RESUMO
Celiac disease (CD) is an autoimmune disease triggered by the ingestion of gluten in genetically predisposed individuals, affecting 1.4% of the world population. CD induces an inflammatory reaction that compromises small intestine villi, leading to nutrient malabsorption, and gastro and extraintestinal manifestations. Although other treatment approaches are being studied, adherence to a gluten-free diet (GFD) is the only effective intervention to date. Despite this, about 50% of patients experience persistent inflammation, often associated with unintentional gluten ingestion through contaminated food. There are regulations for labeling gluten-free foods which specify a limit of 20 mg/kg (20 ppm). The risks of gluten cross-contamination above that level are present throughout the whole food production chain, emphasizing the need for caution. This review explores studies that tested different procedures regarding the shared production of gluten-containing and gluten-free food, including the use of shared equipment and utensils. A literature review covering PubMed, Scielo, Web of Science, VHL and Scopus identified five relevant studies. The results indicate that shared environments and equipment may not significantly increase gluten cross-contamination if appropriate protocols are followed. Simultaneous cooking of gluten-containing and gluten-free pizzas in shared ovens has demonstrated a low risk of contamination. In general, shared kitchen utensils and equipment (spoon, ladle, colander, knife, fryer, toaster) in controlled experiments did not lead to significant contamination of samples. On the other hand, cooking gluten-free and gluten-containing pasta in shared water resulted in gluten levels above the established limit of 20 ppm. However, rinsing the pasta under running water for a few seconds was enough to reduce the gluten content of the samples to less than 20 ppm.
Assuntos
Doença Celíaca , Dieta Livre de Glúten , Contaminação de Alimentos , Manipulação de Alimentos , Glutens , Humanos , Glutens/efeitos adversos , Doença Celíaca/dietoterapia , Doença Celíaca/etiologia , Manipulação de Alimentos/métodos , Contaminação de Alimentos/análise , Culinária/métodosRESUMO
Introducción: La enfermedad celíaca (EC) es una enteropatía autoinmune desencadenada por la ingestión de gluten, en personas con predisposición genética. Su prevalencia está aumentando y el impacto nutricional de la enfermedad y de su tratamiento es objeto de numerosas publicaciones. Objetivo: analizar el estado nutricional integral de los pacientes con EC, atendidos en el Centro de Atención Nutricional Infantil Antímano CANIA, entre 1996 y 2016. Materiales y Métodos: investigación descriptiva, retrospectiva y transeccional. Las variables estudiadas: edad, sexo, diagnóstico nutricional integral, (indicadores antropométricos, de maduración ósea, dietéticos y bioquímicos) y cumplimiento de dieta sin gluten. Resultados: Se evaluaron 55 pacientes con EC, entre 2 y 7 años (58,2 %) con predominio de sexo femenino. El diagnóstico nutricional más frecuente fue la desnutrición en un 56,4 %, un 16,4 % presentó talla baja. El retardo en la maduración ósea se presentó en 33,3 %, y mostró asociación significativa con la desnutrición. El déficit de hierro sérico e hipocalcemia se registraron en 24,4 % y 18,8 % de los pacientes. El cumplimiento de la dieta sin gluten fue reportado en el 78,2 % de los casos. La dieta tuvo una tendencia al déficit de energía, macro y micronutrientes, especialmente grasas y calcio, independiente de su cumplimiento. Conclusión: los resultados evidenciaron que los pacientes son vulnerables desde el punto de vista nutricional. La dieta mostró déficit de energía, macronutrientes y calcio. La mayoría presentó algún grado de desnutrición. La atención nutricional debe ser ofrecida a esta población, desde el mismo momento en que se realiza el diagnóstico independiente de la edad(AU)
ackground: Celiac disease (CD) is an autoimmune enteropathy triggered by the ingestion of gluten, in people with a genetic predisposition. Its prevalence is increasing and the nutritional impact of the disease and its treatment is the subject of numerous publications. Objective: to analyze the comprehensive nutritional status of patients with CD, treated at the Centro de Atención Nutricional Infantil Antímano CANIA, between 1996 and 2016. Methods: descriptive, retrospective and transectional research. The variables studied: age, sex, comprehensive nutritional diagnosis (anthropometric, bone maturation, dietary and biochemical indicators) and compliance with a gluten- free diet. Results: 55 patients with CD were evaluated, the majority between 2 and 7 years (58.2%) with a predominance of females. The most frequent nutritional diagnosis was malnutrition in 56.4%, 16.4% had short stature. The delay in bone maturation occurred in 33.3%, and showed a significant association with malnutrition. Serum iron deficiency and hypocalcemia were recorded in 24.4% and 18.8% of patients. Compliance with the gluten-free diet was reported in 78.2% of cases. The diet had a tendency towards a deficit of energy, macro and micronutrients, especially fats and calcium, regardless of compliance. Conclusion: the results showed that patients are vulnerable from a nutritional point of view. The diet showed a deficit of energy, macronutrients and calcium. The majority presented some degree of malnutrition. Nutritional care must be offered to this population, from the moment the diagnosis is made, regardless of age(AU)
Assuntos
Humanos , Masculino , Feminino , Recém-Nascido , Lactente , Pré-Escolar , Criança , Adolescente , Doença Celíaca/etiologia , Estado Nutricional , Doenças Autoimunes , Criança , GlutensRESUMO
The small intestine has a high rate of cell turnover under homeostatic conditions, and this increases further in response to infection or damage. Epithelial cells mostly die by apoptosis, but recent studies indicate that this may also involve pro-inflammatory pathways of programmed cell death, such as pyroptosis and necroptosis. Celiac disease (CD), the most prevalent immune-based enteropathy, is caused by loss of oral tolerance to peptides derived from wheat, rye, and barley in genetically predisposed individuals. Although cytotoxic cells and gluten-specific CD4+ Th1 cells are the central players in the pathology, inflammatory pathways induced by cell death may participate in driving and sustaining the disease through the release of alarmins. In this review, we summarize the recent literature addressing the role of programmed cell death pathways in the small intestine, describing how these mechanisms may contribute to CD and discussing their potential implications.
