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Introduction: Introduction: celiac patients suffer deficiencies before and during their maintenance of a gluten-free diet. This is due to malabsorption, associated with the disease, and to non-enriched, mostly processed foods high in saturated fats and deficient in the minerals typically present in wheat. Objectives: the main objective of this review was to determine the molecular basis of celiac disease and the nutritional deficiencies that gluten-free diet entails, as well as an assessment of gluten-free diet and its nutritional deficiencies once the intestinal microvilli have been restored. Material and methods: a bibliographic search was carried out through electronic databases. The content of the review focuses on the pathogenesis of celiac disease and the assessment of gluten-free diet when established for treatment. Results: the main deficiencies that occur in untreated celiac patients are (calcium, iron, fiber, folic acid, omega-3, vitamin B12, and vitamin D). It has been observed that the quality of life of celiac patients, after starting treatment, is reduced, and this leads to low adherence to gluten-free diet. In addition, these gluten-free diets without proper follow-up by a nutritionist entail other deficits such as: an increase in the risk of cardiovascular, metabolic, overweight and obesity diseases. Conclusion: gluten-free diet, as followed by celiac patients, usually entails certain deficiencies such as group-B vitamins, vitamin D, calcium, iron, folic acid, and fiber, which is mainly due to the poor nutritional quality of gluten-free products as compared to their equivalents with gluten, and a scarce monitoring by health professionals.

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., (Copyright © 2017 Asociación Mexicana de Gastroenterología. Publicado por Masson Doyma México S.A. All rights reserved.)

Introduction: The aim of this study is to determine the prevalence of coeliac disease in patients of a basic health area in Valencia, on the Mediterranean coast, and describe their sociodemographic and clinical features., Material and Methods: A descriptive, cross-sectional, observational study was conducted on a target population of the inhabitants of the Basic Health Area 14 th , Health Department Xàtiva-Ontinyent, in Valencia, comprising the municipalities of Ontinyent, Aielo de Malferit, and Fontanars dels Alforins., Inclusion Criteria: the patient belongs to a quota of Primary Care in the basic health area and the diagnosis of coeliac disease was active in the computerised medical records., Exclusion Criteria: the patient did not have any serology or intestinal biopsy compatible with coeliac disease. The study included 115 patients, selected to complete an interviewer-administered questionnaire. As 9 patients did not respond, the study was performed with 106 people., Results: The prevalence of coeliac disease is 0.26%, and higher among women than among men (2.31: 1), with a statistically significant difference. The mean age of the patients was 29.71 years. The mean diagnostic delay was 5.15 years, and among the paediatric population it was 0.68 years. There were no statistically significant differences between patients (60) born in spring and summer, and the 46 born in autumn and winter. The prevalence of coeliac disease among first-degree relatives was 7.06%., Conclusions: Coeliac disease is an underdiagnosed condition in our environment, especially among adults, so knowledge and awareness about this disease by general practitioners is necessary., (Copyright © 2015 Sociedad Española de Médicos de Atención Primaria (SEMERGEN). Publicado por Elsevier España, S.L.U. All rights reserved.)

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.

The prevalence of Celiac disease in the general population is approximately 1% and remains undiagnosed in a significant proportion of individuals. Its clinical presentation includes the classical malabsorption syndrome, unspecific and extra-intestinal manifestations, and silent celiac disease. The serologic diagnosis has an elevated sensitivity and specificity and, at least in adult population, it must be confirmed by biopsy in every case. Diagnosis in subjects already on gluten free diet includes HLA typing and gluten challenge with posterior serologic and histologic evaluation. The core of the treatment is the gluten free diet, which must be supervised by an expert nutritionist. Monitoring must be performed with serology beginning at 3-6 months, and with histology two years after the diagnosis, unless the clinical response is poor. Poor disease control is associated with complications such as lymphoma and small bowel adenocarcinoma. In the future, it is likely that new pharmacologic therapies will be available for the management of celiac disease.

