Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four weanling swine fed for 4 weeks a commercial ration adequate in selenium and vitamin E, but supplemented with 0.5% silver acetate, developed lesions typical of selenium-vitamin E deficiency. Clinically, the pigs fed this high level of silver had anorexia, diarrhea, and growth depression; 3 of 4 pigs died. At necropsy, hepatic lesions of hepatosis dietetica were present in 4 of 4 silver-fed pigs, and 1 of 4 pigs had cardiac and skeletal muscle lesions characteristic of selenium-vitamin E deficiency. Development of lesions and mortality was prevented in 2 pigs fed the silver diet supplemented with alpha-tocopherol (100 IU/kg of diet), but not in 2 pigs fed the ration supplemented with selenium as selenite (1 ppm). Four pigs fed a lower dose level of silver (0.2% silver acetate) for 6 weeks failed to develop clinical or pathologic features of selenium-vitamin E deficiency. However, hepatic selenium content was significantly increased in pigs fed the silver-supplemented ration.
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PMID:Induction of lesions of selenium-vitamin E deficiency in pigs fed silver. 99 68

Seventy-five ducklings belonging to nine species of wild ducks were kept in a large floor pen. At about 8 weeks of age, a pintail and two shovelers showed clinical signs of anorexia, diarrhea, and leg weakness before death. Gross pathologic alterations included a pale discoloration of gizzard musculature and pale streaks in the leg muscle. Microscopic alterations in gizzard smooth-muscle cells included hyalinization, mineralization of sarcoplasmic debris in necrotic smooth-muscle fibers, and macrophagic invasion and phagocytosis of sarcoplasmic debris. Similar alterations were present in sections of skeletal leg muscle. The pathological lesions were characteristic of selenium-vitamin E deficiency.
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PMID:Selenium-vitamin E deficiency in captive wild ducks. 687 Jul 28

Over a period of 5 mo, seven out of eight American white pelicans (Pelecanus erythrorhynchos) housed on a spring-fed pond at a zoo died or were euthanized. Clinical signs included inability to stand, anorexia, and weight loss. Clinicopathologic findings included heterophilic leukocytosis and elevated creatine kinase and aspartate aminotransferase. Histopathologic findings on all pelicans demonstrated severe, chronic, diffuse rhabdomyofiber degeneration and necrosis, making vitamin E deficiency a differential diagnosis despite routine supplementation. Based on tissue and pond water assays for the cyanobacterial toxin, microcystin, toxicosis is suspected as the inciting cause of death in these cases. We hypothesize that vitamin E exhaustion and resultant rhabdomyodegeneration and cardiomyopathy were sequelae to this toxicosis.
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PMID:MYONECROSIS AND DEATH DUE TO PRESUMED MICROCYSTIN TOXICOSIS IN AMERICAN WHITE PELICANS (PELECANUS ERYTHRORHYNCOS). 3254 72