eMedicine Specialties > Hematology > Red Blood Cells and Disorders

Cold Agglutinin Disease: Differential Diagnoses & Workup

Author: Sharon Georgy, MD, Resident Physician, Department of Internal Medicine, University of South Florida
Coauthor(s): Richard F Lockey, MD, University Distinguished Health Professor, Professor of Medicine, Pediatrics and Public Health, Joy McCann Culverhouse Chair in Allergy and Immunology, University of South Florida College of Medicine; Director, Division of Allergy and Immunology, James A Haley Veterans' Hospital; Rajalaxmi McKenna, MD, FACP, Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems; Harry L Messmore, Jr, MD, Professor, Department of Medicine, Division of Hematology/Oncology, Loyola University Stritch School of Medicine
Contributor Information and Disclosures

Updated: Feb 16, 2009

Differential Diagnoses

Cholangitis

Other Problems to Be Considered

  • Cryoglobulinemia: This condition has almost none of the features of cold agglutinin disease, except for a history of Raynaud syndrome and an elevated IgM level in some cases, but without hemolysis.
  • Warm antibody–mediated autoimmune hemolytic anemia (AIHA): This must be differentiated from cold agglutinin disease, especially when no symptoms or findings suggest cold-induced acrocyanosis or Raynaud-type phenomenon. The cold agglutinin titer is a specific differentiating test, and a positive IgG-specific Coombs test result would exclude cold agglutinin disease. Examination of the peripheral blood smear is less specific, but finding typical RBC clumps would be unlikely in AIHA, unless it is a mixed IgG-IgM warm/cold autoimmune hemolytic anemia.13,16
  • Episodic hemoglobinuria following cold exposure: This can occur in more severe cases of cold agglutinin disease, so that confusion may exist as to whether it is paroxysmal cold hemoglobinuria or cold agglutinin disease. The cold agglutinin titer is less than 1:64 in paroxysmal cold hemoglobinuria, and the result of the Donath-Landsteiner test for cold hemolysis is positive. The age of the patient is very important; a diagnosis of paroxysmal cold hemoglobinuria is more probable in a child.9 March hemoglobinuria (episodic) is clearly related to exertion.
  • Neoplasms, especially of the lymphoid type: These may be associated with a cold agglutinin or a cryoglobulin, giving rise to symptoms of Raynaud syndrome. If the cold agglutinin titer is elevated and a complement-specific Coombs test result is positive, the patient may have a neoplastic clone of lymphocytes producing the cold agglutinin disease. This would be important in terms of therapy and prognosis, because the underlying lymphoma may be responsive to treatment. Often, the more severe forms of CAD are associated with lymphoid malignancy.45
  • Drug-induced immune hemolytic anemia: This condition may be a source of confusion, particularly when the direct Coombs test result is positive only for complement, but the specific drug use and low cold-agglutinin titer should help to distinguish it from cold agglutinin disease.
  • Rheumatologic diseases manifesting Raynaud syndrome
  • Heparin-induced thrombocytopenia/thrombosis syndrome: Patients may have painful digits. Anemia could be due to bleeding, but other manifestations are different.
  • Systemic vasculitis, sometimes with hemolysis (systemic lupus and scleroderma)
  • Erythromelalgia in association with primary thrombocythemia and painful fingers and toes
  • Drug-induced hemolytic anemia: A positive result from the Coombs test (methyldopa) is possible.
  • Infections (eg, malaria)

Workup

Laboratory Studies

  • Complete blood cell (CBC) count with differential leukocyte count and platelet count
    • If the cold agglutinin is operative at room temperatures, then falsely high mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC) with a low RBC count are obtained due to agglutination of RBCs in the cold, automated counter.
    • Agglutination may also be seen in anticoagulated blood at room temperature. This agglutination worsens with storage and cooling of blood to 4°C and disappears rapidly upon warming the blood to 37°C, unlike with rouleaux formation. Repeating the CBC count after warming the blood to 37°C avoids this problem. Thus, the clinical laboratory is frequently the first to report the presence of a cold agglutinin. Agglutination in the cold may also interfere with typing and cross-matching of blood.
    • Review of a peripheral blood smear may reveal the presence of RBCs in clumps (see Image 1 and below).
      Peripheral blood smear showing several clumps of ...

      Peripheral blood smear showing several clumps of RBCs with the largest in the center. These are typical of aggregates seen in persons with cold agglutinin disease.

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      Peripheral blood smear showing several clumps of ...