Cereals are considered a basic food. Through the development of cooking, the human being has produced high- gluten-content food, so that it could make the most of its nutritional properties. Wheat is becoming one of the key elements of the Mediterranean diet. Amongst gluten- intake-related pathologies- gluten is present mainly in wheat, barley and rye- celiac disease (CD) is the most well-known. CD is a chronic inflammatory condition which affects gastrointestinal tract which develops in genetically predisposed individuals. The most common manifestation of CD is nutrients malabsorption. This protein trigger other pathology, wheat allergy (WA), which is an adverse immunological effect to gluten due to E immunoglobulin. A recent increased in non celiac gluten sensitivity (NCGS) has also been noticed, defined as the emergence of a range of gluten-intake related symptoms in patients for which celiac disease and wheat allergy have been ruled out. This article discusses these three conditions with their phatogenic mecanisms and the different clinic manifestations., (Copyright AULA MEDICA EDICIONES 2014. Published by AULA MEDICA. All rights reserved.)

Unlabelled: The Non Communicable Complex Disease (NCCD) are the leading causes of death in the world, causing more deaths each year than all other combined causes. The approximately 80% of deaths were caused by NCCD and occured in low and middle income countries. However, NCCD deaths could be avoided by prevention programs and early diagnosis. The challenge of the multifactorial phenotypes is to achieve a valid strategy for identifying risk individuals at the population. These strategies may be addressed to screening population or generating causal predictive models for early detection, interpreting the root causes that create the condition. The aim of this paper is to describe the characteristic of complex chronic diseases and some of the current methods of study of these in the health area ., Conclusions: Interdisciplinary work, a team of health professionals belonging to different areas allows for an adequate management of complex diseases. The application of graph models, such as DAG's, is a valuable tool for a better adjustment of the statistical model, which allows an appropriate correspondence with the actual health model of these illnesses. And the best methodological strategy for complex diseases is the early diagnosis and the monitoring of risk groups and therapy monitoring of patients diagnosed.

The global prevalence of celiac disease is of one person per 250 inhabitants. The disease is induced by gluten, a peptide contained in wheat, rye and barley that during small intestinal digestion generates smaller peptides. Some of these are resistant to hydrolysis and cross through the epithelium into the mucosa, inducing a cascade of immune reactions leading to the appearance of the disease in susceptible individuals. Gluten appeared as a consequence of agricultural practices initiated 10000 years ago in the Fertile Crescent of southwest Asia. Celiac disease epidemiology is complicated since consumption of gluten differs depending on the origin of populations. Treatment of celiac disease consists of withdrawing gluten from the diet, a task that becomes difficult in the long term. The concept of gluten-free food has changed along time. This article updates the concept of celiac disease, the history of gluten consumption in the world, the characteristics of a gluten free diet and the difficulties to adhere to it.

Celiac disease is characterized by small intestinal mucosal injury and nutrient malabsorption in genetically susceptible individuals following dietary ingestion of gluten. The pathogenesis of the disease involves interactions between environmental, genetic, and immunologic factors. Transient infections or increased permeability of the mucosa may facilitate disease onset induced by the uptake of gluten peptides into a microenvironmental milieu in the small intestinal mucosa. We present two patients with onset of celiac disease after resolution of acute hepatitis B virus infection. The physiopathology of celiac disease is discussed and possible explanations for this association are proposed.

Celiac disease (CD), with a 1% worldwide prevalence, is an enteropathy caused by an autoimmune reaction to gluten in genetically susceptible individuals, which codify for histocompatibility molecules HLA DQ-2/DQ-8. From the anatomical point of view, CD is characterized by intestinal villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis (IELs) and leukocyte infiltration of the lamina propriety. Patients achieve a complete clinical and endoscopic remission with a gluten free diet. However, symptoms and anatomical alterations recur when this protein is reintroduced in the diet. The pathogenic mechanisms in this disease are not yet well understood, but it is clear that genetic, environmental and immunological factors play a role. The latter are the focus of this review, since this is the only autoimmune disease whose precipitating factor for immunological tissue damage is known.

