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T1211 Clinical Relevance of IgG Antibodies Against Food Antigen in Crohn's Disease - a Double Blind Cross Over Diet Intervention Study
Abstract and Figures
Environmental factors are thought to play an important role in the development of Crohn's disease (CD). Immune responses against auto-antigens or food antigens may be a reason for the perpetuation of inflammation.
In a pilot study, 79 CD patients and 20 healthy controls were examined for food immunoglobulin G (IgG). Thereafter, the clinical relevance of these food IgG antibodies was assessed in a double-blind cross-over study with 40 patients. Based on the IgG antibodies, a nutritional intervention was planned. The interferon (IFN)gamma secretion of T cells was measured. Eosinophil-derived neurotoxin was quantified in stool.
The pilot study resulted in a significant difference of IgG antibodies in serum between CD patients and healthy controls. In 84 and 83% of the patients, respectively, IgG antibodies against processed cheese and yeast were detected. The daily stool frequency significantly decreased by 11% during a specific diet compared with a sham diet. Abdominal pain reduced and general well-being improved. IFNgamma secretion of T cells increased. No difference for eosinophil-derived neurotoxin in stool was detected.
A nutritional intervention based on circulating IgG antibodies against food antigens showed effects with respect to stool frequency. The mechanisms by which IgG antibodies might contribute to disease activity remain to be elucidated.
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... In fact, other studies have also highlighted the complexity underlying this relationship between serum serology and dietary sensitivity. In a double-blind crossover study, Bentz et al. attempted to reduce gastrointestinal inflammation by creating CD patientspecific diets by excluding food antigens, like yeast, in those with ASCA antibodies [36]. Patients with ASCA positivity adhering to a yeast-free diet experienced improved stool frequency, abdominal pain, and overall well-being compared to patients on a regular diet [36]. ...
... In a double-blind crossover study, Bentz et al. attempted to reduce gastrointestinal inflammation by creating CD patientspecific diets by excluding food antigens, like yeast, in those with ASCA antibodies [36]. Patients with ASCA positivity adhering to a yeast-free diet experienced improved stool frequency, abdominal pain, and overall well-being compared to patients on a regular diet [36]. Even in ASCA-positive CD patients not reporting dietary yeast sensitivity, the omission of yeast and other highly antigenic foods provided significant symptomatic improvement [36]. ...
... Patients with ASCA positivity adhering to a yeast-free diet experienced improved stool frequency, abdominal pain, and overall well-being compared to patients on a regular diet [36]. Even in ASCA-positive CD patients not reporting dietary yeast sensitivity, the omission of yeast and other highly antigenic foods provided significant symptomatic improvement [36]. These data were supported by another crossover study of 19 CD patients by Barclay et al. in 1992 [37]. ...
Inflammatory bowel disease represents a wide range of pathologies and disease states including Crohn’s Disease (CD) and Ulcerative colitis (UC). Despite extensive research, the exact immunopathogenesis of Crohn’s disease remains unclear, but a variety of studies over the years have pointed to yeast as a potential source antigen of uncertain significance. The aim of this review is to summarize the current literature investigating the association between Crohn’s disease patients and their responses to yeast. To do this, we performed a literature review by looking at clinical and translational research regarding the immunopathogenesis of Crohn’s disease, yeast and its associated biomarkers, and overall patient response to dietary yeast published between 1 January 1990 and 1 October 2024 that were indexed on PubMed and Google Scholar with the majority written in English. It was found that antibodies against Saccharomyces cerevisiae (ASCA) have proven to be highly specific for CD during the workup of IBD and may have diagnostic value for the purpose of excluding ulcerative colitis. For CD patients, there appears to be a dysregulated immune response to antigens like yeast that results in abnormal mucosal permeability and thus increases antigen presentation to the immune system. In addition, ASCA and its immunoglobulin modifications have been shown to have significant potential in the prediction of CD onset and disease course. Interestingly, although other abnormally structured antibodies can be found in CD patients’ serum for years preceding diagnosis, there appears to be no relation between ASCA and dietary yeast sensitivity by CD patients. In conclusion, significant research efforts have been made in recent years to explore the role of diet in the disease course and management of patients with Crohn’s disease. The immunological role of antigens including yeast in CD is complex and may represent an important pathogenetic factor in addition to influencing the specific phenotype of the disease. Unfortunately, no single specific diet is superior for the management of IBD, and individualized patient treatment by experts in the field is best for adjunctive therapy. New studies characterizing the microbiome of CD patients and also using immune markers/gene modifications to predict disease outcomes have shown to be quite promising. However, further research is required to investigate the CD yeast response and its role in the pathogenesis, diagnosis and treatment of CD.
