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Abstract: “Gluten sensitivity” has become commonplace among the public. Wheat allergy (WA) and celiac disease (CD) are well‐defined entities, but are becoming a fraction of individuals following a gluten‐free diet (GFD). Wheat allergy has a prevalence of <0.5%. Wheat, specifically its omega‐5 gliadin fraction, is the most common allergen implicated in food‐dependent, exercise‐induced anaphylaxis. CD is a non‐IgE hypersensitivity to certain cereal proteins: gluten in wheat, secalin in rye, hordein in barley, and to a lesser extent avenin in oat. It is a rare disease, with an estimated prevalence that varied widely geographically, being higher in Northern Europe and the African Saharawi region than in South‐East Asia. In addition to suggestive symptoms, serologic testing has high diagnostic reliability and biopsy is a confirmatory procedure. Patients with CD have extra‐intestinal autoimmune comorbid conditions more frequently than expected. A third entity is nonceliac gluten sensitivity, which has been created because of the increasing number of subjects who claim a better quality of life or improvement of their variety of symptoms on switching to a GFD. The phenomenon is being fueled by the media and exploited by the industry. The lack of a specific objective test has been raising substantial controversy about this entity. Allergists and gastroenterologists need to pay attention to the multitudes of individuals who elect to follow a GFD. Many such subjects might have WA, CD, or another illness. Providing them with appropriate evaluation and specific management would be of great advantages, medically and economically. [ABSTRACT FROM AUTHOR]

Several seeds have been increasingly incorporated in various food items, with consequent risk of hypersensitivity reactions that are often severe. Identification of the specific seed as the culprit is often not explored or is difficult to verify. In this article, we reviewed the English literature from January 1930 to March 2016 using PubMed and Google Scholar searching for publications relevant to hypersensitivity to common edible seeds, namely sesame, sunflower seed, poppy seed, pumpkin seed, flaxseed, and mustard seed. Considering the worldwide consumption of those seeds, the number of published articles on the subject was relatively small and was mainly as case reports rather than large series. Allergy to sesame was more reported than to other seeds, with an estimated prevalence of 0.1-0.2%. In this review, we summarize the information relevant to each of the six seeds and their oils regarding the manifestations, routes of exposure, identified major allergens, and cross-reactivity with other seeds or other foods. We also addressed the important role of a thorough history taking in suspecting seed allergy, the limited reliability of routine diagnostic procedures, and the importance of verification by appropriate challenge tests. At present, management is basically dietary avoidance and the use of symptomatic medications that may include epinephrine auto-injectors. We did not encounter any well-designed studies on immunotherapy for seed allergy, but it is hoped that such a gap be filled by the development of safe effective protocols in the near future. [ABSTRACT FROM AUTHOR]

To cite this article: Craig TJ, Bewtra AK, Bahna SL, Hurewitz D, Schneider LC, Levy RJ, Moy JN, Offenberger J, Jacobson KW, Yang WH, Eidelman F, Janss G, Packer FR, Rojavin MA, Machnig T, Keinecke H-O, Wasserman RL. C1 esterase inhibitor concentrate in 1085 Hereditary Angioedema attacks - final results of the I.M.P.A.C.T.2 study. Allergy 2011; 66: 1604-1611. Abstract Background: The placebo-controlled study International Multicentre Prospective Angioedema C1-INH Trial 1 (I.M.P.A.C.T.1) demonstrated that 20 U/kg C1 esterase inhibitor (C1-INH) concentrate (Berinert®; CSL Behring, Marburg, Germany) is effective in treating acute abdominal and facial Hereditary Angioedema (HAE) attacks. Methods: I.M.P.A.C.T.2 was an open-label extension study of I.M.P.A.C.T.1 to evaluate the safety and efficacy of long-term treatment with 20 U/kg C1-INH for successive HAE attacks at any body location. Efficacy outcomes included patient-reported time to onset of symptom relief (primary) and time to complete resolution of all symptoms (secondary), analysed on a per-patient and per-attack basis. Safety assessments included adverse events, vital signs, viral safety and anti-C1-INH antibodies. Results: During a median study duration of 24 months, 1085 attacks were treated in 57 patients (10-53 years of age). In the per-patient analysis, the median time to onset of symptom relief was 0.46 h and was similar for all types of attacks (0.39-0.48 h); the median time to complete resolution of symptoms was 15.5 h (shortest for laryngeal attacks: 5.8 h; 12.8-26.6 h for abdominal, peripheral and facial attacks). Demographic factors, type of HAE, intensity of attacks, time to treatment, use of androgens and presence of anti-C1-INH antibodies had no clinically relevant effect on the efficacy outcomes. There were no treatment-related safety concerns. No inhibitory anti-C1-INH antibodies were detected in any patient. Conclusions: A single dose of 20 U/kg C1-INH concentrate is safe and provides reliable efficacy in the long-term treatment of successive HAE attacks at any body location. [ABSTRACT FROM AUTHOR]

