Cord blood‐IgE as risk factor and predictor for atopic diseases

Edenharter,; Bergmann,; Wahn,; Forster,; Zepp,

doi:10.1046/j.1365-2222.1998.00241.x

Cited by 102 publications

(79 citation statements)

References 26 publications

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“…The literature is ambivalent about whether cord blood IgE is predictive for the later development of atopy or not. However, the concentration of total IgE in umbilical cord blood was found in several studies to be positively associated with later development of atopy (7,8,36,37), the sibling effect may have its origin (at least partly) in utero. If this hypothesis were correct, neonatal IgE would be expected to be negatively associated with increasing parity.…”

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confidence: 99%

Determinants of neonatal IgE level: parity, maternal age, birth season and perinatal essential fatty acid status in infants of atopic mothers

Gool

Thijs

Dagnelie

et al. 2004

Allergy

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Objective:The hygiene hypothesis suggests that the protective 'siblings effect' against atopic diseases such as atopic dermatitis, allergic asthma and hay fever is a result of recurrent infections during early childhood. A recent study and review have indicated that this protective effect may already arise in utero. Lower n-3 essential fatty acid (EFA) status is associated with increased parity, and EFA status has also been related to atopy. The present study confirms the negative association between parity and neonatal immunoglobulin E (IgE) levels and further unravel the role of perinatal EFA status. Methodology: In a prospective cohort study in 184 atopic mothers and their neonates, we simultaneously measured serum total IgE and EFA levels in plasma phospholipids, both in the mother at 34-36 weeks of gestation and in the neonate at the age of 1 week. Linear regression analysis was used to estimate the effect of parity on maternal and neonatal IgE and EFA status, and the independent effects of parity and EFA status on IgE, controlling for confounding factors such as maternal age and birth season. Results: Parity was associated with lower neonatal IgE level (P < 0.01), as well as with lower docosahexanoic acid (DHA, 22:6n-3) status of the mother (P = 0.01) but not of the neonate (P > 0.69). In the multivariate analysis, higher parity, higher maternal IgE, lower maternal age and birth in the first 3 months of the year were independently associated with neonatal IgE level. No association was detected between maternal or neonatal EFA status and neonatal IgE. Conclusions: As neonatal total serum IgE is predictive of later atopy, our results support the hypothesis that the sibling effect in atopy is already being programmed in utero. Our data also confirm earlier findings that DHA status is lower in multiparous women, but this did not confound the relation between parity and neonatal IgE.

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confidence: 99%

Determinants of neonatal IgE level: parity, maternal age, birth season and perinatal essential fatty acid status in infants of atopic mothers

Gool

Thijs

Dagnelie

et al. 2004

Allergy

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“…More direct evidence of in utero sensitisation of the fetal immune system to peanut allergen, in the form of the detection of peanut-specific IgE in cord blood, remains absent. Furthermore, studies of non-peanut allergens suggest that the sensitivity and positive predictive value of such an observation for subsequent allergic disease would be low (24) . The one study that attempted to detect peanut-specific IgE in cord blood was unable to do so in twenty-three neonates who subsequently developed peanut allergy (12) .…”

