Kawasaki Disease Medication

  • Author: Noah S Scheinfeld, MD, JD, FAAD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Jan 5, 2012
 

Medication Summary

The goals of pharmacotherapy in Kawasaki disease are to reduce inflammation and platelet activation. Early and aggressive intervention improves outcome. Standard treatment includes intravenous immunoglobulin (IVIG) to treat inflammation and to prevent consequences of coronary artery disease.

Aspirin has traditionally been part of standard treatment. Although its value has been called into question, most experts use high-dose aspirin for a variable period, followed by lower-dose aspirin for its antiplatelet effects. Other anticoagulants or antiplatelet agents (eg, warfarin, dipyridamole) are occasionally used.

Ibuprofen antagonizes aspirin's antiplatelet activity and should be avoided.

Because these children will take aspirin for a variable period, vaccination against influenza and varicella must be ensured.

Corticosteroids have been used, typically in patients who do not respond to standard therapies. Their use in primary treatment is controversial. Treatment of IVIG-resistant Kawasaki disease with methotrexate or cyclophosphamide has been reported to be effective. Refractory Kawasaki disease with coronary aneurysms has been treated with infliximab.[81]

Patients who are at increased risk for thrombus with significant coronary involvement have been treated with various types of medications in addition to the routine aspirin therapy. Antiplatelet medications such as clopidogrel and dipyridamole antagonize adenosine diphosphate and have a synergistic effect when given with aspirin.

Anticoagulants such as warfarin and low molecular weight heparin are used in patients with large aneurysms in whom the risk of thrombus is high. The goal is to maintain an international normalized ratio (INR) of 2-2.5.

Patients who have thrombosis and acute coronary occlusion should be treated with medical therapy because of the risk of rupture if interventional cardiac catheterization is attempted. In addition to standard treatments and warfarin, thrombolytics are given.

Because the potential exists for allergic complications with the use of streptokinase in patients who have had streptococcal pharyngitis in the last 6 months and because the triggering factor for Kawasaki disease remains uncertain, this medication is best avoided. Other drugs in this category, such as tissue plasminogen activator, tenecteplase-tissue plasminogen activator, and urokinase, may be more appropriate.

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Immunomodulatory agents

Class Summary

IVIG is a purified preparation of gamma globulin. It is derived from large pools of human plasma comprising 4 subclasses of antibodies, approximating the distribution of human serum.

These agents are used to improve clinical and immunologic aspects of Kawasaki disease. They may decrease autoantibody production and increase solubilization and removal of immune complexes.

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Immune globulin, intravenous (Carimune, Gammagard, Gamunex-C, Octagam)

 

IVIG is generally recommended as first-line therapy. It neutralizes circulating myelin antibodies by means of anti-idiotypic antibodies; downregulates proinflammatory cytokines, including interferon-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; and promotes remyelination. It may increase cerebrospinal fluid IgG levels (10%).

IVIG reduces the prevalence of coronary abnormalities. It leads to rapid defervescence and more rapid normalization of acute-phase reactants.

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Nonsteroidal Anti-Inflammatory Agents/Salicylates (NSAIDs)

Class Summary

These agents inhibit prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2. Adequate anti-inflammatory therapy requires that aspirin be combined with gamma globulin. Children with coronary artery disease have received aspirin for prolonged periods.

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Aspirin (Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin, Ecotrin)

 

Aspirin is used to decrease inflammation, inhibit platelet aggregation, and improve complications of venous stasis and thrombosis. It irreversibly inactivates cyclooxygenase, ultimately preventing thromboxane A2 production in platelets. Platelet function does not fully recover until new platelets are made (in 7-10 days). It is first-line therapy, along with IVIG.

Oral absorption may decrease in Kawasaki disease to < 50% (vs typical bioavailability of 85-90%). Altered bioavailability may explain why higher doses are required to achieve a salicylate serum concentration >20 mg/dL.

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Antiplatelet Agents, Hematologic

Class Summary

Besides aspirin, dipyridamole may be used to prevent microthrombus formation.

