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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In view of the increasing pollution of our environment and forest decline, growing interest has been focused on aluminum toxicity. Aluminum is one of the most abundant metals and commonly present in tap water, beverages, food, cosmetics, and pharmaceutical preparations. Thus everybody is exposed to aluminum to a greater or lesser extent. It is now beyond any doubt that aluminum intoxication may cause encephalopathy, fracturing vitamin D resistant osteomalacia, and microcytic anemia in patients with chronic renal insufficiency as well as in experimental animals. The risk of aluminum intoxication has also to be considered in several other groups. These include elderly individuals with physiologically impaired excretory renal function who are treated with aluminum-containing antacids, patients with chronic liver disease, infants who are fed highly aluminum-contaminated formula at a time when their excretory renal function has not jet fully developed, patients on total parenteral nutrition, and, possibly, patients with Alzheimer's disease.
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PMID:[Aluminum toxicity]. 251 13

The consequences of renal functional impairment on aluminum (Al) excretion are not clear inasmuch as little is known about its glomerular filtration, tubular reabsorption, or secretion. The association of Al and the etiology of the dialysis encephalopathy syndrome and osteomalacia among patients with uremia suggests that renal functional impairment is a prerequisite for increased body Al stores. However, considerable evidence argues against the concept that tissue Al accumulation occurs as a simple consequence of renal failure. Many dialysis patients have high parathyroid hormone (PTH) concentrations that have been associated with neurologic abnormalities, bone disease, and anemia. The toxicity of PTH could be either direct or indirect by influencing the metabolism of potentially toxic substances such as Al. Our studies in normal rats suggest that gastrointestinal Al absorption and specific tissue burdens are enhanced by PTH, but not irreversibly, because the withdrawal of PTH resulted in Al egress. Dialysis patients are often treated with vitamin D analogs to prevent or control consequences of hyperparathyroidism and impaired 1,25-dihydroxycholecalciferol synthesis. Although some reports suggest that high bone Al in osteomalacia may be responsible for vitamin D resistance, our studies with normal rats suggest that its metabolites may also increase tissue Al burdens independent of PTH action. Thus, several factors operative in uremia other than impaired renal function may contribute to altered Al metabolism and, consequently, to its toxicity.
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PMID:Impaired renal function and aluminum metabolism. 661 95

Aluminium removal by desferrioxamine chelation has been demonstrated in three long-term haemodialysis patients with dialysis encephalopathy and fracturing renal osteodystrophy. Aluminium concentrations in serum and in both bone marrow and bone trabeculae, determined separately in transiliac biopsy specimens, fell significantly over the treatment period. Bone aluminium removal was confirmed by specific histochemical staining. In two patients osteomalacia disappeared, and in two patients osteitis fibrosa emerged but improved in one following vitamin D therapy. We conclude that desferrioxamine is capable of mobilising aluminium from bone and that the calcification defect in fracturing renal osteodystrophy may be overcome.
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PMID:Treatment of fracturing renal osteodystrophy by desferrioxamine. 687 34

Nine patients on long-term hemodialysis with dialysis encephalopathy were studied, with sex matched control subjects for eight of the patients. Each patient with dialysis encephalopathy and control subject were contemporaries in a similar dialysis environment. Rib and other fractures were found in excess in the patients with dialysis encephalopathy (p less than 0.005 and p less than 0.01). These patients had less radiographic hyperparathyroid bone disease, and no more osteopenia as measured by metacarpal thickness than did their control counterparts. Severe osteomalacia was documented by bone biopsy in four of te patients. In a retrospective review of clinical, biochemical and pharmacologic differences, the patients with dialysis encephalopathy were significantly older at the start of dialysis (45.6 years versus 38.6 years, p less than 0.02) and had higher mean concentrations of blood urea nitrogen (BUN) and lower serum hemoglobin in the first year of dialysis than the control subjects. Blood pressure weight, creatinine, calcium, phosphate, alkaline phosphatase and a number of transfusions did not differ significantly. There was no difference in prescribed vitamin D and elemental aluminum in phosphate binders. This study demonstrates that patients with dialysis encephalopathy had more rib fractures without more parathyroid or osteopenic bone disease than did the control subjects and suggests that the etiology of dialysis encephalopathy and osteomalacia is multifactorial.
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PMID:Dialysis encephalopathy and osteomalacic bone disease: a case-controlled study. 703 24

