Sections

Medication

Medication Summary

The overall aim of therapy is treatment of any underlying condition and general suppression of the immune response. Mild anti-inflammatory medications (eg, NSAIDs) are effective in mild cases, and corticosteroid therapy is reserved for the more severe or refractory cases. Patients who require potent immunosuppression or other more aggressive therapies for severe disease should be treated by a specialist. Cyclophosphamide may be used as a steroid-sparing agent or administered concomitantly in severe cases of vasculitis, particularly in patients with renal disease. Azathioprine is commonly used as a steroid-sparing agent, and chlorambucil has also been used for severe vasculitis.

Class Summary

NSAIDs such as ibuprofen, naproxen, and indomethacin have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. NSAIDs may have additional mechanisms, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions. NSAIDs are used to reduce the resultant inflammatory response of cryoglobulin precipitation.

Ibuprofen (Advil, Motrin, Excedrin IB, Ibuprin)

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NSAIDs are the DOC in patients with mild symptoms of arthralgia or fatigue. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Class Summary

These medications are used to reduce the resultant immune response from cryoglobulin precipitation, particularly in patients with more severe symptoms or some evidence of organ damage.

Prednisone (Sterapred)

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DOC in patients with evidence of acute vasculitis.

Class Summary

These are commonly used as steroid-sparing agents.

Cyclophosphamide (Cytoxan, Neosar)

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Chemically related to nitrogen mustards. As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, interfering with growth of normal and neoplastic cells.

Azathioprine (Imuran)

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Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.

Chlorambucil (Leukeran)

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Alkylates and cross-links strands of DNA, inhibiting DNA replication and RNA transcription.

Class Summary

These agents are naturally produced proteins with antiviral, antitumor, and immunomodulatory actions. IFN-alfa is generally administered subcutaneously.

Interferon alfa-2b (Intron A)

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Protein product manufactured by recombinant DNA technology. Mechanism of antitumor activity is not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles. Has antiviral activity in HCV infection.

Peginterferon alfa-2a (Pegasys)

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Used in combination with ribavirin to treat patient with chronic HCV infection who have compensated liver disease and have not received IFN-alfa previously. Consists of interferon alfa-2a attached to a 40-kD branched PEG molecule. Predominantly metabolized by the liver.

Peginterferon alfa 2b (PEG-Intron)

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Escherichia coli recombinant product. Used to treat chronic HCV infection in patients not previously treated with INF-alfa who have compensated liver disease. Exerts cellular activities by binding to specific membrane receptors on cell surface, which, in turn, may suppress cell proliferation and may enhance phagocytic activity of macrophages. May also increase cytotoxicity of lymphocytes for target cells and inhibit virus replication in virus-infected cells.

Class Summary

Nucleoside analogs are initially phosphorylated by viral thymidine kinase to eventually form a nucleoside triphosphate. These molecules inhibit herpes simplex virus (HSV) polymerase with 30-50 times the potency of human alpha-DNA polymerase.

Ribavirin (Virazole)

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Antiviral nucleoside analogs. Chemical name is 1-beta-D-ribofuranosyl-1H-1,2,4-triazole-3-carboxamide. Given alone, has little effect on the course of HCV infection. When used with IFN, significantly augments rate of sustained virologic response.

Class Summary

This agent inhibits the viral reverse transcriptase enzyme, which limits viral replication.

Entecavir (Baraclude)

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Guanosine nucleoside analogue with activity against HBV polymerase. Competes with natural substrate deoxyguanosine triphosphate to inhibit HBV polymerase activity (ie, reverse transcriptase). Less effective for lamivudine-refractory HBV infection. Indicated for treatment of chronic hepatitis B infection. Available as tab and oral solution (0.05 mg/mL; 0.5 mg = 10 mL).

Class Summary

These agents inhibit cell growth and proliferation.

Rituximab (Rituxan)

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Genetically engineered human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.

Immunomodulates response against malignant cells.