      Peripheral blood smear showing several clumps of RBCs with the largest in the center. These are typical of aggregates seen in persons with cold agglutinin disease.

    • In those with chronic cold agglutinin disease, a mild to moderate stable anemia is present. Occasionally, the anemia is severe.
    • Leukocytosis may be evident during hemolytic episodes.
  • Reticulocyte count
    • The results of the count are usually increased, with polychromasia in the peripheral blood smear.
    • Spherocytes may be present, although less prominently than in warm autoantibody–induced hemolytic anemias.
  • Urinalysis
    • Perform urinalysis with microscopic assessment for RBCs and a chemical test for hemoglobin to differentiate between hematuria and hemoglobinuria.
    • Processing only fresh urine samples is important to avoid in vitro hemolysis of RBCs in the urine, leading to an incorrect diagnosis of hemoglobinuria.
    • Urine immunoelectrophoresis should be performed if serum globulins are abnormal; only a 24-hour urine sample can be used to conclusively exclude the presence of light chains.
  • Biochemical tests of the serum and plasma
    • Lactic dehydrogenase (LDH) and total and direct bilirubin values are elevated, depending on the extent of hemolysis.
    • The haptoglobin level may be reduced when hemolysis is active and ongoing with an intravascular spillover from a massive extravascular process and in the absence of significant liver disease.
  • Serum electrophoresis and serum immunoelectrophoresis
    • Perform serum protein electrophoresis and serum immunoelectrophoresis (immunofixation) as initial tests to look for a dysproteinemia.
    • Quantitation of serum levels of IgG, IgA, and IgM should follow when a dysproteinemia is suggested based on results from the first 2 tests. These test results may be normal or abnormal (increased IgM with kappa or lambda light chains).
    • Careful sample processing, avoiding exposure of blood to the cold, and maintaining it at 37°C before testing is essential. If the blood sample is cooled and not kept warm from the time it is collected to the time it is tested, the cold agglutinin attaches to the RBCs and is removed from the serum, with a false-negative result.
  • Special tests
    • The direct Coombs test (DAT, direct antiglobulin test) should be performed with samples at 35-37°C, using polyspecific and monospecific Coombs sera, including monospecific anti-C3 and IgG antisera.
    • With the cold agglutinin titer, a titer of greater than 1:64 is considered abnormal when blood is tested at 4°C. Obtain the cold agglutinin titers also at 30°C and 37°C when needed. Testing at temperatures higher than 4°C is extremely valuable, particularly if the patient is to undergo hypothermia for surgery.Cold agglutinin disease is usually associated with very high cold agglutinin titers of greater than 1:10,000 at 4°C, with a thermal amplitude of up to 30-32°C. The addition of bovine serum albumin (BSA) while testing for the cold agglutinin titer and thermal amplitude results in a better correlation with clinical hemolytic anemia as compared with when data are obtained in the absence of BSA, using saline-suspended cells.7
    • Donath-Landsteiner screening tests are warranted only if hemoglobinuria is detected.
    • Cryoglobulin levels should be tested only if vascular purpura or other atypical findings such as elevated levels of IgM and/or hepatitis virus antibodies are found. Again, proper handling of the sample, by keeping it warm until the test is run, is essential to avoid premature loss of the cryoglobulin.
    • Perform tests for infectious diseases, if such are considered.
      • Infectious mononucleosis (EBV)
      • Anti-influenza antibody
      • Anti–mycoplasmal pneumonia antibodies
      • HIV antibodies
      • Antihepatitis antibodies
      • CMV antibodies
      • Review of thick and thin smears for malaria, as indicated
    • Perform blood tests for collagen vascular disease if the condition is a possibility.
      • Systemic lupus erythematosus (SLE)
      • Rheumatoid arthritis
      • Scleroderma (systemic sclerosis)

Imaging Studies

  • Perform a chest radiograph if pneumonia is suggested. Findings may also indicate lymphadenopathy.
  • Computed tomography (CT) scans of the chest and abdomen are performed to assess for lymphadenopathy and splenomegaly when lymphoma is suggested.

Procedures

  • Perform bone marrow aspiration and biopsy only when needed to exclude certain neoplastic or immunoproliferative diseases. Flow cytometry studies of bone marrow are helpful to define the presence of an abnormal monoclonal population of lymphocytes.
  • A lymph node biopsy is necessary when unexplained lymphadenopathy is present. Fine-needle aspiration is not reliable compared to excision of the largest lymph node for diagnostic purposes because nodal architecture is important to making an accurate diagnosis and is preserved in a lymph node biopsy. The addition of flow cytometry to define the presence of abnormal monoclonal lymphocyte population(s) is also useful.

