A Rare Case of Autoimmune Hemolytic Anemia Caused by Warm-reacting IgM-class Antibodies Associated with Mycoplasma Pneumoniae Infection

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S166-S166
Author(s):  
M Abdelmonem ◽  
H Wasim ◽  
M Abdelmonem
Keyword(s):  
Hemolytic Anemia ◽  
Mycoplasma Pneumoniae ◽  
Autoimmune Hemolytic Anemia ◽  
Hemoglobin Level ◽  
Cytotoxic Agents ◽  
Cold Agglutinin ◽  
Packed Red Blood Cells ◽  
Thermal Amplitude ◽  
History Of

Abstract Introduction/Objective Warm autoantibodies are usually IgG-class and/or IgA-class immunoglobulins. may be classified as agglutinins or hemolysins, which may be incomplete or complete, depending on in vitro serology; they almost always bind complement. Autoimmune hemolytic anemia with only warm IgM autoantibodies is extremely rare. Methods A 91-year-old Caucasian male with hypertension presented with non-productive cough for two weeks, associated with shortness of breath and fatigue. He has a paste history of medical history of high degree AV block with sick sinus syndrome and bradycardia. Results He had blood pressure of 111/53 and heart rate of 50. Laboratory investigations showed leukocytes count of 7, Hemoglobin level of 5.6 g/dl, hematocrit level of 15.5%, platelets count of 267, total bilirubin of 5.6 mg/dL, direct bilirubin of 0.7 mg/dL, and lactate dehydrogenase (LDH) of 372 U/L and IgM titer for Mycoplasma pneumoniae was 1493 units/mL (Ref < 770). He was transfused four units of packed red blood cells as emergency release due to a positive antibody screen. His hemoglobin level increased from 5.6 g/dL to 7.2 g/dL then it decreased from 8.2 g/dL to 5.6 g/dL the next two days. Direct antiglobulin test was 3+ positive for C3d and Negative for IgG. He finished a 7-day course of antibiotic treatment. The results the Cold-agglutinin titer and thermal amplitude test were suggestive of an IgM warm autoantibody and a cold agglutinin of a moderate titer. The results exclude a diagnosis of cold agglutinin syndrome. Conclusion Mycoplasma pneumonia is mainly associated with cold agglutinin syndrome but it is very rare to be associated with WAIHA. WAIHA with a DAT positive for C3 only is relatively rare with an incidence ranging between 6% and 13% and can have a clinical picture ranging from mild to severe anemia. Severe symptomatic hemolysis can be treated with Rituximab, cytotoxic agents or plasmapheresis.

scholarly journals Cold Agglutinin-Mediated Autoimmune Hemolytic Anemia in Association with Antiphospholipid Syndrome

2021 ◽  
pp. 1-4
Author(s):  
Ram Gelman ◽  
Fadi Kharouf ◽  
Yuval Ishay ◽  
Alexander Gural
Keyword(s):  
Hemolytic Anemia ◽  
Antiphospholipid Syndrome ◽  
Complement Activation ◽  
Autoimmune Hemolytic Anemia ◽  
Cold Agglutinin ◽  
Primary Antiphospholipid Syndrome ◽  
Unique Case ◽  
Hematologic Disorders ◽  
Clear Association ◽  
Immune Mediated

Antiphospholipid syndrome and cold agglutinin-mediated autoimmune hemolytic anemia are 2 distinct immune-mediated hematologic disorders. While no clear association exists between these 2 entities, complement activation is known to occur in both of them. Herein, we report a unique case of cold agglutinin hemolytic anemia in a patient with a known primary antiphospholipid syndrome.