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Dipyridamole (Persantine)

 

Dipyridamole is a platelet-adhesion inhibitor that possibly inhibits red blood cell uptake of adenosine, itself an inhibitor of platelet reactivity. It may inhibit phosphodiesterase activity, leading to increased cyclic adenosine monophosphate (cAMP) levels in platelets and formation of potent platelet activator thromboxane A2.

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Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

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Prednisolone acetate (Prelone, Flo-Pred, Millipred)

 

Prednisolone is indicated for the treatment of steroid-responsive inflammation of the palpebral and bulbar conjunctiva, cornea, and anterior segment. It decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Methylprednisolone A-Methapred, Medrol, Solu-Medrol)

 

Methylprednisolone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

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Immunosuppressants

Class Summary

These agents inhibit key factors that mediate immune reactions.

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Infliximab (Remicade)

 

Infliximab may be added to treatment if steroids and other immunosuppressant drugs are ineffective in achieving or maintaining remission. Infliximab is a chimeric IgG1k monoclonal antibody that neutralizes cytokine TNF-α and inhibits its binding to the TNF-α receptor. It reduces the infiltration of inflammatory cells and TNF-α production in inflamed areas.

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Contributor Information and Disclosures
Author

Noah S Scheinfeld, MD, JD, FAAD  Assistant Clinical Professor, Department of Dermatology, Columbia University College of Physicians and Surgeons; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, and New York Eye and Ear Infirmary; Private Practice

Noah S Scheinfeld, MD, JD, FAAD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Optigenex Consulting fee Independent contractor

Coauthor(s)

Elena L Jones, MD  Clinical Assistant Professor of Dermatology, Columbia University College of Physicians and Surgeons; Clinic Chief, Department of Dermatology, St Luke's-Roosevelt Hospital Center

Disclosure: Nothing to disclose.

Paul R Ogershok, MD  Allergist, Allergy, Asthma, and Immunology Clinic, Southwest Regional Medical Center

Paul R Ogershok, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma and Immunology, Pennsylvania Medical Society, and West Virginia State Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Jeffrey Glenn Bowman, MD, MS Consulting Staff, Highfield MRI, Columbus, Ohio

Disclosure: Nothing to disclose.

Lawrence H Brent, MD Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Genentech Honoraria Speaking and teaching; Genentech Grant/research funds Other; Amgen Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Abbott Immunology Honoraria Speaking and teaching; Takeda Honoraria Speaking and teaching; UCB Speaking and teaching; Omnicare Consulting fee Consulting; Centocor Consulting fee Consulting

Herbert S Diamond, MD Professor of Medicine, Temple University School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Kristine M Lohr, MD, MS Professor, Department of Internal Medicine, Center for the Advancement of Women's Health and Division of Rheumatology, Director, Rheumatology Training Program, University of Kentucky College of Medicine

Kristine M Lohr, MD, MS is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Nothing to disclose.

Catherine V Parrillo, DO, FACOP, FAAP, Retired, Clinical Assistant Professor, Department of Pediatrics, Philadelphia College of Osteopathic Medicine

Catherine V Parrillo, DO, FACOP, FAAP, is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

Disclosure: Nothing to disclose

Steven J Parrillo, DO, FACOEP, FACEP Associate Professor, Emergency Medicine, Jefferson Medical College and Philadelphia College of Osteopathic Medicine; Medical Director, Department of Emergency Medicine, Einstein Elkins Park; Chair, Emergency Management Committee, Albert Einstein Healthcare Network; Adjunct Professor, School of Health and Science, Philadelphia University; Medical Director and Faculty, Disaster Medicine and Management Masters Program, Philadelphia University

Steven J Parrillo, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Osteopathic Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Martin Weisse, MD Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Grace M Young, MD Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians

Disclosure: Nothing to disclose.

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Patchy generalized macular erythema, which is also typical of some viral exanthems.
Peeling and erythema of the fingertips.
Strawberry tongue.
Pediatrics, Kawasaki disease. Note the appearance of the hand and lips. Photo courtesy of Sam Richardson, MD.
Clinical manifestations and time course of Kawasaki disease.
Oral manifestations of Kawasaki disease: red lips and strawberry tongue.
 
 
 
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