eMedicine Specialties > Rheumatology > Vasculitis

Serum Sickness: Treatment & Medication

Author: Hassan M Alissa, MD, Fellow in Rheumatology, Department of Internal Medicine, Loyola University Medical Center
Coauthor(s): Elaine Adams, MD, Chief of Medical Service, Chief of Rheumatology Section, Hines Veterans Affairs Hospital; Associate Chief, Associate Professor, Department of Internal Medicine, Loyola University School of Medicine; Rochella Abaygar Ostrowski, MD, Assistant Professor, Department of Medicine, Division of Rheumatology, Loyola University Medical Center; Staff Physician, Department of Medicine, Division of Rheumatology, Edward Hines Jr Veterans Affairs Hospital; Richard Hariman, MD, Fellow, Department of Rheumatology, Loyola University Medical Center
Contributor Information and Disclosures

Updated: Jun 22, 2009

Treatment

Medical Care

Withdrawal of the offending agent is the mainstay of treatment in serum sickness. Anti-inflammatories and antihistamines provide symptomatic relief. Severe cases (multisystem involvement with significant symptomatology5 ) may warrant a brief course of corticosteroids.

In some cases, plasmapheresis can attenuate serum sickness.9

Consultations

The presenting features of fever, rash, and joint pain may be observed in numerous infectious and autoimmune diseases. Consider a consultation with an allergist or a rheumatologist.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Nonsteroidal anti-inflammatory drugs

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may also exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.


Ibuprofen (Motrin, Ibuprin)

Decreases inflammation by blocking prostaglandin synthesis and reduces fever by acting on the hypothalamic temperature-regulating center. Usually administered for mild symptoms of arthralgia, myalgia, or fever.

Adult

200-800 mg PO qid; not to exceed 3200 mg

Pediatric

<12 years: 5-10 mg/kg PO qid
>12 years: Administer as in adults

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and toxicity; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, asthma, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Antihistamines

agents act by competitive inhibition of histamine at the H1 receptor. This mediates the wheal and flare reactions, bronchial constriction, mucous secretion, smooth muscle contraction, edema, hypotension, CNS depression, and cardiac arrhythmias.


Diphenhydramine HCL (Benadryl)

Blocks histamine H1 receptors on the target tissue. For urticarial rash.

Adult

25-50 mg PO/IM qid

Pediatric

5 mg/kg/d PO/IV/IM divided tid/qid

Potentiates effect of CNS depressants; because of alcohol content, do not administer syrup dosage form to patient taking medications that can cause disulfiramlike reactions

Documented hypersensitivity; MAOIs

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in neonates and nursing mothers; may exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, urinary tract obstruction, asthma

Corticosteroids

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


Prednisone (Deltasone, Orasone, Sterapred)

Acts by altering the number and availability of leukocytes, reducing vascular permeability, and suppressing cytokines. Mainstays of treatment in severe cases; usually administered in moderate doses for 1-2 weeks. This or other oral forms of corticosteroids (eg, prednisolone) are useful in managing mild-to-moderate serum sickness treated in an outpatient setting.

Adult

20-40 mg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve

Pediatric

0.2-0.5 mg/kg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

More on Serum Sickness

Overview: Serum Sickness
Differential Diagnoses & Workup: Serum Sickness
Treatment & Medication: Serum Sickness
Follow-up: Serum Sickness
References
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References

  1. Pichler, WJ. Drug hypersensitivity. In: Rich RR, ed. Clinical Immunology Principles and Practice. 3rd ed. St Louis, Mo: Mosby/Elsevier; 2008:714.

  2. Mannik M. Serum sickness and pathophysiology of immune complexes. In: Rich RR, ed. Clinical Immunology Principles and Practice. St. Louis, Mo: Mosby; 1996:1062-71.

  3. Dixon FJ, Cochrane CC. Immune complex injury. In: Samter M, ed. Immunological Diseases. 4th ed. New York, NY: Little, Brown and Company; 1988:233.

