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Biomedical subjects

Erkki Savilahti

Publications and source records attributed to Erkki Savilahti.

At least 19 recordsLinked to original sources
PubMed2007

Undiagnosed coeliac disease and nutritional deficiencies in adults screened in primary health care.

OBJECTIVE: To compare the nutritional parameters of individuals with a previous diagnosis of coeliac disease (CD) with those of screen-detected patients in a large cohort of adults in primary care. MATERIAL AND METHODS: A cohort of 1900 adults (aged 18-64 years) was screened for tissue transglutaminase antibodies (TG2A) in primary care in the capital region of Finland. IgA-endomysium antibodies (EmA), HLADQ2/8 associated with CD were determined in positive individuals. Folate, iron, and transferrin receptor in sera were assessed in patients reporting a previous diagnosis of CD and patients positive for the above tests. RESULTS: Twenty-two out of 1900 (1%) patients reported a previous diagnosis of CD (biopsy-based 16/22 cases; 6/22 cases diagnostic criteria unknown). Among the screen-detected cases with TG2A> or = the cut-off value, 14/32 cases were considered to have CD based on high levels of both TG2A and EmA, DQ2/8 genotype and/or biopsy results. The prevalence of CD was as high as 1:53 in the total study population (36/1900), and in women even 1:46 (2.2%). Nutritional deficiencies were rare among CD patients diagnosed earlier (low iron = 1; low folate n=1) but common among those who had an undiagnosed CD (low folate n=6; p<0.005; concomitant iron deficiency n=2). One-third of the screen-detected CD patients were obese. Screen-detected patients did not present more abdominal symptoms than those with no CD. CONCLUSIONS: CD is common, the proportion among women possibly being as high as 2.2%. Although the great majority of screen-detected patients do not present any gastrointestinal symptoms at primary care, nutritional deficiencies such as low folate levels and iron deficiency are common.

Adolescent↗
PubMed2006

Probiotics and prebiotic galacto-oligosaccharides in the prevention of allergic diseases: a randomized, double-blind, placebo-controlled trial.

BACKGROUND: The increase in allergic diseases is attributed to a relative lack of microbial stimulation of the infantile gut immune system. Probiotics, live health-promoting microbes, might offer such stimulation. OBJECTIVE: We studied the effect of a mixture of 4 probiotic bacterial strains along with prebiotic galacto-oligosaccharides in preventing allergic diseases. METHODS: We randomized 1223 pregnant women carrying high-risk children to use a probiotic preparation or a placebo for 2 to 4 weeks before delivery. Their infants received the same probiotics plus galacto-oligosaccharides (n = 461) or a placebo (n = 464) for 6 months. At 2 years, we evaluated the cumulative incidence of allergic diseases (food allergy, eczema, asthma, and allergic rhinitis) and IgE sensitization (positive skin prick test response or serum antigen-specific IgE level >0.7 kU/L). Fecal bacteria were analyzed during treatment and at age 2 years. RESULTS: Probiotic treatment compared with placebo showed no effect on the cumulative incidence of allergic diseases but tended to reduce IgE-associated (atopic) diseases (odds ratio [OR], 0.71; 95% CI, 0.50-1.00; P = .052). Probiotic treatment reduced eczema (OR, 0.74; 95% CI, 0.55-0.98; P = .035) and atopic eczema (OR, 0.66; 95% CI, 0.46-0.95; P = .025). Lactobacilli and bifidobacteria more frequently (P < .001) colonized the guts of supplemented infants. CONCLUSION: Probiotic treatment showed no effect on the incidence of all allergic diseases by age 2 years but significantly prevented eczema and especially atopic eczema. The results suggest an inverse association between atopic diseases and colonization of the gut by probiotics. CLINICAL IMPLICATIONS: The prevention of atopic eczema in high-risk infants is possible by modulating the infant's gut microbiota with probiotics and prebiotics.

Bifidobacterium↗
PubMed2006

Molecularly defined adult-type hypolactasia in school-aged children with a previous history of cow's milk allergy.

