Leukemia & Lymphoma
ISSN: 1042-8194 (Print) 1029-2403 (Online) Journal homepage: http://www.tandfonline.com/loi/ilal20
Lenalidomide-associated hemolytic anemia Ming Y. Lim, Jay S. Raval, Kristy L. Richards, Joshua F. Zeidner & Matthew C. Foster To cite this article: Ming Y. Lim, Jay S. Raval, Kristy L. Richards, Joshua F. Zeidner & Matthew C. Foster (2015) Lenalidomide-associated hemolytic anemia, Leukemia & Lymphoma, 56:9, 2717-2719, DOI: 10.3109/10428194.2014.1003558 To link to this article: http://dx.doi.org/10.3109/10428194.2014.1003558
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Date: 05 November 2015, At: 19:18
Leukemia & Lymphoma, September 2015; 56(9): 2717–2719 © 2015 Informa UK, Ltd. ISSN: 1042-8194 print / 1029-2403 online DOI: 10.3109/10428194.2014.1003558
Letter to the Editor
Lenalidomide-associated hemolytic anemia Ming Y. Lim1, Jay S. Raval2, Kristy L. Richards1, Joshua F. Zeidner1 & Matthew C. Foster1 1Division of Hematology/Oncology, Department of Medicine and 2Division of Transfusion Medicine, Department of Pathology
Leukemia & Lymphoma 2015.56:2717-2719.
and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA
Immune-mediated hemolytic anemia secondary to drugs is rare, with an estimated occurrence of 1 per million of the population [1]. There are currently about 125 drugs that show reasonable evidence to suggest drug-induced immune hemolytic anemia [1]. Lenalidomide (Revlimid; Celgene Corporation, Summit, NJ) has been reported to be associated with autoimmune hemolytic anemia (AIHA); however, these patients typically had underlying lymphoid neoplasms or myelodysplastic syndrome (MDS) that may cause AIHA in the absence of the drug [2–6]. In addition, multiple myeloma has also been reported to be associated with AIHA in the presence of lenalidomide [7]. We present the case of a patient who developed hemolytic anemia following initiation of lenalidomide for the treatment of acute myeloid leukemia (AML), a malignancy not typically associated with hemolytic anemia. A 69-year-old Caucasian gentleman was diagnosed with AML in September 2012. Cytogenetics revealed a trisomy 8 abnormality, and the patient underwent induction chemotherapy with 7 3 (daunorubicin 90 mg/m2 intravenously on days 1–3, cytarabine 100 mg/m2 continuous infusion on days 1–7) and achieved a complete remission. The patient then enrolled in a dose-finding clinical study (NCT 01578954) evaluating lenalidomide as a consolidation and maintenance therapy for patients with AML in complete remission who were not eligible for intensive consolidation chemotherapy. The patient began lenalidomide 25 mg daily in November 2012. Nine days post-initiation of lenalidomide, he presented to the clinic with a 2-day history of light-headedness, generalized fatigue and cola-colored urine. At the time of presentation, his medication list included lenalidomide 25 mg once daily, digoxin 125 mg once daily, propafenone 225 mg every 8 h, rivaroxaban 20 mg once daily and lorazapem 1 mg as needed. The patient had been on these medications for at least a month, with the exception of lenalidomide. Physical examination was unremarkable except for mild sinus tachycardia of 104. Initial laboratory testing revealed anemia with hemoglobin 9.9 g/dL (normal range: 13.5–17.5 g/dL), hematocrit 26.9% (normal range: 41.0–53.0%), mean corpuscular volume (MCV) 93 fL