FcγRIII (CD16)-Deficient Mice Show IgG Isotype-Dependent Protection to Experimental Autoimmune Hemolytic Anemia

Blood ◽  
1998 ◽  
Vol 92 (11) ◽  
pp. 3997-4002 ◽  
Author(s):  
Dirk Meyer ◽  
Carsten Schiller ◽  
Jürgen Westermann ◽  
Shozo Izui ◽  
Wouter L. W. Hazenbos ◽  
...  
Keyword(s):  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Knock Out ◽  
Effector Cells ◽  
Igg Isotypes ◽  
Knock Out Mice ◽  
Deficient Mice ◽  
Experimental Autoimmune

Abstract In autoimmune hemolytic anemia (AIHA), there is accumulating evidence for an involvement of FcγR expressed by phagocytic effector cells, but demonstration of a causal relationship between individual FcγRs and IgG isotypes for disease development is lacking. Although the relevance of IgG isotypes to human AIHA is limited, we could show a clear IgG isotype dependency in murine AIHA using pathogenic IgG1 (105-2H) and IgG2a (34-3C) autoreactive anti–red blood cell antibodies in mice defective for FcγRIII, and comparing the clinical outcome to those in wild-type mice. FcγRIII-deficient mice were completely resistent to the pathogenic effects of 105-2H monoclonal antibody, as shown by a lack of IgG1-mediated erythrophagocytosis in vitro and in vivo. In addition, the IgG2a response by 34-3C induced a less severe but persistent AIHA in FcγRIII knock-out mice, as documented by a decrease in hematocrit. Blocking studies indicated that the residual anemic phenotype induced by 34-3C in the absence of FcγRIII reflects an activation of FcγRI that is normally coexpressed with FcγRIII on macrophages. Together these results show that the pathogenesis of AIHA through IgG1-dependent erythrophagocytosis is exclusively mediated by FcγRIII and further suggest that FcγRI, in addition to FcγRIII, contributes to this autoimmune disease when other IgG isotypes such as IgG2a are involved.

scholarly journals A Case of Warm Autoimmune Hemolytic Anemia and a Pulmonary Embolus in a Patient Treated with Triple Therapy

2019 ◽  
Vol 2019 ◽  
pp. 1-3
Author(s):  
Gurchetan Randhawa ◽  
Chia-Yu Chiu ◽  
Thanunthorn Suban Na Ayutthaya
Keyword(s):  
Medical History ◽  
Triple Therapy ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Pulmonary Embolus ◽  
Hodgkin's Lymphoma ◽  
Pulmonary Emboli ◽  
Past Medical History ◽  
Non Hodgkin's Lymphoma ◽  
History Of

Autoimmune hemolytic anemia (AIHA) can be caused by a variety of etiologies. AIHA is associated with the development of coagulopathy, leading to potentially fatal pulmonary emboli. Here, we present a case of a 66-year-old female with a past medical history of non-Hodgkin’s lymphoma and gastritis treated with triple therapy that developed warm AIHA. The patient later succumbed to a suspected pulmonary embolus.

Cold Agglutinin Syndrome in Post-Liver Transplant Patients on Tacrolimus.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 967-967
Author(s):  
Wendy Wong ◽  
Jason Merker ◽  
Christine Nguyen ◽  
William Berquist ◽  
Bertil Glader ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Liver Transplant ◽  
Hemolytic Anemia ◽  
Peripheral Blood ◽  
Blood Smear ◽  
Peripheral Blood Smear ◽  
Cold Agglutinin ◽  
Severe Anemia ◽  
Thermal Amplitude ◽  
Antiglobulin Test