Administration of vitamins or metals may cause severe side effects. Retinoids (derivatives of vitamin A) used for the treatment of various skin disorders are teratogenic, hepatotoxic and may induce a substantial increase in serum lipids. A case report demonstrates that vitamin D supplementation in a patient under total parenteral nutrition can cause hypercalcemia. The isolated administration of vitamin B1, without concomitant vitamin B6 and nicotinamide may precipitate potentially life-threatening pellagra encephalopathy. Repeat blood transfusions may produce clinically overt organ hemosiderosis, e.g. cirrhosis of the liver, diabetes mellitus or myocardiopathy. The literature contains reports on a few cases of sarcoma associated with orthopedic metal implants. The controversial issue of the potential dangers of dental amalgams is briefly mentioned.
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PMID:[Vitamins and metals: possible hazards for humans]. 866 74

Various vitamins and minerals play roles in HIV infection. There is evidence that a number of HIV+ patients suffer from deficiencies in vitamins B12, B6, A, and D; folate, zinc and selenium; and carotenoids such as beta-carotene, betacryptoxanthin, and lutein. Vitamin B12 deficiency can result in peripheral neuropathy, encephalopathy, cognitive dysfunction and anemia. Lowered levels of vitamins B6 and A can lead to impaired immune function and, in the latter, an increased rate of perinatal transmission. Low levels of vitamin D have been linked to weight loss and wasting. Folate deficiencies are related to anemia, and low levels of zinc and/or selenium have been linked to impaired immune function. Information on the carotenoids, which have been found to be associated with cellular immune function, is mostly derived from recent research. Studies have shown that the levels of carotenoids are decreased in HIV+ people even in the early stages of infection, but the greatest deficiencies appeared in patients with the most advanced disease. Other clinical trials seem to indicate that administration of beta-carotene improves immune function, causing an increase in CD4 counts over baseline levels. Clinical trials conducted in response to all of these deficiencies have found multivitamin supplementation to be beneficial. Therefore, it is recommended that all HIV-infected patients receive a multivitamin supplement to assist in reversing the damage caused by these vitamin and mineral deficiencies.
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PMID:Update on vitamins, minerals, and the carotenoids. 1136 98

Calcium deficiency due to insufficient nutritional intake, poor intestinal absorption or excessive urinary loss leading to secondary hyperparathyroidism, increase of calcium influx into nerve cells causing cell death may lead to neuronal dysfunction and cell death as in dialysis encephalopathy with EEG changes and decrease of nerve conduction velocity in chronic renal failure and Alzheimer's disease in aging. Intracellular free calcium (Ca i) is increased in nerve cells showing neurofibrillar tangles associated with tau protein in Alzheimer's disease. Increase of Ca i facilitates presenilin mutation with consequent augmentation of short chain amyloid beta production which further increase Ca i. Peroxide radical production by amyloid beta and metals such as Fe, Cu and Mn is prompted by an increase of Ca i. Plasma membrane damage caused by lipid peroxidation further increases Ca i. Neurotoxic action of apolipoprotein E(4) increasing the risk for Alzheimer's disease may be explained by lipid peroxidation and rise of Ca i. Beneficial effect of estrogen in preventing Alzheimer's disease may also be explained by its anti-oxidant effect and stimulation of intestinal calcium absorption. By increasing calcium intake and administration of active form of vitamin D which cannot be sufficiently supplied by the aging kidney, one step forward should be made in the prevention and treatment of Alzheimer's disease.
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PMID:[Alzheimer disease and calcium]. 1557 64

