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Pretibial Myxedema

  • Author: Ranjodh Singh Gill, MD, FACP, CCD; Chief Editor: Dirk M Elston, MD  more...
Updated: Feb 02, 2016


Pretibial myxedema (PTM) or, more appropriately, thyroid dermopathy is a term used to describe localized lesions of the skin resulting from the deposition of hyaluronic acid, usually as a component of thyroid disease. Thyroid dermopathy occurs rarely. Although PTM is most often confined to the pretibial area, it may occur anywhere on the skin, especially the ankle, dorsum of the foot, knees, shoulders, elbows, upper back, pinnae, nose, and neck.[1] It is nearly always associated with autoimmune thyroid disease (ie, Graves Disease for more information).



Pretibial myxedema (PTM) occurs as a result of the deposition of hyaluronic acid in the dermis and subcutis. The precise cause of this phenomenon remains uncertain. A leading theory proposes that fibroblasts are stimulated to produce abnormally high amounts of glycosaminoglycan under the influence of cytokines due to exposure to thyrotropin receptor antibody (TRAB) and antigen-specific T cells. TRAB-binding sites are found in the plasma membranes of fibroblasts derived from the skin of patients with PTM. TRAB is present in the serum of most patients with PTM (80-100%), but it has also been found in the serum of patients without PTM.[2]

Research published in 2006 suggests that it may not be just the high level of glycosaminoglycans, but the change in percentage of the constituents of the glycosaminoglycans in the blood that leads to the development of PTM. Thyroid hormones, by means of their influence on prostaglandin metabolism, alter the synthesis and degradation of glycosaminoglycans. Prostaglandin degradation may be what is changed in the course of Graves disease, based on findings that glycosaminoglycan synthesis is reduced, as is extracellular matrix assembly in vitro with exposure to T3 excess.[3]

Cell-mediated immunity, using differentially expressed T-cell surface receptors in localized PTM, has also been proposed as having a causative role.[4] The fact that PTM frequently develops in areas of injury suggests that trauma may contribute to local fibroblast activation. In addition, extrathyroid manifestations of Graves disease often occur in the skin and eyes—fibroblasts within the orbits and skin were found to have phenotypic differences from other fibroblasts throughout the body.



US frequency

Pretibial myxedema (PTM) occurs in 0.5-4.3% of patients with Graves disease. PTM has also been reported, but much less frequently, in patients with Hashimoto thyroiditis, primary hypothyroidism, and euthyroidism. Peak incidence occurs in the fifth to sixth decades of life.


Women are affected more frequently than men, with a female-to-male ratio of 3.5:1.


PTM may occur in children and young adults, but most cases occur in older adults, with a peak age at onset in the fifth to sixth decades of life.

Contributor Information and Disclosures

Ranjodh Singh Gill, MD, FACP, CCD Associate Professor of Medicine, Division of Endocrinology, Virginia Commonwealth University School of Medicine and McGuire Veterans Administration Medical Center; Consulting Staff, Department of Internal Medicine, Virginia Commonwealth University Health System

Ranjodh Singh Gill, MD, FACP, CCD is a member of the following medical societies: American Association of Physicians of Indian Origin, American College of Physicians, Endocrine Society, International Society for Clinical Densitometry, Medical Society of Virginia, North American Sikh Medical and Dental Association, Richmond Academy of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

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

Disclosure: Nothing to disclose.

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

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, American Academy of Dermatology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Additional Contributors

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.

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, Association of Military Dermatologists

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, Uniformed Services Academy of Family Physicians

Disclosure: Nothing to disclose.


Purnima Sau, MD Associate Professor, Department of Clinical Dermatology, Uniformed Services University of the Health Sciences

Disclosure: Nothing to disclose.

Laurel R Stearns, DO ResidentPhysician, Department of 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.

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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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