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

Refractory coeliac disease (RCD) is a rare diagnosis made after the exclusion of any disorder mimicking CD and after initial or subsequent failure of a strict gluten-free diet (GFD) to restore normal intestinal architecture. In the past, treatments such as steroids, cyclosporin and azathioprine have been tried, but literature on this subject consists mainly of case reports. Interleukin-10 (IL-10) may be beneficial in RCD because of its inhibitory effect on T-lymphocyte- and monocyte-driven immune responses. We performed a pilot, non-randomized, open label study to evaluate recombinant human IL-10 in RCD. IL-10 (8 mcg/kg) was administered subcutaneously, three times a week for 3 months in 10 RCD patients. Small bowel biopsies were taken at T = 0, T = 3 months and T = 9 months. The mucosal histopathology at 3 months was the primary end point for evaluation of efficacy. Evaluations of clinical features, malabsorption parameters and safety were made prior to, during and after treatment. Before treatment, all RCD patients had partial to total villous atrophy (Marsh III ABC). Two patients dropped out of the study: one because of headaches, the other because of thrombocytopenia. In the remaining eight patients, after 3 months of IL-10 treatment histology was unchanged in five patients, improved in two patients and deteriorated in one patient. Disappearance of villous atrophy was seen in only one patient. Three patients reported a clinical response, i.e. relief of fatigue, abdominal complaints and diarrhoea. After stopping IL-10 treatment the symptoms recurred. The laboratory parameters remained the same during treatment and in follow-up. In conclusion, in our study group of 10 RCD patients, IL-10 in the given dosage was not overall effective in our study group of RCD patients. Two dropped out because of side effects and in only one patient did we see a normalization of villous architecture.
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PMID:A pilot study of recombinant human interleukin-10 in adults with refractory coeliac disease. 1171 74

Malnutrition is a common complication of chronic diseases in children and may lead to growth impairment (stunting). Malnutrition in cystic fibrosis (CF) results from increased energy expenditure, decreased energy intakes, malabsorption of ingested nutrients because of pancreatic insufficiency and chronic inflammation. Malnutrition and high levels of inflammatory cytokines affect IGF-1 production through interrelated mechanisms. Nutritional support was shown to improve both nutritional status and outcome in CF. However, some nutrients have a direct effect on the disease. n-3 fatty acids supplementation is able to correct lipid abnormalities resulting from a primary mechanism. Moreover, n-3 fatty acids have a direct effect on the inflammatory response, decreasing eicosanoid synthesis and modulating nuclear transcriptional factors nuclear factor kappaB and peroxisome proliferator-activated receptors gamma. Nutritional support may be considered part of the care of the CF patient together with antibiotics, pancreatic enzymes and physiotherapy, influencing significantly the evolution of the disease.
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PMID:Nutrition and growth in cystic fibrosis. 1237 8

Gluten-sensitive enteropathy or, as it is more commonly called, celiac disease, is an autoimmune inflammatory disease of the small intestine that is precipitated by the ingestion of gluten, a component of wheat protein, in genetically susceptible persons. Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of celiac disease. Recent studies in the United States suggest that the prevalence of celiac disease is approximately one case per 250 persons. Gluten-sensitive enteropathy commonly manifests as "silent" celiac disease (i.e., minimal or no symptoms). Serologic tests for antibodies against endomysium, transglutaminase, and gliadin identify most patients with the disease. Serologic testing should be considered in patients who are at increased genetic risk for gluten-sensitive enteropathy (i.e., family history of celiac disease or personal history of type I diabetes) and in patients who have chronic diarrhea, unexplained anemia, chronic fatigue, or unexplained weight loss. Early diagnosis and management are important to forestall serious consequences of malabsorption, such as osteoporosis and anemia.
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PMID:Gluten-sensitive enteropathy (celiac disease): more common than you think. 1250 63

Primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) are chronic cholestatic liver diseases that affect 0.5 to 40 per 100,000 and 1 to 6 per 100,000 Americans, respectively. Prompt recognition and management of the clinical manifestations of these diseases is essential for the patients' well-being and ultimate outcome. Ursodeoxycholic acid (UDCA), 13 to 15 mg/kg per day, is the standard therapy for PBC and should be offered to every patient. It has been shown to slow progression of the disease and prevent the need for liver transplantation, which is the last recourse for patients with end-stage disease. However, there is no effective therapy for PSC yet. Patients are managed symptomatically, with surgical or endoscopic interventions as needed in cases of significant biliary obstruction. Complications of chronic cholestasis are seen in both PBC and PSC, with pruritus and fatigue being the most common complaints. The first choice for the treatment of pruritus is still cholestyramine, starting at 4 g/d. The pathogenesis of fatigue is poorly understood in this population; unrecognized hypothyroidism should be excluded. The use of antidepressants is currently under evaluation, but there is no specific therapy for fatigue as of yet. For prevention of severe osteoporosis, we recommend supplementation with 800 IU vitamin D and 1500 mg calcium/d. In patients with PBC and established osteoporosis, the use of alendronate and vitamin K appears to cause an increase in bone mineral density. Further studies are necessary before either of these drugs is routinely recommended. Finally, fat-soluble vitamin deficiencies are noted with more advanced disease. We recommend that serum levels be checked in high-risk patients, and that vitamins are replaced as appropriate with water-soluble supplements. However, other causes of malabsorption must be ruled out, including pancreatic insufficiency and celiac sprue.
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PMID:Treatment Options for Primary Biliary Cirrhosis and Primary Sclerosing Cholangitis. 1262 68