Section: Discussionmentioning

confidence: 99%

Peanut sensitisation and allergy: influence of early life exposure to peanuts

et al. 2010

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The aim of the present systematic review was to evaluate the influence of early life exposure (maternal and childhood) to peanuts and the subsequent development of sensitisation or allergy to peanuts during childhood. Studies were identified using electronic databases and bibliography searches. Studies that assessed the impact of non-avoidance compared with avoidance or reduced quantities of peanuts or peanut products on either sensitisation or allergy to peanuts, or both outcomes, were eligible. Six human studies were identified: two randomised controlled trials, two casecontrol studies and two cross-sectional studies. In addition, published animal and mechanistic studies, relevant to the question of whether early life exposure to peanuts affects the subsequent development of peanut sensitisation, were reviewed narratively. Overall, the evidence reviewed was heterogeneous, and was limited in quality, for example, through lack of adjustment for potentially confounding factors. The nature of the evidence has therefore hindered the development of definitive conclusions. The systematic review of human studies and narrative expert-led reviews of animal studies do not provide clear evidence to suggest that either maternal exposure, or early or delayed introduction of peanuts in the diets of children, has an impact upon subsequent development of sensitisation or allergy to peanuts. Results from some animal studies (and limited evidence from human subjects) suggest that the dose of peanuts is an important mediator of peanut sensitisation and tolerance; low doses tend to lead to sensitisation and higher doses tend to lead to tolerance.Peanut allergy: Diet: Prenatal exposure: Childhood exposure Onset of peanut allergy typically occurs in childhood, with 70-100 % (1) of peanut-allergic children being reported to react upon their first known dietary exposure to peanuts. Because IgE-mediated allergic reactions require prior exposure and immunological sensitisation to the allergen, this suggests that sensitisation has already been acquired, either in utero, or by unrecognised oral exposure or non-oral (cutaneous or respiratory) routes. As many as one in fiftyfive children in the UK may currently show evidence of an allergic reaction to peanuts (2) ; indeed, peanut allergy is the most common cause of severe allergic reaction to foods, causing 30 % of all cases of anaphylaxis outside hospital (3) . Data from the Isle of Wight UK Birth Cohort Study suggest a threefold rise in the prevalence of peanut sensitisation and allergy in children born between 1989-90 and 1994 -6 (4,5) . Recent data from children born in 2001 -2 show no further increases in the prevalence of peanut sensitisation and allergy (6) .In 1998 the UK Government issued precautionary advice to mothers whose children have a family history of allergic diseases, that they may wish to avoid peanut consumption during pregnancy and breast-feeding and avoid giving the child peanuts and peanut products until the child is 3 years of age (7) . The precautionary advice was...

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“…Although the production of IgE starts in the 11th week of gestation, no specific sensitization to food or inhalant allergens as measured by elevated serum IgE antibodies can be detected in cord blood via standard methods. Early findings describing elevated cord blood IgE concentrations as a predictor for clinical manifestations of atopy have not been confirmed [6,7].…”

Section: Natural History Of Atopic Manifestationsmentioning

confidence: 99%

Primary prevention of allergy: avoiding risk or providing protection?

Hamelmann

Beyer

Grüber

et al. 2007

Clin Experimental Allergy

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SummaryPrimary prevention strategies of allergy so far have been aimed to fight allergy causes, by avoiding risk factors and inhibiting their mechanisms of action. The results of trials testing food or airborne allergen avoidance as a prevention strategy were, however, rather disappointing. A reverse approach for primary prevention of allergies aims to facilitate exposure to protecting factors which promote the induction of immunologic tolerance against innocuous antigens. These factors are associated with farming environment and a 'traditional lifestyle', but identification of these factors is quite difficult. Major candidates include foodborne microbes, helminths or their components, which are able to stimulate mucosal immunity, particularly in the gut. Similarly, new preventive and therapeutic strategies are being tested to induce specific food-allergen oral tolerance through the ingestion of progressively increasing doses of the offending food. This shifting of allergy prevention research from avoidance to tolerance induction will hopefully allow us to reverse the epidemic trend of allergy diseases.

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Cord blood‐IgE as risk factor and predictor for atopic diseases

Abstract: We conclude that even when elevated cord blood-IgE levels are identified as a strong risk factor for sensitization, their poor predictive performance may make them useless as a basis for preventive measures.

Cited by 102 publications

References 26 publications

Determinants of neonatal IgE level: parity, maternal age, birth season and perinatal essential fatty acid status in infants of atopic mothers

Determinants of neonatal IgE level: parity, maternal age, birth season and perinatal essential fatty acid status in infants of atopic mothers

Peanut sensitisation and allergy: influence of early life exposure to peanuts

Primary prevention of allergy: avoiding risk or providing protection?

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