(normal range: 80–100 fL), red cell distribution width (RDW) of 18.0% (normal range: 12.0–15.0%), white blood cells 9.6 109/L (normal range: 4.5–11.0 109/L) and thrombocytopenia with a platelet count of 79 109/L (normal range: 150–440 109/L). Prior to the initiation of lenalidomide, his hemoglobin was 13.4 g/dL with a hematocrit of 38.1% and his platelet count was 239 109/L. Additional laboratory evaluation of the anemia and thrombocytopenia was significant for elevated lactate dehydrogenase (LDH) 2367 U/L (normal range: 338–610 U/L) and total bilirubin 2.2 mg/dL (normal range: 0.0–1.2 mg/dL). Given the strong temporal relationship between lenalidomide initiation and the patient’s hemolytic anemia, lenalidomide was discontinued. During follow-up 2 days later, repeat laboratory testing revealed worsening anemia with hemoglobin 8.9 g/dL, hematocrit 24.9%, MCV 94 fL, RDW 19.3%, white blood cells 7.8 109/L and platelet count of 91 109/L. Additional testing revealed improving but still elevated LDH at 1721 U/L, total bilirubin 1.6 mg/dL that was predominantly unconjugated (unconjugated bilirubin 1.3 mg/dL [normal range: 0.0–1.2 mg/dL] and conjugated bilirubin 1.3 mg/dL [normal range: 0.0–0.1 mg/dL]), undetectable haptoglobin 14 mg/ dL (normal range: 30–200 mg/dL), reticulocyte percentage 4.4% (normal range: 0.8–2.0%) and absolute reticulocyte count 123.6 109/L (normal range: 27.0–120.0 /L), with a reticulocyte production index (RPI) of 1.2%. A peripheral blood smear demonstrated anisocytosis, polychromasia and poikilocytosis, but no spherocytes, schistocytes or target cells, and normal leukocyte and platelet morphology. The patient’s blood type was O with a negative antibody screen, and the direct antiglobuin test (DAT) was non-reactive with anti-immunoglobulin G (IgG) and anti-C3d antibodies. Testing for drug antibodies by reacting the patient’s serum with lenalidomide-treated red blood cells (RBCs) as well as normal RBCs in the presence of lenalidomide was also negative. An eluate was not performed. Oral prednisone 1 mg/kg daily 5 days was administered. Over the next few days, laboratory findings of hemolysis improved with an increase in hemoglobin and a decrease in LDH (Figure 1), despite an increase in the RPI to 2.3%.
Correspondence: Matthew C. Foster, University of North Carolina School of Medicine, Division of Hematology/Oncology, Physicians Office Bldg. CB# 7305, 170 Manning Drive, Chapel Hill, NC 27599-7305, USA. Tel: 919-966-4431. Fax: 919-966-6735. E-mail: [email protected] Received 13 November 2014; revised 20 December 2014; accepted 24 December 2014
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LDH (U/L)
Hgb (g/L), Platelet (109/L) and Absolute reticulocyte count (109/L)
2718 M. Y. Lim et al.
500
90 70
0 –5
Day
0
5
10
Lenalidomide 25 mg daily
Platelet
15
20
25
30
Prednisone 1mg/kg
Hgb
Absolute Retic Count
LDH
Leukemia & Lymphoma 2015.56:2717-2719.
Figure 1. Temporal relationship between hemoglobin (Hgb), platelet count, reticulocyte count and lactate dehydrogenase (LDH) during the time of lenalidomide initiation. The x-axis shows the day from time of lenalidomide initiation (Day 0).