  4. Sicherer SH, Leung DYM. Serum sickness. In: Kliegman, ed. Nelson Textbook of Pediatrics. 18th ed. Online Edition, Chapter 149.

  5. Erffmeyer JE. Serum sickness. Ann Allergy. Feb 1986;56(2):105-9. [Medline].

  6. King BA, Geelhoed GC. Adverse skin and joint reactions associated with oral antibiotics in children: the role of cefaclor in serum sickness-like reactions. J Paediatr Child Health. Dec 2003;39(9):677-81. [Medline].

  7. Abraham E, Wunderink R, Silverman H, et al. Efficacy and safety of monoclonal antibody to human tumor necrosis factor alpha in patients with sepsis syndrome. A randomized, controlled, double-blind, multicenter clinical trial. TNF-alpha MAb Sepsis Study Group. JAMA. Mar 22-29 1995;273(12):934-41. [Medline].

  8. Karliner JS, Belaval GS. Incidence of reactions following administration of antirabies serum; study of 526 cases. JAMA. Aug 2 1965;193:359-62. [Medline].

  9. Frank, MM, Lawley TJ. Immune complexes and allergic disease. In: Middleton E Jr, ed. Allergy Principles and Practice. 5th ed. St Louis, Mo: Mosby; 1998:704-6.

  10. Lawley TJ, Frank MM. Immune complexes and allergic diseases. In: Middleton E Jr, ed. Allergy Principles and Practice. 4th ed. St. Louis, Mo: Mosby; 1993:990.

  11. Lawley TJ, Bielory L, Gascon P, Yancey KB, Young NS, Frank MM. A prospective clinical and immunologic analysis of patients with serum sickness. N Engl J Med. Nov 29 1984;311(22):1407-13. [Medline].

  12. Pilette C, Coppens N, Houssiau FA, Rodenstein DO. Severe serum sickness-like syndrome after omalizumab therapy for asthma. J Allergy Clin Immunol. Oct 2007;120(4):972-3. [Medline].

  13. Disperati P, Hicks LK, Buckstein R. Rituximab-induced serum sickness in a patient with follicular lymphoma. Leuk Lymphoma. Aug 2007;48(8):1633-5. [Medline].

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Further Reading

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Keywords

serum sickness, hypersensitivity vasculitis, drug-induced vasculitis, immune complex disease, foreign serum, serum protein, serum disease, serum reaction, foreign proteins, haptens, antigens, leukocytoclastic vasculitis, secondary serum sickness, antirabies serum, tetanus antitoxin

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Contributor Information and Disclosures

Author

Hassan M Alissa, MD, Fellow in Rheumatology, Department of Internal Medicine, Loyola University Medical Center
Hassan M Alissa, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Elaine Adams, MD, Chief of Medical Service, Chief of Rheumatology Section, Hines Veterans Affairs Hospital; Associate Chief, Associate Professor, Department of Internal Medicine, Loyola University School of Medicine
Elaine Adams, MD is a member of the following medical societies: American College of Physicians and American College of Rheumatology
Disclosure: Nothing to disclose.

Rochella Abaygar Ostrowski, MD, Assistant Professor, Department of Medicine, Division of Rheumatology, Loyola University Medical Center; Staff Physician, Department of Medicine, Division of Rheumatology, Edward Hines Jr Veterans Affairs Hospital
Rochella Abaygar Ostrowski, MD is a member of the following medical societies: American College of Physicians and American College of Rheumatology
Disclosure: Nothing to disclose.

Richard Hariman, MD, Fellow, Department of Rheumatology, Loyola University Medical Center
Richard Hariman, MD is a member of the following medical societies: American College of Rheumatology
Disclosure: Nothing to disclose.

Medical Editor

John Varga, MD, Professor, Department of Internal Medicine, Division of Rheumatology, Northwestern University
John Varga, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology, Central Society for Clinical Research, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Elliot Goldberg, MD, Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine
Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

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: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; West Penn Allegheny Health System None Board membership

 
 
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