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

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.
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PMID:[Current problems in the diagnosis and treatment of small intestinal diseases]. 204 28

The authors interpret a case report on a secondary amyloidosis involving the whole gastrointestinal tract, and manifested in a rare clinical phenomenon, the malabsorption syndrome. Their histological observations advance the understanding of the pathomechanism of malabsorption.
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PMID:[Malabsorption causing secondary gastrointestinal amyloidosis associated with rheumatoid arthritis]. 264 88

The prognosis of juvenile rheumatoid arthritis (JRA) is generally good, although premature death occurs in a subset of children. Secondary infections, chronic amyloidosis, and heart disease have been reported as common causes. Our experience indicates that JRA can also herald the development of a severe immune enteropathy. In the case presented, typical JRA was followed by fulminant hepatitis; skin rashes; recurrent, severe, watery diarrhea; malabsorption; and ultimately death. Biopsies of the small bowel exposed to the patient's serum revealed deposition of complement and immunoglobulins in the epithelium. Although not widely appreciated, JRA can herald a multisystem syndrome characterized by severe immune enteropathy.
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PMID:Fatal multisystem disease with immune enteropathy heralded by juvenile rheumatoid arthritis. 270 56

We retrospectively analyzed the small bowel radiographies, performed by enteroclysis in 73 patients presenting a malabsorption disease. The etiology are: celiac disease (44 cases), abetalipoprotidemia (2 cases), Whipple's disease (7 cases), mastocytosis (1 case), amyloidosis (1 case), ischemia enteritis (4 cases), radiation injury (4 cases), lymphangiectasia (4 cases), Crohn's disease (4 cases) and NH lymphoma (2 cases). With enteroclysis, the radiological diagnosis of malabsorption disease is improved and it is able to differentiate malabsorption diseases based on radiological features: increased or decreased number of folds (celiac disease, mastocytosis, abetalipoprotidemia), nodularity of folds (Whipple's disease) and wall thickness (amyloidosis, lymphangiectasia, ischemic enteritis and radiation injury). It is no possible to differentiate NH lymphoma from Crohn's disease.
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PMID:[Enteroclysis in malabsorption syndrome in adults. Apropos of 73 cases]. 273 73

Systemic amyloidosis involving the digestive tract is described in an 11-year-old Morgan stallion. The disease was characterized clinically by weight loss, ptyalism, anaemia, persistent mature neutrophilia, hypoalbuminaemia and hypergammaglobulinaemia. The D-xylose absorption test indicated malabsorption. Necropsy revealed oral, oesophageal and gastric ulcers and reddened segments of small bowel mucosa with scant haemorrhages. Microscopically, amyloid deposits were found throughout all tissue layers of the digestive tract, except the serosa. Deposits of amyloid were most apparent in the small bowel mucosa and submucosal arteries. Amyloid was also present in the spleen and lymph nodes and to a lesser extent in the liver, kidneys, lungs, pancreas and bone marrow. All amyloid deposits gave the typical histochemical reaction for AA amyloid with the KMnO4-Congo red stain procedure and immunohistochemical cross-reactivity was demonstrated with antisera to both canine and bovine protein AA by the peroxidase-antiperoxidase technique. The cause of the amyloidosis was not identified, although the haematological and serological data were compatible with an underlying chronic inflammatory process.
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PMID:AA amyloid-associated gastroenteropathy in a horse. 337 53

Systemic amyloidosis is a rare complication in psoriatic arthritis, 16 cases only were published until now. Our case report is characteristic of gastrointestinal symptoms like chronic diarrhea, malabsorption, and intestinal pseudoobstruction. In addition, in this connection the first report of segmental pseudomembranous enteritis is given. Discussing the findings, observations and literature, the difference between psoriatic enteropathy, malabsorption in systemic amyloidosis and pseudomembranous enteritis in amyloidosis is shown. In this connection the basic different pathophysiological mechanisms are demonstrated.
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PMID:[Gastrointestinal disorders in psoriatic arthritis]. 378 27

