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)

A patient is presented who developed a granulomatous hepatitis and pleuritis approximately 7 months after an ileal bypass procedure for morbid obesity. Although the etiological agent was presumed to be Mycobacterium tuberculosis no pathogenic organism was grown from the liver, pleura, bone marrow, sputum, or gastric aspirate. The possibly increased susceptibility of these patients to mycobacterial infections is discussed. The value of obtaining serum levels of ethambutol, isoniazid, and rifampin, in patients with malabsorption is stressed. Although this patient seemed to respond to antituberculous therapy, other possible causes for the granulomatous process are explored.
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PMID:Granulomatous hepatitis and pleuritis after ileal bypass for obesity. 71 72

A case of alpha-chain disease is presented. Diagnosis was clinched by the discovery of typical heavy alpha-chains on analysis of serum proteins. The clinical picture included non-gluten-dependent semi-coeliac malabsorption, Hippocratic fingers, flattened villi, plasma cell infiltration of the jejunal mucosa, alpha- and beta-globulin dysprotidaemia, and abdominal masses; these signs are indicative of, but not conclusive evidence of alpha-chain disease. The presence of Coccidioides organules in the mucosa and glandular tuberculosis rises aetiopathogenetic questions that suggest that due attention be given to microbiological examination. Rapid progression to neoplasia following immunodepressive management underscores the risks associated with the administration of immunodepressors in patients with immunitary deficiencies. It is still not clear whether alpha-chain disease should be regarded as a self-perpetuating immunoproliferative disease, or as a form neoplasia ab initio, with a protracted, though of inevitably fatal, course.
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PMID:[Clinico-pathological study of a case of alpha chain disease]. 82 71

Small bowel enteroscopy in 1991 is now feasible in two clinical situations: in the case of malabsorption or diffuse intestinal disease, it is easier to visualise the small bowel with the "push enteroscopy methods". The most proximal and distal ends of the small intestine can be viewed through standard instruments or better with videocoloscope beyond the ligament of Treitz. The ileocecal valve can be intubated after total colonoscopy for the evaluation of Crohn's disease, tuberculosis and small bowel lymphoma. In the case of occult gastrointestinal hemorrhage small bowel enteroscopy now permits visualization of large amounts of small intestinal. When the gastrointestinal bleeding is severe, we recommend intraoperative enteroscopy. When the bleeding is not severe and chronic, it is possible to perform a non surgical total small bowel enteroscopy with an enteroscope or videoenteroscopoe. Prototypes are under development. The procedure is safe an can be performed on an outpatient basis. The limitations of the procedure are the impossibility of intervention and inability to inspect the total mucosal surface. It is not a "first line" or "second line" investigation in these situations. It should be considered after previous investigations have been negative. Push enteroscopy should be performed by general endoscopists, non surgical and total enteroscopy should be reserved, for instance for skills and motivated team endoscopists.
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PMID:[Endoscopy of the small intestine in 1991: is it the end of the tunnel?]. 141 52

Four patients with acute paracoccidioidomycosis, hypoalbuminemia, ascites and associated infections are reported. They have been admitted to hospital 35 times, 4 of them due to active paracoccidioidomycosis, 14 to associated infections, 14 to ascites, edema and diarrhoea and 3 to herniorrhaphy. Two of them recovered after sepsis and central nervous system, muscular and subcutaneous cryptococcosis. The remaining two died. One had infectious diarrhoea (S. flexneri), peritoneal tuberculosis and sepsis (S. epidermidis); the other had bacterial meningitis, erysipelas, beta-hemolytic Streptococcus sepsis and miliary tuberculosis. Their immunodeficiency was attributed to enteric protein loss and/or malabsorption and malnutrition and was recognized by reduced response to delayed hypersensitivity skin tests in four patients and hypogammaglobulinemia in three of them. The authors discuss the need for prospective studies to be carried out, aiming at the mechanisms involved in secondary infections. Alternatives for maintaining the patients' adequate nutritional state should be investigated, to guarantee proper immune response and thus the ability to control intervening infections in patients with juvenile paracoccidioidomycosis.
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PMID:Immunodeficiency secondary to juvenile paracoccidioidomycosis: associated infections. 148 Feb 6

To define the extent and nature of mycobacterial infection in patients on an adult dialysis unit whose catchment population contains a large proportion of non-Caucasian subjects, a retrospective survey of all new patients accepted onto our maintenance dialysis programme between January 1987 and December 1989 was carried out. Twenty-six Asian, 13 Afro-Caribbean, two Oriental and 170 Caucasian patients were accepted onto the dialysis programme in the three-year recruitment period. Eight of the 26 Asian patients, but none of the others, had developed mycobacterial infection by the end of December 1990. One patient had a cerebral tuberculoma with miliary mottling on chest X-ray, one pulmonary tuberculosis, one tuberculous adenitis and 5 tuberculous peritonitis (four due to Mycobacterium tuberculosis and one Mycobacterium kansasii). All the patients had been living in the UK for an average of 15 (range 6-24) years, with no known recent exposure to tuberculosis. Five patients are now alive and well, one developed malabsorption following M. kansasii peritonitis, but two with tuberculous peritonitis died before treatment could be instituted. Mycobacterial infections were associated with a high level of mortality and morbidity. No Asian patient developed mycobacterial infection during post-transplant immunosuppressive therapy in the study period, probably because of the routine anti-tuberculous chemoprophylaxis employed in this group of patients. The diagnosis of mycobacterial infection should be suspected when an Asian dialysis patient develops a pyrexia of unknown origin. It is likely, though not proven, that anti-tuberculous chemoprophylaxis might reduce this high incidence of tuberculous infection in Asian dialysis patients.
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PMID:Mycobacterial infection is an important infective complication in British Asian dialysis patients. 168 37