The main cause of lack of response to a gluten-free diet is continued, usually inadvertent, gluten intake. Diagnosis of refractory celiac disease is established on the basis of exclusion of other disorders, persistence of malabsorption and villous atrophy. Refractory celiac disease affects a heterogeneous group of patients, usually adults and, fortunately, is infrequent (<5% of the population). Detection of alterations in the intraepithelial lymphocyte population is essential for diagnosis. Some alterations in these lymphocytes, such as the absence of T cell surface receptor expression (CD3 and CD), indicate an aggressive form of the disease with the potential for malignant transformation (type II refractory celiac disease). Treatment is based on adequate nutritional support and on the use of corticosteroids and/or immunosuppressive agents (mainly azathioprine and infliximab). Because of the high risk of progression to intestinal T cell lymphoma, patients diagnosed with type 2 refractory disease require different -generally more aggressive- therapeutic strategies. At present, no treatment has been demonstrated to be effective in the long term, but two options that should be considered in type II disease are immunotherapy with anti-CD52 or similar agents, and autologous bone marrow transplantation. Trials with antibodies that block epithelial secretion of interleukin-15, a key molecule in the pathogenesis of the disease, are promising.

Celiac disease is manifested by an enteropathy caused by intolerance to gluten, a family of proteins found in wheat and other cereals. Following intestinal T-cell activation in predisposed individuals, different inflammatory mechanisms are triggered under the control of the cytokine balance including those with a pro-inflammatory Th1 pattern such as IFNgamma, TNFalpha, IL-15 and IL-18; and regulatory cytokines such as TGFbeta and IL-10. These cytokines, besides increasing the intensity of the activation and the number of immune cells within the intestinal mucosa, regulate the activity of epithelial growth factors and metalloproteinases, a group of molecules involved in the maintenance and turnover of the intestinal mucosa structure; in inflammatory conditions, they also induce the intestinal lesion responsible for malabsorption syndrome.

The differentiation, architecture and function of the mucosa of the digestive tract is the result of close interactions between the epithelial cells and their underlying connective tissue. This interaction not only plays a role in the normal morphological organization of the intestinal mucosa but also in the organization and maturation of the enterocytes, the development of some of their enzymatic activities, the transport of nutrients and the restitution of the epithelium following denudation of the surface of villi due to loss of enterocytes. It is thought that disturbances of the cells of the connective tissue, especially of the myofibroblasts as well as of some of the above mentioned mechanisms, participate in the pathogenesis of some gastrointestinal diseases, celiac disease among them. This review summarizes some of the knowledge in this area.

Objective: To determine the prevalence of coeliac disease amongst the population with unexplained chronic hypertransaminasemia in our region., Patients and Methods: A prospective study was carried out on 147 consecutive patients with chronic hypertransaminasemia, having previously discarded alcoholic cause, hepatotoxic drugs, B, C and Delta viral infections, autoimmune hepatitis, primary biliary cirrhosis, Jemochromatosis, alfal-antitrypsin deficiency, Wilson's disease, congestive liver and illicit drug use. Serum Ig A to gliadin and endomysium antibodies were determined. Intestinal biopsy was carried out in cases those positive for one or both antibodies., Results: One patient was positive for both IgA to gliadin and to endonisyum antibodies, whereas another three patients were positive to IgA to gliadin only. A duodenal biopsy proved normal in two, a total villous atrophy in one and subtotal atrophy in other., Conclusions: 1. The prevalence of coeliac disease amongst the population with unexplained chronic hypertransaminasemia in our region is 1.4%. 2. In our region, screening for coeliac disease in unexplained chronic hypransaminasemia should take a secondary place.

Coeliac disease can by defined as a chronic disease characterized by a typical mucosal lesion of the small intestine and an impaired nutrient absorption which improves on withdrawal of gluten from the diet. The prevalence rate has increased over the last decades and just 1/3 of cases are diagnosed in childhood. There is a striking association with class II histocompatibility antigens, HLA-DR3 and HLA-DQ2. Cellular immune response mediated by intraepithelial and lamina propria lymphocytes is the primary event in the small intestine damage. Up to 50% of adult coeliac patients don't present intestinal symptoms being more frequent subclinic forms. The immunological markers of coeliac disease are antigliadin, antireticulin and antiendomysial antibodies, being the last one the most specific. Mortality of coeliac patient is increased mainly for malignancies, being the most frequent the intestinal T lymphoma.