... There is conflicting evidence in the literature regarding the link between IgG4 levels and dietary modification. It has been postulated that food components in blood stimulate high IgG4 levels and that these in turn may play a role in the inflammatory pathways of IBD, though exact mechanisms are unclear [39]. A large retrospective database of 282 patients found an association of serum IgG4 and disease outcomes in patients with IBD was inconclusive [40]. ...
Background
The efficacy of highly restrictive dietary therapies such as exclusive enteral nutrition (EEN) in the induction of remission in Crohn’s disease (CD) are well established, however, ongoing issues exist with its poor palatability, restrictions, and adherence. The primary aim of this review is to evaluate the current evidence for the efficacy of exclusively solid food diets on the induction and maintenance of clinical and biochemical remission in CD. Secondary aims include impact on endoscopic healing and quality of life.
Methods
A systematic review of all randomised controlled trials (RCTs), open-label randomised trials and head-to-head clinical trials assessing solid food diet intervention in patients with active or inactive Crohn’s disease was conducted. Studies included adult and paediatric patients with a verified disease activity index at baseline and follow up (Harvey Bradshaw Index, HBI; Crohn’s disease activity index, CDAI and paediatric CDAI, PCDAI). Additional secondary endpoints varied between studies, including endoscopic and biochemical responses, as well as quality of life measures. Two authors independently performed critical appraisals of the studies, including study selection and risk of bias assessments.
Results
14 studies were included for review, with several studies suggesting clinically significant findings. Clinical remission was achieved in a paediatric population undertaking the Mediterranean diet (MD) (moderate risk of bias). In adults, the Crohn’s disease exclusion diet (CDED) was comparable to the CDED with partial enteral nutrition (PEN) diet in induction of remission (moderate risk of bias). A low fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) diet was also shown to decrease symptoms in patients with quiescent or mildly active CD (high risk of bias), however, this was not corroborated by other low FODMAP diet studies.
Conclusions
There are promising outcomes for the MD and CDED in inducing clinical remission in mild to moderate CD. The results need to be interpreted with caution due to design limitations, including issues with combining outcomes among CD and UC patients, and small sample size. The current evidence for solid food dietary therapy in CD is limited by the lack of high quality studies and moderate to high bias. Future well designed studies are needed to confirm their efficacy.
... Interestingly, a large RCT found that in patients 84 Cox, 85 Pederson, 86 Heterogeneous in nature, each study eliminated: red meat -Allenberg et al, 78 food selected based on IgG antigenetic profile. 79,80 on stable medical therapy for IBD still experiencing mildmoderate disease activity, the SCD was comparable to Mediterranean diet in achieving symptomatic remission. 81 While, neither diet significantly lowered patients' C-reactive protein levels, fecal calprotectin was significantly lowered in the SCD arm. ...
There remains a paucity of data on the efficacy of nutritional interventions in luminal gastrointestinal disorders. This review appraises the evidence supporting dietary modification in gastroesophageal reflux disease (GERD), irritable bowel syndrome, Celiac disease, and inflammatory bowel disease.
Alhough the use of elimination diets; high fat/low carb; low fermentable oligosaccharides, disaccharides, monosaccharides and polyols; and lactose-free diets in GERD have been studied, the evidence supporting their efficacy remains weak and mixed. Patients with GERD should avoid eating within 3 hours of lying recumbent.
Studied dietary interventions for disorders of gut-brain interaction include low fermentable oligosaccharides, disaccharides, monosaccharides and polyols and gluten-restricted and lactose-free diets. While all can be effective in carefully, individually selected patients, the evidence for each intervention remains low.
In patients with inflammatory bowel disease, enteral nutrition is established in pediatric populations as useful in reducing inflammation and partial enteral nutrition has a growing evidence base for use in adults and children. Specific carbohydrate diets and the Crohn’s disease exclusion diet show promising evidence but require further study to validate their efficacy prior to recommendation.
Overall, the evidence supporting nutritional therapy across luminal gastrointestinal disorders is mixed and often weak, with few well-designed randomized controlled trials (RCTs) demonstrating consistent efficacy of interventions. RCTs, particularly cross-over RCTs, show potential to compare dietary interventions.