Repeat laboratory testing 3 weeks later revealed normalization of all clinical and laboratory findings of hemolysis. The patient was rechallenged with a lower dose of lenalidomide at 10 mg daily without any further complications. The patient was diagnosed with antibody-negative lenalidomideassociated hemolytic anemia and has since not had any evidence of hemolysis. Lenalidomide is a small-molecule immunomodulatory derivative of thalidomide that is currently approved for the treatment of patients with relapsed multiple myeloma and mantle cell lymphoma, and patients with transfusiondependent anemia due to low- or intermediate-1 risk MDS associated with a deletion 5q cytogenetic abnormality. The drug is also in clinical development for other malignant hematologic indications. The most commonly reported adverse event for lenalidomide is myelosuppression, mainly neutropenia and thrombocytopenia [8]. Venous thromboembolism is the most frequent non-hematological adverse event [8]. As far as we are aware, there have been no reported cases of lenalidomide causing hemolytic anemia in patients whose underlying malignancy itself is not associated with AIHA. However, there have been two reported cases of AIHA occurring in patients with de novo AML that were not drug-induced [9]. Several lines of evidence suggest that lenalidomide was responsible for the hemolytic anemia observed in our patient, although not proof of causality. First, there was a temporal relationship between lenalidomide initiation and occurrence of hemolysis. Second, hematological resolution occurred after lenalidomide was discontinued. However, it is notable that the patient was rechallenged with lenalidomide, albeit at a lower dose, which was well tolerated. Given the negative DAT, we are not able to definitively diagnose this as drug-induced immune hemolytic anemia. Confirmation of an immune hemolytic anemia usually requires a positive DAT, although DAT-negative AIHA is a well-described phenomenon [10]. Such cases of negative DATs in patients with drug-induce immune hemolytic
anemia can be explained by massive acute intravascular hemolysis or transfusions before the DAT was performed [1], neither of which occurred in our patient. However, lenalidomide has protean immunomodulatory properties, capable of augmenting immune responses, chiefly by acting on T- and natural killer (NK)-cells, resulting in production of interleukin-2 (IL-2) and interferon-g (INF-g) [11]. Lenalidomide has been reported to result in flares of various autoimmune diseases (ADs) such as myocarditis [12], aplastic anemia [13], hypothyroidism [14] and interstitial lymphocytic dermatitis [15]. Similarly, non-humoral autoimmunity may be the mechanism for developing lenalidomide-induced immune hemolytic anemia, as seen in our patient. More recently, the potential for lenalidomide to cause AD was reported in a retrospective study of 140 patients with multiple myeloma [7]. The absolute risk of developing AD was 4.3%, with six cases observed: grade III AIHA with positive DAT, Evans syndrome with grade III DAT-positive anemia and thrombocytopenia, immune thrombocytopenia (ITP), autoimmune thyroiditis, optic neuritis and polymyositis. In the same retrospective study, patients with multiple myeloma treated with thalidomide (n 474), another immunomodulatory agent, had an absolute risk of developing AD of only 0.4% [7]. This seems to suggest that even though multiple myeloma has been rarely associated with ADs on its own, the role of lenalidomide in causing autoimmune diseases, particularly autoimmune cytopenia, cannot be ignored. Our patient’s clinical course further supports this, as following lenalidomide initiation, there was a significant decrease in platelet count that improved with corticosteroids (Figure 1), suggestive of immune thrombocytopenia. However, as the platelet count did not return to baseline until many months later and the patient was restarted on low-dose lenalidomide, we cannot exclude the possibility of drug-induced thrombocytopenia versus Evans syndrome. In summary, to our knowledge, this is the first report documenting that lenalidomide can induce hemolytic anemia in myeloid malignancies. Although this is likely a rare event,
Letter to the editor 2719 lenalidomide is increasingly being used in many malignant hematologic indications, which may lead to a rise in cases seen. As such, this case raises the awareness that hemolytic anemia should be considered in the differential diagnosis in patients who present with acute anemia while on lenalidomide therapy. Potential conflict of interest: Disclosure forms provided by the authors are available with the full text of this article at www.informahealthcare.com/lal.
Leukemia & Lymphoma 2015.56:2717-2719.
References [1] Garratty G. Immune hemolytic anemia associated with drug therapy. Blood Rev 2010;24:143–150. [2] Darabi K, Kantamnei S, Wiernik PH. Lenalidomide-induced warm autoimmune hemolytic anemia. J Clin Oncol 2006;24:e59. [3] Oren H, Ucar C, Gulen H, et al. Autoimmune hemolytic anemia occurring with myelodysplastic syndrome: report of a pediatric case and review of the literature. Ann Hematol 2001;80:540–542. [4] List A, Kurtin S, Roe DJ, et al. Efficacy of lenalidomide in myelodysplastic syndromes. N Engl J Med 2005;352:549–557. [5] Sun WL, Kock L, Walder A, et al. Successful treatment of MDS with lenalidomide, complicated by transient autoimmune hemolysis. Ann Hematol 2010;89:327–329.