AIM: To assess the role of lactase non-persistence/persistence in school-aged children and their milk-related symptoms. METHODS: The genotypes for the C/T(-13910) variant associated with lactase non-persistence/ persistence were determined using PCR-minisequencing in a group of 172 children with a mean age of 8.6 years (SE = 0.02, 93 boys) participating in a follow-up study for cow's milk allergy. The parents were asked to assess their children's milk consumption and abdominal symptoms. RESULTS: The presence of allergy to cow's milk was not associated with the C/C(-13910) genotype related with a decline of lactase enzyme activity during childhood (lactase non-persistence). The frequency of the C/C(-13910) genotype (16%) was similar to published figures for the prevalence of adult-type hypolactasia in Finland. The majority of the children (90%) in this series consumed milk but 26% of their families suspected that their children had milk-related symptoms. Forty-eight percent of the children with the C/C(-13910) genotype did not drink milk at all or consumed a low lactose containing diet prior to the genotyping (P < 0.004 when compared to the other genotypes). CONCLUSION: Analysis of the C/T(-13910) polymorphism is an easy and reliable method for excluding adult-type hypolactasia in children with milk-related symptoms. Genotyping for this variant can be used to advise diets for children with a previous history of cow's milk allergy.

Child↗
PubMed2006

Fecal calprotectin remains high during glucocorticoid therapy in children with inflammatory bowel disease.

OBJECTIVE: Fecal calprotectin is a promising marker for the assessment of gastrointestinal inflammation. Fecal calprotectin levels were followed-up in children with inflammatory bowel disease (IBD) who were introduced to glucocorticoid therapy. The aim of this study was to assess whether the changes in fecal calprotectin levels reflect therapeutic responses. MATERIAL AND METHODS: Fecal calprotectin was measured by enzyme immunoassay in 57 children (mean age 9.8 years, range 0.9-18 years) who underwent colonoscopies (IBD n=31, non-IBD disease n=13, normal n=13) and followed-up in 15 children (mean age 13 years, range 3.6-18 years) who were introduced to glucocorticoid therapy because of active IBD at 0, 2, and 4 weeks and at 4-week intervals until one month after discontinuation of the therapy. RESULTS: Fecal calprotectin was <100 microg/g in 70% of the children with normal findings on colonoscopy or a non-IBD disease. Fecal calprotectin was >100 microg/g in all but one child with active IBD and in 13/15 of those children who were introduced to glucocorticoids by the clinicians. Fecal calprotectin values decreased within 4 weeks in line with clinical improvement in 7 children and normalized in 4/15 children during the follow-up. Fecal calprotectin increased in 5/8 of the non-steroid-dependent children after discontinuation of glucocorticoids. CONCLUSIONS: Fecal calprotectin is a sensitive marker for chronic colitis. In active disease treated with glucocorticoids, fecal calprotectin levels declined in line with the clinical improvement but seldom fell within the normal range, which suggests ongoing inflammation in a clinically silent disease. The measurement of fecal calprotectin may provide new tools for the assessment of the level of gut inflammation in children with chronic colitis in the follow-up of clinical responses.

Adolescent↗
PubMed2006

Effect of probiotics on vaccine antibody responses in infancy--a randomized placebo-controlled double-blind trial.

Probiotics are immunomodulatory and may thus affect vaccine antibody responses. With the accumulating evidence of their health-promoting effects, probiotics are increasingly administered in allergy-prone infants. Therefore, we studied the effect of probiotics on antibody responses to diphtheria, tetanus and Haemophilus influenzae type b (Hib) vaccines in 6-month-old infants participating in a randomized placebo-controlled double-blind allergy-prevention trial. Mothers of unborn children at increased risk for atopy used a combination of four probiotic strains, or a placebo, for 4 wk before delivery. During 6 months from birth, their infants received the same probiotics and galacto-oligosaccharides, or a placebo. The infants were immunized with a DTwP (diphtheria, tetanus and whole cell pertussis) at ages 3, 4, and 5 months, and with a Hib polysaccharide conjugate at 4 months. Serum diphtheria, tetanus, and Hib IgG antibodies were measured at 6 months. In the probiotic group, protective Hib antibody concentrations (>/=1 microg/ml) occurred more frequently, 16 of 32 (50%) vs. six of 29 (21%) (p = 0.020), and the geometric mean (inter-quartile range) Hib IgG concentration tended to be higher 0.75 (0.15-2.71) microg/ml than in the placebo group 0.40 (0.15-0.92) microg/ml (p = 0.064). In these respective groups, diphtheria, 0.38 (0.14-0.78) vs. 0.47 (0.19-1.40) IU/ml (p = 0.449), and tetanus, 1.01(0.47-1.49) vs. 0.81 (0.56-1.39) IU/ml (p = 0.310), IgG titers were comparable. In conclusion, in allergy-prone infants probiotics seem not to impair antibody responses to diphtheria, tetanus, or Hib, but may improve response to Hib immunization.

