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

Urinary oxalate excretion was measured in healthy persons and patients with Crohn's disease, colitis ulcerosa, sprue and other diseases accompanied with malabsorption, and patients with insufficiency of the exocrine pancreas gland. Further measurements were made in patients after resection of parts of the small intestine or the colon. We found a clear increase of urinary oxalate excretion in patients with resected parts of the small intestine, sprue or other malabsorption syndromes. In 4 patients with resected parts of small intestine or pancreas we even found urolithiasis. Urinary oxalate excretion correlated significantly with steatorrhoea and increased if larger parts of small intestine were resected. Increased resorption of oxalate from food causes increased urinary excretion. Details about the patho-mechanism of this increased excretion are not known yet; an important factor seems to be the reduced absorption of fat in the small intestine.
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PMID:[Hyperoxaluriaas a complication of intestinal diseases (author's transl)]. 99 43

Giardia lamblia infestation can cause severe diarrhea and malabsorption, and the diagnosis is usually made by identification of cysts in the feces, but small intestinal biopsy or smears may be required. A wide spectrum of roentgen changes may be seen. In patients with a normal immune status, the small bowel is normal or shows an inflammatory bowel disease pattern. Eradication of the parasite reverses these changes. In some patients with IgA deficiency, nodular lymphoid hyperplasia occurs, and this is usually not reversible. Other patients with hypogammaglobulinemia or dysgammaglobulinemia and giardiasis may show a sprue pattern. This pattern most often persists after eradication of the parasite. Although the triad of giardiasis, IgA deficiency, and nodular lymphoid hyperplasia has a particularly high association, these, together with diarrhea, malabsorption, and various altered immune states may occur in any combination.
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PMID:Current perspectives on giardiasis. 110 21

The author reports the successful treatment with Vivasorb, the bulk-free, balanced synthetic diet, of patients with severe forms of ulcerative colitis and Crohn's disease, indigenous sprue and condition after small bowel resection, and of one patient with a Cronkhite Canada syndrome. The duration of the treatment was from a few weeks to 34 months. The patients received between 320 and 640 g/day, according to their requirements and their tolerance. Because of the relatively low content of essential fatty acids, long-term exclusive administration of Vivasorb may lead to symptoms of essential fatty acid deficiency, which disappear after the administration of Lipofundin S. The successful treatment of patients with malabsorption syndrome was verified histologically. Particles of mucosa taken from different small bowel sections showed the development of villi after only four weeks of treatment, whereas, before the treatment, subtotal villi atrophy had been observed.
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PMID:[Long term feeding with a chemically defined diet]. 118 91

The vitamin A absorption test and its interaction with the secretin-pancreozymin test, the d-xylose absorption test, fecal fat content and the small intestine biopsy are estimated on their significance in the diagnosis and course of sprue and pancreatic insufficiency. The investigation includes 39 patients with different stages of pancreatic insufficiency and 10 patients with sprue. First it results relatively wide spread normal values in a control collective with sometimes unexplained low values, the significance of the vitamin A absorption test as screening test therefore is limited. Secondly the absent rise after vitamin A ingestion in serum after 3 and 6 hours favours the diagnosis of sprue, correlates with the histological findings of the mucosa and appears more reliable than the d-xylose test. Thirdly this test seems to allow the differentiation between malabsorption and maldigestion when steathorroe is proved: In contrast to sprue-syndromes pancreatic insufficiency shows significant reduced 3 hour values at subnormal 6 hour values after vitamin A ingestion.
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PMID:[Vitamin A absorption test. I. Pancreatic insufficiency and sprue (author's transl)]. 118 78

It is reported on the estimation of the vitamin A absorption test in 17 patients with chronic liver diseases, 26 patients with diseases of the extrahepatic biliary system, and in 12 patients with diseases of the stomach. In the latter there are no changes in the vitamin A test. On the contrary patients with diseases of the liver and biliary system show differences in the serum vitamin A levels. A separate consideration of active liver cirrhosis and active cholangitis indicates individualities in the constellation of the 3 and 6 hour values after vitamin A ingestion: in liver cirrhosis the first value is normal while the 6 hour value seems significant lowered so that the maximum vitamin A concentration is found near 3 hours. In active cholangitis both values are reduced, the first one more than the second one. The reason is to be seen in a decrease of the conjugated bile acids, whereas in the group of liver diseases an interpretation is somewhat problematic. It is to discuss whether these results depend on the development of portal hypertension, while the intestinal absorption seems normal and liver damage only of secondary importance. The fact that this test is influenced by diseases of the liver and biliary system shortens its significance as a screening test for malabsorption or maldigestion though a further differentiation between sprue and pancreatic insufficiency seems possible.
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PMID:[Vitamin A absorption test. II. Diseases of the liver, the extrahepatic biliary system and the stomach (author's transl)]. 118 79

