ABSTRACT
Malabsorption to lactose is caused by the inability to digest sugar due to the decrease in the activity of intestinal lactase. Malabsorption may be due to a primary or secondary disorder. Adult type primary hypolactasia is an autosomal recessive disorder, characterized by the progressive loss of lactase after weaning. The secondary hypolactasia is a transitory disorder, which will be corrected after the cure of the basic pathology. For lactose malabsorption diagnosis, the hydrogen and methane exhaled tests after lactose overload stand out and, in the case of the primary adult type, the molecular test of the simple nucleotide polymorphism (SNP C / T-13910). However, the diagnosis of lactose intolerance requires the presence of symptoms after consumption. The treatment of primary adult-type hypolactasia consists in decreasing the lactose in the diet below the trigger dose. A significant percentage of individuals with malabsorption tolerate habitual amounts of consumption. Practically 99% of them tolerate yogurt or fermented dairy products, thus allowing to cover the daily recommendations of calcium and vitamin D intake. In addition, nutritional strategies that reduce the lactose load, gastric emptying time and / or intestinal transit time or increase lactic activity and colonic compensation, will allow a greater tolerance.
La malabsorción de la lactosa se produce por la incapacidad para la digestión del azúcar debido a la disminución de la actividad de la lactasa intestinal tras un desorden primario o secundario a otras patologías.La hipolactasia primaria tipo adulto es un trastorno autosómico recesivo, caracterizado por la pérdida progresiva de lactasa tras el destete, mientrasque la secundaria es un trastorno transitorio que se corregirá tras la curación de la patología de base. Para el diagnóstico de la malabsorción a la lactosa destacan los test de hidrógeno y metano espirado tras sobrecarga. En el déficit primario tardío de lactasa puede realizarse el test molecular del polimorfismo de nucleótido simple (SNP C/T-13910). El diagnóstico de la intolerancia precisa de la presencia de sintomatología tras el consumo de lactosa.El tratamiento de la hipolactasia primaria tipo adulto consiste en disminuir la lactosa de la dieta por debajo de la dosis gatillo. Un porcentaje importante de individuos con malabsorción toleran cantidades habituales de consumo y prácticamente el 99% toleran yogur o derivados lácteos fermentados, lo que permite así cubrir las recomendaciones diarias de ingesta de calcio y vitamina D. Además, estrategias nutricionales que reduzcan la carga de lactosa, el tiempo de vaciamiento gástrico y/o el tiempo de tránsito intestinal o que incrementen la actividad lactásica y la compensación colónica van a permitir una mayor tolerancia.
Subject(s)
Diet , Lactose Intolerance/diet therapy , Yogurt , Calcium, Dietary , Humans , Lactose Intolerance/diagnosisABSTRACT
La malabsorción de la lactosa se produce por la incapacidad para la digestión del azúcar debido a la disminución de la actividad de la lactasa intestinal tras un desorden primario o secundario a otras patologías. La hipolactasia primaria tipo adulto es un trastorno autosómico recesivo, caracterizado por la pérdida progresiva de lactasa tras el destete, mientras que la secundaria es un trastorno transitorio que se corregirá tras la curación de la patología de base. Para el diagnóstico de la malabsorción a la lactosa destacan los test de hidrógeno y metano espirado tras sobrecarga. En el déficit primario tardío de lactasa puede realizarse el test molecular del polimorfismo de nucleótido simple (SNP C/T-13910). El diagnóstico de la intolerancia precisa de la presencia de sintomatología tras el consumo de lactosa. El tratamiento de la hipolactasia primaria tipo adulto consiste en disminuir la lactosa de la dieta por debajo de la dosis gatillo. Un porcentaje importante de individuos con malabsorción toleran cantidades habituales de consumo y prácticamente el 99% toleran yogur o derivados lácteos fermentados, lo que permite así cubrir las recomendaciones diarias de ingesta de calcio y vitamina D. Además, estrategias nutricionales que reduzcan la carga de lactosa, el tiempo de vaciamiento gástrico y/o el tiempo de tránsito intestinal o que incrementen la actividad lactásica y la compensación colónica van a permitir una mayor tolerancia