Significant differences exist in the prevalence of most gastroenterological emergencies in tropical compared with temperate countries. Both ethnic and environmental (often clearly defined geographically) factors are relevant. The major oesophageal lesions which can present acutely in tropical countries are varices and carcinoma; bleeding and obstruction are important sequelae. Peptic ulcer disease (and its complications), often associated (not necessarily causally) with Helicobacter pylori infection, has marked geographical variations in incidence. Emergencies involving the small intestine are dominated by severe dehydration, and its sequelae, resulting from secretory diarrhoea, most notably cholera. However, enteritis necroticans ('pig bel' disease), paralytic ileus (sometimes caused by antiperistaltic agents) and obstruction (secondary to luminal helminths, volvulus and intussusception) are other important problems, especially in infants and children. Enteric fever is occasionally complicated by perforation and haemorrhage; the former (which is notoriously difficult to manage) is accompanied by significant mortality. Ileocaecal tuberculosis is a major cause of right iliac fossa pathology--sometimes associated with malabsorption; amoeboma is an important clinical differential diagnosis. The colon can be involved in invasive Entamoeba histolytica infection (which, like complicated enteric fever, is difficult to manage if the fulminant form, with perforation, ensues), shigellosis, volvulus and intussusception. Acute colonic dilatation occasionally follows Salmonella sp., Shigella sp., Campylobacter jejuni, Yersinia enterocolitica and rarely E. histolytica infections. Acute hepatocellular failure is a major cause of morbidity and mortality in the tropics and subtropics. It usually results from viral hepatitis (HBV, sometimes complicated by HDV, and HCV), but there is a long list of differential diagnoses. Hepatotoxicity resulting from herbs, chemotherapeutic agents or alcohol also occurs not infrequently. Chronic liver disease and its sequelae (often long-term results of viral hepatitis) are commonplace. Haematemesis and hepatocellular failure are usually very difficult to manage due to a lack of sophisticated support techniques in developing countries. Invasive hepatic amoebiasis usually responds well to medical management; however, spontaneous perforation can occur and the consequences of this are serious. Pyogenic liver abscess, although far less common than amoebic 'abscess', carries a bad prognosis whatever the method(s) of management. Hydatidosis and schistosomiasis also involve the liver, and helminthiases are important in the context of biliary tract disease. Gall stones are unusual in most tropical settings. Acute pancreatitis is overall unusual, but chronic calcific pancreatitis can present as an acute abdominal emergency.
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PMID:Gastroenterological emergencies in the tropics. 176 26

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.
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PMID:Intrinsic factor secretion and cobalamin absorption. Physiology and pathophysiology in the gastrointestinal tract. 177 33

138 Indian patients with megaloblastic haemopoiesis were studied. All were lifelong vegetarians. The diagnosis was nutritional cobalamin deficiency in 95 and pernicious anaemia in 20; only 4 patients had folate deficiency. A third had intestinal malabsorption, 20 had features of osteomalacia, and 87 were iron deficient. Tuberculosis was diagnosed in 17. Cobalamin deficiency may have contributed to these complications via intestinal malabsorption and impaired bacterial killing of phagocytosed bacilli by cobalamin-deficient macrophages. The frequency of pernicious anaemia was the same in Indian subjects as in Caucasians.
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PMID:Megaloblastic anaemia in a vegetarian Hindu community. 286 24

We describe a patient who underwent inadvertent gastroileostomy, and subsequently developed malabsorption, granulomatous hepatitis, arthritis, and reactivation of tuberculosis accompanied by circulating immune complexes and lowered C1q. Surgical correction resulted in marked improvement, with disappearance of arthritis, return to normal of complement levels, and absence of demonstrable circulating immune complexes. Arthritis has not been documented in the spectrum of abnormalities described after gastroileostomy.
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PMID:"Bypass arthritis" after gastroileostomy. 337 26

A 14 year-old boy with coeliac disease and poorly treated diabetes mellitus and pulmonary tuberculosis due to INH resistant BK presented with a permanent malabsorption of rifampicin. Pharmacokinetics of rifampicin was studied after oral administration and intravenous injection. Treatment of diabetes and coeliac disease did not improve the situation. Tuberculosis was cured by pyrazinamide and ethambutol.
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PMID:[Permanent malabsorption of rifampicin in a diabetic with celiac disease]. 377 4


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