... If there are circulating antibodies present, these may affect different patients in different ways. It can be beneficial to test in the case of certain conditions, 35 such as irritable bowel syndrome (IBS), [36][37][38] major depressive disorder, migraine, 39-41 eczema or other skin rashes, 42 aching joints, 43 autoimmune diseases, 44 Crohn's disease, 45 or obesity. 46 The presence of circulating IgG antibodies may indicate increased intestinal permeability, known as "leaky gut syndrome", triggering an immune response, which can cause the production of IgG antibodies to certain food types. ...
Acne vulgaris is a skin condition that can occur in patients of any age. The outcome depends on genetic regulation in terms of hormone level control, sebum excretion, keratinization, and the level of immunological response. However, it is also possible that factors such as hygiene and diet can affect acne, while some recent studies have revealed links between certain specific food types and the onset or severity of acne. Therefore, this case study reports the effectiveness of the integrative approach in treating acne vulgaris in a young man who showed a rapid response to the combination of topical therapies and Intense Pulse Light (IPL) therapy with the removal of certain foods in line with the results of food intolerance testing. It was reported that the patient showed significant improvements following treatment for a three-month period, suggesting the strong potential of the integrative approach for acne treatment.
Diet therapy for inflammatory bowel disease (IBD) is an international research priority but guidance for IBD-specific diet trial design is lacking. This review critically evaluates key elements of prospective IBD food-based intervention trials and identifies gaps. Electronic databases were searched for interventional IBD diet studies. Prospective primary studies/trials were included if used food-based dietary strategies. Forty studies/trials evaluating 29 food-based strategies as therapy for IBD were identified. Considerable heterogeneity in diets, trial design, and methodology exists. Thirty-one trials (78%) intended the diet to modulate inflammation but 14/31 (46%) did not have a primary endpoint measuring an objective change in inflammatory activity and 20/31 (65%) controlled for medication stability prior to application of diet at baseline. Higher-quality IBD diet trials used symptom-based assessment tools coupled with an objective evaluation of inflammatory activity. Dietary advice trials are the most common. One-third of trials developed and administered diet education without a dietitian. Evaluation and reporting on adherence to diet therapy occurred in <60% of trials. Failure to include or report on key elements of trial design reduced the interpretability and validity of the results. This is a considerable limitation to advancing scientific knowledge in this area. Diet therapy trials should adhere to similar rigorous quality standards used to develop other IBD therapies. Therefore, a set of practical recommendations was generated to provide the authors’ perspective to help inform the future design of high-quality IBD diet trials.
Food is one of the most underrated entities with respect to diseases. Food or Diet plays a vital role in healing or recovery of a patient which brings forth the need of analyzing disease and diets associations. The study of such associations is crucial for recommending appropriate diets to patients but is an arduous task due to the complex interdependencies as is evident in literature. Thus, it becomes necessary to automate the analysis and make it available as a service. The main aim of this work is to efficiently collate and analyze disease‐diet associations and provide it as an accessible and adaptable service using a combination of advanced techniques. Complex disease‐diet interdependencies are curated from the literature and transformed into a network offering various parameters for further analysis. The analysis is done using machine learning algorithms to predict accurate and robust recommendations. Cloud computing aids this analysis by providing sufficient resources and making it more accessible. Thus, the recommendations are constructed using amalgamation of techniques including network analysis, machine learning, and cloud computing. The deduced associations from the analysis of medical data using these technologies would aid doctors and healthcare institutions in decision making thereby improving the prognosis of a disease.
Die Bezeichnung Nahrungsmittelunverträglichkeit (NMU) stellt den Oberbegriff für alle reproduzierbaren Reaktionen des menschlichen Organismus dar, die regelmäßig oder chronisch im Zusammenhang mit dem Verzehr eines definierten Nahrungsmittels auftreten. In der Regel führt die Aufnahme dieser Nahrungsmittel zu einer lokalen Symptomatik im Verdauungstrakt, die Unverträglichkeit kann aber auch andere Organe wie die Haut, die Atemwege oder das Nervensystem betreffen oder sich als systemische Befindlichkeitsstörung äußern. Aus Sicht des Laien werden gemeinhin alle belastenden Reaktionen, die mit dem Verzehr von Nahrungsmitteln in Verbindung gebracht werden, als Allergien bezeichnet. Diese Einschätzung bedeutet allerdings oftmals eine Fehlinterpretation, weil auch andere nahrungsmittelassoziierte Pathomechanismen als die klassische IgE-vermittelte Nahrungsmittelallergie für das Auftreten der Symptome verantwortlich sein können. Leider verwenden auch Therapeuten häufig die Begriffe „Unverträglichkeit“, „Allergie“, oder „Intoleranz“ irrtümlicherweise synonym und verursachen dadurch Verwirrung beim Patienten.
