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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An investigation was carried out on 61 children suffering from symptomatic giardiasis with the object of verifying the incidence and entity of lactose malabsorption. Furthermore, the possibility of a substitutive yogurt diet was verified in the lactose malabsorbers. The subjects, all children older than 1 year, were studied according to a schedule that included a lactose hydrogen breath test (BT) performed prior to therapy and a further BT 60 days following therapy. The subjects were divided in two groups: group A, 40 children, received a dose of 250 ml of cow's milk; group B, 21 children, received a stress dose of 2 g/kg lactose (max 50 g). Those subjects who were lactose malabsorbers at the 60 day follow-up were also given a BT at 75 days, and in the case of persistent malabsorption, a further BT was performed after 24 h with the administration of yogurt (450 g containing 12.1 g of lactose). Furthermore, 40 subjects matched for age and sex but without any GI complaints served as controls. The results showed lactose malabsorption to be frequent in children with Giardia lamblia symptomatic infection. According to the BT with a standard lactose load, all patients were malabsorbers; when testing lactose absorption with 250 ml of cow's milk, 45% of patients were found to be malabsorbers. In the latter subjects, the oral load of yogurt was uniformly well tolerated and gave rise to no H2 increment on the BT. We conclude that the occurrence of lactose malabsorption of nutritional relevance is common in children suffering or having suffered from giardiasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lactose malabsorption in children with symptomatic Giardia lamblia infection: feasibility of yogurt supplementation. 261 15

It is usual to consider that the greatest part of the black African population is lactose intolerant. Also, milk lactose malabsorption was studied by a breath hydrogen technique in 87 Gabonese children and 20 Gabonese adults (central Africa). The prevalence of malabsorption was 64.2% in rural schoolchildren, 65% in the urban hospitalized, and 60% in adults. Twelve children and six adults had clinical symptoms after a lactose load. All subjects were Bantus, with no tradition of consuming dairy products. These data must be considered in programs of nutritional support in Africa.
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PMID:Milk lactose malabsorption in Gabon measured by the breath hydrogen test. 272 48

The breath hydrogen test for carbohydrate malabsorption has been proved to be sensitive, specific and noninvasive. This study was performed to determine its applicability in the newborn period. Postprandial hydrogen excretion in the first 5 days of life was measured in 105 full-term normal newborns, who were either artificially or breast fed. Samples of expired air were collected via a nasopharyngeal catheter at 30 min intervals between feeds. Some babies showed no hydrogen production after 5 days, while others produced high (200 parts/10(6] levels. The incidence of hydrogen production increased postnatally--more than 80% of babies produced hydrogen by 5 days of age. None of the babies was unwell or developed frequent or loose stools suggestive of clinical carbohydrate malabsorption. It is therefore postulated that these high hydrogen levels reflect biochemical evidence of clinically insignificant carbohydrate malabsorption in this age group. This study shows clearly that an interfeed interval of 4 h in these babies is insufficient to cause breath hydrogen levels to fall in a predictable way. The ethical and practical difficulties in fasting these infants for longer periods suggest that conventional carbohydrate challenges with breath hydrogen estimations will be difficult in the neonate.
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PMID:Development of hydrogen excretion between feeds in breast and artificially fed full-term normal neonates. 273 86

The retention of the gamma-emitting 75Se-homotaurocholic acid (SeHCAT) after 72 and 168 h was assessed in 10 patients after ileal resection for radiation injury (group I). 6 patients suffering from chronic postirradiation diarrhea (group II) and 6 patients in whom the ileum had been resected for other indications (group III) were also examined. The retention of SeHCAT was abnormally low (less than 50%) in all cases after 72 h and below 20% in 19 out of 21 cases after 168 h. The length of resected small bowel (groups I and III) was inversely related with SeHCAT retention after 72 h (r = 0.63; p = 0.015), but not after 168 h. There was no correlation between the diarrhea score and the extent of bowel resection, SeHCAT retention or xylose absorption. Hydrogen breath test with lactulose revealed a significantly shortened orocecal transit time in group I, compared to groups II and III. Xylose absorption was significantly reduced in patients with positive 5 g xylose-H2 breath test. In groups I and III, however, xylose absorption tended to improve with increasing time interval following resection (r = 0.79; p = 0.003). It is concluded that radiation injury in addition to small-bowel resection contributes significantly to malabsorption and diarrhea in patients after ileal resection for radiation sequelae. The chronic radiation damage seems to act mainly through impaired motility.
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PMID:Small bowel function after surgery for chronic radiation enteritis. 274 45

The aim of the present study was to determine whether changes in orocaecal transit time (OCTT) affect the magnitude of the breath hydrogen (H2) excretion after ingestion of unabsorbable carbohydrate. We studied eight healthy subjects by interval sampling of end expiratory H2 concentration for 12 hours after ingestion of: (1) 10 g lactulose (L); (2) 10 g L with 20 mg metoclopramide (M) as tablets; (3) 20 g L, and (4) 20 g L with 7.5 mg diphenoxylate (D) as tablets, in random order. In spite of significant changes in OCTT after M and D, there were no significant changes, compared for the same dose of lactulose, with respect to area under the breath H2 excretion curves, peak increments of H2 concentration or timing of the peak increment. We conclude that, within the ranges observed, the OCTT does not significantly affect the shape of the H2 concentration versus time curves. In comparative studies estimates of the degree of carbohydrate malabsorption on the basis of breath H2 concentration may be valid in spite of differences in OCTT.
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PMID:Influence of orocaecal transit time on hydrogen excretion after carbohydrate malabsorption. 275 6