Histologic Findings

Depending on the underlying precipitating illness, changes may be seen in the bone marrow and lymph nodes. The presence of a malignant lymphoproliferative disorder may also be evident in these biopsy samples. Clumps of RBCs may be observed in the peripheral smear, as is discussed in Laboratory Studies (see Image 1 and below).


Peripheral blood smear showing several clumps of ...

Peripheral blood smear showing several clumps of RBCs with the largest in the center. These are typical of aggregates seen in persons with cold agglutinin disease.

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Peripheral blood smear showing several clumps of ...

Peripheral blood smear showing several clumps of RBCs with the largest in the center. These are typical of aggregates seen in persons with cold agglutinin disease.


Staging

Staging of cold agglutinin disease is applicable only if an underlying malignant disorder is present.

More on Cold Agglutinin Disease

Overview: Cold Agglutinin Disease
Differential Diagnoses & Workup: Cold Agglutinin Disease
Treatment & Medication: Cold Agglutinin Disease
Follow-up: Cold Agglutinin Disease
Multimedia: Cold Agglutinin Disease
References
Further Reading
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References

  1. Landsteiner K. [Uber beziehunger dem Blutserum und den Korperzellen] [German]. Munch med Wochenschr. 1903;50:1812.

  2. Schobuthe H. Antikorperbedingte hamolytische anamian. Vehr Dtsch Ges Inn Med. 1952;50:679.

  3. Schubothe H. The cold hemagglutinin disease. Semin Hematol. Jan 1966;3(1):27-47. [Medline].

  4. Dacie J, The auto-immune haemolytic anaemias. The Haemolytic Anaemias. Vol 3. 3rd ed. Edinburgh, United Kingdom: Churchill Livingstone; 1992:210-362.

  5. Harboe M, van Furth R, Schubothe H, Lind K, Evans RS. Exclusive occurrence of K chains in isolated cold haemagglutinins. Scand J Haematol. 1965;2(3):259-66. [Medline].

  6. Angevine CD, Andersen BR, Barnett EV. A cold agglutinin of the IgA class. J Immunol. Apr 1966;96(4):578-86. [Medline].

  7. Garratty G, Petz LD, Hoops JK. The correlation of cold agglutinin titrations in saline and albumin with haemolytic anaemia. Br J Haematol. Apr 1977;35(4):587-95. [Medline].

  8. Wortman J, Rosse W, Logue G. Cold agglutinin autoimmune hemolytic anemia in nonhematologic malignancies. Am J Hematol. 1979;6(3):275-83. [Medline].

  9. Petz LD, Garratty G, eds. Acquired Immune Hemolytic Anemias. New York, NY: Churchill Livingstone; 1980:37-50.

  10. Rosse WF, Adams JP. The variability of hemolysis in the cold agglutinin syndrome. Blood. Sep 1980;56(3):409-16. [Medline]. [Full Text].

  11. Roelcke D. The Lud cold agglutinin: a further antibody recognizing N-acetylneuraminic acid-determined antigens not fully expressed at birth. Vox Sang. Nov-Dec 1981;41(5-6):316-8. [Medline].

  12. Crisp D, Pruzanski W. B-cell neoplasms with homogeneous cold-reacting antibodies (cold agglutinins). Am J Med. Jun 1982;72(6):915-22. [Medline].

  13. Sokol RJ, Hewitt S, Stamps BK. Autoimmune hemolysis: mixed warm and cold antibody type. Acta Haematol. 1983;69(4):266-74. [Medline].

  14. Roelcke D. Reaction of anti-Gd, anti-Fl and anti-Sa cold agglutinins with p erythrocytes. Vox Sang. 1984;46(3):161-4. [Medline].

  15. Agarwal SK, Ghosh PK, Gupta D. Cardiac surgery and cold-reactive proteins. Ann Thorac Surg. Oct 1995;60(4):1143-50. [Medline].

  16. Packman CH, Leddy JP. Cryopathic hemolytic syndromes. In: Beutler E, Lichtman M, Coller B, Kippst, eds. Williams Hematology. 5th ed. New York, NY: McGraw-Hill; 1995:685-91.

  17. Jacobs A. Cold agglutinin hemolysis responding to fludarabine therapy. Am J Hematol. Dec 1996;53(4):279-80. [Medline].

