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PubMed source set — UC milk allergy oral tolerance digest

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PubMed source set — UC milk allergy oral tolerance digest

A CONTROLLED THERAPEUTIC TRIAL OF VARIOUS DIETS IN ULCERATIVE COLITIS.

[No abstract available via PubMed.]

CIRCULATING ANTIBODIES TO DIETARY PROTEINS IN ULCERATIVE COLITIS.

[No abstract available via PubMed.]

Circulating antibodies to cow’s milk proteins in ulcerative colitis.

Sera from patients with ulcerative colitis (51), Crohn’s disease (30), hypolactasia (13), untreated adult coeliac disease (11), irritable colon syndrome (24), and sera from 38 healthy control subjects were tested for antibodies to the principal cow’s milk proteins-casein, alpha-lactalbumin, and beta-lactoglobulin. The red-cell-linked antigen-antiglobulin reaction was used to determine the titres of direct agglutinating antibodies and IgA and IgG incomplete antibodies. Apart from patients with coeliac disease, direct agglutinating antibodies were found infrequently and then in low titres. Approximately 50% of subjects had low titres of IgA and IgG antibodies. However, the titres found in sera from patients with ulcerative colitis did not differ from those found in the control subjects or in patients with Crohn’s disease, hypolactasia, or irritable colon syndrome. Patients with untreated coeliac disease frequently had high antibody titres to the milk proteins. In all subjects tested, incomplete antibodies of IgA or IgG immunoglobulin class occurred with equal frequency. The frequent occurrence in adults of low titres of antibodies to the milk proteins may be due to continued absorption of minute amounts of protein. Absorption of allergens may be facilitated by mucosal damage, such as that of coeliac disease, with stimulation of antibody production. At the present time, however, there is little evidence to suggest that milk allergy is a factor in the aetiology of ulcerative colitis.

Dietary allergy and specific IgE in ulcerative colitis.

  • PMID: 7230244
  • Year: 1981
  • Journal: Journal of the Royal Society of Medicine
  • DOI: 10.1177/014107688107400411
  • PMC: PMC1438360
  • URL: https://pubmed.ncbi.nlm.nih.gov/7230244/
  • Publication types: Journal Article

Previous authors have considered that allergy to certain foodstuffs may play an important role in the aetiology of ulcerative colitis, but immunological evidence for dietary allergy in ulcerative colitis is inconclusive. A study is reported of 22 patients with ulcerative colitis, with matched controls, in whom total serum IgE and specific IgE to certain foodstuffs have been estimated by the Phadebas PRIST and RAST (Pharmacia) techniques. Allergens tested were egg-white, milk, wheat, rye, oat, fish (cod) and peanut. There was no significant difference in the total serum IgE levels and the food specific IgE activity between the two groups.

Serum antibodies to cow’s milk proteins in ulcerative colitis and Crohn’s disease.

  • PMID: 3792784
  • Year: 1987
  • Journal: Gastroenterology
  • DOI: 10.1016/0016-5085(87)90145-4
  • PMC: n/a
  • URL: https://pubmed.ncbi.nlm.nih.gov/3792784/
  • Publication types: Journal Article, Research Support, Non-U.S. Gov’t, Research Support, U.S. Gov’t, P.H.S.

Serum antibodies of immunoglobulin G, immunoglobulin M, and immunoglobulin A isotypes to five major proteins of cow’s milk, casein, bovine serum albumin, alpha-lactalbumin, beta-lactoglobulin A, and beta-lactoglobulin B, were measured using enzyme-linked immunosorbent assay in 51 patients with ulcerative colitis, 49 with Crohn’s disease, and 20 age-matched controls. Immunoglobulin G and immunoglobulin M antibodies to cow’s milk proteins were significantly elevated in patients with inflammatory bowel disease as compared to controls. In contrast, no significant increase in immunoglobulin A antibodies to 3 of 5 proteins was noted. The increased titers of antibodies to milk proteins seem to be specific and not due to a polyclonal immunoglobulin activation, as naturally occurring blood group antibodies were not elevated in patients with ulcerative colitis and Crohn’s disease. A good correlation of disease activity, as measured by serum alpha 1-acid glycoprotein concentrations, and immunoglobulin G and immunoglobulin A antibody titers against certain cow’s milk proteins could be demonstrated in Crohn’s disease, but not ulcerative colitis. These findings suggest that production of antibodies to cow’s milk proteins reflects specific immunization with these antigens. The study of antibody isotypes and correlation with disease activity may provide better insight into the immune response to dietary antigens and its possible role in the pathogenesis of inflammatory bowel diseases.

