Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-seven patients undergoing routine investigation for malabsorption were given radio-opaque pellets (ROP) which were compared with polyethylene glycol and chromic oxide as continuous faecal markers. Percentage recovery of all markers showed a wide range. The recovery of all markers was very similar, and radio-opaque pellet-corrected daily faecal fat correlated very closely with PEG-and chromic oxide-corrected fat results. Estimation of ROP is precise, simple, and minimises faecal handling. ROP are suitable for routine use in faecal fat studies and have advantages over markers used at present.
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PMID:Radio-opaque pellets as faecal markers for faecal fat estimation in malabsorption. 48 54

The influence of malabsorption of lactose, as a result of primary lactase deficiency, on the absorption of the nutrients in milk was tested in four healthy controls and four subjects with lactase deficiency. An ileal perfusion technique was used to quantify arrival in the ileum of nutrients and a nonabsorbable marker (polyethylene glycol, PEG 4000) ingested as a test meal of milk. The meal was 250 ml of whole milk or milk in which the lactose had been hydrolyzed to glucose and galactose. In the fasting state, ileal flow of volume, protein, carbohydrate, and electrolytes was small and not different in controls and lactase-deficient subjects. Ileal flow increased in all subjects after the test meal of milk; more fluid and nutrient was recovered from the ileum in lactase-deficient subjects after whole milk than in control subjects or in lactase deficiency after hydrolyzed milk. Two deficient subjects showed marked malabsorption of lactose (35 and 50%); two did not. Protein, calcium, magnesium, and phosphorus were also recovered from the ileum in greater quantities in lactase deficients after whole milk. However, apart from decreased absorption of lactose, the nutritional consequences of malabsorption in association with primary lactase deficiency in adults are probably minimal.
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PMID:Absorption of nutrients in lactase deficiency. 58 2

Primary hypoparathyroidism caused by lymphocytic parathyroiditis was diagnosed in a cat. Other causes of hypocalcemia (ethylene glycol toxicosis, phosphate enema administration, pancreatitis, renal insufficiency, and malabsorption) were ruled out on the basis of history, clinicopathologic data, and lack of supportive clinical signs, which in this cat included inappetence and tetanic muscle spasms. The diagnosis was confirmed by histologic examination of a surgically excised thyroparathyroid lobe that comprised lack of recognizable parathyroid tissue and a lymphocytic plasmacytic infiltrate adjacent to the cranial pole. A treatment regimen similar to that for iatrogenic postthyroidectomy hypoparathyroidism was successful in controlling clinical signs of the disease.
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PMID:Primary hypoparathyroidism in a cat. 233 77

Polyethylene glycol (PEG) 4000 is one of numerous substances used as non-absorbable markers to correct for variable faecal output when assessing daily faecal losses of nutrients. The introduction of enteric coated micro-encapsulated pancreatic enzyme (EMPE) preparations has greatly improved the control of fat malabsorption in cystic fibrosis and chronic pancreatitis patients. Unfortunately, these enzyme preparations contain significant quantities of PEG 4000 or polyvinyl pyrrolidine (PVP) as components of the enteric coating and thus PEG 4000 cannot be used either as a faecal marker, or in intubation studies, if these enzyme preparations are being used.
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PMID:Markers for faecal fat estimation in monitoring steatorrhoea in cystic fibrosis. 319 6

The differential passive permeation of polymers of different lengths across the intestinal mucosa has been proposed as a probe to test mucosal integrity under a variety of physiologic and pathologic conditions. Polyethylene glycol (PEG) 400 contains a series of polymers whose pattern of urinary recovery after oral administration has been used to characterize intestinal mucosal function. To extend this method to the low levels of PEG polymers found in the urine of children with diarrhea, we have introduced three methodologic innovations. These alterations involve (1) formulation of a balanced PEG polymer mixture, (2) improved isolation, derivatization, and gas chromatography techniques, and (3) a new quantification of the pattern of PEG urinary recoveries. Urinary recovery of orally administered PEG was assessed in four normal adults, six hospitalized infants without gastrointestinal complains, two infants with prolonged diarrhea and carbohydrate malabsorption, and two children with cystic fibrosis. A parameter characterizing the urinary recovery of PEG, N1/2, which is the theoretical number of subunits in the polymer whose recovery is reduced to 50% of the value of the polymer whose recovery is maximal, gave stable, reproducible, and consistent results in normal adults and infants.
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PMID:Polyethylene glycol polymers of low molecular weight as probes of intestinal permeability. I. Innovations in analysis and quantitation. 395 71

