ABSTRACT. Objective. Celiac disease (CD), or gluten sensitivity, is considered to be a state of heightened immunologic responsiveness to ingested gluten proteins in genetically predisposed individuals. The gastrointestinal manifestation suggests a severe enteropathy of the small intestine with malabsorption, steatorrhea, and weight loss because of a deranged mucosal immune response. Neurologic complications occur, especially epilepsy, possibly associated with occipital calcifications or folate deficiency and cerebellar ataxia. There have been reports of brain white-matter lesions as an extraintestinal manifestation in Crohn disease and ulcerative colitis but not in CD.Methods. In this study, 75 diet-treated mainly pediatric patients with biopsy-proven CD underwent prospectively clinical neurologic examinations, laboratory investigations, electroencephalography, computed tomography, and magnetic resonance imaging. The age range was 2.8 to 24.2 years with a mean of 11.6 years. The mean period of gluten exposure was 2.4 years.Results. Ten patients had neurologic findings such as febrile seizures, single generalized seizures, mild ataxia, and muscular hypotonia with retarded motor development. No folate deficiency was found. The hippocampal regions showed no abnormalities. Computed tomography did not reveal any cerebral calcifications, but magnetic resonance imaging detected unilateral and bilateral T2-hyperintensive white-matter lesions in 15 patients (20%). There was no correlation between these lesions and dietary compliance or neurologic or electroencephalographic abnormalities. The mean gluten exposure time of these patients was slightly increased (not significant).Conclusions. Focal white-matter lesions in the brain may represent an extraintestinal manifestation of CD. They may be ischemic in origin as a result of a vasculitis or caused by inflammatory demyelination. They seem to be more typical of pediatric CD than cerebral calcifications. Their prognostic value is unclear and needs to be elucidated in additional studies. CD should be suggested as a differential diagnosis in children with unclear white-matter lesions even without intestinal symptoms. Pediatrics 2001;108(2). URL: http://www.pediatrics.org/ cgi/content/full/108/2/e21; celiac disease, neurologic complications, brain white-matter lesions, child.ABBREVIATIONS. CD, celiac disease; EEG, electroencephalography; CT, computed tomography; MRI, magnetic resonance imaging; AU, arbitrary units. C eliac disease (CD), or gluten sensitivity, is considered to be a state of heightened immunologic responsiveness to ingested gluten proteins in genetically predisposed individuals. The gastrointestinal manifestation implies a severe enteropathy of the small intestine with malabsorption, steatorrhea, and weight loss associated with characteristic lesions of the small bowel mucosa, which improve after withdrawal of gluten from the diet. It often is associated with the presence of antiendomysial and antigliadin antibodies. The pathologic mucosal immune response has a ...

Demographic characteristics and risk factors were similar to those previously described in international literature. Clinical presentation was early in life, and digestive symptoms predominated. OFC was underused for diagnosis, and most of the tests requested did not change management.