[6] Brauer DL, Edelman B, Rapoport AP, et al. Plasma exchange and rituximab treatment for lenalidomide-associated cold agglutinin disease. Transfusion 2012;52:2432–2435. [7] Montefusco V, Galli M, Spina F, et al. Autoimmune diseases during treatment with immunomodulatory drugs in multiple myeloma: selective occurrence after lenalidomide. Leuk Lymphoma 2014;55:2032–2037. [8] Dimopoulos M, Spencer A, Attal M, et al. Lenalidomide plus dexamethasone for relapsed or refractory multiple myeloma. N Engl J Med 2007;357:2123–2132. [9] Tamura H, Ogata K, Yokose N, et al. Autoimmune hemolytic anemia in patients with de novo acute myelocytic leukemia. Ann Hematol 1996;72:45–47. [10] Kamesaki T, Toyotsuji T, Kajii E. Characterization of direct antiglobulin test-negative autoimmune hemolytic anemia:a study of 154 cases. Am J Hematol 2013;88:93–96. [11] Zeidner JF, Foster MF. Immunomodulatry drugs: IMIDs in acute myeloid leukemia (AML). Special issue: Targets for immunotherapy in acute leukemia. Curr Drug Targets 2015; in press. [12] Carver JR, Nasta S, Chong EA, et al. Myocarditis during lenalidomide therapy. Ann Pharmacother 2010;44:1840–1843. [13] Dasanu CA, Alexandrescu DT. A case of severe aplastic anemia secondary to treatment with lenalidomide for multiple myeloma. Eur J Haematol 2009;82:231–234. [14] Menon S, Habermann T, Witzig T. Lenalidomide-associated hypothyroidism. Leuk Lymphoma 2007;48:2465–2467. [15] Deng A, Harvey V, Sina B, et al. Interstitial granulomatous dermatitis associated with the use of tumor necrosis factor alpha inhibitors. Arch Dermatol 2006;142:198–202.
ISSN: 1042-8194 (Print) 1029-2403 (Online) Journal homepage: http://www.tandfonline.com/loi/ilal20
Lenalidomide-associated hemolytic anemia Ming Y. Lim, Jay S. Raval, Kristy L. Richards, Joshua F. Zeidner & Matthew C. Foster To cite this article: Ming Y. Lim, Jay S. Raval, Kristy L. Richards, Joshua F. Zeidner & Matthew C. Foster (2015) Lenalidomide-associated hemolytic anemia, Leukemia & Lymphoma, 56:9, 2717-2719, DOI: 10.3109/10428194.2014.1003558 To link to this article: http://dx.doi.org/10.3109/10428194.2014.1003558
View supplementary material
Accepted author version posted online: 03 Feb 2015. Published online: 02 Mar 2015. Submit your article to this journal
Article views: 72
View related articles
View Crossmark data
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ilal20 Download by: [University of Sheffield]
Date: 05 November 2015, At: 19:18
Leukemia & Lymphoma, September 2015; 56(9): 2717–2719 © 2015 Informa UK, Ltd. ISSN: 1042-8194 print / 1029-2403 online DOI: 10.3109/10428194.2014.1003558
Letter to the Editor
Lenalidomide-associated hemolytic anemia Ming Y. Lim1, Jay S. Raval2, Kristy L. Richards1, Joshua F. Zeidner1 & Matthew C. Foster1 1Division of Hematology/Oncology, Department of Medicine and 2Division of Transfusion Medicine, Department of Pathology
Leukemia & Lymphoma 2015.56:2717-2719.
