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I Polanco

Publications and source records attributed to I Polanco.

9 recordsLinked to original sources

HLA-DR and -DQ genotypes of celiac disease patients serologically typed to be non-DR3 or non-DR5/7.

The susceptibility to develop celiac disease (CD) seems to be primarily associated to a particular HLA-DQ alpha/beta heterodimer encoded by the DQA1*0501 and DQB1*0201 alleles, in cis position on the DR3-DQ2 haplotype or in trans position by DR5-DQ7/DR7-DQ2 heterozygotes. However, exceptional patients exist who are neither DR3 nor DR5/DR7, particularly among Southern European populations. We therefore examined the DRB1, DQA1, and DQB1 alleles of 13 Spanish CD patients who were serologically typed to be neither DR3 nor DR5/DR7. Five patients were found to carry the DQA1*0501 and DQB1*0201 alleles either in cis or in trans position, three of them had previously been serologically mistyped. However, two of these patients carried DQA1*0501 and DQB1*0201 on haplotypes other than DR3 or DR5 in combination with DR7. One of the latter patients carried an unusual DR4-DQ2 haplotype, while another had an unusual DR8-DQ2 haplotype. Four of the remaining eight patients carried DR4-DQ8 haplotypes. Taken together, our findings provide further evidence that the DQ alpha/beta heterodimer encoded by the DQA1*0501 and the DQB1*0201 alleles confers the primary HLA-associated susceptibility to develop CD. However, our studies also corroborate that a second (and "weaker") HLA-associated CD susceptibility gene may be present on some DR4-carrying haplotypes.

Adolescent

Current status of digestive intolerance to food protein.

Digestive intolerance to food proteins may occur in childhood as a result of a wide range of etiologic and pathophysiologic mechanisms. Cow milk protein intolerance is the most common form of food intolerance in children. Food allergy and food intolerance may be confused because both produce similar symptoms, especially in young children with clinical manifestations of food allergy localized to the gastrointestinal tract. On the other hand, food-sensitive enteropathy may be defined as the clinical food-related syndromes associated with an abnormal small intestinal mucosa. Although several foods have been reported to damage the small intestinal mucosa in infancy (soy, rice, fish, chicken meat, egg), cow milk-sensitive enteropathy is the most common cause. Whatever the mechanisms, digestive intolerance to food proteins with or without enteropathy is primarily a temporary condition of infancy, in contrast to most forms of food allergy. In children with these disorders, symptoms usually resolve by 1 to 3 years of age. The variation in prevalence rates of this disorder in different countries can be explained by different diagnostic criteria. The classic food-sensitive enteropathy syndromes with chronic diarrhea and failure to thrive in infancy have become rarer in some European countries, including Spain. Some risk factors for the development of these conditions appear to be early exposure to cow milk feedings, acute infectious diarrhea, and malnutrition. Breast-feeding appears to be at least partially protective.

Diarrhea, Infantile

Helicobacter pylori infection in children: clinical, endoscopic, and histologic correlations.

We have assessed 270 consecutive patients (age range 0.8-20 years) referred for endoscopic study because of abdominal pain during 32 months. Helicobacter pylori (HP) was detected by culture in 91 cases (33.7%). HP colonization increased significantly with age (p less than 0.01). Nine patients less than 5 years of age were colonized by HP. A previous history of peptic ulcer disease in first-degree relatives was significantly more frequent in the HP-positive group (p less than 0.001). The frequency of HP positiveness as related to diagnosis was: normal, 3.3%; nonactive chronic gastritis, 100%; active chronic gastritis, 97.2%; gastric ulcer, 75%; and duodenal ulcer, 90.9% (p less than 0.001). Endoscopic nodular antritis was a frequent (67%) and specific finding; this presence was associated with that of lymphoid follicles in the histopathological study. Signs of histological activity were observed in 55.9% of the HP-positive patients. The histological colonization by HP was assessed semiquantitatively, and a significantly greater HP colonization score was observed in patients with signs of histological activity (p less than 0.001). A significant correlation was found between HP colonization score and histological score (rs = 0.574), with a significant association between the degree of HP colonization and the histologic categories (p less than 0.001). The present study suggests a pathogenic role of HP in the development of gastroduodenal disease in children.

Adolescent

Growth in malnutrition related to gastrointestinal diseases: coeliac disease.