Bifidobacterium↗
PubMed2006

Dietary insulin as an immunogen and tolerogen.

We have shown that exposure to bovine insulin (BI) in cow's milk (CM) formula induces an insulin-specific immune response in infants. Here we studied the role of human insulin (HI) in breast milk as a modulator of the immune response to insulin. In a group of 128 children participating in the TRIGR pilot study, maternal breast milk samples were collected 3-7 days and/or 3 months after delivery. After exclusive breast-feeding, the children received either CM formula or casein hydrolysate during the first 6-8 months of life. Insulin concentration in breast milk and immunoglobulin G (IgG) antibodies to BI in plasma samples were measured by EIA. The levels of insulin in breast milk samples were higher in mothers affected by type 1 diabetes than in non-diabetic mothers (p = 0.007 and p < 0.001). The concentration of insulin in breast milk correlated inversely with the plasma levels of IgG antibodies to BI at 6 months of age in children who received CM formula (r = -0.39, p = 0.013), and at 12 months of age in all children (r = -0.25, p = 0.029). The levels of breast milk insulin were higher in the mothers of nine children who developed beta-cell autoimmunity when compared with autoantibody-negative children (p = 0.030); this holds true also when only children of diabetic mothers were included (p = 0.045). BI in CM induces higher levels of IgG to insulin in infants than does HI in breast-fed children. Instead, HI in breast milk seems to be tolerogenic and may downregulate the IgG response to dietary BI. However, our results in infants who developed beta-cell autoimmunity suggest that in this subgroup of children breast milk insulin does not promote tolerance.

Animals↗
PubMed2005

Mutations in the translated region of the lactase gene (LCT) underlie congenital lactase deficiency.

Congenital lactase deficiency (CLD) is a severe gastrointestinal disorder characterized by watery diarrhea in infants fed with breast milk or other lactose-containing formulas. We initially assigned the CLD locus by linkage and linkage disequilibrium on 2q21 in 19 Finnish families. Here we report the molecular background of CLD via characterization of five distinct mutations in the coding region of the lactase (LCT) gene. Twenty-seven patients out of 32 (84%) were homozygous for a nonsense mutation, c.4170T-->A (Y1390X), designated "Fin(major)." Four rare mutations--two that result in a predicted frameshift and early truncation at S1666fsX1722 and S218fsX224 and two point mutations that result in substitutions Q268H and G1363S of the 1,927-aa polypeptide--confirmed the lactase mutations as causative for CLD. These findings facilitate genetic testing in clinical practice and enable genetic counseling for this severe disease. Further, our data demonstrate that, in contrast to common adult-type hypolactasia (lactose intolerance) caused by a variant of the regulatory element, the severe infancy form represents the outcome of mutations affecting the structure of the protein inactivating the enzyme.

DNA Mutational Analysis↗
PubMed2005

Clinical course and prognosis of cow's milk allergy are dependent on milk-specific IgE status.

BACKGROUND: Large, prospective population-based studies on clinical course, development of tolerance, and risk for other atopy in children with cow's milk allergy (CMA) are lacking. OBJECTIVE: We investigated the development of tolerance and the risk for asthma, rhinoconjunctivitis, atopic dermatitis, and sensitization in children with CMA followed to school age. METHODS: We followed 118 children with CMA until recovery and repeatedly measured their sensitization to cow's milk (CM). At age 8.6 years, 94 allergic subjects and 80 control subjects from the same cohort were studied for atopic diseases and sensitization. In addition, the parents of 12 allergic subjects and 26 control children returned a questionnaire on atopy, respectively. RESULTS: IgE-mediated CMA was detected in 86 (73%) children; at age 8.6 years, 13 (15%) had persistent CMA. All children with IgE-negative CMA were tolerant by age 5.0 years (P < .0001). Risk factors for persistent CMA at age 2.0 years were sensitization to CM at age 1.6 years (odds ratio, 6.3; 95% CI, 2.6-15.2), urticaria at diagnostic challenge (odds ratio, 3.3; 95% CI, 1.4-7.8), CM exposure at the maternity hospital (odds ratio, 3.2; 95% CI, 1.4-7.8), and early sensitization to egg (odds ratio, 2.8; 95% CI, 1.2-6.6). By age 8.6 years, children with IgE-positive CMA more frequently had asthma (31% vs 13%, P < or = .01), rhinoconjunctivitis (66% vs 21%, P < or = .001), atopic eczema (81% vs 26%, P < or = .001), and sensitization to any allergen (88% vs 39%, P < or = .001) than control subjects. CMA and family history of atopy were independent risk factors for atopic diseases, and CMA was also a risk factor for sensitization to inhalant allergens. CONCLUSION: IgE-mediated CMA often persists to school age and is a risk factor for other atopy; non-IgE-mediated CMA, by contrast, is a benign infantile condition.