Background: Given the importance of airway inflammation in asthma, there has been an effort to incorporate inflammatory markers into its management. Measurement of fractional exhaled nitric oxide (FeNO) is a noninvasive marker of airway inflammation; however, the use of the available FeNO analyzer is limited by several factors including its cost and lack of transportability. The aim of this study was to compare the performance of a new hand-held FeNO measuring device (NIOX MINO) to the current clinical standard – the chemiluminescence FeNO analyzer (NIOX). Methods: Subjects 6 years and older presenting to an allergy and asthma clinic underwent FeNO evaluation by NIOX and each of three NIOX MINOs. The mean of two acceptable measurements from the NIOX and the first approved measurement from each NIOX MINO were used for analysis. Results: One hundred ten patients aged 6–86 years completed the study. Intrasubject FeNO levels obtained by each of the three NIOX MINOs revealed no significant difference between the measurements ( P = 0.59). There was a very strong correlation between FeNO measurements by NIOX and by NIOX MINO ( r = 0.98, P < 0.0001). The mean intrasubject FeNO difference between NIOX and NIOX MINO was −0.5 p.p.b. which was not statistically significantly different from zero ( P = 0.21). Conclusions: Fractional exhaled nitric oxide measurements by the NIOX MINO showed a strong correlation and a high degree of agreement with the current standard stationary device. The NIOX MINO may be reliably used in clinical practice. [ABSTRACT FROM AUTHOR]

Allergic (immune-mediated) reactions to cow milk and other dietary proteins encountered during infancy are responsible for some of the adverse symptoms and syndromes observed in infants intolerant to cow milk, infant formulas and occasionally human milk. Iron deficiency anemia associated with gastrointestinal blood loss, protein losing enteropathy, enterocolitis, colitis, and malabsorption syndrome are examples of putative allergic reactions to dietary antigens which occur in infancy. A number of symptoms referable to the gastrointestinal tract such as, vomiting, colic and chronic non-specific diarrhea occur in infants both with and without immune-mediated reactions to dietary antigens. Verification of adverse reactions to dietary antigens, including allergic reactions, should be accomplished through the use of double-blind, placebo-controlled food challenge, with the dietary antigen to be tested presented in a liquid vehicle or, in older children, in capsule form. Approximately 8%-25% of children with immediate hypersensitivity to cow milk have been found to be allergic to soy products. Soy and other intact protein substitutes for cow milk, such as beef and lamb based formulas, have produced anaphylactic reactions both in human infants and in animal models. Hypoallergenic formulas should have a chemically modified protein base which demonstrates significant reduction in antigenicity when tested in the laboratory both in vitro and in vivo. Such formulas should meet rigorous standards for hypoallergenicity in clinical testing in human allergic infants or infants at high risk for developing allergy before being labelled hypoallergenic. [ABSTRACT FROM AUTHOR]

