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Results for “Fructose Intolerance”

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At least 433 records · Page 24Linked to original sources
PubMed1992

[Fructose malabsorption and dysfunctional gastrointestinal manifestations].

BACKGROUND: Individuals with impaired intestinal absorption of fructose may exhibit recurrent abdominal discomfort after the ingestion of fructose-containing foods. We report on patients with this disorder in whom the diagnosis was made by the fructose hydrogen breath test. METHODS: We investigated 293 patients with recurrent abdominal pain, meteorism or diarrhea in connection with the ingestion of fruits, apple juice or soft drinks. Mixed expired air was collected before and at 30 minute intervals after a fructose load and analysed thereafter by a hydrogen sensitive electrochemical cell. Incomplete absorption of fructose was defined as a peak rise in breath hydrogen of > 20 ppm. RESULTS: 108 out of 293 patients showed an abnormal peak rise after fructose (mean 71.8 ppm, SD 31.4). This malabsorption of fructose was associated with clinical symptoms in 79 of them. Sensitivity and specificity of the fructose hydrogen breath test were 98 or 86 per cent respectively. 19 patients with an abnormal breath test and symptoms following fructose were reexamined after a load with equimolar concentrations of glucose and fructose. Hydrogen breath test was normal in all of them, none developed abdominal discomfort. CONCLUSION: A considerable number of individuals suffer from dysfunctional gastrointestinal problems due to fructose malabsorption. The fructose hydrogen breath test is a simple, sensitive and noninvasive method for the diagnosis for this disorder. Possible means of treatment are dietary fructose restriction or a modification of the diet in which fructose-containing foods are exchanged for those with equal concentrations of glucose and fructose.

Abdominal Pain↗
PubMed2004

[Fructose].

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Fructose↗
PubMedDate not supplied

Etiology of hyperuricemia.

Hyperuricemia is a common laboratory finding with significant clinical implications. It is easily detected, but its mechanisms may not be clearly elucidated. A scheme of pathogenesis has been outlined and diagrammed but much is conjectural; therefore, the classification is merely tentative. About 45 diseases or categories of conditions, 20 drugs, and nine states of intoxication have been surveyed. Hyperuricemia can be a multifactorial genetic disorder or a discrete response to a specific stimulus. It may be governed by a complex interplay of biochemical disorders for a lifetime duration, or it may be determined by environmental forces for a very transient course. Some conditions have both increased production of uric acid as well as decreased renal outflow. For many patients, the underlying mechanisms have not yet been elucidated.

Anemia↗
PubMed1991

Diet and the irritable bowel syndrome.

Food intake plays a key role in triggering or perpetuating symptoms in patients with IBS. Evaluation of the impact of diet in the individual patient requires a precise dietary history and a 7-day prospective dietary analysis, which should include the quality and quantity of food consumed, chronologic sequence and nature of symptoms, and the frequency and consistency of bowel movements. The caloric density of the meal, total fat intake, the quantity and quality of lactose-containing foods, sorbitol, fructose, and the nature and quantity of soluble and insoluble fiber intake must be noted. Patients with reflux esophageal symptoms should eliminate foods that decrease LES pressure, such as chocolate, peppermint, alcohol, and coffee. Direct esophageal mucosal irritants such as tomatoes, citrus juices, sharp condiments, and alcohol should be limited. Gastric emptying is slowed with the ingestion of fats and soluble fiber. Small bowel motility is slowed by soluble fiber and fatty foods. Gaseous syndromes may be reduced by avoidance of smoking, chewing gum, excessive liquid intake, and carbonated drinks. The reduced intake of large amounts of lactose-containing foods, sorbitol, and fructose may limit postprandial bloating. Flatus production can be lowered by reducing fermentable carbohydrates such as beans, cabbage, lentils, brussel sprouts, and legumes. Soluble and insoluble fiber ingestion will reduce sigmoidal intraluminal pressures and overcome spastic constipation when given in progressive graded doses. Effective dietary manipulations remain a key factor in reducing symptoms in IBS.

Colonic Diseases, Functional↗
PubMed1988

[Small intestine biopsies in children with malabsorption syndrome. Autoradiographic studies with 3H-thymidine].

Bioptic material of the small intestine is suitable for short-time in-vitro incubation in 3H-thymidine labelled medium followed by autoradiography. Histological and autoradiographic investigations of the small intestine of 45 children yielded the following characteristic findings: 1. 93 per cent of the healthy controls (n = 14) showed normal mucous membrane (Type I according to Shmerling) and a mean 3H-thymidine labelling index of 13 per cent. 2. Normal histological findings but a mean autoradiographic labelling index of 22 per cent were recorded from 87 per cent of children with cow's milk or fructose incompatibility (n = 12). 3. Mucous membrane of Shmerling Type I and a labelling index of enterocytes of 32 per cent was recorded from 50 per cent of children with coeliac disease (n = 19) after diet periods of seven or three to five months. Other children with coeliac disease but without therapy up to that time showed in 80 per cent the Shmerlings Type III and in 20 per cent Type II accompanied by the highest labelling index of 35 per cent. The increase of proliferative activity of enterocytes in coeliac disease shown by autoradiography and histological observations (villous atrophy) suggested an increased rate of cell death which led to the need for high cell replacement. This autoradiographic method used complementarily to usual histological diagnosis, has proved to help saving an enormous amount of time in the diagnosis of coeliac disease.

Adolescent↗
PubMed1985

The dietary management of inborn errors of metabolism.

Many inborn errors have now been described that can be treated by alterations in diet. Such treatment requires an understanding of both the biochemistry of the defect and of normal nutritional requirements. The principal strategies are cofactor therapy, steps to prevent accumulation of toxic metabolites and the replacement of essential nutrients that are deficient as a result of the metabolic block. It is essential to make sure that any diet used for more than a brief period is complete and capable of sustaining normal growth and development. The treatment of disorders of carbohydrate and amino acid metabolism including organic acidaemias and disorders of the urea cycle and of fat oxidation are discussed.

Acute Disease↗