Abstract Following liver transplantation, patients require immunosuppressive medications to prevent graft rejection. However, these drugs can have significant side effects including severe anemia. Tacrolimus is now commonly used in pediatrics patients after liver transplantation. Case reports indicate that tacrolimus rarely can cause microangiopathic hemolytic anemia and also hemolytic anemia due to cold reactive IgM antibodies (cold agglutinin disease). We have seen 4 patients with symptomatic cold agglutinins thought to have been triggered by tacrolimus. Four patients, 6 to 26 months post-ABO-compatible liver transplant, presented with severe anemia (hemoglobin < 6g/dL), indirect hyperbilirubinemia, reticulocytosis and low serum haptoglobin (Table 1). Peripheral blood smear exhibited marked autoagglutination but no evidence of microangiopathic changes. The direct antiglobulin test (DAT) initially was strongly positive in all 4 patients (Table 2). After warm saline washes, the DAT remained positive for complements in 3 out of 4 patients. Cold agglutinin titers were low (1:4 – 1:16) but thermal amplitude studies were positive at 37°C in the two tested patients. Viral serologies significant for cold agglutinin syndrome were negative. None of the patients had clinical evidence of post-transplant lymphoproliferative disorder. All 4 patients had brisk hemolysis requiring multiple uncrossmatched packed red blood cells (PRBC) transfusions. Favorable resolution of the hemolytic anemia occurred following steroids, plasmapheresis and withdrawal of tacrolimus. Subsequently, patients were placed on cyclosporin and none exhibited liver rejection or recurrence of their hemolytic anemia. The above observation indicates that acute cold-agglutinin induced hemolysis occurs in patients following liver transplantation and these events appear to have temporally associated with tacrolimus administration. Patient Profiles Patient Age Diagnosis Months after transplant Presenting hemoglobin (g/dL) Reticulocyte (%/Abs k/μL Total/Direct Bilirubin Treatments (in addition to withdrawal of tacrolimus) ND=not done. MP=methylprednisolone 1 8 mos Neonatal iron storage disease 6 2.8 41%/469 4.2/0.6 MP 4mg/kg/d plus
 30mg/kg/d x 3 days.
 Plasmapheresis x 6. 2 13 mos Biliary atresia Idiopathic 6 5.3 8%/250 3.2/0.4 MP 4mg/kg/d.
 Plasmapheresis x 15. 3 2 yrs 5 mos fulminant hepatic failure 14 4.6 19.5%/237 2.6/0.3 MP 10mg/kg/d.
 Plasmapheresis x 10. 4 4 yrs Biliary atresia 26 5.3 5%/ND 8.8/0.5 MP 2mg/kg/d→ 4mg/kg/d.
 Plasmapheresis x 10. Immunohematology Profiles Admission DAT Patient 1 Patient 2 Patient 3 Patient 4 Admission DAT Pre/post saline wash Pre/post saline wash Pre/post saline wash Pre/post saline wash DAT-Direct antiglobulin test, M-microscopically, NT-not tested, +-positive, 0-negative, Polyspecific 3+/0 1+/M+ 4+/4+ 3+/1+ Anti-IgG 2+/0 M+/0 4+/1+ 3+/1+ Anti-C3 2+/0 2+/1+ 4+/4+ 3+/1+ Saline Control 2+/0 1+/0 1+/0 1+/0 Eluate 0 NT Panreactive 1+ Panreactive 1+ Cold agglutinin titer at 4°C in saline NT 4 8 16 Thermal amplitude screen at 30°C NT NT Reactive Reactive Donath-Landsteiner Test NT NT Negative Negative Admission peripheral blood smear 4+ polychromatophilia. 4+ microcytosis 4+ autoagglutination. 3+ polychromatophilia. 3+ spherocytes. 3+ microcytes 3+ autoagglutination. 3+ polychromatophilia. 3+ spherocytes. 2+ macrocytes 4+ autoagglutination. 4+ spherocytes. 2+ polychromatophilia. 2+ macrocytes

Rituximab Treatment for Autoinmune Hemolitic Diseases,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3168-3168
Author(s):  
Natalia Schutz ◽  
Jorge Arbelbide ◽  
Walter Skordo ◽  
Susana Viñuales ◽  
Elsa Nucifora ◽  
...  
Keyword(s):  
Partial Response ◽  
Median Time ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Response Rate ◽  
Complete Response ◽  
Infectious Complications ◽  
Hemoglobin Level ◽  
Published Data ◽  
Steroid Dependence

