Pretibial Myxedema Clinical Presentation

  • Author: George E vonHilsheimer, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Nov 28, 2011
 

History

  • The onset of PTM most commonly occurs 1-2 years after the diagnosis of Graves disease, but it may occur earlier or later. PTM in the absence of Graves disease is uncommon. Most patients who develop PTM also have Graves ophthalmopathy, with the onset of dermopathy typically following the onset of ophthalmopathy by 6-12 months. The natural history of PTM is not well defined. Available data indicate that about 10-26% of patients eventually experience complete remission, and about 24% have partial remission.
  • Skin lesions or areas of nonpitting edema appear on the anterior or lateral aspects of the legs or in sites of old or recent trauma in patients with Graves disease.
  • Otherwise unexplained skin lesions or areas of nonpitting edema occur in patients with thyroid disease.
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Physical

Pertinent physical findings of PTM are limited to the skin. However, physical findings consistent with Graves thyrotoxicosis are significant because they are indicative of PTM as the etiology of the skin lesions. This observation is especially true regarding the finding of proptosis because nearly all patients who develop PTM have thyroid ophthalmopathy. Ophthalmopathy usually occurs prior to dermopathy.[3] Thyroid acropachy occurs in 1% of patients with Graves disease. It is clinically characterized by clubbing of the fingers and the toes, periosteal proliferation of the shafts of the phalanges and other distal long bones, and swelling of the soft tissues overlying affected bony structures. When present, acropachy usually follows dermopathy. Graves dermopathy and acropachy appear to be markers of severe ophthalmopathy.

Bilateral erythematous infiltrative plaques in theBilateral erythematous infiltrative plaques in the pretibial areas.
  • Primary lesion
    • Early lesions are bilateral, firm, nonpitting, asymmetrical plaques or nodules.
    • Hair follicles are sometimes prominent, giving a peau d'orange texture.
    • Areas of nonpitting edema may develop.
    • In the elephantiasic form of PTM, lesions may coalesce to give the entire extremity an enlarged, verruciform appearance.
    • Overlying hyperhidrosis or hypertrichosis may be present in these cases.
  • Distribution
    • Lesions characteristically appear on the lateral or anterior aspect of the legs, but they may occur on the thighs,[4] the shoulders, the hands, the forehead, or any other skin surface.
    • Lesions often occur in areas of recent or prior trauma or skin graft donor sites.
  • Color: Lesions are characteristically shiny pink to purple-brown.
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Causes

  • The cause is unknown.
  • PTM is generally considered a cutaneous manifestation of thyroid disease.
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Contributor Information and Disclosures
Author

George E vonHilsheimer, MD  Assistant Professor of Dermatology, Uniformed Services University of the Health Sciences; Chief, Staff Dermatologist, Department of Medicine, Martin Army Community Hospital, Fort Benning, Georgia

George E vonHilsheimer, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Association of Military Dermatologists

Disclosure: Nothing to disclose.

Coauthor(s)

Laurel R Stearns, DO  Resident in Dermatology, National Capital Consortium

Laurel R Stearns, DO is a member of the following medical societies: American Academy of Dermatology and Association of Military Osteopathic Physicians and Surgeons

Disclosure: Nothing to disclose.

Kathryn K Garner, MD  Staff Physician, Family Health Clinic, Ehrling Bergquist Clinic, Offutt AFB, NE

Kathryn K Garner, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Physicians, and Uniformed Services Academy of Family Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Gregory J Raugi, MD, PhD  Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Christen M Mowad, MD  Associate Professor, Department of Dermatology, Geisinger Medical Center

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

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 author, Purnima Sau, MD, to the development and writing of this article.

References

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  9. Shinohara M, Hamasaki Y, Katayama I. Refractory pretibial myxoedema with response to intralesional insulin-like growth factor 1 antagonist (octreotide): downregulation of hyaluronic acid production by the lesional fibroblasts. Br J Dermatol. Nov 2000;143(5):1083-6. [Medline].

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Bilateral erythematous infiltrative plaques in the pretibial areas.
Deposition of mucin in the reticular dermis (hematoxylin and eosin stain, original magnification X25).
Blue staining of mucin with colloidal iron stain (original magnification X25).
 
 
 
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