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Blood, 1 May 2006, Vol. 107, No. 9, pp. 3489-3491. Prepublished online as a Blood First Edition Paper on January 26, 2006; DOI 10.1182/blood-2005-10-4148. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-10-4148v1 107/9/3489    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Comenzo, R. L. Articles by Teruya-Feldstein, J. Search for Related Content PubMed PubMed Citation Articles by Comenzo, R. L. Articles by Teruya-Feldstein, J. Related Collections Immunobiology Neoplasia Brief Reports Clinical Trials and Observations Related Letter in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CLINICAL TRIALS AND OBSERVATIONS Brief report Seeking confidence in the diagnosis of systemic AL (Ig light-chain) amyloidosis: patients can have both monoclonal gammopathies and hereditary amyloid proteins Raymond L. Comenzo, Ping Zhou, Martin Fleisher, Bradly Clark, and Julie Teruya-Feldstein From the Hematology Service, Division of Hematologic Oncology, Department of Medicine, Sloan-Kettering Institute, and the Department of Pathology and the Department of Clinical Laboratories, Memorial Sloan-Kettering Cancer Center, (MSKCC) New York, NY. Investigators in the United Kingdom have shown that hereditary amyloidosis can be misdiagnosed as Ig light-chain (AL) amyloidosis because family history is an ineffective screen, and tissue staining used to type amyloid is unreliable. Misdiagnosis of AL can lead to inappropriate use of chemotherapy and failure to diagnose a hereditary disease. Over a 3-year period we sought to determine how often both possible sources of amyloidosis occurred in the same patient. We employed an algorithm based on established data and patterns of amyloidosis in order to focus the screening effort. Of 178 consecutive patients referred for amyloidosis, 54 were screened by polymerase chain reaction techniques with primers designed to detect transthyretin, apolipoprotein AI, apolipoprotein AII, fibrinogen A, and lysozyme variants. Three patients (6% of those screened and 2% of symptomatic patients) had both a monoclonal gammopathy and a hereditary variant. These results justify further study of screening for hereditary variants in patients with apparent AL, and highlight the need for practical techniques for identifying fibrils extracted from tissue. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Letter in Blood Online: Misclassification of amyloidosis is unwarranted Alan Solomon, Charles L. Murphy, Per Westermark, and Raymond L. Comenzo Blood 2006 108: 776-777. [Full Text] [PDF] This article has been cited by other articles: F. Bergesio, A. M. Ciciani, M. Santostefano, R. Brugnano, M. Manganaro, G. Palladini, A. M. D. Palma, M. Gallo, P. L. Tosi, M. Salvadori, et al. Renal involvement in systemic amyloidosis--an Italian retrospective study on epidemiological and clinical data at diagnosis Nephrol. Dial. Transplant., June 1, 2007; 22(6): 1608 - 1618. [Abstract] [Full Text] [PDF] L. M. Dember Amyloidosis-Associated Kidney Disease J. Am. Soc. Nephrol., December 1, 2006; 17(12): 3458 - 3471. [Abstract] [Full Text] [PDF] G. Merlini and M. J. Stone Dangerous small B-cell clones Blood, October 15, 2006; 108(8): 2520 - 2530. [Abstract] [Full Text] [PDF] A. Solomon, C. L. Murphy, P. Westermark, and R. L. Comenzo Misclassification of amyloidosis is unwarranted. Blood, July 15, 2006; 108(2): 776 - 777. [Full Text] [PDF]

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