Passage through the small intestine was significantly accelerated after intramuscular injection of ceruletide (synthetic caerulein, F.I. 6934), 0.50 to 0.75 mug/kg body-weight. Average passage took 62 +/- 41 min (106 patients, with various suspected or demonstrated small-intestinal involvement, excluding malabsorption syndrome, sprue or collagen diseases) after caerulein, while in a control group of 83 patients with radiologically normal small intestine it was 126 +/- 62 min (P less than 0.001). In 75% of patients there was no evidence of induced change in radiological pattern of the small intestine. Increased local contractions were observed in a quarter of patients, but did not impair the diagnostic interpretation.
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PMID:[Acceleration of passage through the small intestine by caerulein (author's transl)]. 120 25

Thirty-eight specimens obtained by jejunal biopsy from 22 children suffering from mucoviscidosis were examined by histochemical techniques. In 27% of the patients the findings were within normal limits. In 18% of cases, associated coeliacal sprue was disclosed. The remaining cases displayed slight morphological abnormalities associated with trehalase and/or lactase deficiency, and in 41% there was hypersecretion of viscous mucus filling up dilated crypts and adhering to the surface of villi. The findings as observed in enterobiopsis are not pathognostic of mucoviscidosis. They however, should make one to think of it, particularly if trehalase and/or lactase deficiency is found associated with hypersecretion of viscous mucus and an almost normal morphological appearance. Neither normal findings nor that of coeliacal sprue exclude the diagnosis of mucoviscidosis. It appears that malabsorption in mucoviscidosis is not only pancreatogenic; the intestinal mucosa may be contributory to a various degree as well.
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PMID:[Jejunal mucosa in children with mucoviscidosis]. 120 86

According to the computerized ICD registration, 20 new cases of non-tropical sprue were detected in our outpatient clinic between 1979 and 1990. 8 of these patients had an oligo- or asymptomatic form of this disease (40%). The clinical presentation and spectrum of abnormal laboratory findings in these 8 cases are described in detail. It is concluded that laboratory parameters indicating malabsorption, especially hematologic changes, are helpful for the detection of the oligo- and asymptomatic form of non-tropical sprue, and that, in cases with undetermined anemia, this form of sprue must be considered in etiologic differential diagnosis. Finally, it seems advisable to perform a biopsy as a routine procedure during endoscopy in cases with unclear anemia.
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PMID:[How does oligo- en asymptomatic non-tropical sprue present itself?]. 147 59

We report coexistent collagenous colitis and collagenous sprue in a 62-year-old woman with diarrhea. Investigations suggested malabsorption, and small intestinal biopsies demonstrated a flattened mucosa with subepithelial collagen deposition. Colonic biopsies also showed a thickened subepithelial collagen band as well as a striking lamina propria inflammatory cell infiltrate. Symptomatic remission was induced with a gluten/lactose-free diet, oral prednisone, and sulfasalazine and has been maintained with gluten restriction alone. Repeat biopsies after 2 months demonstrated restoration of normal small intestinal and colonic collagen bands; only a chronic inflammatory cell infiltrate (consistent with microscopic/lymphocytic colitis) persisted in colonic biopsies. We propose that, in this instance, collagenous enterocolitis represented a diffuse manifestation of gluten sensitivity.
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PMID:Collagenous enterocolitis: a manifestation of gluten-sensitive enteropathy. 150 Jun 61

The authors report the first case of collagenous sprue in Hungary. This condition is characterized by coeliac type small bowel malabsorption, resistant to gluten free diet and other therapeutic efforts, associated with poor prognosis. The diagnosis depends on the histological demonstration of extensive collagenization of the lamina propria in the flat jejunal mucosa. This disease must be kept in mind at differential diagnosis of chronic diarrhoea with progressive malabsorption, especially if it is resistant to gluten withdrawal than conventional coeliac disease.
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PMID:[Collagen sprue--a rare form of adult celiac disease]. 150 54


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