The effect of proctocolectomy on serum antibody levels against cow’s milk proteins in patients with chronic ulcerative colitis, with special reference to liver changes.

BACKGROUND: The levels of antibodies against cow’s milk proteins in ulcerative colitis (UC) were used to study whether mucosal inflammation leads to immune recognition, as a marker of enhanced permeability, of dietary proteins. A further purpose was to study the effect of proctocolectomy on the serum antibody levels against cow’s milk proteins and their relation to biochemical and histologic liver abnormalities associated with ulcerative colitis. METHODS: Serum antibody levels against six cow’s milk proteins, alpha-casein, alpha-lactalbumin (LA), beta-lactoglobulin A (LGA), beta-lactoglobulin B (LGB), bovine serum albumin (BSA), and whole milk powder (MP) were determined before and after (mean, 24 months) proctocolectomy in 15 patients with ulcerative colitis. Simultaneously, serum liver enzymes were analyzed. A liver biopsy specimen was also obtained at proctocolectomy. RESULTS: Before proctocolectomy IgA antibody levels were significantly increased against all antigens except BSA. Increased levels of IgM antibodies against LGA, LGB, and BSA were also detected. IgG antibodies were significantly increased only against LGA. After proctocolectomy IgA and IgM antibody levels decreased significantly (p < 0.05) against LGA, LGB, and LA, whereas IgG antibodies increased significantly (p < 0.01). In the patient group with abnormal liver histology (n = 9) the IgA antibodies to all cow’s milk proteins were significantly higher (p < 0.02) than in the group with normal liver histology both before and after proctocolectomy. The IgA antibody levels showed a significant positive correlation with alanine amino-transferase and gamma-glutamyltransferase (r value from 0.460 to 0.721, p value from < 0.05 to < 0.01), but not with alkaline phosphatase. CONCLUSIONS: These results suggest that the inflamed mucosa in UC allows the antigenic contents of the bowel to escape. Proctocolectomy alters the antibody levels against certain milk proteins, which may serve as a model to suggest that proctocolectomy, probably by eliminating inflammation, may have positive effects by reducing the foreign pathogenic antigen and immune complex load.

Antibodies to cow’s milk in ulcerative colitis.

[No abstract available via PubMed.]

Type I allergy to cow milk proteins in adults. A retrospective study of 34 adult milk- and cheese-allergic patients.

  • PMID: 8241802
  • Year: 1993
  • Journal: International archives of allergy and immunology
  • DOI: 10.1159/000236589
  • PMC: n/a
  • URL: https://pubmed.ncbi.nlm.nih.gov/8241802/
  • Publication types: Journal Article, Research Support, Non-U.S. Gov’t