We report the treatment of steatorrhea with pancreatic enzymes in four pancreatic endocrine tumors treated in our hospital. All four patients were males, with a mean age of 50 +/- 4.6, a basal steatorrhea of 10.8 +/- 3.7 g/24 h (N: less than 5 g/24 h), and a defecation rate of 1.8 +/- 0.8 (mean +/- SD). They were treated for one week with Pankreon 700 in the form of pills of 700 mg pancreatin (28,000 U lipase PIF, 22,000 U amylase PIF and 1,500 U protease PIF). They were given 15 pills/day divided into three doses. The mean steatorrhea dropped to 7.1 +/- 1.5 g/24 h. Then the patients were given Creon capsules with 300 mg pancreatin in pellets (8,000 U lipase PIF, 9,000 U amylase PIF and 450 U protease PIF). They were given six capsules/day divided into three doses, and the steatorrhea dropped to 7.2 +/- 4.1 g/24 h, while the rate of defecation dropped to 1/day. On comparison of the two products (Pankreon-- a classic form of pancreatin, and Creon-- a modern galenical in pellets), it was found that Creon achieved the same results as Pankreon 700 in a doses 2.5 times lower. This pilot study demonstrates that exocrine pancreatic insufficiency can be frequent in endocrine tumors of the pancreas, and although underestimated, it can be partially corrected with pancreatic enzymes.

Intestinal protein loss was determined in a group of patients with gastric resection by measuring the faecal radioactivity in the stools of 4 days, after intravenous administration of Cl3Cr51. The patients studied were divided in three groups: a) 10 healthy control subjects, b) 5 patients with gastrectomy BII without steatorrhoea, c) 15 patients with gastrectomy BII with steatorrhoea. In group (a) faecal radioactivity was 0.36 +/- 0.26% of the administrated dosis; in group (b) the value was 1.24 +/- 1.07% and in group (c) the activity was 1.40 +/- 1%. Statistically significative difference between groups (a) and (b) ((p less than 0.05) was found between groups (a) and (c) the difference was highly significative (p less than 0.001). However there was no significative difference between groups (b) and (c) (p less than 0.8). We think that serum protein intestinal loss may be, one of the causes of the hipoalbuminemia present in some patients who underwent partial gastrectomy because of gastroduodenal ulcer. Otherwise we did not find a relation between protein loss and steatorrhoea.

We have made a comparative cross study of 30 patients with chronic pancreatitis and steatorrhea. The aim of the study has been to compare the effectiveness of a new galenic form of pancreatin, in pellets, with the common galenic presentation, in tablets. In all the cases the cause of pancreatic failure was alcoholism. In both groups the treatment was administered during seven days, after a period of wash out. We evaluated steatorrhea and clinical symptoms, including the typical abdominal pain. (The doses administrated were 12 tablets/day or 9 pellets/day.) Statistically there was a significant decrease of steatorrhea p less than 0.01.

Malabsorption of pancreatic origin has been traditionally treated with pancreatic enzymes, but the effectiveness of treatment has been limited, related to the scant enzymatic activity of preparations, enzyme lability to acid attack and deficient mixing with the intestinal bolus, among other factors. We studied the efficacy of a new pancreatic enzyme preparation in the form of pellets, which mix easily with the intestinal bolus, are protected against gastric acid attack and have a high lipase concentration (Creon, Kalichemie-Pharma), as compared to traditional unprotected pancreatin in the form of tablets (Pankreon 700). The study was open, comparative and crossover, and included 12 patients. The diagnosis was chronic alcoholic pancreatitis in 10 cases and idiopathic pancreatitis in 2, with a steatorrhea of more than 10 g/24 h and a basal gastric pH less than 2.5. The duration of treatment was 3 weeks, using a diet containing 100 g of fat. The first week served as a control, and in the 2nd and 3rd treatment was given in the form of 7 capsules of Creon (2.1 g pancreatin and 70,000 UFIP lipase) or 17 tablets of Pankreon 700 (11.9 g pancreatin and 476,000 UFIP lipase) by randomized assignment. Our results confirm the beneficial effects observed by others. Steatorrhea was significantly reduced, up to 45.6% with Pankreon 700 and 57% with Creon, in spite of a dose that had 6.8 times less lipase activity, 5.6 times less pancreatin weight and 2.4 times fewer units ingested (capsules/tablets). Patients showed significant weight gain. At 30 days of treatment with Creon, steatorrhea had declined 70% and the weight gain was significant.(ABSTRACT TRUNCATED AT 250 WORDS)