Die Vielfältigkeit der verschiedenen Formen einer NMU lässt die exakte Diagnosefindung manches Mal der Suche nach der berühmten Nadel im Heuhaufen gleichen. Mit einiger allergologischer und ernährungstherapeutischer Erfahrung kann sich jedoch die Ursachenforschung einer NMU auch wie das gekonnte Zusammenfügen eines Mosaiks aus vielen kleinen Informationen gestalten. In diesem Sinne basiert die Diagnosefindung bestenfalls auf vier Säulen: die Krankengeschichte (inkl. Ernährungsanamnese), aussagekräftige diagnostische Testverfahren (inkl. Nachweis der klinischen Relevanz), die diagnostische Eliminationsdiät, eine nachfolgende Provokation (Reexposition).
Aus labormedizinischer Sicht ist es wichtig, dem Therapeuten ein strukturiertes und zielgerichtetes differentialdiagnostisches Regime zur Beurteilung fraglicher NMU an die Hand zu geben. Im Folgenden sollen dem geneigten Leser die verschiedenen Möglichkeiten einer NMU vorgestellt und jeweils dafür geeignete labordiagnostische Tests empfohlen werden.
Most adverse reactions to food are patient self-reported and not based on validated tests but nevertheless lead to dietary restrictions, with patients believing that these restrictions will improve their symptoms and quality of life. We aimed to clarify the myths and reality of common food intolerances, giving clinicians a guide on diagnosing and treating these cases. We performed a narrative review of the latest evidence on the widespread food intolerances reported by our patients, giving indications on the clinical presentations, possible tests, and dietary suggestions, and underlining the myths and reality. While lactose intolerance and hereditary fructose intolerance are based on well-defined mechanisms and have validated diagnostic tests, non-coeliac gluten sensitivity and fermentable oligosaccharide, disaccharide, monosaccharide, and polyol (FODMAP) intolerance are mainly based on patients’ reports. Others, like non-hereditary fructose, sorbitol, and histamine intolerance, still need more evidence and often cause unnecessary dietary restrictions. Finally, the main outcome of the present review is that the medical community should work to reduce the spread of unvalidated tests, the leading cause of the problematic management of our patients.
CD4 � CD25 � T cells have been identified as a population of immunoregulatory T cells, which mediate suppression of CD4 � CD25 � T cells by cell-cell contact and not secretion of suppres- sor cytokines. In this study, we demonstrated that CD4 � CD25 � T cells do produce high levels of transforming growth factor (TGF)- � 1 and interleukin (IL)-10 compared with CD4 � CD25 � T cells when stimulated by plate-bound anti-CD3 and soluble anti-CD28 and/or IL-2, and se- cretion of TGF- � 1 (but not other cytokines), is further enhanced by costimulation via cyto- toxic T lymphocyte-associated antigen (CTLA)-4. As in prior studies, we found that CD4 � CD25 � T cells suppress proliferation of CD4 � CD25 � T cells; however, we observed here that such suppression is abolished by the presence of anti-TGF- � . In addition, we found that CD4 � CD25 � T cells suppress B cell immunoglobulin production and that anti-TGF- � again abolishes such suppression. Finally, we found that stimulated CD4 � CD25 � T cells but not CD4 � CD25 � T cells express high and persistent levels of TGF- � 1 on the cell surface. This, plus the fact that we could find no evidence that a soluble factor mediates suppression, strongly suggests that CD4 � CD25 � T cells exert immunosuppression by a cell-cell interaction
Two hundred patients (156 women) with the irritable bowel syndrome were treated with dietary exclusion for three weeks. Of the 189 who completed this study, 91 (48.2%) showed symptomatic improvement. Subsequent challenge with individual foods showed that 73 of these 91 responders were able to identify one or more food intolerances and 72 remained well on a modified diet during the follow up period (mean (SD), 14.7 (7.98) months). Of the 98 patients who showed no symptomatic improvement after three weeks of strict exclusion only three were symptomatically well at follow up (mean (SD), 12.48 (8.09 months). There was no close correlation between response and symptom complex. There was a wide range of food intolerance. The majority (50%) identified two to five foods which upset them (range 1-14). The foods most commonly incriminated were dairy products (40.7%) and grains (39.4%).