and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA
Immune-mediated hemolytic anemia secondary to drugs is rare, with an estimated occurrence of 1 per million of the population [1]. There are currently about 125 drugs that show reasonable evidence to suggest drug-induced immune hemolytic anemia [1]. Lenalidomide (Revlimid; Celgene Corporation, Summit, NJ) has been reported to be associated with autoimmune hemolytic anemia (AIHA); however, these patients typically had underlying lymphoid neoplasms or myelodysplastic syndrome (MDS) that may cause AIHA in the absence of the drug [2–6]. In addition, multiple myeloma has also been reported to be associated with AIHA in the presence of lenalidomide [7]. We present the case of a patient who developed hemolytic anemia following initiation of lenalidomide for the treatment of acute myeloid leukemia (AML), a malignancy not typically associated with hemolytic anemia. A 69-year-old Caucasian gentleman was diagnosed with AML in September 2012. Cytogenetics revealed a trisomy 8 abnormality, and the patient underwent induction chemotherapy with 7 3 (daunorubicin 90 mg/m2 intravenously on days 1–3, cytarabine 100 mg/m2 continuous infusion on days 1–7) and achieved a complete remission. The patient then enrolled in a dose-finding clinical study (NCT 01578954) evaluating lenalidomide as a consolidation and maintenance therapy for patients with AML in complete remission who were not eligible for intensive consolidation chemotherapy. The patient began lenalidomide 25 mg daily in November 2012. Nine days post-initiation of lenalidomide, he presented to the clinic with a 2-day history of light-headedness, generalized fatigue and cola-colored urine. At the time of presentation, his medication list included lenalidomide 25 mg once daily, digoxin 125 mg once daily, propafenone 225 mg every 8 h, rivaroxaban 20 mg once daily and lorazapem 1 mg as needed. The patient had been on these medications for at least a month, with the exception of lenalidomide. Physical examination was unremarkable except for mild sinus tachycardia of 104. Initial laboratory testing revealed anemia with hemoglobin 9.9 g/dL (normal range: 13.5–17.5 g/dL), hematocrit 26.9% (normal range: 41.0–53.0%), mean corpuscular volume (MCV) 93 fL
(normal range: 80–100 fL), red cell distribution width (RDW) of 18.0% (normal range: 12.0–15.0%), white blood cells 9.6 109/L (normal range: 4.5–11.0 109/L) and thrombocytopenia with a platelet count of 79 109/L (normal range: 150–440 109/L). Prior to the initiation of lenalidomide, his hemoglobin was 13.4 g/dL with a hematocrit of 38.1% and his platelet count was 239 109/L. Additional laboratory evaluation of the anemia and thrombocytopenia was significant for elevated lactate dehydrogenase (LDH) 2367 U/L (normal range: 338–610 U/L) and total bilirubin 2.2 mg/dL (normal range: 0.0–1.2 mg/dL). Given the strong temporal relationship between lenalidomide initiation and the patient’s hemolytic anemia, lenalidomide was discontinued. During follow-up 2 days later, repeat laboratory testing revealed worsening anemia with hemoglobin 8.9 g/dL, hematocrit 24.9%, MCV 94 fL, RDW 19.3%, white blood cells 7.8 109/L and platelet count of 91 109/L. Additional testing revealed improving but still elevated LDH at 1721 U/L, total bilirubin 1.6 mg/dL that was predominantly unconjugated (unconjugated bilirubin 1.3 mg/dL [normal range: 0.0–1.2 mg/dL] and conjugated bilirubin 1.3 mg/dL [normal range: 0.0–0.1 mg/dL]), undetectable haptoglobin 14 mg/ dL (normal range: 30–200 mg/dL), reticulocyte percentage 4.4% (normal range: 0.8–2.0%) and absolute reticulocyte count 123.6 109/L (normal range: 27.0–120.0 /L), with a reticulocyte production index (RPI) of 1.2%. A peripheral blood smear demonstrated anisocytosis, polychromasia and poikilocytosis, but no spherocytes, schistocytes or target cells, and normal leukocyte and platelet morphology. The patient’s blood type was O with a negative antibody screen, and the direct antiglobuin test (DAT) was non-reactive with anti-immunoglobulin G (IgG) and anti-C3d antibodies. Testing for drug antibodies by reacting the patient’s serum with lenalidomide-treated red blood cells (RBCs) as well as normal RBCs in the presence of lenalidomide was also negative. An eluate was not performed. Oral prednisone 1 mg/kg daily 5 days was administered. Over the next few days, laboratory findings of hemolysis improved with an increase in hemoglobin and a decrease in LDH (Figure 1), despite an increase in the RPI to 2.3%.