Abstract Abstract 3168 INTRODUCTION: Steroids are the first line treatment for Autoimmune Hemolytic Anemia (AHA) and Immune Thrombocytopenic Purpura (ITP). Second line treatments for patients with partial reponses or steroid dependence are controversial and have changed during the last decades. Several authors have proposed the use of Rituximab in these patients although published data are still sparse. OBJECTIVES: We reviewed the medical records of all the patients treated in our hospital with Rituximab in order to evaluate the response rate and security of this treatment. MATHERIALS AND METHODS: We included in the study all the patients older than 18 years with diagnoses of Immune Thrombocytopenia or Autoimmune Hemolytic Anemia treated with Rituximab. Patients with oncologic diseases that required specific chemotherapy apart from AHA or ITP were excluded. Rituximab was administered at a dose of 375mg/m3 weekly for 4 weeks. In patients with AHA we assessed the response according to the following criteria: complete response a hemoglobin level higher than 12 g/dl without hemolysis (normal bilirubin, LDH and haptoglobin) and partial response at least 2g/dl increase from the basal hemoglobin level with improvement in the hemolysis parameters. In patients with ITP we defined complete response as >100.000 platelets/mm3 and partial response >50.000 platelets/mm3. In both cases patients should be tapering steroids (less than 10mg/day of prednisone) and without transfusions. RESULTS: We performed 55 treatments with Rituximab in 37 pts., 19 AHA (12 cold hemolytic anemia) and 18 ITP. The median age was 60 years (26 – 86) and 31 pts. were female. Five patients had other autoimmune diseases (lupus, sjogren, autoimmune hepatitis), and six patients had an underlying onco-hematologyc disease (CLL, indolent lymphoma). All patients had been treated with steroids before and most of them had also received azathioprine, cyclophosphamide or gamaglobuline. The median of previous treatments was 3. Eight patients had undergone also splenectomy. The reason for the treatment was steroid dependence in 16 patients, partial response 6 patients and no response to previous treatment in 15 patients. The overall response rate was 79% for AHA and 94% for ITP, with 8pts (42%) and 13pts (72%) achieving a complete response and 7pts (37%) and 4pts (22%) achieving a partial response respectively. The median time to the complete response was 14 days for ITP and 28 days for AHA. The treatment was well tolerated with only one infusion related serious adverse event and one pulmonary thromboembolism during the period of treatment. Fourteen patients relapsed (8 AHA and 6 PTI). The response rate to Rituximab at relapsed for those patients that received a second or even third course of treatment were similar to the observed before. The median time of follow up was 50 months with and event free survival at 1 year of 34% (median 11,9 months) for AHA vs. 60% for PTI (median 38 months) (p 0,23). The overall survival at 5 years was 39% (median 53 months) vs. 86% (median not reached) (p 0,18) respectively. Seven patients with AHA and 2pts with ITP died, mostly of infectious complications. CONCLUSIONS: Rituximab is an effective treatment for ITP and AHA patients with no response to previous treatments or corticoid dependence. There were few serious adverse effects related to the treatment with Rituximab itself. The mortality rate was higher in patients with AHA although it wasn`t statistically significant. The main cause of death was related to infectious complications but most of the patients had a long history of immunosuppression treatment. Patients who relapsed and were treated again with rituximab had very good response rate. Disclosures: No relevant conflicts of interest to declare.

FcγRIII (CD16)-Deficient Mice Show IgG Isotype-Dependent Protection to Experimental Autoimmune Hemolytic Anemia

Blood ◽  
1998 ◽  
Vol 92 (11) ◽  
pp. 3997-4002 ◽  
Author(s):  
Dirk Meyer ◽  
Carsten Schiller ◽  
Jürgen Westermann ◽  
Shozo Izui ◽  
Wouter L. W. Hazenbos ◽  
...  
Keyword(s):  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Knock Out ◽  
Effector Cells ◽  
Igg Isotypes ◽  
Knock Out Mice ◽  
Deficient Mice ◽  
Experimental Autoimmune

In autoimmune hemolytic anemia (AIHA), there is accumulating evidence for an involvement of FcγR expressed by phagocytic effector cells, but demonstration of a causal relationship between individual FcγRs and IgG isotypes for disease development is lacking. Although the relevance of IgG isotypes to human AIHA is limited, we could show a clear IgG isotype dependency in murine AIHA using pathogenic IgG1 (105-2H) and IgG2a (34-3C) autoreactive anti–red blood cell antibodies in mice defective for FcγRIII, and comparing the clinical outcome to those in wild-type mice. FcγRIII-deficient mice were completely resistent to the pathogenic effects of 105-2H monoclonal antibody, as shown by a lack of IgG1-mediated erythrophagocytosis in vitro and in vivo. In addition, the IgG2a response by 34-3C induced a less severe but persistent AIHA in FcγRIII knock-out mice, as documented by a decrease in hematocrit. Blocking studies indicated that the residual anemic phenotype induced by 34-3C in the absence of FcγRIII reflects an activation of FcγRI that is normally coexpressed with FcγRIII on macrophages. Together these results show that the pathogenesis of AIHA through IgG1-dependent erythrophagocytosis is exclusively mediated by FcγRIII and further suggest that FcγRI, in addition to FcγRIII, contributes to this autoimmune disease when other IgG isotypes such as IgG2a are involved.