Skeletal muscle disorders manifested by muscle pain, fatigue, proximal weakness, and serum creatine kinase (CK) elevation have been reported in patients with selenium deficiency. The object of this report was to review the conditions in which selenium deficiency is associated with human skeletal muscle disorders and to evaluate the importance of mitochondrial alterations in these disorders. A systematic literature review using the Medline database and Cochrane Library provided 38 relevant articles. The main conditions associated with selenium deficiency fell into three categories: (1) insufficient selenium intake in low soil-selenium areas; (2) parenteral or enteral nutrition, or malabsorption; and (3) chronic conditions associated with oxidative stress, such as chronic alcohol abuse and human immunodeficiency virus (HIV) infection. In low soil-selenium areas, reversibility of muscle symptoms was similar after selenium supplementation and placebo administration, suggesting a role for other factors in the development of disease. In parenteral or enteral nutrition, or malabsorption, muscle symptoms improved after selenium supplementation in 18 of 19 patients (median delay: 4 weeks). The reason that only a minority of selenium-deficient patients present with skeletal muscle disorders is unclear and is possibly related to cofactors, such as viral infections and drugs. Prospective studies of selenium-deficient myopathies would be useful in critically ill patients, alcohol abusers, and HIV-infected patients.
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PMID:Skeletal muscle disorders associated with selenium deficiency in humans. 1276 76

In this case report, a 56-year-old woman with a reversible multiple organ disease with septic fever, arthritis, rash, weight loss, thrombocytopenia, severe disturbance of liver function, renal tubular dysfunction, general muscular weakness, pleural and pericardial effusions and elevated CRP, leukocytosis and a striking hyperferritinemia is presented. An autoimmune disease and a septic process were excluded. Because of the significantly decreased plasma phosphorus concentration (0.2 mmol/l), caused by malabsorption after Whipple's operation with lowered vitamin D and secondary hyperparathyroidism and by chronic alcoholism, severe phosphate deficiency was diagnosed. By substitution of phosphorus, all symptoms disappeared and laboratory findings normalized. Except for the patient's age, all criteria for the diagnosis of Still's disease were fulfilled. So we reflected upon Still's disease to be rather a disturbance of energy metabolism with secondary immunologic changes than an inflammatory rheumatic disease. Significant weight loss in Still's disease and osteopenia might be signs of decreased energy supply. Besides hypophosphatemia, deficiency of magnesium, which is involved in all ATP-dependent processes, and mitochondrial diseases cause disturbances of energy metabolism.
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PMID:[Adult Still's disease as a manifestation of severe hypophosphatemia. Still's disease--a disturbance of energy metabolism?]. 1282 5

Intolerance of gluten, resposible for Coeliac disease, is essentially shown by an auto-immune enteropathy, even if the cutaneous manifestation (herpetiform dermatitis) and perhaps certain neurological signs (cerebral syndrome, peripheral neuropathy) may be independent as well as associated with the intestinal illness. This affection is of immunological nature, occuring in a genetic field that predisposes to the illness (familial form: concordance of 70% in homozygote twins; 90% of patients show an HLA molecule of type DQ2, DQ8 in almost all the other cases. The exogenous factor is the gluten content contained in wheat, rye and barley, more precisely by the intermediary "the prolamines" which are the "reactive" element that induces a the same time an inflammatory reaction of type TH11 locally (expressed by the histological aspect of a duodenal biopsy evolving as villous atrophy) and a humoral response with production of anti-gliadine and anti-transglutaminase antibodies (the role of the latter enzyme is intervention in the local transformation of antigens to make them antigenic). It is an illness of adults as well as children and this point must now be emphasized. Recent epidemiological studies insist on a high prevalence (1/300 in Europe). Clinical expression, at the start very polymorphic and so misleading, before the appearance of the more classical signs of malabsorption and development, always feared, towards a lymphoma. These signs are haematological (anemia of various types, hyper platelets by hyposplenism, haemorrhagic signs) cutaneous (herpetiform dermatitis, cutaneous vasculitis) mucosal (aphtose), hepatic (cytolysis), neurophysical (fatigue, troubles of behaviour, cerebral syndrome, neuropathy) and osteo-articulitis (osteopenia, arthralgias, diffuse pains). The association of certain auto-immune illnesses must be emphasized (diabetes, Hashimoto thyroiditis, Gougerot disease, primitive biliary cirrhosis). To think early of the possibility of intolerance to gluten, is to give the means of a very easy diagnosis (measurement of anti-gliadin, anti-endomysium and anti-transglutaminase, and secondarily duodenal biopsy if necessary), and it is early elimination of gluten food which will make the various clinical manifestations disappear and so prevent the risk of evolution to a tumoral pathology.
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PMID:[A great imitator for the allergologist: intolerance to gluten]. 1513 80

