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Results for “Fructose Intolerance”

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PubMed1975

Total parenteral alimentation in childhood general considerations.

The paper presents a discussion of the definition, the indications and some of the difficulties and complications of total long-term parenteral alimentation in infants and children. The problems of protein quality, the inadequacy of the E/T ratio, the quantities and quality of carbohydrates and the metabolic complications due to inappropriate electrolyte and mineral salts composition are reviewed. It is pointed out that the optimal amounts of some of the components used are still under investigation, that there seems to be no imperative reason not to use glucose as the sole carbohydrate in this age group and that most of the possible long-term sequelae and complications of total long-term parenteral alimentation will have to be looked for by prospective studies of the children treated.

Amino Acids↗
PubMed1996

Molecular analysis of the fructose transporter gene (GLUT5) in isolated fructose malabsorption.

Fructose, a naturally occurring monosaccharide, is increasingly used as an added sweetener in processed foods in the form of high fructose corn syrup. Increased fructose intake combined with the identification of children with clinical evidence of isolated fructose malabsorption (IFM) has stimulated interest in possible disorders of fructose absorption. The intestinal absorption of fructose is carried out by the facilitative hexose transporter, which has been designated as GLUT5. Functional properties and tissue distribution of GLUT5 suggest that IFM might be due to mutations in the GLUT5 gene. To test this hypothesis, we screened the GLUT5 gene for mutations in a group of eight patients with IFM and in one subject with global malabsorption, as compared with 15 healthy parents of subjects and up to 6 unrelated controls. No mutations were found in the protein coding region of this gene in any of the subjects. A single G to A substitution in the 5' untranslated region of exon 1 was identified in the subject with global malabsorption. This subject and her healthy mother were heterozygous for the variant sequence, suggesting that it was unlikely to be clinically significant. In addition, sequence analysis of each of the 12 GLUT5 exons was performed in the index case and confirmed the negative single-strand conformation polymorphism findings. These studies demonstrate that IFM does not result from the expression of mutant GLUT5 protein.

Alleles↗
PubMed1981

Defense of HFI study.

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Carbohydrate Metabolism, Inborn Errors↗
PubMed1981

Critique of HFI study.

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Carbohydrate Metabolism, Inborn Errors↗
PubMed2000

Carbohydrate malabsorption and the effect of dietary restriction on symptoms of irritable bowel syndrome and functional bowel complaints.

BACKGROUND: Carbohydrate malabsorption of lactose, fructose and sorbitol has already been described in normal volunteers and in patients with functional bowel complaints including irritable bowel syndrome. Elimination of the offending sugar(s) should result in clinical improvement. OBJECTIVE: To examine the importance of carbohydrate malabsorption in outpatients previously diagnosed as having functional bowel disorders, and to estimate the degree of clinical improvement following dietary restriction of the malabsorbed sugar(s). METHODS: A cohort of 239 patients defined as functional bowel complaints was divided into a group of 94 patients who met the Rome criteria for irritable bowel syndrome and a second group of 145 patients who did not fulfill these criteria and were defined as functional complaints. Lactose (18 g), fructose (25 g) and a mixture of fructose (25 g) plus sorbitol (5 g) solutions were administered at weekly intervals. End-expiratory hydrogen and methane breath samples were collected at 30 minute intervals for 4 hours. Incomplete absorption was defined as an increment in breath hydrogen of at least 20 ppm, or its equivalent in methane of at least 5 ppm. All patients received a diet without the offending sugar(s) for one month. RESULTS: Only 7% of patients with IBS and 8% of patients with FC absorbed all three sugars normally. The frequency of isolated lactose malabsorption was 16% and 12% respectively. The association of lactose and fructose-sorbitol malabsorption occurred in 61% of both patient groups. The frequency of sugar malabsorption among patients in both groups was 78% for lactose malabsorption (IBS 82%, FC 75%), 44% for fructose malabsorption and 73% for fructose-sorbitol malabsorption (IBS 70%, FC 75%). A marked improvement occurred in 56% of IBS and 60% of FC patients following dietary restriction. The number of symptoms decreased significantly in both groups (P < 0.01) and correlated with the improvement index (IBS P < 0.05, FC P < 0.025). CONCLUSIONS: Combined sugar malabsorption patterns are common in functional bowel disorders and may contribute to symptomatology in most patients. Dietary restriction of the offending sugar(s) should be implemented before the institution of drug therapy.

Adult↗
PubMed1979

[Development of ossification in children with chronic digestive insufficiency (author's transl)].

In 84 children suffering from chronic insufficiency of digestion, ossification of both hands was observed by means of fluoroscopic controls for several years. In 48 of 71 patients there was a retarded ossification; in 23 it was normal, or respectively more advanced. 18 boys and girls succeeded in making up for there retardation by means of consequent diet so that it might be regarded as a "spurt of growth". But in 10 of them retardation was constant, and in 14 children it increased. The causes of insufficient improvement were: late diagnosis and therapy, failures of diet, but also additional diseases--different from digestive insufficiency--, and long-term use of corticosteroides. In 30 of 84 children ossification was always normal or advanced. They had received early and consequent diet for years. Only in few cases, slight or moderate diseases were diagnosed. Development of ossification was parallel to body height, but not to weight gain.

Age Factors↗
PubMed2001

Inherited risks for susceptibility to dental caries.

Dental caries incidence is affected by host factors that may be related to the structure of dental enamel, immunologic response to cariogenic bacteria, or the composition of saliva. Genetic variation of the host factors may contribute to increased risks for dental caries. This systematic review examined the literature to address the question, "Is the risk for dental decay related to patterns of genetic inheritance?" Numerous reports have described a potential genetic contribution to the risk for dental caries. Studies on twins have provided strong evidence for the role of inheritance. Establishing a basis for a genetic contribution to dental caries will provide a foundation for future studies utilizing the human genome sequence to improve understanding of the disease process. Inherited disorders of tooth development with altered enamel structure increase the incidence of dental caries. Specific genetic linkage has not been determined for all of the syndromes of altered tooth development. Consequently, genetic screens of large populations for genes or mutations associated with increased caries susceptibility have not been done. Altered immune response to the cariogenic bacteria may also increase the incidence of caries. Association between specific patterns of HLA genetic inheritance and dental caries risk is weak and does not provide a predictable basis for predicting future decay rates. The evidence supporting an inherited susceptibility to dental caries is limited. Genetic linkage approaches on well-characterized populations with clearly defined dental caries incidence will be required to further analyze the relationship between inheritance and dental caries.

Dental Caries↗