Animals↗
PubMed2005

Spectrum of mutations in CFTR in Finland: 18 years follow-up study and identification of two novel mutations.

BACKGROUND: The incidence of cystic fibrosis (CF) is low in the isolated Finnish population and the Finnish CF mutation spectrum has differed from many European countries. METHODS: We have analyzed the mutation spectrum and the geographical distribution of CF mutations in Finland covering the last 18 years (1987-2004). RESULTS: A total of 14 mutations were identified; two of them new, 774insT and S589T (G>C at 1,898). The overall coverage of mutations was 97% (99/102 chromosomes). The most frequent mutations were F508del and 394delTT, found in 36% (37/102) and 35% (36/102) of the CF chromosomes respectively. Of the rare mutations, a mutation of presumable Slavic origin, CFTRdele2.3 (21 kb), was enriched in a rural isolate with a frequency of 5,9% (6/102), and a mutation that possibly indicates Swedish influence, 3659delC, was scattered throughout the country with a similar frequency of 5,9% (6/102). G542X, R1162X, R117H, 3732delA, 1,898 + 3A >C, S1196X, S945L, W57R, 774insT and S589T were each identified in a number of chromosomes from one to three. CONCLUSIONS: Our observations of the Finnish CF mutation spectrum fit well with the characteristics of Finland as a population of multiple local founder effects.

Cystic Fibrosis↗
PubMed2005

Gluten-free diet may alleviate depressive and behavioural symptoms in adolescents with coeliac disease: a prospective follow-up case-series study.

BACKGROUND: Coeliac disease in adolescents has been associated with an increased prevalence of depressive and disruptive behavioural disorders, particularly in the phase before diet treatment. We studied the possible effects of a gluten-free diet on psychiatric symptoms, on hormonal status (prolactin, thyroidal function) and on large neutral amino acid serum concentrations in adolescents with coeliac disease commencing a gluten-free diet. METHODS: Nine adolescents with celiac disease, aged 12 to 16 years, were assessed using the semi-structured K-SADS-Present and Lifetime Diagnostic interview and several symptom scales. Seven of them were followed at 1 to 2, 3, and 6 months on a gluten-free diet. RESULTS: Adolescent coeliac disease patients with depression had significantly lower pre-diet tryptophan/ competing amino-acid (CAA) ratios and free tryptophan concentrations, and significantly higher biopsy morning prolactin levels compared to those without depression. A significant decrease in psychiatric symptoms was found at 3 months on a gluten-free diet compared to patients' baseline condition, coinciding with significantly decreased coeliac disease activity and prolactin levels and with a significant increase in serum concentrations of CAAs. CONCLUSION: Although our results of the amino acid analysis and prolactin levels in adolescents are only preliminary, they give support to previous findings on patients with coeliac disease, suggesting that serotonergic dysfunction due to impaired availability of tryptophan may play a role in vulnerability to depressive and behavioural disorders also among adolescents with untreated coeliac disease.

Adolescent↗
PubMed2005

Induction of inflammation as a possible mechanism of probiotic effect in atopic eczema-dermatitis syndrome.

BACKGROUND: The immunomodulating mechanisms of Lactobacillus GG (LGG) and other probiotics are poorly understood. OBJECTIVE: We studied in vivo the immunologic effects of probiotics in infants with atopic eczema-dermatitis syndrome (AEDS) and cow's milk allergy (CMA). METHODS: Two hundred thirty infants with AEDS and suspected CMA received, concomitant with elimination diet, either LGG, a mixture of 4 probiotic strains (MIX), or placebo for 4 weeks. All available paired pretreatment and posttreatment plasma samples (n = 132) were analyzed for concentrations of IL-2, IL-4, IL-6, IL-10, TNF-alpha, IFN-gamma, soluble intercellular adhesion molecule 1, soluble E-selectin, TGF-beta1, TGF-beta2, and C-reactive protein. RESULTS: In infants with IgE-associated AEDS, treatment with LGG induced higher C-reactive protein levels than in the placebo group (geometric mean, 0.83 microg/mL [95% CI, 0.56-0.81] vs 0.42 microg/mL [95% CI, 0.27-0.65]; P = .021). Concomitantly, IL-6 levels increased after treatment with LGG ( P = .023) but not with MIX or placebo. Soluble E-selectin levels were higher after probiotic than after placebo treatment in infants with IgE-mediated CMA (LGG geometric mean, 86.7 ng/mL [95% CI, 75.2-100]; MIX geometric mean, 91.6 ng/mL [95% CI, 74.8-111.9]; and placebo geometric mean, 64.9 ng/mL [95% CI, 53-79.3]; analysis of covariance, P = .035; LGG vs placebo, P = .023; MIX vs placebo, P = .020). Use of MIX induced an increase in plasma IL-10 levels ( P = .016). CONCLUSION: Probiotics induced systemically detectable low-grade inflammation, which might explain the clinical effects of probiotics in AEDS and CMA.