Peptides containing a dominant T-cell epitope from red cell band 3 have in vivo immunomodulatory properties in NZB mice with autoimmune hemolytic anemia

Blood ◽  
2003 ◽  
Vol 102 (10) ◽  
pp. 3800-3806 ◽  
Author(s):  
Chia-Rui Shen ◽  
Abdel-Rahman Youssef ◽  
Anne Devine ◽  
Laura Bowie ◽  
Andrew M. Hall ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Cell Epitope ◽  
Band 3 ◽  
T Cell Epitope ◽  
Helper Epitope

Abstract The major target of the pathogenic red blood cell (RBC) autoantibodies in New Zealand black (NZB) mice is the anion channel protein band 3, and CD4+ T cells from NZB mice respond to band 3. Here, we demonstrate that a band 3 peptide 861-875, which is the predominant sequence recognized by NZB T cells in vitro, bears a dominant helper epitope able to modulate the autoimmune hemolyic anemia in vivo. The development of RBC-bound autoantibodies and anemia was accelerated in NZB mice injected with peptide 861-874, which is relatively insoluble, and inhalation of the peptide primed T cells for both peptide 861-874 and band 3 responses. By contrast, inhalation of a soluble analog (Glu861, Lys875) of peptide 861-874 deviated the autoimmune response toward a T helper-2 (Th2) profile, with marked increases in the ratio of interleukin-4 to interferon-γ produced by splenic T cells responding in vitro to either peptide 861-874 or band 3. Moreover, in mice that had received such treatment, the proportion of RBC-bound immunoglobulin G (IgG) molecules that were of the Th2-associated IgG1 isotype was also increased, and anemia was less severe. It is concluded that NZB autoimmune hemolytic anemia is helper dependent and that nasal administration of different peptides containing the dominant T-cell epitope can have potentially detrimental or beneficial effects on the disease. (Blood. 2003; 102:3800-3806)

scholarly journals Cold agglutinin-mediated autoimmune hemolytic anemia associated with COVID-19 infection

2021 ◽  
Author(s):  
Chee Yik Chang ◽  
Huang Hin Chin ◽  
Pek Woon Chin ◽  
Masliza Zaid
Keyword(s):  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Supportive Therapy ◽  
Blood Film ◽  
Cold Agglutinin ◽  
Cell Agglutination ◽  
Negative Results ◽  
Systemic Corticosteroids ◽  
Packed Cell Transfusion ◽  
Oropharyngeal Swab

Abstract Cold agglutinin-mediated autoimmune hemolytic anemia (AIHA) is a rare disorder associated with COVID-19 infection. Here, we present a case of COVID-19 pneumonia with concomitant cold agglutinin syndrome (CAS). On admission, the patient was anemic with reticulocytosis and the direct antiglobulin test showed the presence of anti-complement (C3d) antibodies. Peripheral blood film demonstrated red cell agglutination which was dispersible on blood warming. Chest radiography showed bilateral lower zone ground glass appearance. SARS-CoV-2 was detected in the nasopharyngeal and oropharyngeal swab samples by the RT-PCR method. Additional workup for malignancy, autoimmune disease, and other infections yielded negative results. Systemic corticosteroids and oxygen therapy were administered as she developed hypoxic respiratory failure. In addition, she received packed cell transfusion in view of hemolysis. Following corticosteroid and other supportive therapy, she recovered and was discharged well.

scholarly journals Cold Agglutinin Disease Transfusion Practices in the United States: An Electronic Medical Record-Based Analysis

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 3690-3690
Author(s):  
Jun Su ◽  
Rajeshwari Punekar ◽  
Jaime Morales Arias ◽  
Nisha Jain
Keyword(s):  
Medical Record ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Index Date ◽  
Cold Agglutinin ◽  
Cold Agglutinin Disease ◽  
Employment Equity ◽  
Medical Activity ◽  
Equity Ownership ◽  
Rbc Transfusion

