Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Finger clubbing, protein-losing enteropathy, and iron deficiency were documented in three children with severe gastroesophageal reflux. One patient had Sandifer syndrome and the other two had the rumination syndrome. In each case, surgical repair of the gastroesophageal reflux resulted in immediate clearing of signs of the Sandifer syndrome, gastroesophageal reflux, and anemia and the return of serum protein levels to normal. There was definite regression of the finger clubbing during the ensuing year. It is suggested that finger clubbing, protein-losing enteropathy, Sandifer syndrome, and rumination be viewed as parts of an extended syndrome of unusual presentations of gastroesophageal reflux.
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PMID:Gastroesophageal reflux with protein-losing enteropathy and finger clubbing. 98 11

This is a case report of juvenile gastrointestinal polyposis involving the gastrointestinal system from the stomach to the rectum. Only few cases have been reported and extra-intestinal manifestations of this syndrome include macrocephaly, hepatosplenomegaly, hypotonia, clubbing of fingers, anemia and protein-losing enteropathy. The disease usually has a poor prognosis, and the children rarely live more than 2 years.
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PMID:Infantile Cronkhite-Canada syndrome?--Case report. 132 40

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.
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PMID:[Treatment of chronic diseases of the small intestine]. 172 19

Copper deficiency developed in a five-month-old prematurely born infant with an abdominal wall closure defect and a small bowel fistula under long-term parenteral nutrition. The first manifestations were typical bone changes including diffuse osteoporosis, delayed bone age, widened cupped metaphyses with beaks and a fracture, subperiosteal hematomas and ossifications in the shafts of long bones, and a diaphyseal fracture. Other findings that confirmed the diagnosis included edema of the limbs with pseudoparalysis, neurologic abnormalities, anemia, leukoneutropenia, and very low serum levels of copper and ceruloplasmin. Following initiation of copper supplementation, clinical, hematological and biological disorders resolved within a few days and roentgenologic bone abnormalities within four months. Copper deficiency develops only in the presence of specific risk factors, that are often combined in a single patient: inadequate stores due to prematurity, excessive loss due to chronic diarrhea, exudative enteropathy, a proximal stoma, or a biliodigestive fistula; and inadequate intake due to malabsorption or long-term exclusive parenteral nutrition (EPN). Appropriate copper supplementation is needed in all these high risk situations. Early, continuous copper supplementation is required for young children under EPN. Serum copper assays should be included among the periodically monitored biochemical parameters.
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PMID:[Nutritional copper deficiency. Apropos of a case]. 250 Aug 84

In contrast with traumatic intestinal perforation, the late sequelae of lesser small-bowel injury are not readily recognised. A protracted course of protein-losing enteropathy as an intermediate result of traumatic segmental small-intestinal ischaemia, and a fibrotic stricture with anaemia, intestinal obstruction and bezoar formation as a late result, are illustrated.
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PMID:Late presentation of small-bowel injury--hypoproteinaemia, anaemia and obstruction. A report of 2 cases. 334 Sep 71

This is a report of a case of juvenile gastrointestinal polyposis consisting of widespread juvenile polyps encountered from the stomach into the rectum. Only few cases have been reported, and extra intestinal manifestations include clubbing of fingers, macrocephaly, hypotonia, hepatosplenomegaly, anemia, and protein-losing enteropathy. The outcome is usually dismal, the children barely becoming older than 2 years. Modern fibreoptic endoscopy with polypectomies performed via the upper and lower gastrointestinal intestinal tracts and via a midbowel ileostomy may offer a viable form of management.
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PMID:Juvenile gastrointestinal polyposis or the infantile Cronkhite-Canada syndrome. 379 50