To determine the clinical and serological characteristics of type I food allergy to cow milk proteins in adults, we investigated all 34 patients (aged from 16 to 58 years) who were diagnosed between 1981 and 1991 to have IgE-mediated reactions to cow milk and cheese. Women represented 91.2% of the study group and 39% of them suffered from the first symptoms during or soon after a pregnancy. So far, 47% of the patients were nonatopic and showed a monovalent sensitization to cow milk proteins. According to RAST results (score > or = 2) the predominant allergen was casein with a sensitization frequency of 71%, whereas sensitization to whey proteins (alpha-lactalbumin and beta-lactoglobulin) in this adult group was rare. In cow milk allergy (CMA) patients, significantly lower levels of milk-specific IgG were observed than in normal controls. The main organ manifestations of CMA in adults were the respiratory tract and the skin, with gastrointestinal and cardiovascular symptoms occurring less often than in children. Only 28% of CMA adults could enjoy an unlimited symptom-free intake of milk products after 4 years of disease. Compared with the existing studies on CMA in children, the results suggest that allergies to cow milk proteins in adults are less frequent and tend to persist longer. They are likely to be misdiagnosed for years due to symptoms that initially often refer to only one organ system such as the respiratory tract.(ABSTRACT TRUNCATED AT 250 WORDS)

Characteristics of patients suffering from cow milk allergy.

  • PMID: 22722049
  • Year: 2012
  • Journal: International immunopharmacology
  • DOI: 10.1016/j.intimp.2012.06.008
  • PMC: n/a
  • URL: https://pubmed.ncbi.nlm.nih.gov/22722049/
  • Publication types: Journal Article, Research Support, Non-U.S. Gov’t

The most frequent symptoms among the manifestations of cow milk allergy (CMA) are gastrointestinal. CMA pathogenesis involves immunological mechanisms with participation of immunocompetent cells, production of immunoglobulin E (IgE) and immunoglobulin G (IgG). We aim to determine whether cow milk-specific IgE antibodies coexist with cow milk-specific IgG antibodies in CMA patients with diarrhea symptom, and if there is any relationship between both antibody types. 65 CMA patients (average age of 17 years, ranging from 2 to 74 years), all of who had diarrhea symptom of CMA, were enrolled in this study. The total cow IgE and IgG subclass in serum were measured by electrochemiluminescence immunoassay and rate immune scatter turbidimetry, respectively. And also the cow milk-specific IgE was determined by enzyme-linked immunosorbent assay. The number of eosinophils in serum was calculated by Sysmex XE-2100 Hematology Analyzer. Our data showed that both cow milk-specific IgG and IgE levels were significantly elevated in CMA patients compared to those of age-matched control subjects. Out of the 65 CMA patients, 40 showed elevated cow milk-specific IgE antibody level, among which, 28 cases presented highly sensitive reaction to cow milk-specific IgG, along with each six of moderate and mild sensitive reaction to cow milk-specific IgG; while 20 showed elevated total IgG levels. The IgG3 positive rate was 16.9%, which was the highest. A moderate correlation between cow milk-specific IgE and cow milk-specific IgG was found in the CMA patients (r=0.415, P=0.001). The results indicated that cow milk-specific IgE antibodies could coexist with cow milk-specific IgG antibodies in patients suffering from CMA. The aberrant changes in the concentration of cow milk-specific IgE antibodies were associated with cow milk-specific IgG antibodies.

Exploring the Molecular Mechanisms Underlying the Protective Effects of Microbial SCFAs on Intestinal Tolerance and Food Allergy.

  • PMID: 32612610
  • Year: 2020
  • Journal: Frontiers in immunology
  • DOI: 10.3389/fimmu.2020.01225
  • PMC: PMC7308428
  • URL: https://pubmed.ncbi.nlm.nih.gov/32612610/
  • Publication types: Journal Article, Research Support, Non-U.S. Gov’t, Review