Correspondence: Matthew C. Foster, University of North Carolina School of Medicine, Division of Hematology/Oncology, Physicians Office Bldg. CB# 7305, 170 Manning Drive, Chapel Hill, NC 27599-7305, USA. Tel: 919-966-4431. Fax: 919-966-6735. E-mail: [email protected] Received 13 November 2014; revised 20 December 2014; accepted 24 December 2014
2717
250
2500
230 2000
210 190
1500
170 150
1000
130 110
LDH (U/L)
Hgb (g/L), Platelet (109/L) and Absolute reticulocyte count (109/L)
2718 M. Y. Lim et al.
500
90 70
0 –5
Day
0
5
10
Lenalidomide 25 mg daily
Platelet
15
20
25
30
Prednisone 1mg/kg
Hgb
Absolute Retic Count
LDH
Leukemia & Lymphoma 2015.56:2717-2719.
Figure 1. Temporal relationship between hemoglobin (Hgb), platelet count, reticulocyte count and lactate dehydrogenase (LDH) during the time of lenalidomide initiation. The x-axis shows the day from time of lenalidomide initiation (Day 0).
Repeat laboratory testing 3 weeks later revealed normalization of all clinical and laboratory findings of hemolysis. The patient was rechallenged with a lower dose of lenalidomide at 10 mg daily without any further complications. The patient was diagnosed with antibody-negative lenalidomideassociated hemolytic anemia and has since not had any evidence of hemolysis. Lenalidomide is a small-molecule immunomodulatory derivative of thalidomide that is currently approved for the treatment of patients with relapsed multiple myeloma and mantle cell lymphoma, and patients with transfusiondependent anemia due to low- or intermediate-1 risk MDS associated with a deletion 5q cytogenetic abnormality. The drug is also in clinical development for other malignant hematologic indications. The most commonly reported adverse event for lenalidomide is myelosuppression, mainly neutropenia and thrombocytopenia [8]. Venous thromboembolism is the most frequent non-hematological adverse event [8]. As far as we are aware, there have been no reported cases of lenalidomide causing hemolytic anemia in patients whose underlying malignancy itself is not associated with AIHA. However, there have been two reported cases of AIHA occurring in patients with de novo AML that were not drug-induced [9]. Several lines of evidence suggest that lenalidomide was responsible for the hemolytic anemia observed in our patient, although not proof of causality. First, there was a temporal relationship between lenalidomide initiation and occurrence of hemolysis. Second, hematological resolution occurred after lenalidomide was discontinued. However, it is notable that the patient was rechallenged with lenalidomide, albeit at a lower dose, which was well tolerated. Given the negative DAT, we are not able to definitively diagnose this as drug-induced immune hemolytic anemia. Confirmation of an immune hemolytic anemia usually requires a positive DAT, although DAT-negative AIHA is a well-described phenomenon [10]. Such cases of negative DATs in patients with drug-induce immune hemolytic
anemia can be explained by massive acute intravascular hemolysis or transfusions before the DAT was performed [1], neither of which occurred in our patient. However, lenalidomide has protean immunomodulatory properties, capable of augmenting immune responses, chiefly by acting on T- and natural killer (NK)-cells, resulting in production of interleukin-2 (IL-2) and interferon-g (INF-g) [11]. Lenalidomide has been reported to result in flares of various autoimmune diseases (ADs) such as myocarditis [12], aplastic anemia [13], hypothyroidism [14] and interstitial lymphocytic dermatitis [15]. Similarly, non-humoral autoimmunity may be the mechanism for developing lenalidomide-induced immune hemolytic anemia, as seen in our patient. More recently, the potential for lenalidomide to cause AD was reported in a retrospective study of 140 patients with multiple myeloma [7]. The absolute risk of developing AD was 4.3%, with six cases observed: grade III AIHA with positive DAT, Evans syndrome with grade III DAT-positive anemia and thrombocytopenia, immune thrombocytopenia (ITP), autoimmune thyroiditis, optic neuritis and polymyositis. In the same retrospective study, patients with multiple myeloma treated with thalidomide (n 474), another immunomodulatory agent, had an absolute risk of developing AD of only 0.4% [7]. This seems to suggest that even though multiple myeloma has been rarely associated with ADs on its own, the role of lenalidomide in causing autoimmune diseases, particularly autoimmune cytopenia, cannot be ignored. Our patient’s clinical course further supports this, as following lenalidomide initiation, there was a significant decrease in platelet count that improved with corticosteroids (Figure 1), suggestive of immune thrombocytopenia. However, as the platelet count did not return to baseline until many months later and the patient was restarted on low-dose lenalidomide, we cannot exclude the possibility of drug-induced thrombocytopenia versus Evans syndrome. In summary, to our knowledge, this is the first report documenting that lenalidomide can induce hemolytic anemia in myeloid malignancies. Although this is likely a rare event,
Letter to the editor 2719 lenalidomide is increasingly being used in many malignant hematologic indications, which may lead to a rise in cases seen. As such, this case raises the awareness that hemolytic anemia should be considered in the differential diagnosis in patients who present with acute anemia while on lenalidomide therapy. Potential conflict of interest: Disclosure forms provided by the authors are available with the full text of this article at www.informahealthcare.com/lal.