Coeliac disease in children is frequently associated with a slow growth rate. This observation may be linked to the malabsorption that occurs in these patients; however, the underlying mechanism remains unknown. To better understand this phenomenon, we have studied the growth patterns of 153 patients with coeliac disease for 2-9 years. Gastro-intestinal biopsies were performed before and after gluten exclusion. In a second group of 79 children, somatostatin levels and binding properties in the plasma and jejunal mucosa were measured. In a third group of 40 patients we measured insulin-like growth factor I (IGF-I) and IGF-binding protein 3 (IGF-BP3) levels. We found that in children diagnosed before 2 years of age weight was the most affected growth parameter. In children diagnosed after this age, height was more affected. Suppression of gluten intake induced an acceleration of growth velocity. Although plasma levels of somatostatin were not significantly altered, somatostatin concentrations in the jejunal mucosa of patients in the active phase of the disease were significantly elevated (p < 0.05). Children with coeliac disease exhibited significantly lower levels of IGF-BP3 when compared to patients with normal stature and growth velocities. In contrast, these patients showed an increase in IGF-BP3 levels after gluten exclusion from the diet.

Body Height

[A simultaneous study of intestinal permeability and the test of H2 in the expired breath of celiac children].

Permeability test with sugars (PTS) as a non-invasive diagnostic tool is of special interest in pediatric patients. This study evaluated the relationship between PTS and antigliadin antibodies (AA) with the intestinal biopsy and studied whether an altered expired hydrogen test (EHT) could interfere in this relation in celiac patients. Thirty children (13 girls, 17 boys) with diagnosis of celiac disease (ESPGAN criteria) were divided into three groups according to this histopathology: Group A (n = 23) normal biopsy; Group B (n = 7) biopsy grade III or IV; Group C (n = 25) controls. The intestinal permeability test showed significative differences (p < 0.01) of Group B (0.159 +/- 0.03) with Group A (0.048 +/- 0.005) and with the control Group C (0.039 +/- 0.002). The cut-off for the Youden maximum index (0.75) was 0.092 and ROC SE 0.87 +/- 0.7. The results of the AA were related to those of the PTS. The variance analysis showed that the results of the expired hydrogen test do not interfere statistically on the good correlation of PTS with the histology. The PTS is a good indicator of the status of intestinal mucosa. There is a good correlation between PTS and AA in celiac children. A pathological expired hydrogen test seems not to interfere with the correlation found between PTS and histological damage in our series.

Adolescent

[Chronic diarrhea and intestinal cytomegalic inclusion (author's transl)].

A case of chronic diarrhea resistent to treatment is presented. At autopsy a cytomegalic inclusion disease localized only in the gastrointestinal tract was found. This case seems to be a confirmation to the hypothesis that the cytomegalovirus may be cause of gastrointestinal disturbances in infants.

Autopsy

[Malabsorption of carbohydrates in children (author's transl)].

Physiological bases of digestion and absorption of carbohydrates are reviewed, as a preliminary step, in order to draw a general scheme of its patholophysiology. Clasification of different types of carbohydrate malabsorption is presented. Various exploration methods are discussed in terms of autors' own experiences. Relationship between a sugar screening test, faecal lactic acid contents and a simplified lactose tolerance test, is described in detail. Systematic diagnoses of these diseases are established. Different clinical pictures are reviewed. It is not yet well defined if a starch malabsorption can be caused by either a primary or secondary duodenal amylase deficiency. The clinical forms of congenital sucrose-isomaltose intolerance may be more attenuated than its classical form; incertain cases, secondary sucrose intolerance may also be present due to mucosa anatomic lesions. Maltose malabsorption has no clinical implications. As compared to other alpha-glycosidades, the trehalase activity has been not more affected by not using trehalose in feeding. Primary congenital lactase deficiency is not frequent, whereas secondary forms as much more usual and appear, in primary malabsorption syndromes and in the coeliac disease, very often along with clinical tolerance to lactose. In Spain, lactose nonabsorbers in 16.5% for adults 11.2% for adolescents and 18.3% for children, meaning, that it is being favored by environmental factors in the latter. The unspecified sugar malabsorption during the child's first year is still the most frequent cause of carbohydrate intolerance in children and, although certain progress has been achieved in its diagnosis and therapy, its pathogenic mechanism is not satisfactorily known yet.

Adolescent