. Information derived from the compulsory national scheme of medical registration of births in Norway has been utilized in a study of the course and outcome of pregnancy in women with epilepsy. The series comprises 371 pregnancies in women with epilepsy and, as controls, 112530 pregnancies in women reporting no disease before or during the pregnancy. Comparisons indicate that women with epilepsy experience an excess of complications during pregnancy and labour, and that their babies are more frequently born prematurely and of low birth weight, and moreover have an excess of congenital malformations and higher perinatal and neonatal mortality rates. Epileptics, undoubtedly, constitute a high risk group in need of special attention during pregnancy and special care during labour. A proper interpretation of the findings in terms of causation, however, will call for additional data obtainable only through especially designed inquiries. [ABSTRACT FROM AUTHOR]

Background: Adverse reactions to drugs commonly occur sporadically. Certain individuals seem to have an increased susceptibility to develop reactions to multiple drugs. Genetic predisposition has not been elucidated. Our objective was to describe a case of three siblings who developed severe rashes to the same drug simultaneously. Methods: Review of the patients’ medical records for information on the clinical course, and comparing their serum immunoglobulin (Ig) levels initially and during follow-up. Results: The rashes were compatible with erythema multiforme and Stevens-Johnson syndrome and developed in the three siblings within 1–3 weeks after the intake of thiabendazole. Follow-up of serum Ig levels did not show any particular pattern, except for an initial mild to moderate elevation in IgG, IgA and IgM. Conclusions: The occurrence of such severe cutaneous drug reaction in the three siblings to the same drug suggests a genetic predisposition to adverse drug reactions. [ABSTRACT FROM AUTHOR]

The past few decades have witnessed an increasing understanding of the role of food allergy in human disease. Nevertheless, controversies still exist in several aspects of this area. One such controversy concerns the body systems that can be the target of food hypersensitivity reactions. Another is the role of noningestant exposure to food in a nonoccupational setting. Both of these aspects are vividly demonstrated in the case presented here. [ABSTRACT FROM AUTHOR]

The skin is very much exposed to food contact, both in the occupational and nonoccupational settings. Through such an exposure, adverse reactions can occur that may be irritant or immunologic. Both such types of reactions are particularly common in children with atopic dermatitis. Immunologic reactions can be immediate (immunoglobulin E-mediated) or delayed (cell-mediated), and can be localized or systemic. The latter can be life-threatening, even following trivial exposure. Clinical and experimental data are accumulating to indicate that epicutaneous exposure to food can induce de novo systemic immunoglobulin E sensitization., (Copyright 2004 Blackwell Munksgaard)

Serum IgE levels in healthy blood donors who had no history of atopy were measured by a paper-disc RIA and analyzed according to the donors' smoking habits. The IgE geometric mean for regular smokers was 41.7 IU/ml, which was significantly higher than that for nonsmokers (19.3 IU/ml) or rare smokers (22.7 IU/ml). Whereas 28% of smokers had IgE levels greater than 200 IU/ml, none of the rare smokers or nonsmokers did. IgE levels in smokers showed a moderate inverse correlation with the degree of smoking. The mean IgE level was 189.8 IU/ml in those who smoked 1-9 cigarettes/day but only 32.8 IU/ml in those who smoked 10-19 cigarettes per day and 11.1 IU/ml in those who smoked 20 or more cigarettes/day. The number of years a person smoked did not seem to significantly influence the IgE level. The mean IgE level in ex-smokers (50.5 IU/ml) was much lower than in current light smokers but was still higher than in nonsmokers. There was a moderate inverse correlation between IgE levels and duration of cessation of smoking. Our data suggest a characteristic pattern for the influence of cigarette smoking on serum IgE level, namely, a striking rise associated with light smoking and a remarkable drop in heavy smokers, and such changes seemed reversible after the habit was stopped. Smoking status, therefore, appears to be an important consideration in interpreting serum IgE levels and in revising the "norms" of IgE levels.