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)

Literature on the various manifestations of the selenium deficiency in humans and animals is presented. Mechanisms of the biological effects of selenium brought about by glutathione peroxidase are considered. Biogeochemical anomalies, parenteral nutrition, malabsorption syndromes as conditions for the development of hyposelenosis are characterized as well as their manifestations (white-muscular disease, myopathies, cardiomyopathies, Keshan disease, Kashin-Beck disease). Selenium deficiency facilitates the development of the ischemic heart disease, myocardium infarction, certain types of malignancy and so on. The attention is drawn to the link of the selenium deficiency with imbalance of other trace elements.
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PMID:[Hyposelenoses]. 212 81

Selenium deficiency is a rare cause of cardiomyopathy that may be encountered by the forensic pathologist. Selenium deficiency is associated with a cardiomyopathy, myopathy and osteoarthropathy. In Asia and Africa, dietary selenium deficiency is associated with a cardiomyopathy known as Keshan disease and an osteoarthropathy called Kashin-Beck disease. Chronic selenium deficiency may also occur in individuals with malabsorption and long term selenium-deficient parenteral nutrition. Selenium deficiency causes myopathy as a result of the depletion of selenium-associated enzymes which protect cell membranes from damage by free radicals. We present a case of fulminant heart failure in a middle aged woman with a complex medical and surgical history including documented malabsorption and selenium deficiency. Pathological examination of the heart showed features consistent with Keshan disease.
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PMID:Fulminant heart failure due to selenium deficiency cardiomyopathy (Keshan disease). 1184 34

The essential trace mineral selenium is of fundamental importance to human health. It is incorporated in the proteome in the forms of the genetically encoded amino acids selenocysteine and selenomethionine, which are the characteristic components of selenoproteins (SeP) such as glutathione peroxidases (GPx), thioredoxin reductases and iodothyronine deiodinase families. Thyroid is especially sensitive to selenium deficiency, because SeP can modify thyreocytes function by acting as antioxidants and modifying redox status and thyroid hormone metabolism. SeP are also involved in apoptosis, cell growth and modification of the action of cell signalling systems and transcription factors. Some intestinal GPx modulate apoptosis by removing the cells affected by oxidative damage preserving tissue integrity. The malfunctioning of the GPx antioxidant system in intestinal mucosa can trigger a continuous cycle of reactive oxygen species and inflammation. Selenium deficiency is a risk factor, due to the malabsorption, in celiac disease (CD) because the inflammatory damage affects the small intestine; this deficiency can modulate SeP genes expression, with consequent reiteration of inflammation and increase of mucosal damage. In active CD, overexpression of interleukin-15 (IL-15) may increase activation of effector mechanisms of epithelial damage by stimulating T helper 1 cytokine proliferation and production and intraepithelial lymphocytes cytotoxicity by protecting these lymphocytes from apoptosis. Blocking IL-15 has the potential to provide new therapeutic tools to prevent both tissue damage and complication of CD such as autoimmune thyroid diseases (AITD) where IL-15 expression is also increases. In view of the role played by SeP in apoptosis inhibition, the presence of environmental factors such as selenium deficiency can be considered an important direct factor of thyroidal damage in development of AITD.
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PMID:[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]. 1903 61