A body of evidence suggests that food allergy (FA) has increased in prevalence over the past few decades. Novel findings support the hypothesis that some commensal bacteria and particularly microbial metabolites might contribute to development of oral tolerance and prevention from FA. Recently, beneficial effects of short-chain fatty acids (SCFAs), the main class of gut microbiota-derived metabolites, on FA have been proposed. The intestinal SCFAs are major end products during bacterial fermentation of complex and non-digestible carbohydrates such as dietary fiber. The multifaceted mechanisms underlying beneficial effects of SCFAs on the mucosal immune system comprise the regulation of diverse cellular pathways in epithelial, dendritic, and T cells, as well as the impact on the immunometabolism and epigenetic status of regulatory lymphocytes. Of note, SCFAs are effective inhibitors of histone deacetylases (HDACs). As a consequence, SCFAs appear to be implicated in attenuation of intestinal inflammation and autoimmune diseases. In this review, we will discuss the recent development in this research area by highlighting the role of the individual SCFAs acetate, propionate, butyrate, and pentanoate in promoting the differentiation of regulatory T and B cells and their potential beneficial effects on the prevention of FA. In this context, targeted alterations in the gut microbiota in favor of SCFA producers or supplementation of medicinal food enriched in SCFAs could be a novel therapeutic concept for FA.

Food allergy and the gut.

  • PMID: 27999436
  • Year: 2017
  • Journal: Nature reviews. Gastroenterology & hepatology
  • DOI: 10.1038/nrgastro.2016.187
  • PMC: n/a
  • URL: https://pubmed.ncbi.nlm.nih.gov/27999436/
  • Publication types: Journal Article, Review

Food allergy develops as a consequence of a failure in oral tolerance, which is a default immune response by the gut-associated lymphoid tissues to ingested antigens that is modified by the gut microbiota. Food allergy is classified on the basis of the involvement of IgE antibodies in allergic pathophysiology, either as classic IgE, mixed pathophysiology or non-IgE-mediated food allergy. Gastrointestinal manifestations of food allergy include emesis, nausea, diarrhoea, abdominal pain, dysphagia, food impaction, protein-losing enteropathy and failure to thrive. Childhood food allergy has a generally favourable prognosis, whereas natural history in adults is not as well known. Elimination of the offending foods from the diet is the current standard of care; however, future therapies focus on gradual reintroduction of foods via oral, sublingual or epicutaneous food immunotherapy. Vaccines, modified hypoallergenic foods and modification of the gut microbiota represent additional approaches to treatment of food allergy.

Non-IgE Mediated Food Allergy.

Food allergies, defined as an immune response to food proteins, affect as many as 8% of young children and 2% of adults in western countries, and their prevalence appears to be rising like all allergic diseases. In addition to well-recognized urticaria and anaphylaxis triggered by IgE antibody- mediated immune responses, there is an increasing recognition of cell-mediated disorders, such as eosinophilic esophagitis and food protein-induced enterocolitis. Non-IgE-Mediated gastrointestinal food allergies are a heterogeneous group of food allergies in which there is an immune reaction against food but the primary pathogenesis is not a production of IgE and activation of mast cells and basophils. Those diseases tend to affect mainly the gastrointestinal tract and can present as acute (FPIES) or chronic reaction, such as Eosinophilic Esophagitis (EoE), Food Protein-Induced Allergic Proctocolitis (FPIAP). The role of food allergy in Non-EoE gastrointestinal Eosinophilic disorders (Non- EoE EGID) is poorly understood. In some diseases like EoE, T cell seems to play a major role in initiating the immunological reaction against food, however, in FPIES and FPIAP, the mechanism of sensitization is not clear. Diagnosis requires food challenges and/or endoscopies in most of the patients, as there are no validated biomarkers that can be used for monitoring or diagnosis of Non-IgE mediated food allergies. The treatment of Non-IgE food allergy is dependent on diet (FPIES, and EoE) and/or use of drugs (i.e. steroids, PPI) in EoE and Non-EoE EGID. Non-IgE mediated food allergies are being being investigated.

Food Protein-Induced Enterocolitis Syndrome.

Food protein-induced enterocolitis syndrome (FPIES) is a rare, non-immunoglobulin E-mediated gastrointestinal food allergy primarily diagnosed in infancy, but has also been reported in older children and adults. Acute FPIES reactions typically present with delayed, repetitive vomiting, lethargy, and pallor within 1 to 4 hours of food ingestion. Chronic FPIES typically presents with protracted vomiting and/or diarrhea, and weight loss or poor growth. Common foods triggering FPIES include cow’s milk, soy, rice, oats, fish, and egg. More detailed diagnostic criteria may help in increasing awareness of FPIES and reducing delayed diagnoses or misdiagnoses.