Questions

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Media Gallery

Rash on lower extremities typical of cutaneous small-vessel vasculitis due to cryoglobulinemia secondary to hepatitis C infection.
Renal biopsy sample that shows membranoproliferative glomerulonephritis in a patient with hepatitis C–associated cryoglobulinemia (hematoxylin and eosin; magnified X 200).

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Author

Colin C Edgerton, MD Clinical Assistant Professor, Department of Medicine, Medical College of Georgia; Clinical Assistant Professor, Department of Medicine, Uniformed Services University

Colin C Edgerton, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, Clinical Immunology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Lawrence H Brent, MD Associate Professor of Medicine, Sidney Kimmel 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, American College of Rheumatology

Disclosure: Stock ownership for: Johnson & Johnson.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; 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, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Kristine M Lohr, MD, MS Professor, Department of Internal Medicine, Interim Chief, 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, American College of Rheumatology

Disclosure: Nothing to disclose.

Adam M Tritsch, MD Resident Physician, Department of Internal Medicine, Eisenhower Army Medical Center, Fort Gordon, Georgia

Adam M Tritsch, MD is a member of the following medical societies: American College of Physicians

Disclosure: Partner received stocks from Amgen for none.

Acknowledgements

Craig Ainsworth, MD Chief of Medical Residents, Department of Internal Medicine, Eisenhower Army Medical Center

Craig Ainsworth, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Robert John Oglesby, MD Chief of Rheumatology Service, Department of Medicine, Walter Reed Army Medical Center; Associate Professor of Medicine, Uniformed Services University of the Health Sciences

Robert John Oglesby, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology, and Arthritis Foundation

Disclosure: Nothing to disclose.

Timothy M Straight, MD Instructor, Department of Medicine, Uniformed Services University of the Health Sciences

Disclosure: Nothing to disclose.

Cryoglobulinemia Medication

Medication Summary

Nonsteroidal anti-inflammatory drugs

Class Summary

Ibuprofen (Advil, Motrin, Excedrin IB, Ibuprin)

Ibuprofen (Advil, Motrin, Excedrin IB, Ibuprin)

Corticosteroids

Class Summary

Prednisone (Sterapred)

Prednisone (Sterapred)

Immunosuppressive agents

Class Summary

Cyclophosphamide (Cytoxan, Neosar)

Cyclophosphamide (Cytoxan, Neosar)

Azathioprine (Imuran)

Azathioprine (Imuran)

Chlorambucil (Leukeran)

Chlorambucil (Leukeran)

Interferons

Class Summary

Interferon alfa-2b (Intron A)

Interferon alfa-2b (Intron A)

Peginterferon alfa-2a (Pegasys)

Peginterferon alfa-2a (Pegasys)

Peginterferon alfa 2b (PEG-Intron)

Peginterferon alfa 2b (PEG-Intron)

Antiviral agents

Class Summary

Ribavirin (Virazole)

Ribavirin (Virazole)

Antiviral Agent, Oral

Class Summary

Entecavir (Baraclude)

Entecavir (Baraclude)

Antineoplastic agents

Class Summary

Rituximab (Rituxan)

Rituximab (Rituxan)

Cryoglobulinemia Medication

Medication Summary

Nonsteroidal anti-inflammatory drugs

Class Summary

Ibuprofen (Advil, Motrin, Excedrin IB, Ibuprin)

Corticosteroids

Class Summary

Prednisone (Sterapred)

Immunosuppressive agents

Class Summary

Cyclophosphamide (Cytoxan, Neosar)

Azathioprine (Imuran)

Chlorambucil (Leukeran)

Interferons

Class Summary

Interferon alfa-2b (Intron A)

Peginterferon alfa-2a (Pegasys)

Peginterferon alfa 2b (PEG-Intron)

Antiviral agents

Class Summary

Ribavirin (Virazole)

Antiviral Agent, Oral

Class Summary

Entecavir (Baraclude)

Antineoplastic agents

Class Summary

Rituximab (Rituxan)

References

Tables

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