Leucocyte Migration Inhibition in Cow's Milk Protein Intolerance

Khoshoo, Vikram; Bhan, M. K.; Nk, Arora; Sood, D.K.; Kumar, Ramesh; Stintzing, G

doi:10.1111/j.1651-2227.1986.tb10204.x

Cited by 11 publications

(7 citation statements)

References 6 publications

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“…The results confirmed our original hypothesis in that patients with late reacting CMA show greater evidence of delayed type hypersensitivity (DTH), reflected by LIF production, compared with the other patient groups. Minor et al [8], Khoshoo et al [10] and Ashkenazi et al [9] described similar in-vitro features of DTH to milk proteins in some children with CMA, although their findings are not strictly comparable with the results of this study. Minor et al's [8] patients were older and some had less welldefined symptoms attributable to CMA.…”

Section: Discussioncontrasting

confidence: 67%

“…Both these investigators reported a clear distinction between CMA positive and negative patients in the production of leucocyte migration inhibition factor (LIF). Khoshoo [10], in a study of infants with protracted diarrhoea, demonstrated that the leucocytes of patients with CMPI showed significant migration inhibition after in-vitro incubation with ^-lactoglobulin. In these studies [8][9][10], detailed information regarding the volume of milk administered and the nature or time of onset of symptoms after milk challenge was not described.…”

Section: Introductionmentioning

confidence: 99%

“…Khoshoo [10], in a study of infants with protracted diarrhoea, demonstrated that the leucocytes of patients with CMPI showed significant migration inhibition after in-vitro incubation with ^-lactoglobulin. In these studies [8][9][10], detailed information regarding the volume of milk administered and the nature or time of onset of symptoms after milk challenge was not described. Furthermore, the possible influence of prolonged dietary milk exclusion on LIF production was not examined.…”

Section: Introductionmentioning

confidence: 99%

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Clinical manifestations of cows’ milk allergy in childhood. I. Associations with in‐vitro cellular immune responses

Hill

Ball

Hosking

1988

Clin Experimental Allergy

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Summary In this study 51 children who presented with symptoms of cows’ milk allergy (CMA) were categorized clinically by their response to cows’ milk challenge. Forty‐two patients had unequivocal evidence of CMA and nine were milk tolerant. Of the patients with CMA two groups were identified. The first, made up of 32 patients, had immediate‐type hypersensitivity reactions to milk associated with both positive skin‐prick test (SPT) and RAST. The second group of 10 late reacting patients developed symptoms of CMA over several hours or days; significant increases in irritability, frequency of bowel actions, and rhinitis following milk ingestion were noted in this group. Leucocyte inhibition factor (LIF) produced in response to α‐lactalbumin, β‐lactoglobulin and α‐casein was assessed in the immediate and late reacting CMA patients as well as in the milk‐tolerant group. There was no difference in LIF production between the milk‐tolerant group and those with immediate reactions. However, these two groups produced less LIF than the late reacting patients for α‐lactalbumin (P= 002), α‐casein (P= 0.03) and β‐lactoglobulin (P= 0.05). A clinical diary score card was found to be a useful instrument to assess the response of non‐immediate reactions to milk ingestion.

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Section: Discussioncontrasting

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Clinical manifestations of cows’ milk allergy in childhood. I. Associations with in‐vitro cellular immune responses

Hill

Ball

Hosking

1988

Clin Experimental Allergy

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“…Several reports suggest that T-cell mediated reactions play a role in deeluyed reactions to CMP, mainly gastrointestinal and skin reacttions (33). Cellular tests for type IV reactions include in vitro lymphoblast transformation test (172,173), lymphoblastic stimulation test (174,175), and leucocyte migration inhibition test (33,(176)(177)(178)(179). Hill et al (1988) demonstrated an increased production of leucocyte migration inhibitor factor (LIF) in response to ALA, BLG and alpha-CAS in clinically well-defined late reactors, but not in immediate reactors and controls (33).…”

Section: Type IV Cellular Immune Reactionmentioning

confidence: 99%

Cow's milk protein allergy and intolerance in infancy Some clinical, epidemiological and immunological aspects