Assuntos
Apoptose , Doença Celíaca/patologia , Intestino Delgado/patologia , Animais , Doença Celíaca/etiologia , HumanosRESUMO
BACKGROUND: Concomitance of celiac disease (CD) and IgE-mediated wheat allergy is described in some case reports. The objective was to evaluate the frequency of sensitization to wheat, rye, barley, and malt in children and adolescents with CD. METHODS: Measurement of serum levels of specific IgE to wheat, rye, barley, and malt (ImmunoCAP; sensitization IgE ≥0.35 kUA/L) in CD patients followed in specialized clinics to verify allergy history, general characteristics, small bowel biopsy characteristics, compliance with gluten-free diet (GFD), and occurrence of symptoms in case of noncompliance. RESULTS: We evaluated 74 patients; the median of age and age at diagnosis of CD were 8.6 years (5.0-12.8) and 3.6 years (1.6-7.0), respectively. Median time of GFD was 3.5 years (1.4-5.8). History of asthma occurred in 17.3% of subjects, allergic rhinitis in 13.5%, and AD in 5.4%. Frequency of sensitization was 4% for wheat, 10.8% for rye, 5.4% for barley, and 2.7% for malt. There was no association between wheat sensitization and age at diagnosis, time of GFD, small bowel biopsy characteristics, allergy history, and gluten consumption. There was no relationship between sensitization to wheat and occurrence of immediate symptoms when not complying with GFD. CONCLUSION: In conclusion, the frequency of sensitization to wheat, rye, barley, and malt in CD patients was 4, 10.8, 5.4, and 2.7%, respectively. Therefore, to ensure that cutaneous and respiratory contact with wheat is safe, we advise patients with CD to investigate their sensitivity to wheat, rye, and barley because not all patients with CD are allergic to these cereals.
Assuntos
Doença Celíaca/diagnóstico , Doença Celíaca/etiologia , Glutens/efeitos adversos , Hordeum/efeitos adversos , Hipersensibilidade a Trigo/complicações , Hipersensibilidade a Trigo/imunologia , Adolescente , Biópsia , Doença Celíaca/dietoterapia , Criança , Pré-Escolar , Dieta Livre de Glúten , Humanos , Imunização , Imunoglobulina E/sangue , Imunoglobulina E/imunologiaRESUMO
OBJECTIVE: To study the optimal cut-off value for anti-tissue transglutaminase type 2 IgA antibodies (TG2A) in serum to select for diagnostic small bowel biopsies for celiac disease in children with type 1 diabetes mellitus. STUDY DESIGN: Children with type 1 diabetes mellitus with elevated TG2A titers and duodenal biopsies performed during the course of their diabetes treatment were included. Anti-endomysial antibodies were recorded if present. The optimal TG2A cut-off value, expressed as the ratio between obtained value and upper limit of normal (ULN), was determined using receiver operating characteristic curve analysis and compared with the cut-off value used in the European Society for Pediatric Gastroenterology, Hepatology and Nutrition guidelines in terms of sensitivity, specificity, positive and negative predictive value. RESULTS: We included 63 children. The optimal cut-off value for performing biopsies is demonstrated to be 11 times the ULN. Raising the cut-off value from 3 times the ULN to 11 times the ULN changed sensitivity from 96% to 87% and increased specificity from 36% to 73%, increased the positive predictive value from 88% to 94% and lowered negative predictive value from 67% to 53%. The percentage of normal histology was decreased from 12% to 6%. CONCLUSIONS: Increasing the TG2A cut-off value for performing duodenal biopsies in children with type 1 diabetes mellitus and suspected celiac disease leads to a substantial reduction of unnecessary biopsies. We advocate to adapt the European Society for Pediatric Gastroenterology, Hepatology and Nutrition 2012 guidelines for this group of children, including monitoring patients with TG2A levels of less than 11 times the ULN over time.