Biopsy specimens of the gastric antrum, duodenum, and rectum from three patients with secondary amyloidosis were examined by electron microscopy in an attempt to determine the ultrastructural distribution of amyloid filaments and to identify any secondary changes in the covering mucosal epithelial cells. The characteristic amyloid filaments were seen in the walls of submucosal arterioles and mucosal capillaries deposited within the basal lamina surrounding the endothelial cells. Filaments were also sometimes seen within the muscularis mucosa. the overlying gastric and rectal epithelial cells appeared normal, but numerous curved bacilli were seen in close contact with the microvilli of the surface epithelial gastric cells. Duodenal columnar absorptive cells were vacuolated and contained prominent lysosomes. These changes are probably degenerative and may explain, at least in part, the development of malabsorption in some patients with intestinal amyloidosis.
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PMID:Secondary amyloidosis of the gastrointestinal tract: an electron microscopic study. 399 36

Seven patients (five male and two female) with chronic renal failure (CRF) treated by periodical haemodialysis presented with swelling and effusion of more than three months' duration in knees (four bilateral), shoulders (two, one of them bilateral), elbow (one), and ankle (one). Four had a carpal tunnel syndrome both clinically and electromyographically (three bilateral). All patients had hyperparathyroidism secondary to their CRF, which was not due to amyloidosis in any of them. The dialysis duration period varied from five to 14 years, with an average of 8.6 years. Amyloid deposits (Congo red positive areas with green birefringence under polarising microscopy) were shown in six of the seven synovial biopsy specimens of the knee, in five of the sediments of the synovial fluids, and in specimens removed during carpal tunnel syndrome surgery. No amyloid was found in the biopsy specimen of abdominal fat of six of the patients. The finding of amyloid only in the synovial membrane and fluid, and carpal tunnel, its absence in abdominal fat, and the lack of other manifestations of generalised amyloidosis (cardiomyopathy, malabsorption syndrome, macroglossia, etc.) and of Bence Jones myeloma (protein immunoelectrophoresis normal) raises the possibility that this is a form of amyloidosis which is peculiar to CRF treated by periodical haemodialysis.
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PMID:Amyloid arthropathy in patients undergoing periodical haemodialysis for chronic renal failure: a new complication. 406 86

In a longitudinal study, 21 patients with familial amyloidosis with polyneuropathy (FAP) were followed up for more than three years. Gastrointestinal symptoms ultimately evolved in all patients. In the advanced stage of the disease, 13 patients had diarrhea together with anal incontinence. Weight loss was very common and related to both malabsorption and motility disturbances with anorexia and also to muscular atrophy. Steatorrhea was found in 19 patients at least once during the follow-up. The duration of the disease was significantly correlated to fecal fat output. The conclusion was drawn that the gastrointestinal involvement in FAP is very common and of great clinical importance. The consequences of malnutrition also influence the outcome of the disease.
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PMID:Familial amyloidosis with polyneuropathy. A long-term follow-up of 21 patients with special reference to gastrointestinal symptoms. 666 47

Twenty-seven patients with familial amyloidosis with polyneuropathy were studied with regard to the morphology of the small intestine, and this was correlated to symptoms and malabsorption features. The mucosa was normal in all cases investigated by the dissecting microscope, the light microscope, and the scanning electron microscope. Amyloid was demonstrated in 83% of the cases by the presence of green birefringent material in the biopsy specimens stained with alkaline Congo red and examined in polarized light. Nineteen patients had steatorrhea, and 12 had pathological D-xylose test results. The degree of amyloid infiltration did not correlate with these data, nor did the symptomatic state correlate with the amount of amyloid in the biopsy specimens. The surface ultrastructure was normal when investigated by means of the scanning electron microscope in all patients except five in whom the glycocalyx was altered. As a group, however, those five did not differ in any respect from the rest of the patients. Rod-shaped microorganisms were shown to adhere to the surface in one patient. The results suggest that mechanisms other than bowel-wall deposition of amyloid cause the dysfunction of the gastrointestinal tract in familial amyloid polyneuropathy.
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PMID:Relationship between morphological findings and function of the small intestine in familial amyloidosis with polyneuropathy. 667 30


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