The health effects of long-term ingestion of rare earth elements (REEs) on the villagers living in high-REE-background areas in South Jangxi Province, China were studied. Major health complaints from the REE area population included indigestion, diarrhea, abdominal distension, anorexia, weakness, and fatigue, especially after high-fat or high-protein intake. Liver function tests were conducted for adult villagers. Among them, 45 live in a heavy rare earth (HREE) area, 62 in a light rare earth (LREE) area, and 49 in the control area. Test results showed that serum total protein and globulin from both HREE and LREE areas, as well as albumin from the LREE area, were significantly lower (p < 0.01 - 0.01) compared to the results from the control area, whereas albumin from the HREE area showed no significant variance (p > 0.05). The chi-square test showed that Serum-glutamic pyruvic transaminase (SGPT) in both areas were not significant (p > 0.05), whereas the IgM in the HREE area was significantly elevated. It is our conclusion that long-term ingestion of REE affected activities of some digestive enzymes, causing malabsorption and indigestion, and might further lead to a low-protein effect for the villagers in the LREE area. However, the damage to the liver was rather mild. The elevation of IgM was probably the result of stimulation induced by the formation of a large amount of granules as a result of direct binding of REEs to globulin or albumin (combination of REEs with globulin or albumin).
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PMID:Investigation on liver function among population in high background of rare earth area in South China. 1585 27

Coeliac disease is a lifelong intolerance to the gluten found in wheat, barley and rye, and some patients are also sensitive to oats. The disease is genetically determined, with 10% of the first-degree relatives affected and 75% of monozygotic twins being concordant. Of the patients with coeliac disease 95% are human leucocyte antigen (HLA)-DQ2 or HLA-DQ8 positive. Characteristically, the jejunal mucosa becomes damaged by a T-cell-mediated autoimmune response that is thought to be initiated by a 33-mer peptide fragment in A2 gliadin, and patients with this disorder have raised levels of anti-endomysium and tissue transglutaminase antibodies in their blood. Coeliac disease is the major diagnosable food intolerance and, with the advent of a simple blood test for case finding, prevalence rates are thought to be approximately 1:100. Classically, the condition presented with malabsorption and failure to thrive in infancy, but this picture has now been overtaken by the much more common presentation in adults, usually with non-specific symptoms such as tiredness and anaemia, disturbance in bowel habit or following low-impact bone fractures. Small intestinal biopsy is necessary for diagnosis and shows a characteristically flat appearance with crypt hypoplasia and infiltration of the epithelium with lymphocytes. Diet is the key to management and a gluten-free diet effectively cures the condition. However, this commitment is lifelong and many aisles in the supermarket are effectively closed to individuals with coeliac disease. Compliance can be monitored by measuring antibodies in blood, which revert to negative after 6-9 months. Patients with minor symptoms, who are found incidentally to have coeliac disease, often ask whether it is necessary to adhere to the diet. Current advice is that dietary adherence is necessary to avoid the long-term complications, which are, principally, osteoporosis and small bowel lymphoma. However, risk of these complications diminishes very considerably in patients who are on a gluten-free diet.
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PMID:Coeliac disease: a diverse clinical syndrome caused by intolerance of wheat, barley and rye. 1631 85

Celiac disease is a gastrointestinal disorder characterized by inflammation, leading to injury to the mucosal lining of the small intestine. The inflammation occurs when gliadin, a protein found in such gluten-containing foods as wheat, rye, and barley, is ingested by genetically susceptible individuals. The mucosal damage and subsequent malabsorption of nutrients leads to various complications. Researchers estimate that more than 2 million people in the United States have celiac disease-a prevalence that is greater than was previously believed. Approximately 60,000 Americans are diagnosed annually with celiac disease. Until recently, diagnosis has been complicated by the fact that the indicators of celiac disease are nonspecific. However, because of the development of new, easy-to-administer serology tests, diagnosis has become much less complicated. After conducting a review of the literature, the authors recommend a serologic testing sequence for diagnosis of celiac disease and urge that adults and children with an assortment of symptoms be tested for this disease. Common signs and symptoms of celiac disease include anemia, arthralgia, fatigue, infertility, neuropathy, and weight loss, in addition to such gastrointestinal symptomatology as abdominal pain, anorexia, bloating, constipation, and diarrhea. The only treatment for patients with celiac disease remains a gluten-free diet.
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PMID:New strategies for diagnosis and management of celiac disease. 1658 82


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