BIBLIOGRAPHIC UPDATE IN ALLERGY
1. Nut co-reactivity – Elimination recommendations
2. Lip Food Challenge as alternative to Open Food Challenge
3. Immune Mechanisms of Food Allergy
4. Risk of Asthma : Lessons from Amish and Hutterite Children
5. Atopic Dermatitis and Psoriasis : Similarity and Difference
I. NUT Co Reactivity - Elimination Recommendations
Arnon Elizur,et al Allergy 2017 11 Nov Accepted Articles
To examine the co-incidences of allergies among tree-nuts and improve diagnostic testing to minimize the need for OFC, the Israeli pediatricians took charge of eighty three patients prospectively evaluated for walnut, pecan, cashew, pistachio, hazelnut and almond allergy. Standardized skin prick tests (SPT) using finely ground tree-nut solution and basophil activation tests (BAT) were performed. Patients underwent OFC for each tree-nut they eliminated. While most patients were sensitized to 5-6 tree-nuts, over 50% were allergic to only 1-2 tree-nuts. The highest rate of allergy in sensitized patients was observed for walnut (74.6%) and cashew (65.6%). The rate of co-allergy for most tree-nuts was < 30%. Knowledge of co-incident allergies in these pairs along with the combination of SPT and BAT correctly distinguished allergic from tolerant patients forwalnut (87%), pecan (66%), cashew (71%) and pistachio (79%).
In conclusion, these data should assist in differentiating between allergic and tolerant patients, decrease the need for OFC and allow for appropriate elimination recommendations.
II. Lip Food Challenge as alternative to Open Food Challenge
C.Venter et al Ped All. Immun 2017 28 7 707-711
The British pediatricians of the Isle of Wight, using the method of French allergists Rance & Dutau and A. Monneret-Vautrin, performed a Lip Food Challenge (LFC) in many children from birth cohorts followed until 11 years. Skin prick-tests to common food allergens (milk, egg, cod sesame, wheat and peanut ) were evaluated. Then 112 LFCs took place. Four cases although positive were excluded as parents decline to continue the process. So108 LFC were followed up by an open food challenge. A positive labial reaction was noted in 9 challenges. All resulted in positive oral food challenge (OFC). A positive predictive value of 100%, a negative predictive value of 72,7% with 100% specificity were calculated. Side effects of LFC were minimal: urticaria (3 cases), with lip edema (2), rash, rhinorrhea.
These data, despite very limited and including only four food allergens, prove that LFC is highly indicative of a positive OFC (but a negative LFC does not rule out a positive OFC). In conclusion LFC is feasible, reliable and safe.
III. Immune Mechanisms of Food Allergy
Turcanu et al Curr.Op.Immunol 2017October 48 92-98
Environmental factors, dual exposure to allergens, hygiene hypothesis and local microbiota may explain worldwide increase in food allergies. The tolerance is driven by effects of microbiota on gut immune responses whereas skin exposure to foods may promote allergy. As proved by recent studies (Learning Early on Peanut Allergy - LEAP), early intervention by introduction of peanuts in the infants diet, reduces the window-of-risk when children are not protected by tolerance. It conveyed more information on evolution of IgE and IgG4 antibodies responses to food allergens over time. Prevention studies require long-term immunological and clinical follow-up.
IV. Risk of Asthma : Lessons from Amish and Hutterite Children
C.Ober et al Current Op.Immunol 2017 October 48 51-60
It is well known that, since the publications of Erika Von Mutius, children who grow up in traditional farm environments are protected from developing asthma mainly by activating innate pathways, and distinct immune cell phenotypes. Moreover the 17q21 asthma locus confers both protection and risk, depending on exposures.
This ‘farm effect’ can be largely explained by the child's early life contact with farm animals, in particular cows, and their microbes. The recent studies of the authors further demonstrated that although Amish and Hutterites are very similar with respect to ancestry, many lifestyle factors, and farming practices, profound differences exist in the levels of house dust endotoxin, in the prevalence of atopy among school children, and in the proportions, phenotypes, and functions of immune cells. These findings like many previous studies in European farm children have advanced our understanding of the asthma-protective ‘farm effect’.
V. Atopic Dermatitis and Psoriasis : Similarity and Difference
E.Guttman-Yassky et al Current Op.Immunl 2017 October 48 51-60
Psoriasis and atopic dermatitis (AD) are common T-cell mediated inflammatory diseases of the skin that can be treated by specific cytokine antagonists or more broad immunosuppressive drugs. The diseases are similar in that epidermal keratinocytes respond to T-cell derived cytokines by altering growth and differentiation responses. When studied across European-American populations, psoriasis and AD display differing T-cell polarity and different arrays of cytokines. Psoriasis is a disease largely driven by Th17 T-cells and associated IL-17 activation, while AD has a strong Th2 component associated with IL-4 and IL-13 over-production, and both diseases have activation of Th22 T-cells and Th1 pathways with increased IL-22 and IFNγ production, respectively. AD is a disease frequently associated with increased IgE production and over allergies or asthma, most likely due to increased Th2 activation, which is largely lacking in psoriasis. Hence, psoriasis and AD can be viewed as distinct diseases with differing clinical, tissue, and molecular disease phenotypes, but this view does not account for specific subtypes of AD, including Asian-origin, intrinsic, and pediatric AD, that have a prominent IL-17 component and also tissue patterning that overlaps with distinctive psoriasis histopathology. Hence, when considering the range of AD phenotypes, a case can be made that psoriasis and AD exist across a spectrum where polar T-cell axes can be variably present and create some overlapping disease characteristic. So it is necessary to personalize therapies and target multiple T-cell axes to attain similar disease improvement.
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