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Discordance between serum cardiac biomarker and immunoglobulin‐free light‐chain response in patients with immunoglobulin light‐chain amyloidosis treated with immune modulatory drugs
Author(s) -
Dispenzieri Angela,
Dingli David,
Kumar Shaji K.,
Rajkumar S. Vincent,
Lacy Martha Q.,
Hayman Suzanne,
Buadi Frances,
Zeldenrust Stephen,
Leung Nelson,
DetweilerShort Kristen,
Lust John A.,
Russell Stephen J.,
Kyle Robert A.,
Gertz Morie A.
Publication year - 2010
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.21822
Subject(s) - medicine , discontinuation , tolerability , al amyloidosis , biomarker , population , antibody , drug , gastroenterology , immunology , adverse effect , pharmacology , immunoglobulin light chain , biology , biochemistry , environmental health
We evaluated the capability of soluble cardiac biomarkers to predict tolerability and outcomes of IMiD‐containing treatments among 106 patients treated on clinical trials. Baseline elevations in troponin T (TnT) and N‐terminal brain naturietic protein (NT‐proBNP) predicted for an inability to tolerate IMiD‐based regimens. The best predictors for early attrition during cycle 1 were TnT ≥ 0.07 μg/L and NT‐proBNP ≥ 11,939 ng/L. NT‐proBNP‐response underperformed TnT‐response as a predictor for overall survival (OS), but both predicted for early protocol attrition. Despite hematologic response, IMiD‐treated patients were at higher risk for NT‐proBNP rises and early drug discontinuation than a control population but not for early death. These observations prompt two questions: (1) does IMiD‐based therapy lead to increased fluid retention and/or cardiac toxicity and (2) is an NT‐proBNP‐driven cardiac response system valid in IMiD‐treated amyloidosis patients? Recognition of potential drug‐induced cardiac toxicity is important so that increased cardiac surveillance and drug dose‐adjustment or discontinuation may be implemented. Am. J. Hematol. 85:757‐759, 2010. © 2010 Wiley‐Liss, Inc.