Animals↗
PubMed2005

Undiagnosed silent coeliac disease: a risk for underachievement?

OBJECTIVE: Silent coeliac disease is reported in 1% of Caucasian populations, but there is a lack of knowledge of its natural course and the risk of complications. The need for population screening is debated. We sought for complications of untreated coeliac disease in a well-defined cohort of Finnish adults. MATERIAL AND METHODS: Subjects (n=2427, ages 24-39 years) attending the 21-year follow-up visit of the study "Cardiovascular Risk in Young Finns" completed an extensive questionnaire on their health, diet, social situation and family life, and were given a medical examination. Measurement of serum IgA-transglutaminase and IgA-endomysium antibodies identified 21 subjects with silent coeliac disease. RESULTS: The subjects with silent coeliac disease did not differ from the rest of the cohort in age, gender, stature, weight, medical diagnoses (autoimmune, malignant), health concerns, use of alternative medications, physical activity, or in the cause of death their parents. They had lower serum HDL-cholesterol (1.12 versus 1.29 mmol/L; p=0.015), as described for active coeliac disease. Fewer (5.3% versus 22.8%; p=0.047) had a university or college degree or worked in managerial or professional positions (28% versus 45%; p=0.112). CONCLUSIONS: The underachievement in education and working life observed in subjects with silent coeliac disease is a new and intriguing finding and may be related to the increased prevalence of depressive and disruptive behavioural disorders described in teenagers with untreated coeliac disease. Our findings add a new ingredient to the ongoing discussion regarding the need for population screening for silent coeliac disease.

Adult↗
PubMed2005

Metalloelastase (MMP-12) is upregulated in the gut of pediatric patients with potential celiac disease and in type 1 diabetes.

OBJECTIVE: A slight to moderate increase in autoantibodies to transglutaminase 2 (TG2), but no morphological evidence of villous atrophy to confirm the diagnosis of celiac disease (CD) poses a challenge for clinicians. Our aim was to study the matrix metalloproteinase (MMP) profile, proliferative and apoptotic characteristics of jejunal biopsies obtained from such pediatric patients in order to find markers predictive of early changes in extracellular matrix degrading enzymes in the development of CD. MATERIAL AND METHODS: Twenty-eight children with positive screening tests (increase in transglutaminase and/or endomysium antibodies), but minor histological changes in the gut (Marsh grade 0-2), were studied and followed up for 2-3 years. In situ hybridizations for MMP-1, -3 and -12 were performed and sections were immunostained for MMP-19 and -26. Proliferating cells were identified by Ki-67 immunostaining and apoptotic cells using the TUNEL technique. RESULTS: MMP-12 was detected in macrophages in 16/28 samples and its expression was associated with increased autoantibodies for TG2 and densities of CD3 and gammadelta positive T-cells in the epithelium. The number of stromal MMP-26 positive cells was high in patients with high TG2 titers. Expression of MMP-12, MMP-1 and -3 clustered in children with type 1 diabetes (T1D) and the proportion of apoptotic mucosal cells was increased in patients with T1D compared to the others. When children with CD were compared to those who did not develop it, the numbers of IEL, cryptal Ki-67, CD-3, and MMP-12 positive cells were higher and showed the most significant differences. CONCLUSIONS: In pediatric patients, increased numbers of MMP-12 positive macrophages in lamina propria associate with high titers of antibodies to TG2 and proness to CD. A stage of mild inflammation may contribute to the upregulation of MMPs in the gut of patients with T1D.

Adolescent↗
PubMed2005

Probiotic effects on faecal inflammatory markers and on faecal IgA in food allergic atopic eczema/dermatitis syndrome infants.