36 patients with severe neurological diseases (craniocerebral trauma, cerebrovascular insufficiency, meningo-encephalitis, polyneuropathy, paraplegia, intoxication etc.) received for more than 3 months monosaccharides and polyols (Triofusin E 1000) and a 10-%-concentration of crystalline amino acids (Aminofusin L10% kohlenhydratfrei) via the parenteral route in combination with / or exclusively a nutrient-defined diet (Biosorb). Exclusive enteral nutrition was given preference if possible. Numerous laboratory parameters, as for example blood counts, "hepatic enzymes", electrolytes, trace elements, plasma proteins, lipids, urea and creatinine were determined once a week. Substitutions and secondary complications were registered in addition. Iron and plasma proteins had to be substituted most frequently. It could be proved that hypoferremia was caused by insufficient iron supply in case of exclusive/prevailing parenteral nutrition, incorrect application of the iron preparations, inflammatory complications with iron moving into the R.E.S., as well as malabsorption syndromes probably induced by bacteria. Inflammatory complications were also the major cause of protein deficiency syndromes (hypoalbuminemia). In case of relatibely often occurring diarrhea, however, it could clearly be proved that it was not induced by nutrition but was produced by a broad-spectrum antibiosis. Chronically persistent diarrhea with colitis-like colonic changes required enteral feeding with an oligopeptide diet (z.B. Peptisorb) via jejunal feeding tube. Nitrogen balances which were determined after more than 3 months of artificial nutrition formed the basis of a nutritional plan differentiated according to diagnostic groups and stages of disease.
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PMID:[Artificial nutrition in neurology--indications and problems]. 640 43

Macromolecular absorption of food and microbial antigens being enhanced in the intestine under pathological conditions may well be the cause of such diseases as food allergy, coeliac disease, Crohn's disease, atopic eczema, etc. The polyethyleneglycol-4000 (PEG-4000) and food antigens absorption was found to be similar in the animal intestine. The PEG-4000 gastrointestinal permeability is considerably increased in the rats with anaphylaxis, experimental biliary malabsorption and experimental colitis. Fatty acids of the omega-3 and omega-6 series as well as histidine were found to change the permeability for the PEG-4000.
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PMID:[Disordered permeability of the gastrointestinal tract barrier for macromolecules and the possibilities for its experimental dietetic correction]. 840 45

The gastrointestinal (GI) manifestations of cystic fibrosis (CF) are varied and include pancreatic insufficiency, meconium ileus, distal intestinal obstruction syndrome (DIOS), liver disease, and other less common manifestations. Treatment of pancreatic insufficiency consists of providing appropriate pancreatic enzyme replacement therapy and may include raising duodenal pH to allow for optimal action of these enzymes. Despite a number of pancreatic enzyme replacement products, malabsorption cannot be normalized. Management of DIOS depends on the severity of the symptoms; adequate hydration is very important. Polyethylene glycol solutions are being increasingly used. The precipitating cause of the episode of DIOS should be looked for so future episodes can be prevented. Liver disease is relatively silent and annual monitoring of liver function and status is recommended. Treatment is mainly supportive and the role of ursodeoxycholic acid in the prevention of cirrhosis needs to be better defined. Nutritional status is an important part of management of all GI and liver manifestations of CF. A team approach and the assistance of a registered dietitian are extremely valuable in managing the GI and liver manifestations of CF.
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PMID:Treatment of Gastrointestinal Problems in Cystic Fibrosis. 1295 49

Acute oxalate nephropathy can occur due to primary hyperoxaluria and secondary hyperoxaluria. The primary hyperoxalurias are a group of autosomal recessive disorders of endogenous oxalate overproduction. Secondary hyperoxaluria may occur as a result of excess dietary intake, poisoning with oxalate precursors (ethylene glycol), or enteric hyperoxaluria. The differential diagnosis of enteric hyperoxaluria includes inflammatory bowel disease, short bowel syndrome, bariatric surgery (with jejunoileal bypass or Roux-en-Y gastric bypass), celiac disease, partial colectomy, and chronic pancreatitis. The common etiology in all these processes is fat malabsorption, steatorrhea, saponification of calcium, and absorption of free oxalate. Hyperoxaluria causes increased urinary oxalate excretion, urolithiasis (promoted by hypovolemia, decreased urinary pH caused by metabolic acidosis, and decreased citrate and magnesium concentrations in urine), tubulointerstitial oxalate deposits, and tubulointerstitial nephritis. We report a rare case of acute oxalate nephropathy due to pancreatic atrophy and exocrine insufficiency caused by newly diagnosed pancreatic cancer.
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PMID:Acute oxalate nephropathy due to pancreatic atrophy in newly diagnosed pancreatic carcinoma. 2661 99