Latent anaphylactic sensitivity of infants to cow's milk proteins

Mclaughlan, P.; Coombs, R.R.A.

doi:10.1111/j.1365-2222.1983.tb02560.x

Cited by 15 publications

(11 citation statements)

References 14 publications

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“…The discrepancy between our results and those described by May [I 3] may be partly explained by differences in the techniques used for histamine release but also because the earlier study [1] was of children with stich severe asthma that they had been admitted to hospital, suggesting that patient selection may have played a part. The most striking finding was the relatively poor response of leucocytes from patients who were clearly allergic to egg by several criteria; a finding similar to reports published on other types of food allergy [4][5][6][7]. When Dockhorn [7] compared the amount of histamine released in response to inhalant and food antigens using leucocytes taken from patients who had multiple allergies he found that HR to inhalant antigens was consistently higher (38-58",,) than HR to foods (11-21",,).…”

Section: Discussionsupporting

confidence: 83%

Histamine release from peripheral blood leucocytes in egg‐allergic patients

Clinton¹,

Kemeny²,

Amlot³

et al. 1986

Clin Experimental Allergy

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Summary Twelve egg‐allergic patients were selected on the basis of a clinical history of egg allergy and a positive skin‐prick test (SPT) to whole egg. A study was then carried out on the ability of the patients’ washed leucocytes to release histamine in the presence of whole egg, ovomucoid, ovalbumin and ovotransferrin. Histamine release (HR) from washed leucocytes was demonstrated in ten out of twelve patients, but only four out of ten released over 40% of their total histamine. Spontaneous HR ranged from 2·1–14·5% with a mean of 7·5%. There was good agreement between positive and negative HR, skin test and radioallergosorbent test (RAST) results. Concordance between the HR and skin test was found in 83%, HR and RAST in 71% and skin test and RAST in 78% of patients. However there was poor quantitative agreement between these three tests. When skin‐prick tests and HR thresholds were compared, ovomucoid elicited the greatest skin test sensitivity in five out of six patients, whereas five of the same six were more sensitive to ovalbumin when judged by HR.

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Section: Discussionsupporting

confidence: 83%

Histamine release from peripheral blood leucocytes in egg‐allergic patients

Clinton¹,

Kemeny²,

Amlot³

et al. 1986

Clin Experimental Allergy

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“…Our results are comparable with those of McLaughlan and Coombs, however, who reported that only 17% of the group showed no response to IgE antibody. 7 Our results suggest that latent sensitivity to respiratory syncytial virus antigen(s) occurs during the course of infection with respiratory syncytial virus (tables 3 and 5). Both the within group and between group comparisons suggest that challenge with respiratory syncytial virus antigen has a significant effect on release of histamine from whole blood.…”

Section: Latent Sensitisationmentioning

confidence: 60%

“…Latent anaphylactic sensitivity of infants to allergens has been shown experimentally by assay of histamine release from blood on exposure to specific allergens-for example cows' milk proteins. 7 The main aim of the present study was to find out whether latent sensitivity to respiratory Challenge reagents Goat antihuman IgE (E chain specific) was obtained from Sigma Chemicals (minimum titre 1:8).…”

Section: Introductionmentioning

confidence: 99%

Latent sensitisation to respiratory syncytial virus during acute bronchiolitis and lung function after recovery.

Caswell

Thomson

Ashmore

et al. 1990

Archives of Disease in Childhood

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To determine whether latent sensitivity to respiratory syncytial virus antigen(s) occurs after infection, 27 infants with acute bronchiolitis were studied and compared with 15 hospital controls. Blood was collected for whole blood challenge, and histamine release was measured by a high performance liquid chromatography technique with fluorometric detection. There was a significantly greater histamine release to respiratory syncytial virus antigen(s) in those with bronchiolitis than in controls, expressed either in amount (median 154 nmol/l compared with 104 nmol/l) or percentage release (median 20% compared with 3%). There was a significant difference between index and control groups in terms of individual histamine responses. These findings strongly suggest that infants develop latent sensitivity to respiratory syncytial virus antigen(s) during the course of acute bronchiolitis.Serial lung function tests were performed in 15 infants. All infants had abnormalities of lung function at some stage, but the small numbers of subjects precluded comparison between 'sensitised' and 'non-sensitised' infants. Further study is indicated to define the relation of latent sensitisation and subsequent bronchial hyper-responsiveness after respiratory syncytial virus infection in infants.syncytial virus antigen(s) occurs during the course of attacks of acute bronchiolitis in infancy, and whether there may be a relationship between latent sensitivity and lung function (including the responsiveness of airways to histamine) after apparent recovery from the acute illness. Patients and methods LATENT SENSITIVITYPatients Twenty seven infants with bronchiolitis (mean age 17 weeks, range 3-42) were studied during the 1987/8 winter outbreak of respiratory syncytial virus infection. Fifteen infants (mean age 13 weeks, range 1-35), in hospital for nonrespiratory illnesses, were studied as a control group. Six had been born after the end of the 1986/7 winter outbreak of respiratory syncytial virus infection and were studied before the onset of the 1987/8 outbreak.The clinical details and course of the illness were carefully recorded for each index case. Nasopharyngeal aspirates were obtained so that viruses could be identified by indirect immunofluorescence and tissue culture. During venepuncture for routine clinical investigations an additional 2 ml venous blood was obtained for 'challenge' studies.

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“…The concept that SIDS might be due to overwhelming IgE‐mediated anaphylaxis has received some consideration. As 25% of normal infants are reputed to release large amounts of histamine from their basophils in response to milk proteins, the hypothesis that milk aspiration into the lung might trigger fatal anaphylaxis through sensitised mast cells or basophils has been proposed [6]. A study by Mirchandani et al [7] found normal serum levels of both total IgE and IgE specific for house dust mite, mould and milk protein in post‐mortem blood from SIDS subjects.…”

Section: Anaphylaxismentioning

confidence: 99%

Immune and inflammatory responses in sudden infant death syndrome

Forsyth

1999

FEMS Immunology &Amp; Medical Microbiology

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Infancy is a time of unparalleled infection exposure. Coming from the privilege of the uterus, the newborn infant must make appropriate immune responses following infection that eliminates the infection but protects the host. There is evidence that in sudden infant death syndrome (SIDS) subjects there is a background of recent 'trivial' infection and immunological/inflammatory reactivity. This immunological/inflammatory reactivity is seen in enhanced pulmonary immunoglobulins and T-cell activation. It may be that in certain SIDS cases a trivial infection triggers an exaggerated inflammatory response, inducing cytokine cascades and eventual demise of the infant.

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Latent anaphylactic sensitivity of infants to cow's milk proteins

Cited by 15 publications

References 14 publications

Histamine release from peripheral blood leucocytes in egg‐allergic patients

Histamine release from peripheral blood leucocytes in egg‐allergic patients

Latent sensitisation to respiratory syncytial virus during acute bronchiolitis and lung function after recovery.

Immune and inflammatory responses in sudden infant death syndrome

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