Probiotic bacteria are proposed to alleviate intestinal inflammation in infants with atopic eczema/dermatitis syndrome (AEDS) and food allergy. In such infants we investigated effects of probiotic bacteria on faecal IgA, and on the intestinal inflammation markers tumour necrosis factor-alpha (TNF-alpha), alpha1-antitrypsin (AT), and eosinophil cationic protein (ECP). A total of 230 infants with AEDS and suspected cow's milk allergy (CMA) received in a randomized double-blinded manner, concomitant with elimination diet, Lactobacillus GG (LGG), a mixture of four probiotic strains (MIX), or placebo for 4 wk. Four weeks after treatment, CMA was diagnosed with a double-blind placebo-controlled milk challenge. Faecal samples of 102 infants, randomly chosen for analysis, were collected before treatment, after 4-wk treatment, and on the first day of milk challenge. After treatment, IgA levels tended to be higher in probiotic groups than in the placebo group (LGG vs. placebo, p=0.064; MIX vs. placebo, p=0.064), and AT decreased in the LGG group, but not in other treatment groups. After challenge in IgE-associated CMA infants, faecal IgA was higher for LGG than for placebo (p=0.014), and TNF-alpha was lower for LGG than for placebo, but non-significantly (p=0.111). In conclusion, 4-wk treatment with LGG may alleviate intestinal inflammation in infants with AEDS and CMA.

Biomarkers↗
PubMed2005

Maternal consumption of dairy products during pregnancy and lactation, and the development of cow's milk antibodies in the offspring.

OBJECTIVE: To assess whether the maternal consumption of milk and milk products affects development of cow's milk (CM) antibodies in infants. DESIGN: A randomized pilot trial using food frequency questionnaires (mothers) and food records (infants). SETTING: Families with a newborn infant with increased HLA-DQB1-conferred risk of type 1 diabetes and at least one first-degree relative affected by type 1 diabetes from 16 hospitals in Finland between April 1995 and November 1997. SUBJECTS AND INTERVENTION: Infants randomized to receive a hydrolysed formula when breast milk was not available during their first 6-8 mo (n=112). Of these, 13 dropped out by the age of 3 mo and two were excluded due to incomplete CM antibody data. RESULTS: Maternal milk protein intake from cheese during pregnancy was inversely related to IgA-class antibody titres to beta-lactoglobulin (BLG) and casein (CAS) at 3 mo, and to IgA antibody titres to BLG at 6 mo. Maternal consumption of raw milk products during lactation was positively related to the development of IgA antibody titres to CAS at 6 mo, and inversely correlated to IgG antibody titres to bovine serum albumin (BSA) and IgA antibody titres to CAS at 2 y. Maternal cheese consumption was inversely related to the IgG antibody titres to CM formula and CAS and to the IgA antibody titres to CAS in early infancy. CONCLUSIONS: Few associations were established between maternal CM protein intake and CM protein antibody levels in the infants. The milk and milk products taken by the mother differed in their impact on the emerging CM antibody response in the offspring.

Animals↗
PubMed2005

IgA antibodies, TGF-beta1 and -beta2, and soluble CD14 in the colostrum and development of atopy by age 4.

Specific defense factors in breast milk together with length of breast-feeding and genetic predisposition may modulate the development of allergy. We studied whether IgA, soluble CD14 (sCD14), or transforming growth factor (TGF)-beta in colostrum could affect the development of atopy in children up to age 4. From a cohort of 4676, we selected four groups of children with either long or short exclusive breast-feeding (>3.5 or <0.5 mo); these groups further differed in the presence or absence of atopic heredity. In colostrum from mothers, we measured total IgA, IgA antibodies to cow's milk (CM) and casein, sCD14, and TGF-beta1 and -beta2. The children were divided into three groups: those with no atopic symptoms or IgE, those with allergic symptoms, and those with both outcomes. Mothers of infants later showing atopic symptoms or, in addition, having IgE sensitization (verified atopy) had a lower concentration of IgA casein antibodies in their colostrum than did mothers of infants with no indication of atopy at age 4. Low concentration of IgA casein antibodies was a significant risk for verified atopy. sCD14 levels were lower in colostrum of mothers with infants developing atopic symptoms and IgE sensitization than of those of infants with no atopy. Specific IgA antibodies to CM antigens and sCD14 in colostrum significantly associated with the appearance of both symptomatic and verified atopy by age 4.

Animals↗