Leukemia & Lymphoma 2015.56:2717-2719.
References [1] Garratty G. Immune hemolytic anemia associated with drug therapy. Blood Rev 2010;24:143–150. [2] Darabi K, Kantamnei S, Wiernik PH. Lenalidomide-induced warm autoimmune hemolytic anemia. J Clin Oncol 2006;24:e59. [3] Oren H, Ucar C, Gulen H, et al. Autoimmune hemolytic anemia occurring with myelodysplastic syndrome: report of a pediatric case and review of the literature. Ann Hematol 2001;80:540–542. [4] List A, Kurtin S, Roe DJ, et al. Efficacy of lenalidomide in myelodysplastic syndromes. N Engl J Med 2005;352:549–557. [5] Sun WL, Kock L, Walder A, et al. Successful treatment of MDS with lenalidomide, complicated by transient autoimmune hemolysis. Ann Hematol 2010;89:327–329.
[6] Brauer DL, Edelman B, Rapoport AP, et al. Plasma exchange and rituximab treatment for lenalidomide-associated cold agglutinin disease. Transfusion 2012;52:2432–2435. [7] Montefusco V, Galli M, Spina F, et al. Autoimmune diseases during treatment with immunomodulatory drugs in multiple myeloma: selective occurrence after lenalidomide. Leuk Lymphoma 2014;55:2032–2037. [8] Dimopoulos M, Spencer A, Attal M, et al. Lenalidomide plus dexamethasone for relapsed or refractory multiple myeloma. N Engl J Med 2007;357:2123–2132. [9] Tamura H, Ogata K, Yokose N, et al. Autoimmune hemolytic anemia in patients with de novo acute myelocytic leukemia. Ann Hematol 1996;72:45–47. [10] Kamesaki T, Toyotsuji T, Kajii E. Characterization of direct antiglobulin test-negative autoimmune hemolytic anemia:a study of 154 cases. Am J Hematol 2013;88:93–96. [11] Zeidner JF, Foster MF. Immunomodulatry drugs: IMIDs in acute myeloid leukemia (AML). Special issue: Targets for immunotherapy in acute leukemia. Curr Drug Targets 2015; in press. [12] Carver JR, Nasta S, Chong EA, et al. Myocarditis during lenalidomide therapy. Ann Pharmacother 2010;44:1840–1843. [13] Dasanu CA, Alexandrescu DT. A case of severe aplastic anemia secondary to treatment with lenalidomide for multiple myeloma. Eur J Haematol 2009;82:231–234. [14] Menon S, Habermann T, Witzig T. Lenalidomide-associated hypothyroidism. Leuk Lymphoma 2007;48:2465–2467. [15] Deng A, Harvey V, Sina B, et al. Interstitial granulomatous dermatitis associated with the use of tumor necrosis factor alpha inhibitors. Arch Dermatol 2006;142:198–202.