In the decades since the major forms of idiopathic inflammatory bowel disease were defined on the basis of clinical manifestations, investigators have been challenged to identify the fundamental pathophysiologic processes underlying these enigmatic disorders, and clinicians have struggled to provide effective therapy for the often dismaying clinical manifestations. Clinical experience has led to the generally accepted notion that Crohn's disease and ulcerative colitis are distinct, if not discrete, entities. However, whether these are fundamentally different diseases or part of a mechanistic continuum remains an unanswered question, with both conceptual and practical management implications.
Prospectively, serum levels of IgE, specific IgE antibodies (AB) to whole cow milk protein (CMP), bovine se-albumin, bovine immunoglobulin, bovine lactoferrin, bovine lactalbumin and beta-lactoglobulin (BLG), IgG and IgG subclass antibodies to ovalbumin (OA) and BLG, and IgG4 RAST to CMP (bovine whey) were measured in 39 infants with cow milk protein allergy (CMPA) at birth (cord blood), at time of diagnosis and before and after milk challenge at the age of 12 months. Immunological measurements were also undertaken in 33 control infants without CMPA at birth, at 6 months and at 18 months. At no time, were differences found between the levels of IgG and IgG subclass AB to OA and BLG in control versus infants with CMPA. In the 39 infants with CMPA no correlation was found between the levels of IgE, IgG and IgG subclass AB in cord blood and subsequent levels of these values, irrespective of the type of CMPA (IgE-mediated (CMA) or non-IgE-mediated (CMI)), and irrespective of whether remission had occurred. In cord blood 25/33 (76%) of the infants with CMPA had specific IgE-AB to one or more of the bovine milk proteins indicating a prenatal intrauterine sensitization to cow milk protein. At 6 months the frequency of specific IgE-AB to bovine milk proteins was significantly (p<0.05) higher in infants with CMA versus CMI, and at 12 months total serum-IgE and the increase of these specific IGE-AB and RAST to CMP were significantly higher (p<0.05) in infants with persistent CMA. From 6 to 12 months withholding milk resulted in a significant fall in specific IgE-AB to CMP, and IgG, IgG, and IgG4 anti-BLG followed by an increase after milk challenge. Decreasing levels of IgG anti-OA from birth to 6 months reflect passive maternal transfer of IgG through the placenta, and increasing levels of IgG anti-BLG, already from birth to 6 months, may represent an early exposure to CMP in all infants. Significantly higher levels (p<0.05) of IgG anti-OA AB, IgG, and IgG4 anti-BLG AB were found in infants with persistent CMA, indicating a close relation between the synthesis of IgE and IgG and between IgE and IgG subclasses (IgG, and IgG4) in symptomatic cow milk-allergic individuals. Determination of IgG AB and IgG subclass AB (IgG, and IgG4) to BLG and bovine whey in cord blood appears unable to discern infants at high risk of development of CMPA. However, infants with persistent CMPA have an increased antibody response of specific IgE and IgG subclasses (IgG, and IgG4) to CMP exposure.
Baklien, K. & Brandtzaeg, P. Immunohistochemical characterization of local immunoglobin formation in Crohn’s disease of the ileum. Scand. J. Gastroent. 1976, 11, 447-457
Paired direct immunofluorescence was used to localize and differentially enumerate immunocytes containing the various immunoglobulin (Ig) classes in ileal bowel walls of patients with Crohn’s disease. In slightly inflamed mucosa the total number of Ig-containing cells of an average ‘tissue unit’ increased threefold compared with normal controls, but only minor changes occurred in class ratios. In severely inflamed mucosa with persisting glands, the total immunocyte number was increased by a factor of 12.2 compared with the control unit. For IgA, IgM, and IgG cells this increase was 9.0, 12.0, and 60.9, respectively. The immunocyte ratios for these three major Ig classes were 57.5:14.7:27.7 in the inflamed mucosa, and 83.1:11.4: 5.4 in the histologically normal control mucosa. When severely inflamed specimens from the ileum and from the colon were compared, there was no statistically significant difference in absolute immunocyte counts or class distributions. IgD and IgE immunocytes were extremely rare, and no consistent increase was found in the inflamed mucosae. In both the ileum and the colon fairly dense immunocyte populations with a marked IgG-cell predominance were encountered in the deeper layers of the inflamed bowel wall. The possible pathogenetic consequences of the pronounced local ‘over-production’ of IgG in inflammatory bowel disease are discussed.