  18. Terness P, Kirschfink M, Navolan D, et al. Inverse correlation between IgG-antihinge region and antierythrocyte autoantibody in chronic benign and malignant cold agglutination. J Clin Immunol. May 1997;17(3):220-7. [Medline].

  19. Thorpe SJ, Turner CE, Stevenson FK, et al. Human monoclonal antibodies encoded by the V4-34 gene segment show cold agglutinin activity and variable multireactivity which correlates with the predicted charge of the heavy-chain variable region. Immunology. Jan 1998;93(1):129-36. [Medline]. [Full Text].

  20. Ciejka JZ, Cook EB, Lawler D, et al. Severe cold agglutinin disease and cryoglobulinemia secondary to a monoclonal anti-Pr2 IgM lambda cryoagglutinin. Clin Exp Rheumatol. Mar-Apr 1999;17(2):227-31. [Medline].

  21. De Silva BD, McLaren K, Doherty VR. Equestrian perniosis associated with cold agglutinins: a novel finding. Clin Exp Dermatol. Jun 2000;25(4):285-8. [Medline].

  22. Potter KN. Molecular characterization of cold agglutinins. Transfus Sci. Feb-Apr 2000;22(1-2):113-9. [Medline].

  23. Jefferies LC, Carchidi CM, Silberstein LE. Naturally occurring anti-i/I cold agglutinins may be encoded by different VH3 genes as well as the VH4.21 gene segment. J Clin Invest. Dec 1993;92(6):2821-33. [Medline]. [Full Text].

  24. Berentsen S, Beiske K, Tjonnfjord GE. Primary chronic cold agglutinin disease: an update on pathogenesis, clinical features and therapy. Hematology. Oct 2007;12(5):361-70. [Medline]. [Full Text].

  25. Gertz MA. Management of cold haemolytic syndrome. Br J Haematol. Aug 2007;138(4):422-9. [Medline].

  26. McNicholl FP. Clinical syndromes associated with cold agglutinins. Transfus Sci. Feb-Apr 2000;22(1-2):125-33. [Medline].

  27. Maniatis A, Papayannopoulou T, Bertles JF. Fetal characteristics of erythrocytes in sickle cell anemia: an immunofluorescence study of individual cells. Blood. Jul 1979;54(1):159-68. [Medline]. [Full Text].

  28. Gertz MA. Cold agglutinin disease. Haematologica. Apr 2006;91(4):439-41. [Medline]. [Full Text].

  29. Sokol RJ, Booker DJ, Stamps R, Walewska R. Cold haemagglutinin disease: clinical significance of serum haemolysins. Clin Lab Haematol. Dec 2000;22(6):337-44. [Medline].

  30. Delval A, Stojkovic T, Vermersch P. Relapsing sensorimotor neuropathy with ophthalmoplegia, antidisialosyl antibodies, and extramembranous glomerulonephritis. Muscle Nerve. Feb 2006;33(2):274-7. [Medline].

  31. Siddiqui K, Cahalane E, Keogan M, Hardiman O. Chronic ataxic neuropathy with cold agglutinins: atypical phenotype and response to anti-CD20 antibodies. Neurology. Nov 11 2003;61(9):1307-8. [Medline].

  32. Skorupa A, Chaudhary UB, Lazarchick J. Cold agglutinin induced autoimmune hemolytic anemia and NK-cell leukemia: a new association. Am J Hematol. Jul 2007;82(7):668-71. [Medline]. [Full Text].

  33. Cao L, Kaiser P, Gustin D, Hoffman R, Feldman L. Cold agglutinin disease in a patient with uterine sarcoma. Am J Med Sci. Nov 2000;320(5):352-4. [Medline].

  34. Michaux L, Dierlamm J, Wlodarska L, et al. Trisomy 3q11-q29 is recurrently observed in B-cell non-Hodgkin's lymphomas associated with cold agglutinin syndrome. Ann Hematol. May 1998;76(5):201-4. [Medline].

  35. Chng WJ, Chen J, Lim S, et al. Translocation (8;22) in cold agglutinin disease associated with B-cell lymphoma. Cancer Genet Cytogenet. Jul 1 2004;152(1):66-9. [Medline].

  36. Kitamura T, Mizuta K, Kawarasaki H, Sugawara Y, Makuuchi M. Severe hemolytic anemia related to production of cold agglutinins following living donor liver transplantation: a case report. Transplant Proc. Feb 2003;35(1):399-400. [Medline].