HIGHLIGHTS What is already known about this subject?Celiac disease (CD) has a high clinical and histological diversity and the mechanisms underlying this phenomenon remain elusive.H. pylori is a bacterium that chronically infect gastric and duodenal mucosa activating both a Th1/Th17 and T-reg pathways.The role of H. pylori (and the effect of their virulence factors) in CD have not yet completely elucidated.What are the new findings?cagA+ H. pylori strains are associated to milder histological damage in infected CD patients.In active-CD patients the presence of cagA+ H. pylori is associated to an increase in T-reg markers, contrasting with a downregulation in cagA+ infected potential-CD individuals.How might it impact on clinical practice in the foreseeable future?The identification of microbiological factors that could modulate inflammation and clinical expression of CD may be used in the future as preventive strategies or as supplementary treatment in patients that cannot achieve complete remission, contributing to the better care of these patients.Background: Mechanisms underlying the high clinical and histological diversity of celiac disease (CD) remain elusive. Helicobacter pylori (Hp) chronically infects gastric and duodenal mucosa and has been associated with protection against some immune-mediated conditions, but its role (specifically of cagA+ strains) in CD is unclear.Objective: To assess the relationship between gastric Hp infection (cagA+ strains) and duodenal histological damage in patients with CD.Design: Case-control study including patients with active-CD, potential-CD and non-celiac individuals. Clinical presentation, HLA genotype, Hp/cagA gene detection in gastric mucosa, duodenal histology, Foxp3 positive cells and TGF-β expression in duodenal lamina propria were analyzed.Results: We recruited 116 patients, 29 active-CD, 37 potential-CD, and 50 non-CD controls. Hp detection was similar in the three groups (~30–40%), but cagA+ strains were more common in infected potential-CD than in active-CD (10/11 vs. 4/10; p = 0.020) and non-CD (10/20; p = 0.025). Among active-CD patients, Foxp3 positivity was significantly higher in subjects with cagA+ Hp+ compared to cagA- Hp+ (p < 0.01) and Hp- (p < 0.01). In cagA+ Hp+ individuals, Foxp3 positivity was also higher comparing active- to potential-CD (p < 0.01). TGF-β expression in duodenum was similar in active-CD with cagA+ Hp+ compared to Hp- and was significantly downregulated in cagA+ potential-CD subjects compared to other groups.Conclusion: Hp infection rates were similar among individuals with/without CD, but infection with cagA+ strains was associated with milder histological damage in celiac patients infected by Hp, and in active-CD cases with higher expression of T-reg markers. Results suggest that infection by cagA+ Hp may be protective for CD progression, or conversely, that these strains are prone to colonize intestinal mucosa with less severe damage.

Palabras clave:Prolapso rectal, enfermedad celiaca, diarrea crónica ResumenIntroducción: El prolapso rectal (PR) está relacionado a un aumento de presión intrabdominal, patología del piso pélvico o esfinter anal, siendo las causas más frecuentes la constipación, fibrosis quística, tos convulsiva y diarrea disentérica. La enfermedad celiaca no está considerada entre las patologías relacionadas a PR. Objetivo: Dar a conocer una asociación escasamente descrita entre PR y enfermedad celiaca. Casos Clínicos: Se presentan 2 preescolares en quienes el motivo de consulta fue el PR, cuyo estudio se enfocó como diarrea prolongada, debido al antecedente de deposiciones de consistencia pastosa. En los exámenes destacaron títulos de anticuerpos anti-transglutaminasa tisular (Ac anti-tTG) elevados, y biopsias duodenales con atrofia vellositaria y aumento de linfocitos intraepiteliales, compatible con enfermedad celiaca. Ambos tuvieron una excelente respuesta a la dieta libre de gluten, con rápida normalización de las deposiciones, sin nuevos episodios de PR, desarrollo pondoestatural normal y Ac anti-tTG negativos en los controles anuales a 5 años de seguimiento. Conclusiones: Aunque la asociación entre PR y enfermedad celiaca prácticamente no ha sido descrita, debe considerarse en pacientes que se presenten con PR. Keywords:Rectal prolapse, celiac disease, chronic diarrhea Abstract Introduction: Rectal prolapse (RP) is related to an increase of intra-abdominal pressure, pelvic floor disease or anal sphincter. The most common causes of RP are constipation, cystic fibrosis, whooping cough and dysenteric diarrhea. However, celiac disease is not considered among the pathologies related to RP. Objective: To present a scarcely described association between RP and celiac disease. Clinical Cases: We presented 2 preschoolers in whom the reason for consultation was RP, whose study was focused on as prolonged diarrhea, due to the antecedent of pasty consistency of stools. The tests showed elevated anti-tissue transglutaminase (anti-tTG) antibody titers, and duodenal biopsies with villous atrophy and increased intraepithelial lymphocytes, consistent with celiac disease. Both had an excellent response to the gluten-free diet, with rapid normalization of depositions, without presenting any episodes of RP after treatment. Both with normal staturo-ponderal development and anti-tTGnegative controls at the annual 5-year follow-up. Conclusions: Although the association between RP and celiac disease has not been described yet, it should be considered in diagnosis and treatment.

Chile." The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. Additionally, there was an error regarding the affiliations for Yalda Lucero. Affiliation 8 has been removed and the following affiliation has been added instead: