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Is there any effective treatment of pretibial myxoedema/myxedema in someone who is now euthyroid?

Associated tags: Endocrinology, euthyroid, pretibial myxoedema, thyroid dysfunction, treatment options

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Question answered:25/09/02 Warning! this question is over two years old.

We did not find any studies offering treatment for pretibial myxoedema (PTM) in euthyroid patients.

  • We found a case study which states "Pretibial myxedema is typically associated with clinical hyperthyroidism, diffuse goiter, and ophthalmopathy in patients with Graves' disease. A case of biopsy-proved pretibial myxedema was encountered in a clinically euthyroid woman who had neither diffuse goiter nor exophthalmos. Although serum total and free thyroxine hormone concentrations were normal, the thyroid-stimulating hormone response to thyrotropin-releasing hormone was absent. This case illustrates that pretibial myxedema may present without other more common manifestations of Graves' disease. In patients with suspect pretibial skin lesions, the thyrotropin-releasing hormone stimulation test may be required to establish the presence of subtle underlying thyroid gland autonomy and the diagnosis of euthyroid pretibial myxedema." (1)
  • Emedicine, an American online textbook contains a chapter on Pretibial Myxedema, which states: "The lesions of PTM are of primarily cosmetic concern, although severe elephantiasic form may lead to significant limb enlargement and impair function. Surgical treatment should be avoided as scarring may aggravate the dermopathy, and benefits are equivocal. Local application of corticosteroids remains the mainstay of treatment.

Various medical treatments, including plasmapheresis and cytotoxic therapy have been tried, but the efficacy of these therapies is unproven. Intralesional or topical therapy with corticosteroids is currently the only treatment offering demonstrated efficacy. Systemic use should be avoided due to undesirable adverse effects. Newer treatment regimens offering promise but requiring further investigation include ocreotide, a somatostatin analog, and high-dose intravenous immunoglobulin (IVIG)." (2)

We found a number of papers discussing treatment options for PTM. The abstracts are reproduced below:

  • "In this study, we report on the outcomes of 178 patients seen at our institution between January 1969 and November 1995 with thyroid dermopathy who were followed up for an average of 7.9 yr. Nonpitting edema was the most prevalent form of dermopathy (43.3%), and the pretibial area was the region most commonly involved (99.4%). The majority of patients with dermopathy had ophthalmopathy (97.0%). Topical corticosteroids were the most commonly used treatment (53.9%). Patients with milder forms of dermopathy (40.4%) did not receive any therapy for dermopathy. Twenty-six percent of the patients experienced complete remission, 24.2% had moderate improvement (partial remission), and 50.0% had no or minimal improvement of their dermopathy at last follow-up. Patients who did not receive therapy experienced a significantly (P = 0.03) higher rate of complete remission (34.7%) than those who received local therapy (18.7%), although the combined complete and partial remission rates were not significantly different for the treated and untreated groups (P = 0.3). However, the treated and untreated groups were not comparable because our practice is to use therapy for more extensive and severe cases. All five cases of elephantiasis were in the treatment group and were less likely to have remission because of the severity of their skin condition. Patients receiving treatment were more likely to have dermatologic consultation and histologic diagnosis (P < 0.001). The beneficial effect of topical corticosteroid therapy on long-term remission rates remains to be determined." (3)
  • "We reviewed 150 consecutive cases with the diagnosis of pretibial myxedema over a 20-year period in a referral center. Only 1 patient in this group did not have ophthalmopathy, whereas 88% had significant proptosis and 30% required orbital decompression surgery. Dermopathy was a late manifestation of Graves disease, and its onset usually followed the diagnosis of hyperthyroidism and ophthalmopathy. In a few patients, dermopathy preceded diagnosis of hyperthyroidism or onset of ophthalmopathy. Fourteen patients were never clinically hyperthyroid; spontaneous hypothyroidism had developed in 11 in this group. All cases involved the lower extremities, with only 1 patient having combined upper and lower extremity involvement. The most common form of thyroid dermopathy was nonpitting edema, followed by nodular and plaque forms, which occurred with equal frequency. The polypoid form occurred in 1 patient and the elephantiasic form in another; 7.3% had thyroid acropachy. Follow-up was available for 120 patients (range, 3 mo to 19 yr; mean, 3.2 yr), and complete remission was observed in only 12 patients. Topically applied corticosteroid therapy was used in 76 patients, and in this group 38% had sustained long-term partial remission, as opposed to 18% in the group receiving no corticosteroid therapy." (4)
  • "Seven patients affected by Graves' ophthalmopathy and pretibial myxedema (four patients with nodular form, two with diffuse, and one with elephanthiasic form) have been treated with high-dose intravenous immunoglobulins. We have observed (a) clinical improvement of pretibial myxedema and Graves' ophthalmopathy in all patients, (b) a reduction of pretibial skin thickness, by ultrasonography evaluation, in four patients, (c) a reduction of mucopolysaccharide skin content in three patients, (d) disappearance of lymphocytic skin infiltration and IgG deposition in two patients, and (e) a parallel reduction of the titer of circulating autoantibodies as antithyroglobulin, antimicrosomal, anti-TSH receptor, and of non-organ-specific antibodies as antinuclear, anti-smooth muscle cells, and anti-mitochondrial. In comparison two patients with Graves' ophthalmopathy and pretibial myxedema treated with systemic corticosteroids did not present any improvement of the cutaneous ailment." (5)
  • "Pretibial myxedema is a localized dermopathy seen in patients with past or present hyperthyroidism. Massive intradermal deposition of mucin (acid mucopolysaccharide) produces the classic indurated nodules or plaques on the anterior lower legs. Most patients have elevated levels of LATS in their serum; however, this appears to be a marker for the disease, rather than a cause. Mild pretibial myxedema requires no treatment. Topical, intralesional or systemic steroids may be useful in severe cases." (6)

 

  1. Chen JJ Ladensons PW. Euthyroid pretibial myxedema. American Journal of Medicine. 1987; 82(2): 318-20.
  2. Purnima S. Pretibial myxedema. Emedicine.

  1. http://www.emedicine.com/derm/topic347.htm
  2. Schwartz KM et al. Dermopathy of Graves disease (pretibial myxedema): long-term outcome. Journal of Clinical Endocrinology. 2002; 87(2): 438-46.
  3. Fatourechi V et al. Dermopathy of Graves Disease (pretibial myxedema). Review of 150 cases. Medicine. 1994; 73(1): 1-7.
  4. Antonelli A et al. Pretibial myxedema and high-dose intravenous immunoglobulin treatment. Thyroid. 1994; 4(4): 399-408.
  5. Truhan AP. Pretibial myxedema. American Family Physician. 1985; 31(5): 135-8.


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