  37. Tamura T, Kanamori H, Yamazaki E, et al. Cold agglutinin disease following allogeneic bone marrow transplantation. Bone Marrow Transplant. Mar 1994;13(3):321-3. [Medline].

  38. Thomson AW, Bonham CA, Zeevi A. Mode of action of tacrolimus (FK506): molecular and cellular mechanisms. Ther Drug Monit. Dec 1995;17(6):584-91. [Medline].

  39. Oshima M, Maeda H, Morimoto K, Doi M, Kuwabara M. Low-titer cold agglutinin disease with systemic sclerosis. Intern Med. Feb 2004;43(2):139-42. [Medline]. [Full Text].

  40. Torres JR, Villegas L, Perez H, et al. Low-grade parasitaemias and cold agglutinins in patients with hyper-reactive malarious splenomegaly and acute haemolysis. Ann Trop Med Parasitol. Mar 2003;97(2):125-30. [Medline].

  41. Johnson ST, McFarland JG, Kelly KJ, Casper JT, Gottschall JL. Transfusion support with RBCs from an Mk homozygote in a case of autoimmune hemolytic anemia following diphtheria-pertussis-tetanus vaccination. Transfusion. May 2002;42(5):567-71. [Medline].

  42. Gunduz Gedikoglu A, Cantez T. Haemolytic-anaemia relapses after immunisation and pertussis. Lancet. Oct 21 1967;2(7521):894-5. [Medline].

  43. Zupanska B, Lawkowicz W, Gorska B, et al. Autoimmune haemolytic anaemia in children. Br J Haematol. Nov 1976;34(3):511-20. [Medline].

  44. Haneberg B, Matre R, Winsnes R, et al. Acute hemolytic anemia related to diphtheria-pertussis-tetanus vaccination. Acta Paediatr Scand. May 1978;67(3):345-50. [Medline].

  45. Hamblin T. Management of cold agglutination syndrome. Transfus Sci. Feb-Apr 2000;22(1-2):121-4. [Medline].

  46. Teachey DT, Felix CA. Development of cold agglutinin autoimmune hemolytic anemia during treatment for pediatric acute lymphoblastic leukemia. J Pediatr Hematol Oncol. Jul 2005;27(7):397-9. [Medline].

  47. Webster D, Ritchie B, Mant MJ. Prompt response to rituximab of severe hemolytic anemia with both cold and warm autoantibodies. Am J Hematol. Apr 2004;75(4):258-9. [Medline]. [Full Text].

  48. Berentsen S, Ulvestad E, Tjonnfjord GE. B-lymphocytes as targets for therapy in chronic cold agglutinin disease. Cardiovasc Hematol Disord Drug Targets. Sep 2007;7(3):219-27. [Medline].

  49. Hoppe B, Gaedicke G, Kiesewetter H, Salama AR. Response to intravenous immunoglobulin G in an infant with immunoglobulin A-associated autoimmune haemolytic anaemia. Vox Sang. Feb 2004;86(2):151-3. [Medline].

  50. Atkinson VP, Soeding P, Horne G, Tatoulis J. Cold agglutinins in cardiac surgery: management of myocardial protection and cardiopulmonary bypass. Ann Thorac Surg. Jan 2008;85(1):310-1. [Medline].

  51. Inaba H, Geiger TL, Lasater OE, Wang WC. A case of hemoglobin SC disease with cold agglutinin-induced hemolysis. Am J Hematol. Jan 2005;78(1):37-40. [Medline]. [Full Text].

  52. O'Connor BM, Clifford JS, Lawrence WD, Logue GL. Alpha-interferon for severe cold agglutinin disease. Ann Intern Med. Aug 1 1989;111(3):255-6. [Medline].

  53. Hippe E, Jensen KB, Olesen H, Lind K, Thomsen PE. Chlorambucil treatment of patients with cold agglutinin syndrome. Blood. Jan 1970;35(1):68-72. [Medline]. [Full Text].

  54. Aoki A, Kay GL, Zubiate P, Ruggio J, Kay JH. Cardiac operation without hypothermia for the patient with cold agglutinin. Chest. Nov 1993;104(5):1627-9. [Medline].

  55. Robinson KL, Marasco SF, Street AM. Practical management of anticoagulation, bleeding and blood product support for cardiac surgery. Part two: transfusion issues. Heart Lung Circ. 2002;11(1):42-51. [Medline].

  56. Batalias L, Trakakis E, Loghis C, et al. Autoimmune hemolytic anemia caused by cold agglutinins in a young pregnant woman. J Matern Fetal Neonatal Med. Apr 2006;19(4):251-3. [Medline].

