{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,24]],"date-time":"2023-10-24T10:43:38Z","timestamp":1698144218494},"reference-count":14,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,7,11]],"date-time":"2006-07-11T00:00:00Z","timestamp":1152576000000},"content-version":"vor","delay-in-days":5580,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[1991,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The clinical constellation of leukocytosis, thrombocytosis, and low or absent stainable neutrophil alkaline phosphatase (NAP) is considered characteristic of chronic myelogenous leukemia (CML) [1]. CML with eosinophilic differentiation (eosinophilic leukemia) is well described [2], and leukemia and other clonal hematologic malignancies are associated with the syndrome of eosinophilic fasciitis [3]. We describe leukocytosis, thrombocytosis, eosinophilia, mild basophilia, and absent stainable NAP, initially suggesting the diagnosis of CML in a patient with the eosinophilia myalgia syndrome associated with L\u2010tryptophan use, a condition resembling eosinophilic fasciitis. Cytogenetic and molecular genetic studies failed to demonstrate a clonal proliferation of eosinophils.<\/jats:p>","DOI":"10.1002\/ajh.2830360411","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T12:08:38Z","timestamp":1172059718000},"page":"280-281","source":"Crossref","is-referenced-by-count":1,"title":["Absent neutrophil alkaline phosphatase in the eosinophilia myalgia syndrome associated with <scp>L<\/scp>\u2010tryptophan use"],"prefix":"10.1002","volume":"36","author":[{"given":"Jeffrry P.","family":"Jaffe","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elie","family":"Gertner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wesley","family":"Miller","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,11]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"crossref","first-page":"77","DOI":"10.1016\/S0308-2261(21)00550-6","article-title":"The clinical features of chronic granulocytic leukemia","volume":"6","author":"Spiers ASD","year":"1977","journal-title":"Clin Haematol"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1097\/00005792-197501000-00001"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0025-7125(16)30625-3"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.263.11.1502"},{"key":"e_1_2_1_6_2","first-page":"4806","article-title":"Clonal analysis using recombinant DNA probes from the X chromosome","volume":"47","author":"Vogelstein B","year":"1987","journal-title":"Cancer Res"},{"key":"e_1_2_1_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(58)91031-6"},{"key":"e_1_2_1_8_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM196005052621804"},{"key":"e_1_2_1_9_2","first-page":"1641","article-title":"Neutrophil alkaline phosphatase in hypophosphatemia","volume":"312","author":"Stinson RA","year":"1985","journal-title":"N Engl J Med"},{"key":"e_1_2_1_10_2","doi-asserted-by":"crossref","first-page":"1012","DOI":"10.1182\/blood.V58.5.1012.1012","article-title":"A clinicopathologic correlation of the idiopathic hypereosinophilic syndrome. 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