A case of malabsorption and subtotal villous atrophy secondary to pulmonary and intestinal tuberculosis is reported. The patient was a 21-year-old Chinese girl who had active pulmonary tuberculosis, malabsorption, subtotal villous atrophy, atrophic gastritis with hypochlorhydria, ileal stricture, and a severe non-specific anaemia. There was also evidence to suggest protein-losing enteropathy. The association of subtotal villous atrophy and atrophic gastritis with tuberculosis is discussed. When antituberuclous therapy was instituted, improvement was marked not only clinically but also in the tests for intestinal absorption and in the jejunal mucosa.
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PMID:Malabsorption and subtotal villous atrophy secondary to pulmonary and intestinal tuberculosis. 542 99

Multifocal idiopathic stenosing enteritis has been described as a relapsing disease affecting the small bowel. The main anatomical characteristics are multiple non-specific inflammatory strictures. Six cases (4 men, 2 women) presenting this disorder were followed up for 3 to 22 years. Five patients were young. Iterative obstruction or chronic diarrhea and loss of weight were the outstanding clinical features. Hyposideremic anemia and protein-losing enteropathy were common. The anatomical substrate was numerous (2-19) short annular strictures situated in the ileum (75 p. 100). These strictures presented shallow ulcerations and underlying fibrosis which never extended beyond the submucosa. The small bowel wall was otherwise normal and did not show mucosal or vascular abnormalities at microscopic examination. In case of relapse, strictures developed distal to or in close contact with previous suture lines. Cultures for pathogenic bacteria were constantly negative. The natural history of these 6 cases and of 7 other previously published cases suggests that this disease is an autonomous disorder which must be differentiated from other inflammatory bowel disease entities such as Crohn's disease or tuberculosis.
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PMID:[Multifocal cryptogenetic stenosing enteritis: an autonomous entity?]. 652 38

In Dakar, through histopathological biopsies, the author looked for duodenal alterations in four parasitosis: giardiasis, strongyloidiasis, hookworms and ascaridiosis. He gives an overall survey on malabsorption in relation with intestinal parasitosis, including intestinal capillariosis and coccidiosis. He recalls basic concepts concerning each of these parasitic diseases, with a special mention to mucosal invasion and endogenous self reinfection during some parasitosis; he also emphasizes the importance of some diagnosis techniques (such as examination of duodenal fluid in relation to giardiasis). Anatomical lesions (villi atrophia and chorion cellular infiltration) were the starting point to study such as intestinal malabsorption. But these lesions are neither specific nor regular. Other causes must be determined such as direct action of the parasite, bacterial overgrowth, exudative enteropathy. The role played by host factors seems to be of the utmost importance in giardiasis and strongyloidiasis (antibody deficiency proteinic malnutrition). The part played by the parasite biomass is unquestionable in hookworm disease (hypoalbuminuria, anemia) and a great number of worms in ascaridiasis worsens a preexisting condition of malnutrition. Finally, intestinal parasitosis, with a special mention to giardiasis and strongyliasis, may be responsible for a malabsorption syndrome. They must be identified through reliable diagnosis tests, prior to referring to "idiopathic malabsorption syndrome in Tropical areas".
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PMID:[Malabsorption syndrome and intestinal parasitosis]. 664 78

Juvenile polyposis is an uncommon condition characterized by the development of multiple juvenile polyps, predominantly in the colon but also in the rest of the gastrointestinal tract. The condition usually presents in childhood; only 15 per cent of patients present as adults. The rarer and often fatal form, namely, juvenile polyposis of infancy, is typified by diarrhoea, protein-losing enteropathy, bleeding and rectal prolapse. The more common form of juvenile polyposis (affecting the colon, stomach and small bowel) occurs in the first or second decade with rectal bleeding and anaemia. A family history of the condition is found in 20-50 per cent of patients with apparently an autosomal dominant trait. The gene for juvenile polyposis has not yet been identified. Epithelial dysplasia is common and the cumulative risk of colorectal cancer is > 50 per cent. Various extracolonic abnormalities may also occur. Most patients are treated surgically for colonic polyps, although endoscopic polypectomy is also an option. The rest of the gastrointestinal tract should be screened as should asymptomatic first-degree relatives.
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PMID:Juvenile polyposis. 788 43


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