  57. Bossi E, Wagner HP. Autoimmune hemolytic anemia and cytomegalovirus infection in a six-months-old child, treated with azathioprine. Helv Paediatr Acta. Jun 1972;27(2):155-62. [Medline].

  58. Fest T, de Wazieres B, Lamy B, et al. Successful response to alpha-interferon 2b in a refractory IgM autoagglutinin-mediated hemolytic anemia. Ann Hematol. Sep 1994;69(3):147-9. [Medline].

  59. Geffray E, Najman A. [Efficacy of danazol in autoimmune hemolytic anemia with cold agglutinins. 4 cases] [French]. Presse Med. Sep 26 1992;21(31):1472-5. [Medline].

  60. Jefferies LC. Transfusion therapy in autoimmune hemolytic anemia. Hematol Oncol Clin North Am. Dec 1994;8(6):1087-104. [Medline].

  61. Mainwaring CJ, Walewska R, Snowden J, et al. Fatal cold anti-i autoimmune haemolytic anaemia complicating hairy cell leukaemia. Br J Haematol. Jun 2000;109(3):641-3. [Medline].

  62. Pascual V, Victor K, Spellerberg M, et al. VH restriction among human cold agglutinins. The VH4-21 gene segment is required to encode anti-I and anti-i specificities. J Immunol. Oct 1 1992;149(7):2337-44. [Medline].

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Further Reading

Related eMedicine Topics

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Keywords

cold agglutinin disease, cold agglutinin hemolytic anemia, idiopathic acquired hemolytic anemia, autoimmune hemolytic anemia, hemolytic anemia, CAD, acrocyanosis, cold-induced immune hemolytic anemia, mixed autoimmune hemolysis,
Mycoplasma pneumoniae, M pneumoniae, infectious mononucleosis, Epstein-Barr virus, EBV, influenza, human immunodeficiency virus, HIV, cytomegalovirus, CMV, rubella, varicella, varicella zoster virus, mumps, subacute bacterial endocarditis, syphilis, malaria, equestrian perniosis,

lymphoma, Waldenstrom syndrome, chronic lymphocytic leukemia, CLL, lymphoproliferative disease, autoimmune disease, myeloma, Kaposi sarcoma, Kaposi's sarcoma, angioimmunoblastic lymphoma

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Contributor Information and Disclosures

Author

Sharon Georgy, MD, Resident Physician, Department of Internal Medicine, University of South Florida
Sharon Georgy, MD is a member of the following medical societies: Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Richard F Lockey, MD, University Distinguished Health Professor, Professor of Medicine, Pediatrics and Public Health, Joy McCann Culverhouse Chair in Allergy and Immunology, University of South Florida College of Medicine; Director, Division of Allergy and Immunology, James A Haley Veterans' Hospital
Richard F Lockey, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American Association for the Advancement of Science, American College of Chest Physicians, American College of Occupational and Environmental Medicine, American College of Physicians, American Medical Association, and Florida Medical Association
Disclosure: Nothing to disclose.

Rajalaxmi McKenna, MD, FACP, Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Harry L Messmore, Jr, MD, Professor, Department of Medicine, Division of Hematology/Oncology, Loyola University Stritch School of Medicine
Harry L Messmore, Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Angiology, American College of Physicians, American Heart Association, American Society of Hematology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey Lee Kishiyama, MD, Assistant Clinical Professor of Medicine, University of California at San Francisco School of Medicine; Consulting Staff, Allergy and Asthma Associates of Santa Clara Valley Research Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Samuel R Marney, Jr, MD, Director, Associate Professor, Department of Internal Medicine, Division of Allergy and Immunology, Vanderbilt University School of Medicine
Samuel R Marney, Jr, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, American College of Physicians, and Tennessee Medical Association
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michael A Kaliner, MD, Clinical Professor of Medicine, George Washington University School of Medicine; Chief, Section of Allergy and Immunology, Washington Hospital Center; Medical Director, Institute for Asthma and Allergy
Michael A Kaliner, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Allergy, Asthma and Immunology, American Society for Clinical Investigation, American Thoracic Society, and Association of American Physicians
Disclosure: Abbott Consulting fee Consulting; Alcon Consulting fee Consulting; Glaxo Consulting fee Consulting; Greer Consulting fee Consulting; Sanofi Consulting fee Consulting; Schering Consulting fee Consulting; Teva  Consulting; Meda Honoraria Speaking and teaching

 
 
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