Malabsorption to lactose is caused by the inability to digest sugar due to the decrease in the activity of intestinal lactase. Malabsorption may be due to a primary or secondary disorder. Adult type primary hypolactasia is an autosomal recessive disorder, characterized by the progressive loss of lactase after weaning. The secondary hypolactasia is a transitory disorder, which will be corrected after the cure of the basic pathology. For lactose malabsorption diagnosis, the hydrogen and methane exhaled tests after lactose overload stand out and, in the case of the primary adult type, the molecular test of the simple nucleotide polymorphism (SNP C / T-13910). However, the diagnosis of lactose intolerance requires the presence of symptoms after consumption. The treatment of primary adult-type hypolactasia consists in decreasing the lactose in the diet below the trigger dose. A significant percentage of individuals with malabsorption tolerate habitual amounts of consumption. Practically 99% of them tolerate yogurt or fermented dairy products, thus allowing to cover the daily recommendations of calcium and vitamin D intake. In addition, nutritional strategies that reduce the lactose load, gastric emptying time and / or intestinal transit time or increase lactic activity and colonic compensation, will allow a greater tolerance
Subject(s)
Humans , Lactose Intolerance/diet therapy , Lactose Intolerance/diagnosis , Yogurt , Diet , Calcium, DietaryABSTRACT
According to new ESPGHAN guidelines, gluten challenge is considered necessary when there is doubt about the initial diagnosis of celiac disease (CD). The main aim of this study was to quantify intraepithelial lymphocyte (IEL) immunophenotype on celiac patients on gluten-containing diet (GCD) compared to those on gluten-free diet (GFD). Another aim was to evaluate the clinical utility of IELs in the CD diagnosis, especially in selected patients on GFD where diagnostic uncertainty remains. IEL immunophenotype (TCRγDelta and NK-like IELs) were studied by flow cytometry in 111 children with CD (81 children with CD on GCD and 30 celiac patients on GFD) and a control group (10 children). Duration of GFD was 5.4 ± 1.6 years. TCRγDelta IELs in celiac patients receiving a GCD or GFD were significantly higher (p < 0.001) than in the control group. NK-like IELs in patients receiving a GCD or GFD were significantly lower than in the control group (p < 0.001). We observed a permanent decrease of NK-like IELs and an increment of TCRγDelta IELs after following an adequate establishment and compliance of a long-term GFD in celiac patients. Recognition of IELs changes in the intestinal mucosa on celiac patients after long-term establishment of a GFD could constitute a useful tool for CD diagnosis in various situations: in which there is doubt about the initial diagnosis and repeat biopsy is necessary (avoiding the need of gluten challenges), and in those patients with symptoms/signs suggestive of CD who maintain a low gluten diet
Subject(s)
Humans , Male , Female , Child, Preschool , Child , Adolescent , Celiac Disease/diagnosis , Immunophenotyping , Intestinal Mucosa/immunology , Intestine, Small/immunology , Celiac Disease/epidemiology , Asymptomatic Diseases , Biopsy , Celiac Disease/diet therapy , Celiac Disease/pathology , Diet, Gluten-Free , Follow-Up Studies , Hospitals, University , Intestine, Small/pathology , Retrospective Studies , Spain/epidemiologyABSTRACT
According to new ESPGHAN guidelines, gluten challenge is considered necessary when there is doubt about the initial diagnosis of celiac disease (CD). The main aim of this study was to quantify intraepithelial lymphocyte (IEL) immunophenotype on celiac patients on gluten-containing diet (GCD) compared to those on gluten-free diet (GFD). Another aim was to evaluate the clinical utility of IELs in the CD diagnosis, especially in selected patients on GFD where diagnostic uncertainty remains. IEL immunophenotype (TCRγδ and NK-like IELs) were studied by flow cytometry in 111 children with CD (81 children with CD on GCD and 30 celiac patients on GFD) and a control group (10 children). Duration of GFD was 5.4 ± 1.6 years. TCRγδ IELs in celiac patients receiving a GCD or GFD were significantly higher (p < 0.001) than in the control group. NK-like IELs in patients receiving a GCD or GFD were significantly lower than in the control group (p < 0.001). We observed a permanent decrease of NK-like IELs and an increment of TCRγδ IELs after following an adequate establishment and compliance of a long-term GFD in celiac patients. Recognition of IELs changes in the intestinal mucosa on celiac patients after long-term establishment of a GFD could constitute a useful tool for CD diagnosis in various situations: in which there is doubt about the initial diagnosis and repeat biopsy is necessary (avoiding the need of gluten challenges), and in those patients with symptoms/signs suggestive of CD who maintain a low gluten diet.