In autumn 2004, many Japanese patients with renal failure developed cryptogenic encephalopathy by consuming sugihiratake mushroom, a Japanese delicacy. To elucidate the relationship between the cryptogenic cases and this mushroom, we conducted a multivariate analysis of metabolites in 'Probably Toxic' sugihiratake collected from the area of encephalopathy outbreaks, and 'Probably Safe' sugihiratake collected from unaffected areas using UPLC/ToF MS. The results indicate that the presence of milligram quantities of vitamin D-like compounds per 10 g of dried sugihiratake from the areas of encephalopathy outbreaks. Two hypotheses to induce the encephalopathy are proposed: the found metabolites are (1) vitamin D agonists, which induce acute and severe hypercalcemia and/or hyperammonemia and/or vitamin D toxicity, or (2) vitamin D antagonists, which induce acute and severe hypocalcemia.
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PMID:Sugihiratake mushroom (angel's wing mushroom)-induced cryptogenic encephalopathy may involve vitamin D analogues. 1714 93

In 1960s and 1970s when hemodialysis therapy was started in Japan, calcium carbonate was used as a phosphate binder and as the purpose of calcium supplement. Aluminum preparations were widely used in Japan, Europe and United states since the end of 1970s, when these drugs were reported as a strong phosphate binder. After that, some adverse effects such as encephalopathy and bone lesions attributed to Aluminum administration have become serious problems in dialysis patients. As a result, Aluminum administration was prohibited in 1992 in Japan. Oral vitamin D pulse therapy was developed in 1990s as a treatment for secondary hyperparathyroidism in Japan, hypercalcemia have been occurred easily by combination use of vitamin D preparations and calcium carbonate. Since the 2000s, various complications, such as ectopic calcifications, cardiovascular diseases, and reduced life expectancy, which are associated with hypercalcemia and hyperphosphatemia have been clarified. Therefore, sevelamer hydrochrolide, that is non calcium phosphate binder, became available from 2003. Moreover, Lanthanum carbonate, that is another type of non calcium phosphate binder, was effective in Europe and United States, and also developing in Japan. However, there are not any phosphate binders which solved all clinical problems such as phosphate adsorptive power, digestive symptoms, and organ accumulation.
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PMID:[Management of phosphate in chronic kidney disease--Chemistry and history of phosphate binder]. 1918 59

This review is an update of the long-term follow-up of nutritional and metabolic issues following bariatric surgery, and also discusses the most recent guidelines for the three most common procedures: adjustable gastric bands (AGB); sleeve gastrectomy (SG); and roux-en-Y gastric bypass (GBP). The risk of nutritional deficiencies depends on the percentage of weight loss and the type of surgical procedure performed. Purely restrictive procedures (AGB, SG), for example, can induce digestive symptoms, food intolerance or maladaptative eating behaviours due to pre- or postsurgical eating disorders. GBP also has a minor malabsorptive component. Iron deficiency is common with the three types of bariatric surgery, especially in menstruating women, and GBP is also associated with an increased risk of calcium, vitamin D and vitamin B12 deficiencies. Rare deficiencies can lead to serious complications such as encephalopathy or protein-energy malnutrition. Long-term problems such as changes in bone metabolism or neurological complications need to be carefully monitored. In addition, routine nutritional screening, recommendations for appropriate supplements and monitoring compliance are imperative, whatever the bariatric procedure. Key points are: (1) virtually routine mineral and multivitamin supplementation; (2) prevention of gallstone formation with the use of ursodeoxycholic acid during the first 6 months; and (3) regular, life-long, follow-up of all patients. Pre- and postoperative therapeutic patient education (TPE) programmes, involving a new multidisciplinary approach based on patient-centred education, may be useful for increasing patients'long-term compliance, which is often poor. The role of the general practitioner has also to be emphasized: clinical visits and follow-ups should be monitored and coordinated with the bariatric team, including the surgeon, the obesity specialist, the dietitian and mental health professionals.
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PMID:Medical follow up after bariatric surgery: nutritional and drug issues. General recommendations for the prevention and treatment of nutritional deficiencies. 2015 42


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