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Using a population cohort of 5276 infants, Peters et al recently published in The Journal of Allergy and Clinical Immunology (JACI), SPT and sIgE thresholds with 95% PPV for challenge-confirmed peanut, egg and sesame allergy.
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They found that the SPT 95% PPV for peanut and sesame allergy was ≥ 8mm
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It is quite interesting that all 7 failed food challenges were patients screened for sesame allergy as a result of having peanut and tree nut allergies; 4 had previously tolerated sesame but asked to restrict sesame from their diet based on positive results.
Quote from: CMdeux on March 24, 2012, 12:24:06 AM
Wow-- thanks for the update. Unfortunately not good news. But important.
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Lastly, Ho et al. identified a sesame SPT wheal diameter ≥ 8 mm as being predictive of a positive food challenge with > 95% accuracy.
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Ho MH, Heine RG, Wong W, Hill DJ. Diagnostic accuracy of skin prick testing in children with tree nut allergy. J Allergy Clin Immunol. 2006;117(6):1506–8.[PubMed]
Quote from: admin rebekahc on September 09, 2011, 05:04:48 PM
CMdeux
Moderator1
Posted: 08.06.2008 at 01:01:20
the only firm statistical conclusion was that if your RAST <0.35 kU/L that you are really, REALLY unlikely to be allergic
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Notably, 29% of sesame allergic patients had a sesame-specific IgE < 0.35 kUA/L. This is in contrast to the findings of Zavalkoff et al. who reported a cut-off < 0.35 kUA/L as being useful in excluding a diagnosis of sesame allergy.
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Based on our sample, both tests are not good predictors of true sesame allergy as determined by an oral challenge. We were unable to establish a threshold with a 95% positive predictive value for both sesame-specific IgE and SPT.
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We have conducted the first study to evaluate the diagnostic value of sesame-specific IgE. We were unable to establish a threshold, in our population, with a 95% positive predictive value. At a sesame-specific IgE threshold of 7 kUA/L, the positive predictive value was 74.1% and did not increase monotonically at higher thresholds.
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Although our study is limited by a small sample of cases, the sample size is similar to that in the study by Sampson5 of wheat and soy IgE, which also did not predict allergy. It is possible that a larger sample would be successful in establishing a threshold. Another potential limitation of our study is that allergy or tolerance to sesame was usually determined by history rather than the gold standard food challenge. Although history is subject to recall and reporting bias, we applied strict inclusion and exclusion criteria. Furthermore, other studies have relied on clinical history to define their allergic cohort.6, 7, 8 The several year delay between convincing reaction and measurement of sesame-specific IgE is also a limitation of our study because it raises the concern that the sesame allergy may have resolved at the time of the IgE measurement.
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Further, the clinician should be aware of the potential for patients with peanut allergy to be falsely labeled as having sesame allergy if this diagnosis is solely based on the sesame-specific IgE. We suggest that if a patient clearly tolerates sesame, it is not warranted to obtain a sesame-specific IgE. Alternatively, if the patient's history is truly convincing of a significant allergic reaction to sesame, regardless of the SPT result or sesame-specific IgE level, the patient should be considered allergic, because anaphylaxis to sesame has been described with negative SPT and IgE levels.