{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T13:29:57Z","timestamp":1762003797446},"reference-count":0,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2003,8,18]],"date-time":"2003-08-18T00:00:00Z","timestamp":1061164800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Inher Metab Disea"],"published-print":{"date-parts":[[2005,6]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Several markers have been developed for the biochemical monitoring of Gaucher disease. Three of the most commonly used markers are acid phosphatase, angiotensin\u2010converting enzyme (ACE) and chitotriosidase. The rationale for using all three concurrently is not clear. A retrospective study was therefore carried out on data collected from 28 paediatric patients treated with enzyme replacement therapy. All three markers fell with time. However, chitotriosidase showed the steepest time trend, the largest trend by case interaction, and the lowest residual variance, making it the most reliable of the three. ACE correlated strongly with chitotriosidase, but acid phosphatase did not correlate well with either and also had the largest residual variance, indicating that it was too \u2018noisy\u2019 to be informative. The absence of a \u2018gold standard\u2019 for assessing Gaucher disease complicates the interpretation of these findings, but they suggest that acid phosphatase be dropped from routine clinical practice, and that chitriosidase be used in preference to ACE.<\/jats:p>","DOI":"10.1007\/s10545-005-0585-9","type":"journal-article","created":{"date-parts":[[2005,5,17]],"date-time":"2005-05-17T12:50:32Z","timestamp":1116334232000},"page":"585-592","source":"Crossref","is-referenced-by-count":31,"title":["Evaluation of three biochemical markers in the monitoring of Gaucher disease"],"prefix":"10.1002","volume":"28","author":[{"given":"A.","family":"Vellodi","sequence":"first","affiliation":[{"name":"Metabolic Unit  UK"},{"name":"Metabolic Unit Great Ormond Street Hospital for Children NHS Trust  Great Ormond St London WC1N 3JH UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y.","family":"Foo","sequence":"additional","affiliation":[{"name":"Chemical Pathology Great Ormond Street Hospital for Children NHS Trust  London"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T. J.","family":"Cole","sequence":"additional","affiliation":[{"name":"Centre for Paediatric Epidemiology and Biostatistics Institute of Child Health  London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2003,8,18]]},"container-title":["Journal of Inherited Metabolic Disease"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1007\/s10545-005-0585-9","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1007\/s10545-005-0585-9","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,9,15]],"date-time":"2023-09-15T00:22:28Z","timestamp":1694737348000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1007\/s10545-005-0585-9"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2003,8,18]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2005,6]]}},"alternative-id":["10.1007\/s10545-005-0585-9"],"URL":"https:\/\/doi.org\/10.1007\/s10545-005-0585-9","archive":["Portico"],"relation":{},"ISSN":["0141-8955","1573-2665"],"issn-type":[{"value":"0141-8955","type":"print"},{"value":"1573-2665","type":"electronic"}],"subject":[],"published":{"date-parts":[[2003,8,18]]}}}