Granuloma Annulare Workup

  • Author: Ruby Ghadially, MBChB, FRCP(C)Derm; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jan 25, 2012
 

Laboratory Studies

  • Laboratory studies are largely noncontributory in patients with granuloma annulare (GA). With a classic history and unremarkable physical examination findings (other than the presenting lesion[s]), no additional workup is necessary.
    • If, however, a thorough history is not available or systemic disease is considered likely, appropriate laboratory evaluations should be performed to exclude other diagnostic possibilities.
    • For example, in subcutaneous granuloma annulare, a CBC count, an erythrocyte sedimentation rate, and a rheumatoid factor study may assist in excluding other possible causes for nodules.
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Imaging Studies

  • Imaging studies are not generally necessary in diagnosing granuloma annulare. However, radiographs, CT scans, or MRIs may be helpful in the evaluation of atypical subcutaneous lesions.
    • Radiographs of subcutaneous granuloma annulare show a nonspecific soft tissue mass without calcification.
    • On CT scans, subcutaneous granuloma annulare appears as a poorly defined mass with variable attenuation and variable contrast enhancement.
    • On MRIs, subcutaneous granuloma annulare appears as a mass with poorly defined margins that is limited to subcutaneous tissue. MRI findings may be suggestive of, but not diagnostic of, subcutaneous granuloma annulare.[9, 10]
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Procedures

  • Biopsy is recommended for a subcutaneous lesion and for an atypical presentation with respect to history (ie, rapid enlargement, pain) or location of lesion.
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Histologic Findings

Early interstitial or incomplete granuloma annulare lesions show an interstitial pattern characterized by lymphocytes around vessels of the superficial and deep plexuses and by macrophages scattered between reticular dermal collagen bundles that are separated by mucin within which mast cells may be found. Mucin in granuloma annulare is hyaluronic acid and is visible in sections stained with hematoxylin and eosin as faintly basophilic stringy material. Its presence can be confirmed by staining with colloidal iron or Alcian blue at pH 2.5.

Fully evolved granuloma annulare lesions and deep subcutaneous granuloma annulare nodules demonstrate palisaded granulomatous dermatitis or a septal and lobular panniculitis, respectively. Macrophages surround acellular necrobiotic areas in which collagen bundles are thinned, or they sometimes have a pale, homogeneous, light-blue appearance, the latter of which is due to the presence of mucin.

In many cases of subcutaneous granuloma annulare, and in some dermal infiltrates, the centers of granulomas contain degenerated, homogeneous-appearing collagen and are deeply eosinophilic. In some sections, necrotic small vessels in the centers of palisaded foci are surrounded by nuclear dust. Presence of fibrinogen can be shown by direct immunofluorescence in the centers of palisaded granulomas. In perforating lesions, necrobiotic material is extruded through focal perforations. Epidermal hyperplasia at the edge of the perforation forms a pseudochannel communicating with an underlying necrobiotic granuloma.

Rare cases of nonnecrobiotic, sarcoidal, or tuberculoid granuloma annulare are also described.

Actinic annulare, also known as annular elastolytic giant cell granuloma, may lack the classic palisaded arrangement observed in granuloma annulare. Although elastosis is abundant in the mid dermis outside the granuloma, elastic tissue is absent from the center of the annulus. Giant cells frequently abut elastotic tissue, and phagocytosed elastotic fibers are noted in histiocytic cells at the advancing edge. Collagen has a normal appearance outside the lesion but a finely fibrillar pattern within the annulus. Mucin deposition is not increased as it is in granuloma annulare. Thus, actinic annulare can be distinguished histologically from granuloma annulare by a preponderance of giant cells in relation to elastotic tissue, by absence of mucin, and, occasionally, by absence of palisading histiocytes around granulomas.

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Contributor Information and Disclosures
Author

Ruby Ghadially, MBChB, FRCP(C)Derm  Professor, Department of Dermatology, University of California, San Francisco, School of Medicine

Ruby Ghadially, MBChB, FRCP(C)Derm is a member of the following medical societies: American Academy of Dermatology, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Akos Z Szabo, MD  Resident Physician, Department of Obstetrics and Gynecology, University of Heidelberg Medical Center, Germany

Disclosure: Nothing to disclose.

Amit Garg, MD  Director of Clinical Elective in Dermatology, Assistant Professor, Department of Internal Medicine, Division of Dermatology, University of Massachusetts Medical School

Amit Garg, MD is a member of the following medical societies: American Academy of Dermatology and American Medical Student Association/Foundation

Disclosure: Abbott Immunology Honoraria Speaking and teaching; Centocor Grant/research funds Other; RegenRx Grant/research funds Other

Specialty Editor Board

James J Nordlund, MD  Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine

James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Richard P Vinson, MD  Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Rosalie Elenitsas, MD  Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology

Disclosure: Lippincott Williams Wilkins Royalty Textbook editor; DLA Piper Consulting fee Consulting

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.

References

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