Introduction Cold agglutinin disease (CAD) is a rare autoimmune hemolytic anemia (AIHA) accounting for 20% of all cases, with no approved therapies and limited management options for patients. CAD is characterized by immunoglobulin M-mediated erythrocyte agglutination, which triggers activation of the classical complement pathway leading to hemolysis and subsequent anemia. Red blood cell (RBC) transfusions are used as a supportive treatment in CAD to temporarily alleviate anemia, although the transfusion practices are variable among providers treating patients with CAD. Recent RBC transfusion guidelines from the AABB (formerly the American Association of Blood Banks) recommend that transfusions be administered with a restrictive threshold in most clinical scenarios (ie, transfusion is not indicated until hemoglobin [Hb] reaches 7-8 g/dL and/or patients exhibit anemia-related symptoms) to avoid associated complications such as acute reactions, alloantibody development, and hemochromatosis (Carson et al, JAMA, 2016; Carson et al, N Engl J Med, 2017). Because of the dearth of information available regarding trends in RBC transfusion practices among US hematologists, the objective of this longitudinal, retrospective, observational assessment of an electronic medical record database was to evaluate transfusion practices applied to patients with CAD in the US. Methods Patients were retrospectively identified from Optum® de-identified Electronic Health Record (EHR) dataset. Adult patients with ≥1 AIHA-related medical encounter between January 2007 and September 2018 (study period) and ≥3 mentions of CAD-related terms from physician notes ("cold agglutinin disease," "cold autoimmune hemolytic anemia," or "cold agglutinin hemoglobinuria") were included (Broome et al, Blood, 2017). The index date for each patient was the date of first mention of CAD during the study period. The baseline period was defined as the interval from the start of medical activity in the EHR database or study period (whichever occurred later) to the index date, and the follow-up period was defined as the interval from the index date to the end of the study period, end of medical activity, or death (whichever occurred earlier). The study sample was categorized into 2 study groups, the transfusion group (patients with CAD with ≥1 RBC transfusion after the index date) and the non-transfusion group (patients with CAD without any transfusions during the study period). Patients were further grouped based on the following Hb levels (g/dL): <8, ≥8 to ≤10, and >10 to ≤12. The closest Hb level prior to the most recent transfusion (within the prior 15 days and the lowest level) was used for the transfusion group and the lowest Hb level during the study period was used for the non-transfusion group. Descriptive statistics included mean, standard deviation, and median values for continuous variables and frequency (n and percent) for categorical variables. No adjustment was made for this descriptive analysis. Results A total of 903 patients with CAD were identified from the Optum EHR database; most patients were white (n=760 [84%]) and female (n=560 [62%]). Baseline demographics and clinical characteristics of each group can be found in the Table. Of the patients with CAD, 548 (61%) did not receive transfusions and 355 (39%) received ≥1 RBC transfusion. Among patients with CAD who received transfusions, 84% (n=297) had ≥2 RBC transfusions. Out of the 903 patients with CAD, 864 had Hb levels reported and 752 had Hb levels ≤12 g/dL. Forty-four percent (n=329/752) of those CAD patients received ≥1 RBC transfusion. When separated by Hb levels, 18% of patients with Hb >10 to ≤12 g/dL (n=19/108); 41% (n=88/216) of patients with Hb ≥8 to ≤10 g/dL; and 52% (n=222/428) of patients with Hb <8 g/dL received ≥1 RBC transfusion. Of the 423 (56%) patients with CAD and Hb levels ≤12 g/dL who did not receive RBC transfusions, 21% (n=89/423) had Hb levels >10 to ≤12 g/dL; 30% (n=128/423) had Hb levels ≥8 to ≤10 g/dL; and 49% (n=206/423) had Hb levels <8 g/dL. Conclusions Overall, patients with CAD are not a heavily transfused population. Even in those with a significantly decreased Hb (<8 g/dL), approximately half of them (49%) did not receive RBC transfusions. This suggests that the use of transfusions in patients with CAD may not reflect disease severity. Further prospective studies are needed to fully understand the impact of transfusions on patients with CAD. Disclosures Su: Sanofi Genzyme: Employment, Equity Ownership. Punekar:Sanofi: Employment, Equity Ownership. Morales Arias:Sanofi: Employment, Equity Ownership. Jain:Sanofi Genzyme: Employment, Equity Ownership.

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