The role of gastrointestinal permeability in food allergy.

  • PMID: 29803708
  • Year: 2018
  • Journal: Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
  • DOI: 10.1016/j.anai.2018.05.010
  • PMC: n/a
  • URL: https://pubmed.ncbi.nlm.nih.gov/29803708/
  • Publication types: Journal Article, Research Support, Non-U.S. Gov’t, Review

[No abstract available via PubMed.]

The Epithelial Barrier Hypothesis in Food Allergies: The State of the Art.

Recently, the “epithelial barrier hypothesis” has been proposed as a key factor in the development of allergic diseases, such as food allergies. Harmful environmental factors can damage epithelial barriers, with detrimental effects on the host immune response and on the local microbial equilibrium, resulting in chronic mucosal inflammation that perpetuates the dysfunction of the epithelial barrier. The increased epithelial permeability allows allergens to access the submucosae, leading to an imbalance between type 1 T-helper (Th1) and type 2 T-helper (Th2) inflammation, with a predominant Th2 response that is the key factor in food allergy development. In this article on the state of the art, we review scientific evidence on the “epithelial barrier hypothesis”, with a focus on food allergies. We describe how loss of integrity of the skin and intestinal epithelial barrier and modifications in gut microbiota composition can contribute to local inflammatory changes and immunological unbalance that can lead to the development of food allergies.

Food allergy and hypersensitivity reactions in children and adults-A review.

Adverse reactions after food intake are commonly reported and a cause of concern and anxiety that can lead to a very strict diet. The severity of the reaction can vary depending on the type of food and mechanism, and it is not always easy to disentangle different hypersensitivity diagnoses, which sometimes can exist simultaneously. After a carefully taken medical history, hypersensitivity to food can often be ruled out or suspected. The most common type of allergic reaction is immunoglobulin E (IgE)-mediated food allergy (prevalence 5-10%). Symptoms vary from mild itching, stomach pain, and rash to severe anaphylaxis. The definition of IgE-mediated food allergy is allergic symptoms combined with specific IgE-antibodies, and therefore only IgE-antibodies to suspected allergens should be analyzed. Nowadays, methods of molecular allergology can help with the diagnostic process. The most common allergens are milk and egg in infants, peanut and tree nuts in children, and fish and shellfish in adults. In young children, milk/egg allergy has a good chance to remit, making it important to follow up and reintroduce the food when possible. Other diseases triggered by food are non-IgE-mediated food allergy, for example, eosinophilic esophagitis, celiac disease, food protein-induced enterocolitis syndrome, and hypersensitivity to milk and biogenic amines. Some of the food hypersensitivities dominate in childhood, others are more common in adults. Interesting studies are ongoing regarding the possibilities of treating food hypersensitivity, such as through oral immunotherapy. The purpose of this review was to provide an overview of the most common types of food hypersensitivity reactions.

Adult Food Protein-Induced Enterocolitis Syndrome: A Review of Emerging Evidence and Clinical Considerations.

  • PMID: 40716421
  • Year: 2025
  • Journal: Digestive diseases (Basel, Switzerland)
  • DOI: 10.1159/000547494
  • PMC: PMC12490835
  • URL: https://pubmed.ncbi.nlm.nih.gov/40716421/
  • Publication types: Journal Article, Review

BACKGROUND: Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated reaction to food, well known in the allergy and immunology literature, that presents with delayed gastrointestinal symptoms. It is classically diagnosed in children and infants; however, new-onset cases have recently been identified in the adult population. SUMMARY: There is a paucity of literature on FPIES in the gastroenterology literature. This review aimed to bring awareness to this entity as a possible etiology of gastrointestinal symptoms. Symptoms include abdominal pain, diarrhea, repetitive vomiting, and nausea, which occur 1 to 4 h after initial ingestion of food. In adult-onset cases, food triggers most often include seafood (fish, crustacean, and mollusk). Egg, wheat, and cow’s milk have also been identified as triggers for adult-onset FPIES. Oral food challenge is the gold standard for diagnosis. KEY MESSAGES: This review provides an overview of the current literature on adult-onset FPIES. Adult and pediatric patients notably have different presentations of FPIES and different triggers. Providers should be aware of these distinctions when diagnosing this condition.