Assuntos
Doença Celíaca/diagnóstico , Diabetes Mellitus Tipo 1/complicações , Proteínas de Ligação ao GTP/sangue , Transglutaminases/sangue , Adolescente , Anticorpos , Biópsia/efeitos adversos , Doença Celíaca/sangue , Doença Celíaca/etiologia , Criança , Pré-Escolar , Feminino , Humanos , Intestino Delgado/imunologia , Masculino , Proteína 2 Glutamina gama-Glutamiltransferase , Curva ROC , Estudos Retrospectivos , Sensibilidade e Especificidade , Procedimentos DesnecessáriosRESUMO
Celiac disease (CD) is a chronic enteropathy elicited by a Th1 response to gluten peptides in the small intestine of genetically susceptible individuals. However, it remains unclear what drives the induction of inflammatory responses of this kind against harmless antigens in food. In a recent work, we have shown that the p31-43 peptide (p31-43) from α-gliadin can induce an innate immune response in the intestine and that this may initiate pathological adaptive immunity. The receptors and mechanisms responsible for the induction of innate immunity by p31-43 are unknown and here we present evidence that this may reflect conformational changes in the peptide that allow it to activate the NLRP3 inflammasome. Administration of p31-43, but not scrambled or inverted peptides, to normal mice induced enteropathy in the proximal small intestine, associated with increased production of type I interferon and mature IL-1ß. P31-43 showed a sequence-specific spontaneous ability to form structured oligomers and aggregates in vitro and induced activation of the ASC speck complex. In parallel, the enteropathy induced by p31-43 in vivo did not occur in the absence of NLRP3 or caspase 1 and was inhibited by administration of the caspase 1 inhibitor Ac-YVAD-cmk. Collectively, these findings show that p31-43 gliadin has an intrinsic propensity to form oligomers which trigger the NLRP3 inflammasome and that this pathway is required for intestinal inflammation and pathology when p31-43 is administered orally to mice. This innate activation of the inflammasome may have important implications in the initial stages of CD pathogenesis.
Assuntos
Caspase 1/metabolismo , Gliadina/metabolismo , Inflamassomos/metabolismo , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Fragmentos de Peptídeos/metabolismo , Multimerização Proteica , Sequência de Aminoácidos , Animais , Apoptose , Doença Celíaca/etiologia , Doença Celíaca/metabolismo , Modelos Animais de Doenças , Suscetibilidade a Doenças , Gliadina/química , Gliadina/ultraestrutura , Mucosa Intestinal/ultraestrutura , Intestino Delgado , Masculino , Camundongos , Camundongos Transgênicos , Modelos Moleculares , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Fragmentos de Peptídeos/química , Fragmentos de Peptídeos/ultraestrutura , Conformação Proteica , Relação Estrutura-AtividadeRESUMO
INTRODUCTION: Celiac disease (CD) is an autoimmune enteropathy associated with gluten ingestion. In extended families of celiac patients that live in close proximity of one another, shared genetic and environmental factors can predispose them to CD. AIM: The aim of this study was to provide evidence about the genetic and environmental factors involved in the development of CD in the extended family of a pediatric patient. METHODS: The medical history, environmental conditions, and participant weight, height, and peripheral blood samples were evaluated. The HLA-DQ2/DQ8 haplotypes were genotyped through qPCR testing and the IgA anti-gliadin and anti-transglutaminase antibodies were quantified using the ELISA test. RESULTS: Twelve close-living maternal relatives of the index case participated in the study. Eight of them presented with the HLA-DQ2 haplotype, inherited from the grandfather, and 7/12 and 9/12 were positive for IgA anti-gliadin and IgA anti-transglutaminase antibodies, respectively. The main intestinal symptoms stated by the participants were abdominal bloating, excess flatulence, constipation, and gastroesophageal reflux. The most frequent extra-intestinal symptoms were fatigue, stress, and anxiety. In addition, 6/13 participants had bronchial asthma. CONCLUSION: The extended family living in close proximity of one another shared a genetic predisposition, environmental conditions, and asthma, which could have predisposed them to celiac disease.
Assuntos
Asma/complicações , Doença Celíaca/etiologia , Meio Ambiente , Predisposição Genética para Doença , Antígenos HLA-DQ/genética , Adulto , Asma/genética , Doença Celíaca/diagnóstico , Criança , Família , Feminino , Marcadores Genéticos , Haplótipos , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de RiscoRESUMO
Diet is considered an important triggering factor for gastrointestinal symptoms whose physiopathology includes not only measurable, inflammatory reactions, but also functional disorders, where no organic effects may be measured or demonstrated. Moreover, the prevalence of the perceived intolerance to certain foods ranges from 20-25% (within the general population) to 50-70% in diseases like irritable bowel syndrome. This intolerance has been observed particularly after the consumption of milk and dairy products, which are frequently considered as causative of gastrointestinal symptoms, thus limiting their ingestion. However, this behavior reduces the dietary sources of calcium and consequently may lead to malnutrition and bone decalcification, amongst other complications. The true dairy intolerance (intestinal lactase deficiency) explains most of the symptoms ensuing their consumption, but the frequency of such alteration on the different gastrointestinal diseases has not been determined. This review focuses on the most frequent gastrointestinal diseases and the existing evidence regarding the alterations and symptoms related to the consumption of milk or dairy products.