The local response pattern of immunoglobulin-containing cells was compared in Crohn's disease and ulcerative colitis by paired immunohistochemistry on specimens of the large bowel wall. In the "Crohn mucosa" with persisting glands the total cell count was on the average raised more than three times compared with controls. The numbers of IgA, IgM and IgG immunocytes were increased 2.0, 4.8 and 28.6 times, respectively. Only 0-2 IgD- and IgE-containing cells were generally found per section. No consistent differences in the mucosal response pattern were revealed when Crohn's disease was compared with ulcerative colitis. The deeper layers of the bowel wall were in both diseases more or less densely infiltrated by immunocytes-IgG cells compromising about 80%. Immunoglobulin-containing cells in the muscularis propria and subserosa were characteristically found in Crohn's disease. There was no indication of a primary defect in the secretory immunoglobulin system which appeared to be normal in areas with intact glands. The pronounced local humoral immune response, particularly that involving IgG, might be of pathogenetic importance by aggravating and perpetuating in the inflammatory bowel disease.
Gastrointestinal symptoms occur in a large number of patients with food allergies. Immediate hypersensitivity mechanisms may give rise to the nausea, vomiting, abdominal pain, and diarrhea experienced by these patients. However, there are limited human data about the pathophysiological basis for these symptoms. Most of the available information comes from a variety of animal models. This article reviews the literature using models of intestinal food hypersensitivity, as well as human studies, that have contributed to our understanding of the pathophysiological mechanisms in gastrointestinal food hypersensitivity.
Prospectively, serum levels of IgE, specific IgE antibodies (AB) to whole cow milk protein (CMP), bovine se-albumin, bovine immunoglobulin, bovine lactoferrin, bovine lactalbumin and beta-lactoglobulin (BLG), IgG and IgG subclass antibodies to ovalbumin (OA) and BLG, and IgG4 RAST to CMP (bovine whey) were measured in 39 infants with cow milk protein allergy (CMPA) at birth (cord blood), at time of diagnosis and before and after milk challenge at the age of 12 months. Immunological measurements were also undertaken in 33 control infants without CMPA at birth, at 6 months and at 18 months. At no time, were differences found between the levels of IgG and IgG subclass AB to OA and BLG in control versus infants with CMPA. In the 39 infants with CMPA no correlation was found between the levels of IgE, IgG and IgG subclass AB in cord blood and subsequent levels of these values, irrespective of the type of CMPA (IgE-mediated (CMA) or non-IgE-mediated (CMI)), and irrespective of whether remission had occurred. In cord blood 25/33 (76%) of the infants with CMPA had specific IgE-AB to one or more of the bovine milk proteins indicating a prenatal intrauterine sensitization to cow milk protein. At 6 months the frequency of specific IgE-AB to bovine milk proteins was significantly (p less than 0.05) higher in infants with CMA versus CMI, and at 12 months total serum-IgE and the increase of these specific IGE-AB and RAST to CMP were significantly higher (p less than 0.05) in infants with persistent CMA. From 6 to 12 months withholding milk resulted in a significant fall in specific IgE-AB to CMP, and IgG, IgG1 and IgG4 anti-BLG followed by an increase after milk challenge. Decreasing levels of IgG anti-OA from birth to 6 months reflect passive maternal transfer of IgG through the placenta, and increasing levels of IgG anti-BLG, already from birth to 6 months, may represent an early exposure to CMP in all infants. Significantly higher levels (p less than 0.05) of IgG anti-OA AB, IgG1 and IgG4 anti-BLG AB were found in infants with persistent CMA, indicating a close relation between the synthesis of IgE and IgG and between IgE and IgG subclasses (IgG1 and IgG4) in symptomatic cow milk-allergic individuals.(ABSTRACT TRUNCATED AT 400 WORDS)
IgG and IgG subclass antibodies to cow's milk casein, egg albumin, and gliadin appear to rise in circumstances in which the absorption of undigested protein rises and to remain low when these specific foods are excluded from the diet.