Goblet cell associated antigen passages are inhibited during Salmonella typhimurium infection to prevent pathogen dissemination and limit responses to dietary antigens.

  • PMID: 29445136
  • Year: 2018
  • Journal: Mucosal immunology
  • DOI: 10.1038/s41385-018-0007-6
  • PMC: PMC6037413
  • URL: https://pubmed.ncbi.nlm.nih.gov/29445136/
  • Publication types: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov’t

Dietary antigen acquisition by lamina propria (LP) dendritic cells (DCs) is crucial to induce oral tolerance and maintain homeostasis. However, encountering innocuous antigens during infection can lead to inflammatory responses, suggesting processes may limit steady-state luminal antigen capture during infection. We observed that goblet cell (GC) associated antigen passages (GAPs), a steady-state pathway delivering luminal antigens to LP-DCs, are inhibited during Salmonella infection. GAP inhibition was mediated by IL-1β. Infection abrogated luminal antigen delivery and antigen-specific T cell proliferation in the mesenteric lymph node (MLN). Antigen-specific T cell proliferation to dietary antigen was restored by overriding GAP suppression; however, this did not restore regulatory T cell induction, but induced inflammatory T cell responses. Salmonella translocation to the MLN required GCs and correlated with GAPs. Genetic manipulations overriding GAP suppression, or antibiotics inducing colonic GAPs, but not antibiotics that do not, increased dissemination and worsened outcomes independent of luminal pathogen burden. Thus, steady-state sampling pathways are suppressed during infection to prevent responses to dietary antigens, limit pathogen entry, and lessen the disease. Moreover, antibiotics may worsen Salmonella infection by means beyond blunting gut microbiota colonization resistance, providing new insight into how precedent antibiotic use aggravates enteric infection.

The role of commensal bacteria in the regulation of sensitization to food allergens.

  • PMID: 24791655
  • Year: 2014
  • Journal: FEBS letters
  • DOI: 10.1016/j.febslet.2014.04.026
  • PMC: PMC4216641
  • URL: https://pubmed.ncbi.nlm.nih.gov/24791655/
  • Publication types: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov’t, Review

The prevalence of life-threatening anaphylactic responses to food is rising at an alarming rate. The emerging role of the gut microbiota in regulating food allergen sensitization may help explain this trend. The mechanisms by which commensal bacteria influence sensitization to dietary antigens are only beginning to be explored. We have found that a population of mucosa-associated commensal anaerobes prevents food allergen sensitization by promoting an IL-22-dependent barrier protective immune response that limits the access of food allergens to the systemic circulation. This early response is followed by an adaptive immune response mediated in part by an expansion of Foxp3(+) Tregs that fortifies the tolerogenic milieu needed to maintain non-responsiveness to food. Bacterial metabolites, such as short-chain fatty acids, may contribute to the process through their ability to promote Foxp3(+) Treg differentiation. This work suggests that environmentally induced alterations of the gut microbiota offset the regulatory signals conferred by protective bacterial species to promote aberrant responses to food. Our research presents exciting new possibilities for preventing and treating food allergies based on interventions that modulate the composition of the gut microbiota.

A microbiota signature associated with experimental food allergy promotes allergic sensitization and anaphylaxis.