Høst

1994

Pediatric Allergy Immunology

259

140

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Reproducible clinically abnormal reactions to cow's milk protein (CMP) may be due to the interaction between one or more milk proteins and one or more immune mechanisms, possibly any of the four basic types of hypersensitivity reactions. At present, evidence for type I, III and IV reactions against CMP has been demonstrated. Immunologically mediated reactions, mainly immediate IgE‐mediated reactions are defined as cow's milk protein allergy (CMPA). Non immunologically reactions against CMP are defined as cow's milk protein intolerance (CMPI). Many studies on “cow's milk allergy” have not investigated the immunological basis of the clinical reactions. It is not possible to differentiate between CMPA and CMPI solely on clinical symptoms. No single laboratory test is diagnostic of CMPA/CMPI. Therefore, the diagnosis still has to be based on strict well‐defined elimination and milk challenge procedures. Before 1950 CMPA/CMPI was rarely diagnosed. Since 1970 widely varying estimates of the incidence from 1.8% to 7.5% have been reported, mainly reflecting differences in diagnostic criteria and study design. Based on strict diagnostic criteria the incidence of confirmed CMPA/CMPI in infancy seems to be about 2–5% in developed countries. Symptoms suggestive of CMPA/CMPI may be encountered in about 5–15% of infants emphasizing the importance of controlled elimination/milk challenge. In breastfed infants reproducible clinical reactions to CMP in human milk have been reported in about 0.5%. Most infants with CMPA/CMPI develop symptoms before one month of age, often within one week after introduction of cow's milk based formula. The majority have ≥ 2 symptoms and symptoms from ≥ 2 organ systems. About 50%–70% have cutaneous symptoms, 50–60% gastrointestinal symptoms, and about 20–30% respiratory symptoms. In exclusively breast‐fed infants with CMPA/CMPI severe atopic eczema is a predominant symptom. Debut of CMPA/CMPI after 12 months is extremely rare. The basic treatment is complete avoidance of CMP. In infancy a proven hypoallergenic CM substitute is needed. Due to clinically important residual allergenicity in some hypoallergenic formulae controlled clinical testing is necessary in each case before use. Goat's milk proteins share identity with CMP. Raw untreated cow's milk and unhomogenized cow's milk is as allergenic as normal pasteurized and homogenized milk products. The prognosis of CMPA/CMPI is good with a remission rate about 45–50% at one year, 60–75% at two years, and 85–90% at three years. Associated adverse reactions to other foods develop in about 50%, and allergy against inhalants in 50–80% before puberty. High levels of IgE to CMP are associated with an increased risk of persisting CMPA, persisting allergy to other foods and inhalant allergy. The degree of antibody response to CMP exposure is a better predictor of persisting CMPA than a single finding of an elevated antibody level which can occur in normal infants without CMPA/CMPI. Cow's milk proteins are absorbed from the gut and can be measured in the bloo...

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“…Since its variable symptomatology may render CMAI difficult to diagnose clinically, reliable laboratory methods are required to aid the diagnosis. Prick, scratch and epicutaneous tests, determination of specific IgE antibodies, lymphocyte transformation test, leucocyte migration inhibition assay and histamine release test have been utilized as diagnostic tools in immunologically mediated cow's milk allergy (CMA) [2][3][4][5][6][7][8][9][10][11][12][13][14]. In the present study we used five different in vitro and in vivo tests measuring immediate and delayed responses to CM in 22 children with challenge-proven CMAI.…”

Section: Introductionmentioning

confidence: 99%

Diagnostic value of skin and laboratory tests in cow's milk allergy/intolerance

Räsänen

Lehto

Reunala

1992

Clin Experimental Allergy

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The applicability of a panel of five skin and laboratory tests in the diagnosis of cow's milk allergy/intolerance (CMAI) was investigated. The tests used were prick and patch tests, RAST, basophil histamine release test (BHRT) and lymphocyte proliferation test (LPT). Twenty-two atopic children who had experienced either immediate or delayed cutaneous symptoms upon challenge with cow's milk (CM), and 12 non-milk-allergic controls with atopic dermatitis (AD) were included in the study. RAST, prick test, BHRT and LPT to CM and patch test to alpha-casein were positive in the CMAI group and non-milk-allergic atopic controls as follows: 59% and 33%, 57% and 0%, 55% and 17%, 77% and 17%, 33% and 0%. RAST, prick test and BHRT were more often positive in children exhibiting immediate reactions, and patch test and LPT more often positive in those having delayed reactions to CM. The panel of five tests detected 21/22 children with CMAI and gave false-positive results in 5/12 of non-milk allergic controls. The sensitivity and specificity of the panel in the diagnosis of CMAI were 95% and 58%, respectively.

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Leucocyte Migration Inhibition in Cow's Milk Protein Intolerance

Cited by 11 publications

References 6 publications

Clinical manifestations of cows’ milk allergy in childhood. I. Associations with in‐vitro cellular immune responses

Clinical manifestations of cows’ milk allergy in childhood. I. Associations with in‐vitro cellular immune responses

Cow's milk protein allergy and intolerance in infancy Some clinical, epidemiological and immunological aspects

Diagnostic value of skin and laboratory tests in cow's milk allergy/intolerance

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