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Query: UMLS:C0024523 (
malabsorption
)
7,319
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Multimodality and differentiated treatment of small-intestinal diseases is to combine methods of etiological action with pathogenetic treatment of the main clinical syndromes: chronic diarrhea,
malabsorption syndrome
, hypercatabolic exudative enteropathy. Each nosological form should be treated specifically. Pathogenetic treatment involves diet therapy, chemotherapeutic correction of metabolic processes (vitamin administration, recovery of normal protein and lipid metabolism, water and electrolyte balance, anemia), management of chronic diarrhea. Treatment regimens are specified for gluten enteropathies, total variable immunodeficiency, Whipple disease, small-intestinal diverticulosis,
Crohn's disease
, amyloidoses, intestinal lymphoma and retroperitoneal lymph nodes. Clinical experience justifies the above methods as highly effective.
...
PMID:[Treatment of chronic diseases of the small intestine]. 172 19
PAF-acether (PAF) is a phospholipid mediator with potent biological effects on the digestive tract. We report the presence of PAF in stool of patients with active
Crohn's disease
(39.1 +/- 13.5 ng/g of stool, mean +/- SEM, N = 19) and its absence in patients with irritable bowel syndrome with diarrhea and diarrhea with
malabsorption
. Fecal PAF acetylhydrolase activity was higher (P less than 0.04) in patients with
Crohn's disease
as compared to patients with irritable bowel syndrome with diarrhea and diarrhea with
malabsorption
. We also report a solid-phase extraction of fecal PAF using silica minicolumns, which yielded results highly correlated with those obtained with a high-performance liquid chromatography method (r = 0.86, P less than 0.001, N = 16). These findings may allow us to implicate PAF in the onset and perpetuation of digestive tract inflammatory symptoms observed during
Crohn's disease
. They would warrant to investigate the influence of various therapeutic agents, including PAF antagonists, on fecal PAF levels during inflammatory digestive ailments.
...
PMID:PAF-acether and acetylhydrolase in stool of patients with Crohn's disease. 173 66
Intrinsic factor is produced by the gastric parietal cell. Its secretion is stimulated via all pathways known to stimulate gastric acid secretion: histamine, gastrin, and acetylcholine. There is, however, a different mode of secretion for both substances: atropine, vagotomy, and H2 receptor antagonists inhibit both intrinsic factor and acid secretion, but secretin and the hydrogen-potassium ATPase antagonist omeprazole have no effect on intrinsic factor while substantially reducing acid secretion. Cobalamin in food is bound to animal protein. Cobalamin deficiency due to inadequate dietary intake is rarely seen in extreme vegetarians (vegans). In the stomach cobalamin is liberated from its protein binding by peptic digestion and bound to R-proteins. Hypochlorhydria or achlorhydria, whether medically induced or not, may impair cobalamin uptake. The cobalamin-R-protein complex is split by pancreatic enzymes in the duodenum, where cobalamin is bound to intrinsic factor. Pancreatic insufficiency may lead to cobalamin deficiency. Lack of intrinsic factor is the commonest cause of cobalamin deficiency; very rarely, aberrant forms of intrinsic factor are produced, but the clinical syndrome is similar. Gram-negative anaerobe bacteria bind the cobalamin-intrinsic factor complex, and bacterial overgrowth of the small intestine diminishes cobalamin resorption. Parasitic infections with fish tape-worm and Giardia lamblia are also associated with cobalamin
malabsorption
. The cobalamin-intrinsic factor complex binds to the ileal receptors in the terminal ileum. Cobalamin absorption may be impaired after resection or by diseases affecting more than 50 cm of the terminal ileum, such as
Crohn's disease
, coeliac disease, tuberculosis, lymphoma or radiation. There is clearly a wide diversity in the aetiology of cobalamin deficiency, which requires a versatile diagnostic approach.
...
PMID:Intrinsic factor secretion and cobalamin absorption. Physiology and pathophysiology in the gastrointestinal tract. 177 33
Gallstones are usually present in patients with
Crohn's disease
involving the distal ileum. This may be due to disturbances of the enterohepatic circulation, with bile salt
malabsorption
and secondary precipitation of cholesterol in the gallbladder. The article describes three patients who were cholecystectomized for cholelithiasis, and where
Crohn's disease
was found incidentally during laparotomy.
...
PMID:[Crohn disease found incidentally during cholecystectomy. Report of 3 cases with pronounced biliary tract problems]. 186 26
In 53 patients with chronic diarrhea ileoscopy was done following colonoscopy. Beside the microscopic examination, terminal ileum biopsies and mucosal smears were also performed. Endoscopy of the terminal ileum was abnormal in eight patients (15.1%); biopsy itself was diagnostic in 22 patients (41.5%): primary bile acid
malabsorption
with mucosal atrophy and reduced retention of 75ScHCAT (10), mucosal atrophy after cholecystectomy (4),
Crohn's disease
(6), backwash ileitis in ulcerative colitis (1), and postirradiation ileitis (1). Biopsies were normal but mucosal smear indicated the cause of diarrhea in a further 10 patients: giardiasis was found in 7, and candidiasis in 3 patients. All in all, endoscopy, biopsy and mucosal smear of terminal ileum showed a sensitivity of 58.5%. In 38 patients in whom laboratory, roentgenologic and endoscopic investigation failed to establish the etiology of diarrhea, the sensitivity of ileoscopy itself was 0%, of ileoscopy with biopsy 36.8% and ileoscopy with biopsy and mucosal smear 47.4%. We conclude that endoscopy, biopsy and mucosal smear of the terminal ileum are indicated in the investigation of patients with chronic diarrhea.