  • PMID: 23201093
  • Year: 2013
  • Journal: The Journal of allergy and clinical immunology
  • DOI: 10.1016/j.jaci.2012.10.026
  • PMC: PMC3860814
  • URL: https://pubmed.ncbi.nlm.nih.gov/23201093/
  • Publication types: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov’t, Research Support, U.S. Gov’t, Non-P.H.S.

BACKGROUND: Commensal microbiota play a critical role in maintaining oral tolerance. The effect of food allergy on the gut microbial ecology remains unknown. OBJECTIVE: We sought to establish the composition of the gut microbiota in experimental food allergy and its role in disease pathogenesis. METHODS: Food allergy-prone mice with a gain-of-function mutation in the IL-4 receptor α chain (Il4raF709) and wild-type (WT) control animals were subjected to oral sensitization with chicken egg ovalbumin (OVA). Enforced tolerance was achieved by using allergen-specific regulatory T (Treg) cells. Community structure analysis of gut microbiota was performed by using a high-density 16S rDNA oligonucleotide microarrays (PhyloChip) and massively parallel pyrosequencing of 16S rDNA amplicons. RESULTS: OVA-sensitized Il4raF709 mice exhibited a specific microbiota signature characterized by coordinate changes in the abundance of taxa of several bacterial families, including the Lachnospiraceae, Lactobacillaceae, Rikenellaceae, and Porphyromonadaceae. This signature was not shared by similarly sensitized WT mice, which did not exhibit an OVA-induced allergic response. Treatment of OVA-sensitized Il4raF709 mice with OVA-specific Treg cells led to a distinct tolerance-associated signature coincident with the suppression of the allergic response. The microbiota of allergen-sensitized Il4raF709 mice differentially promoted OVA-specific IgE responses and anaphylaxis when reconstituted in WT germ-free mice. CONCLUSION: Mice with food allergy exhibit a specific gut microbiota signature capable of transmitting disease susceptibility and subject to reprogramming by enforced tolerance. Disease-associated microbiota may thus play a pathogenic role in food allergy.

Ulcerative colitis in children 10 years old or younger.

  • PMID: 8350209
  • Year: 1993
  • Journal: Journal of pediatric gastroenterology and nutrition
  • DOI: 10.1097/00005176-199307000-00004
  • PMC: n/a
  • URL: https://pubmed.ncbi.nlm.nih.gov/8350209/
  • Publication types: Journal Article, Research Support, Non-U.S. Gov’t

The onset and course of ulcerative colitis diagnosed in 38 children at or before 10 years of age were reviewed. The mean age at onset was 5.9 years. A family history of inflammatory bowel disease was present in 24% of patients, and 13% had a history of cow milk allergy in infancy. Initially, by radiologic or colonoscopic studies, 71% had total colonic disease, 13% had left-sided colitis, and 6% had proctitis; extensive examination was not performed in 4 patients. Four patients (11%) presented with severe colitis, 14 (37%) with moderate colitis, and 20 (53%) with mild colitis. The most frequent symptoms were abdominal pain (94%), diarrhea (84%), and rectal bleeding (84%). Between 2 and 10 years after diagnosis, 89% of children had total colonic disease and 11% had left-sided disease. All four patients with severe disease at onset responded to medical therapy with one having a colectomy 15 years later with pathology consistent with Crohn’s disease. Of those with moderate disease, half had infrequent moderate recurrences and half had intermittent mild disease. One patient had colectomy at 21 years for intractable disease. Of the 20 with mild disease, 16 continued to have intermittent mild recurrences, 1 had chronic mild disease, 2 had moderate recurrent disease, and 1 has remained asymptomatic for 5 years. Psychiatric disturbances requiring therapy were identified in 5 (13%) children. Results are encouraging: after the first 2 years of illness, two thirds of the children have had subsequent mild colitis with infrequent relapses and three quarters consider their life to be of good quality.

Additional old milk/UC source records

Ulcerative colitis provoked by milk.

[No abstract available via PubMed.]

Circulating antibodies to milk proteins in ulcerative colitis.

[No abstract available via PubMed.]

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