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The prevalence of peanut allergy appears to have increased in recent decades.
However, apart from a family history of peanut allergy and the presence of atopy, there are no known risk factors.
In this study, researchers from England used data from a geographically defined cohort of 13,971 preschool children to identify those with a history of peanut allergy. The team also assessed a subgroup that reacted to a double-blind peanut challenge.
The team prospectively collected data on the whole cohort. They then collected information by interview from the parents of children with peanut reactions, and of children from 2 groups of controls.
The controls were randomly selected from the cohort, and from children whose mothers had a history of eczema and who had had eczema themselves in their first 6 months.
 | | Development of peanut allergy was associated with the use of skin preparations containing peanut oil. | New England Journal of Medicine |
Overall, 49 children had a history of peanut allergy. This was confirmed by peanut challenge in 23 of 36 children tested.
The research team found no evidence of prenatal sensitization from the maternal diet. They also determined that peanut-specific IgE was not detectable in the cord blood.
They found that peanut allergy was independently associated with intake of soy milk or soy formula (OR 2.6), rash over joints and skin creases (OR 2.6), and oozing, crusted rash (OR 5.2).
In addition, analysis of interview data showed that the use of skin preparations containing peanut oil was an independent factor in the development of peanut allergy (OR 6.8).
Dr Gideon Lack's team concluded, "Sensitization to peanut protein may occur in children through the application of peanut oil to inflamed skin".
"The association with soy protein could arise from cross-sensitization through common epitopes."
"Confirmation of these risk factors in future studies could lead to new strategies to prevent sensitization in infants who are at risk for subsequent peanut allergy."
In the same publication, a further article looks at the effect of anti-IgE therapy in patients with peanut allergy.
Peanut-induced anaphylaxis is an IgE-mediated condition that is estimated to affect 1.5 million people. It causes between 50 and 100 deaths per year in the United States.
TNX-901 is a humanized IgG1 monoclonal antibody against IgE. It recognizes and masks an epitope in the CH3 region of IgE responsible for binding to the high-affinity Fcepsilon receptor on mast cells and basophils.
In this study, researchers from the United States conducted a double-blind, randomized, dose-ranging trial in 84 patients with a history of hypersensitivity to peanut.
The team confirmed hypersensitivity in all patients. They then established the threshold dose of encapsulated peanut flour using a double-blind, placebo-controlled oral food challenge.
The researchers randomly assigned patients to receive either TNX-901 (150, 300, or 450 mg) or placebo subcutaneously every 4 weeks for 4 doses.
The patients then underwent a final oral food challenge within 2 to 4 weeks after the fourth dose.
The research team determined a mean baseline threshold of sensitivity of 178 to 436 mg of peanut flour in the various groups.
They found that mean increases in the oral-food-challenge threshold were 710 mg in the placebo group, 913 mg in the 150 mg TNX-901 group, 1650 mg in the 300 mg TNX-901 group, and 2627 mg in the 450 mg TNX-901 group.
The team found that TNX-901 was well tolerated.
Dr Donald Leung's team concluded, "A 450-mg dose of TNX-901…increased the threshold of sensitivity to peanut on oral food challenge from a level equal to approximately half a peanut (178 mg) to one equal to almost 9 peanuts (2805 mg)".
This is "An effect that should translate into protection against most unintended ingestions of peanuts".
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