Enhanced excretion of urinary leukotriene E4 in mevalonic aciduria is not caused by an impaired peroxisomal degradation of cysteinyl leukotrienes

Journal of Inherited Metabolic Disease

Volumn 20, Issue 5, 1997, Pages 721-722

  Mayatepek, E ^a  

^a UNIVERSITY HOSPITAL HEIDELBERG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

LEUKOTRIENE E4; MEVALONIC ACID;

ACIDURIA; ARTICLE; CLINICAL ARTICLE; CONTROLLED STUDY; ENZYME DEFICIENCY; HUMAN; URINARY EXCRETION;

CYSTEINE; HUMANS; LEUKOTRIENE E4; LEUKOTRIENES; MEVALONIC ACID; MICROBODIES; PHOSPHOTRANSFERASES (ALCOHOL GROUP ACCEPTOR);

EID: 0030800465     PISSN: 01418955     EISSN: None     Source Type: Journal    
DOI: 10.1023/A:1005351215690     Document Type: Article

References (4)

1. Biardi L, Sreedhar A, Zokaei A, et al (1994) Mevalonate kinase is predominantly localised in peroxisomes and is defective in patients with peroxisome deficiency disorders. J Biol Chem 269: 1197-1205.
2. Hoffmann GF, Charpentier C, Mayatepek E, et al (1993) Clinical and biochemical phenotype in eleven patients with mevalonic aciduria. Pediatrics 91: 915-921.
3. 4 in patients with mevalonate kinase deficiency. J Pediatr 123: 96-98.
4. Mayatepek E, Lehmann WD, Fauler J, et al (1993b) Impaired degradation of leukotrienes in patients with peroxisome deficiency disorders. J Clin Invest 91: 881-888.