...
PMID:[The terminal ileum and chronic diarrhea: endoscopy, histology and parasitology]. 192 64
To study cholesterol metabolism in
Crohn's disease
and especially the effect of ileum resection, liver biopsy specimens were obtained from patients undergoing partial ileal resection because of
Crohn's disease
(n = 17) and patients with Crohn's colitis undergoing colectomy (n = 3). Gallstone-free patients (n = 16) undergoing cholecystectomy because of adenomyomas or polyps of the gallbladder served as controls. The mean levels of cholesterol 7 alpha-hydroxylase activity and 3-hydroxy-3-methylglutaryl coenzyme A reductase activity, rate-determining enzymes in bile acid, and cholesterol synthesis, respectively, were twofold to threefold higher in the ileum-resected patients than in the controls. Significant positive correlations were obtained between length of resected ileum and cholesterol 7 alpha-hydroxylase activity. Provided patients who had received total parenteral nutrition preoperatively were excluded from analysis, a significant correlation was also observed between length of resected ileum and 3-hydroxy-3-methylglutaryl coenzyme A reductase activity. Significant positive correlations were also obtained between length of resected ileum and serum levels of 7 alpha-hydroxycholesterol (a marker for bile acid biosynthesis) and lathosterol (a marker for cholesterol synthesis). The plasma levels of total and low-density lipoprotein cholesterol were negatively correlated to the length of resected ileum. The expression of hepatic low-density lipoprotein-receptor binding activity was determined in five of the patients and in three of the controls. A significant positive correlation was observed between 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and low-density lipoprotein-receptor binding activity. The results show that
malabsorption
of bile acids leads to parallel stimulation of cholesterol synthesis, cholesterol degradation, and low-density lipoprotein-receptor expression in human liver. The resulting effect in the present patients was a significant reduction in low-density lipoprotein cholesterol.
...
PMID:Hepatic metabolism of cholesterol in Crohn's disease. Effect of partial resection of ileum. 200 2
Autonomic nerve function was evaluated in 33 patients with
Crohn's disease
(age range, 19-66 years; mean, 36 years) by three established non-invasive tests based on the heart reactions to deep breathing (E/I ratio) and to tilt (acceleration and brake indices). Peripheral nerve function was evaluated neurographically and by measuring thresholds to vibration and temperature changes. None of the patients were diabetic, and all had normal thyroid function. In spite of normal peripheral nerve function, almost half of the patients, 48% (16/33), showed signs of autonomic neuropathy (AN). The occurrence of AN was not related to duration or severity of
Crohn's disease
or to biochemical evidence of inflammation or
malabsorption
of vitamins and trace elements. We conclude that autonomic nerve dysfunction is a feature of
Crohn's disease
which may be relevant with regard to the frequent disturbance in bowel function in patients with this disorder.
...
PMID:Disturbed autonomic nerve function in patients with Crohn's disease. 203 89
Crohn's disease
is a chronic inflammatory granulomatous disorder affecting any part of the gastrointestinal tract, particularly the terminal ileum and the colon. Familiar complications are strictures, fistulae, perforation, haemorrhages and
malabsorption
due to multiple resections. A patient with two rare complications of
Crohn's disease
is described. A 16-year-old female with ileocaecal
Crohn's disease
presented with anaemia and ileus. This ileus was caused by some 40 tablets of ferrosulphate with a non-soluble matrix, in the presence of an existing stenosis of the ileum due to
Crohn's disease
. An ileocaecal resection was performed. During an exacerbation of
Crohn's disease
she developed hepatic vein thrombosis with a Budd-Chiari syndrome (upper abdominal pain, hepatomegaly and ascites). Prescription of tablets with a non-soluble matrix is contraindicated in patients with a partial stenosis of the intestine. Patients with active
Crohn's disease
are predisposed to thromboembolic complications. Hepatic vein thrombosis in our patient may have been the result of hypercoagulability during the exacerbation of her disease.
...
PMID:[Intestinal obstruction caused by non-absorbable tablets and Budd-Chiari syndrome in a patient with Crohn's disease]. 204 72
Based on the data obtained during clinical examination of 1,026 patients with small intestinal diseases the authors provide the portion of laboratory and instrumental methods employed in the diagnosis of different disease entities. The clinical picture of small intestinal diseases is mainly determined by the gravity of
malabsorption
. Histological examination of the small intestinal mucosa is a method of choice in the diagnosis of gluten enteropathy, Whipple's disease, primary lymphangiectasis and amyloidosis. Immunoassays play the key role in recognition of variable immunodeficiencies and disease of heavy alpha-chains. Meanwhile in differential diagnosis of
Crohn's disease
, small intestinal tumors, congenital abnormalities of rotation and in some others, the leading part is played by x-ray methods. The authors describe the treatment schedule based on the pathogenetic approach, that makes it possible to reach a stable clinical remission and recovery of the working capacity even in part of patients with stage III
malabsorption
.
...
PMID:[Current problems in the diagnosis and treatment of small intestinal diseases]. 204 28
A 51-year-old man who had undergone several partial bowel resections for
Crohn's disease
presented with progressively decreased night vision. Electroretinography showed a flat scotopic response and a diminished, delayed photopic response. Measurement of stool fat showed marked fat
malabsorption
. Treatment with parenteral nutrition, including administration of vitamin A, resulted in marked improvement in the scotopic and photopic response and subjective improvement in his night vision. Patients with
malabsorption
states should be followed to avoid irreversible visual loss.
...
PMID:Reversal of progressive nyctalopia in a patient with Crohn's disease. 211 31
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