As the 50 g of lactose in the usual clinical test is unphysiologic both because it is equivalent to 1 L milk and because the usual dietary intake is not the purified sugar, but milk, we undertook a prospective comparison of the absorption of lactose after both lactose and milk ingestion with an equivalent lactose content. We studied 51 healthy volunteers, using the hydrogen breath test technique. All patients received 25 g lactose in aqueous solution. Subjects with an abnormal test had the test repeated with 500 ml whole cow's milk, whereas subjects with a normal test repeated the test after ingesting the unabsorbable sugar lactulose to detect the capacity of their colonic flora to produce the gas. Symptoms of gastrointestinal intolerance were also recorded. Compared to an equivalent lactose amount, milk lactose is better absorbed (8% of the entire population malabsorbed 500 ml whole milk, whereas 33.33% malabsorbed 25 g lactose) and induces intolerance in fewer subjects. We conclude that milk rather than pure lactose must be used in clinical evaluation of lactose malabsorption and intolerance.
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PMID:Breath hydrogen excretion after lactose and whole milk ingestion. A prospective comparison in lactase deficiency. 275 15

Pulmonary hydrogen gas (H2) concentrations were used to assess the malabsorption of dietary nutrients in preruminating calves inoculated with Cryptosporidium sp. Normal values were established in five control calves and seven calves (principals) were inoculated with 1.0 x 10(8) Cryptosporidium sp. oocysts. Hydrogen concentrations and wet fecal weights were measured at three stages: before Cryptosporidium sp. inoculation (stage 1), three days after the onset of diarrhea (stage 2), and after the resolution of diarrhea (stage 3). Mean end-breath and total-breath H2 concentrations in the principal calves were higher (P less than 0.025 and P less than 0.05) for stage 2, when compared to control values. Both end-breath and total-breath H2 concentrations were increased (P less than 0.001 and P less than 0.025, respectively) in the principal calves during stage 2 when compared to values obtained for stages 1 and 3. Concurrently, Cryptosporidium sp. infection was associated with increased (P = 0.06) fecal output during stage 2, only. The increased H2 concentrations and cumulative fecal output show that Cryptosporidium sp. caused malabsorption of fermentable nutrients.
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PMID:Pulmonary excretion of H2 in calves with Cryptosporidium-induced malabsorption. 276 7

Individuals with sufficient intestinal lactase hydrolyze ingested lactose to galactose and glucose and these monosaccharides are absorbed. Lactose is not digested completely when intestinal lactase activity is low and the disaccharide is malabsorbed. Breath hydrogen excretion after lactose ingestion is used commonly to diagnose lactose malabsorption. However, no direct tests are currently used to assess lactose absorption. We tested a new method of assessing lactose absorption in 26 healthy individuals. Each subject ingested 50 g of lactose. Participants were evaluated for lactose malabsorption using a standard 3-h breath hydrogen test. In addition, the urinary excretions of galactose, lactose, and creatinine were quantitated for 3-5 h after lactose ingestion. On the basis of breath hydrogen analysis after lactose ingestion, 12 individuals were lactose malabsorbers (defined as a rise in the breath hydrogen concentration of greater than 20 parts per million above the baseline value). The 14 subjects who did not malabsorb lactose by breath hydrogen testing (defined as a rise in the breath hydrogen concentration of less than or equal to 20 parts per million above the baseline value), had significantly more galactose in their urine 1, 2, and 3 h after lactose ingestion than lactose malabsorbers. The ratio of excreted lactose to excreted galactose was significantly decreased in lactose absorbers compared with lactose malabsorbers (p less than 0.001). Determination of the ratio of urinary galactose to urinary creatinine separated lactose absorbers from lactose malabsorbers completely (p less than 0.001). We conclude from this study that the determination of urinary galactose, urinary lactose/galactose ratio, and urinary galactose/creatinine ratio may be used to assess lactose digestion and absorption in healthy adults.
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PMID:Assessment of lactose absorption by measurement of urinary galactose. 277 42

Glucomannan (Propol), a potent gel forming dietary fibre, was added to a carbohydrate rich breakfast in eight patients with previous gastric surgery suffering from postprandial hypoglycaemia. Addition of only 2.6 g and 5.2 g glucomannan to the meal dose dependently improved reactive hypoglycaemia from 2.3 (0.2) mmol/l to 3.3 (0.2) mmol/l (p less than 0.0005) after 2.6 g and 4.1 (0.2) mmol/l (p = 0.0005) after 5.2 g, and decreased postprandial rise in plasma insulin (p less than 0.05). Expiratory breath hydrogen excretion tended to decrease reflecting improvement of carbohydrate metabolism. Addition of glucomannan to an intraduodenal sucrose solution significantly raised plasma glucose nadirs, indicating glucomannan to be effective during the intestinal phase. It is concluded that small amounts of glucomannan may be beneficial to patients with reactive postprandial hypoglycaemia, without the disadvantage of unpalatability and carbohydrate malabsorption.
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PMID:Glucomannan prevents postprandial hypoglycaemia in patients with previous gastric surgery. 284 Mar 65

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
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PMID:Consequences of phosphate imbalance. 306 Jan 61


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