanut-specific IgE and Ara h 2 levels fared suboptimally in our population. Maximum PPVs for this study population were found at SPT 11 mm, peanut IgE 15 kU/L and ImmunoCAP Ara h 2 of 8 kU/L, but these adjusted levels still had suboptimal PPVs in Xhosa subjects. Severe peanut allergy was associated with increased median peanut IgE and Ara h 2. CONCLUSIONS: The component Ara h 2 was useful for differentiating allergy from tolerance in both ethnic groups in this SA cohort. Ninety-five percent PPVs for peanut allergy tests may need to be revised, especially in Xhosa patients. An SPT result ≥11 mm as well as Ara h 2 ≥8 kU/L had the best predictive value for peanut allergy.