Turnip rapeseed does not worsen atopic eczema in most sensitized children

To the Editor, Turnip rapeseed oil – rich in essential fatty acids and vitamin E – is a significant source of vegetable oils in the diet. Its fatty acid composition is ideal, and in addition to its current use in baby foods and margarines, components of turnip rapeseed may be increasingly used in the future. The seeds containing 20% protein are also used to high-protein animal feed and to produce biodiesel. Turnip rape and oilseed rape – sources of canola oil – grow in cool temperature and their cultivation is rapidly increasing in the Northern Hemisphere. Turnip rape and oilseed rape pollens may cause hay fever in sensitized individuals, primarily in cultivators. Turnip rape and oilseed rape have been proposed as potential food allergens. Sensitization to turnip rapeseed was earlier reported to be up to 10% among children with atopic eczema in Finland (1). The clinical importance of the sensitization is, however, remains controversial. Whether purified oil extracted from the seeds by crushing plays any role in the sensitization and in the development of eczema is debated. In an open food challenge performed to 28 Finnish children sensitized to turnip rapeseed, clinical allergy was diagnosed in 22 (89%) with immediate labial/facial urticaria, or delayed flare-up of eczema, asthma, and abdominal complaints (1). An open challenge performed to turnip rapeseed-sensitized children with eczema revealed high rate of clinical allergy in Finland 14/14 (100%). In France, clinical allergy was less frequent 5/14 (36%) (2). Eczema in infancy is frequently associated with IgE-mediated sensitization to foods (3), but symptomatic food allergy confirmed by double-blind placebo-controlled food challenge (DBPCFC) is less common in eczema patients. To prevent unnecessary avoidance of turnip rapeseed oil or other rapeseed products in the future, we deemed it important to conduct a DBPCFC with turnip rapeseed in sensitized children. At the Helsinki University Skin and Allergy Hospital, children (aged 0–16 yr) with atopic eczema and strongly sensitized (skin prick test ≥6 mm) to turnip rapeseed were recruited to participate in a study with a crossover DBPCFC. At the hospital, the child received 10 mg, 100 mg, and 1 g of purified and milled turnip rapeseeds, or placebo with 30-min intervals. In the absence of immediate symptoms, the patient was discharged. A daily dose of 1 g continued for 4 days at home. The parents filled in symptom diaries. Between the two 5-day challenges, there was a 7-day washout period. Any known allergy to the ingredients of the vehicle led to exclusion. We assessed the severity score of atopic dermatitis (SCORAD) (4) at baseline and after each challenge, performed skin prick tests to a panel of food allergens and measured specific IgE against oilseed rape, mustard, birch, peanut 2S albumin Ara h 2, peanut birch pollen homology Ara h 8, profilins in birch Bet v 2, and peach Pru p 4 (ImmunoCAP; Thermo Fisher, Uppsala, Sweden). Sera of fourteen age-matched non-atopic children served as negative controls. The ethics committee at the Helsinki University Central Hospital for Children and Adolescents approved the study protocol. One of the parents signed a written informed consent. To study cross-reactive allergens of turnip rapeseed, we performed an ISAC 112 microarray (ThermoFisher, Uppsala, Sweden) inhibition. To inhibit IgE-binding of solid-phase allergens by turnip rapeseed extract (1:3 w/v in phosphate buffer), we used a mixture of 27 sera from patients with specific IgE against 2S albumins (sesame Ses i 1, buckwheat Fag e 2, peanut Ara h 2 and Ara h 6, walnut Jug r 1, and Brazil nut Ber e 1), 7S and 11S globulins, lipid transfer proteins (LTP) (peanut Ara h 9, hazelnut Cor a 8, walnut Jug r 3, peach Pru p 3, mugwort Art v 3, olive pollen Ole e 7, and plane tree Pla a 3), and profilins (birch Bet v 2, timothy Phl p 12, annual mercury Mer a 1, and latex Hev b 8). The microarray contains no rapeseed-specific allergens. Our primary outcome measure was the number of positive DBPCFCs. The estimated 60% positive turnip rapeseed challenges and 5% positive placebo challenges with the 0.8 power and probability of 0.05 gave us a sample of 15 (McNemar test). The sample size calculation was based on the expected 89% rate of positive open challenges among turnip rape-sensitized individuals (1). McNemar test was used to compare the number of positive active and placebo challenges. Related samples Wilcoxon’s signed rank test was used to compare SCORAD. Of 1751 children screened with a panel of skin prick tests between 2009 and 2011, 11.8% was sensitized (≥3 mm) to turnip rapeseed. Of the 62 strongly sensitized (≥6 mm) children, 16 (10 males and 6 females) entered the study. Their median (range) age was 3.15 (1.18–13.6) yr, and SCORAD was 19.5 (3.5–83.5) at baseline. Fourteen children underwent the DBPCFC. No difference occurred in the number of positive reactions between active 1/14 (7%) and placebo 3/14 (21%) challenges (p = 0.4795). One child had immediate skin symptoms at both challenges, and two experienced worsening of eczema during placebo. The median (range) SCORAD was 12.9 (3.6–83.5) after active and 13.5 (3.6–57) after placebo challenge. Parentally reported symptoms did not differ between active and placebo challenges (data not shown). The children had multiple sensitizations: mustard 13/14 (93%), peanut 11/14 (78%), soy 10/14 (71%), egg white 11/ 14 (78%), wheat 5/14 (36%), cow’s milk 5/14 (36%), and turnip rapeseed oil 0%. Serum-specific IgE analyses appear in Table 1. In the microarray analysis, turnip rapeseed extract strongly inhibited IgE-binding of the profilins. Bet v 2 was inhibited 97%, Hev b 8 95%, Mer a 1 98%, and Phl p 12 100%. No inhibition was detected in the 2S albumins (0%), Abbreviations DBPCFC, Double-blind placebo-controlled food challenge; SCORAD, Severity score of atopic dermatitis; LTP, Lipid transfer protein.