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Further in-vitro studies of pretibial fibroblasts have illustrated enhanced sensitivity to the serum of patients with pretibial myxedema, which may explain the reason for the site predilection.5 There have been some conflicting reports of thickening of the skin on the extensor surfaces of the forearms, a clinical counterpart of pretibial myxedema.6,7 Skin biopsies of pretibial myxedema reveal increased deposition of glycosaminoglycans, notably hyaluronic acid, in the dermis and distortion of collagen bundles into fibers, which are widely separated. One histologic study mentions biopsy reports of patients without Graves’ disease as having features of stasis dermatitis in addition to the mucin deposition.8 The glycosaminoglycans or mucin accumulation involves the papillary and reticular dermis of patients without thyroid disease as opposed to just the reticular dermis in patients with Graves’ disease. There are no specific laboratory studies specific for the diagnosis of pretibial myxedema.
Pretibial myxedema is not a life-threatening condition and may resolve spontaneously after many years. Treatment of the underlying hyperthyroidism does not necessarily eradicate the skin lesions of pretibial myxedema, which occasionally become more pronounced after the treatment of the thyrotoxicosis. Mild pretibial myxedema does not require treatment. The standard form of therapy involves topical or intralesional corticosteroids particularly for moderate to severe pretibial myxedema.9 The long-term remission rates from corticosteroid therapy are unknown.1 Compression bandages can provide additional benefit. A preliminary trial with pentoxifylline 400mg intravenously followed by 800mg by mouth daily for a week diminished the size of pretibial myxedema lesions.10
Third-line therapy involving intravenous immunoglobulins have shown some benefit in the treatment of pretibial myxedema as well as ophthalmopathy according to one study.11 Surgical excision has been shown to be effective in a minority of cases. Three cases were successfully treated with octreotide therapy, a somatostatin analogue, at 100µg subcutaneous three times daily. The mechanism of action is postulated as inhibition of insulin-like growth factor.12 Overall, patients diagnosed with pretibial myxedema have good prognoses.
The patient in this case report was treated conservatively with compression stockings and cadexomer iodine gel dressings. Her ulcers healed completely within three weeks. The patient is on oral prednisone for her severe asthma history, and the dosage has not been modified. The authors continue to monitor her thyroid function and will order antimicrosomal and antithyroglobulin antibodies for further analysis of thyroid disease.
1. What laboratory value is specific for pretibial myxedema?
A. Antimicrosomal antibody
B. Antithyroglobulin antibody
C. No specific value
D. Serum hyaluronic acid
2. What distinguishes euthyroidal pretibial myxedema versus pretibial myxedema associated with Graves’ disease?
A. Collagen fiber appearance
B. Location of myxedema lesions
C. The distribution of mucin in the dermis
D. The clinical appearance of pretibial myxedema
3. What is the standard form of therapy in the treatment of pretibial myxedema?
A. Intravenous immunoglobulins
B. Octreotide therapy
C. Intralesional/topical corticosteroid
4. What areas are affected by pretibial myxedema?
A. Bilateral shins
B. Head, neck, and arms in rare cases
C. The shoulders and the shins
D. A and B
5. The distribution of mucin in the pretibial myxedema patients with Graves’ occurs most commonly in:
A. Both superficial and deep dermis
B. Papillary dermis only
C. Dermal-epidermal junction and deep dermis
D. Reticular dermis
6. Name a third-line form of therapy in pretibial myxedema:
References 1. Schwartz KM, Fatourechi V, Ahmed DD, et al. Dermopathy of Graves’ disease (pretibial myxedema): Long-term outcome. J Clin Endocrinol Metab 2002;87:438–46. 2. Georgala S, Katoulis AC, Georgala C, et al. Pretibial myxedema as the initial manifestation of Graves’ disease. J Eur Acad Dermatol Venereol 2002;16:380–3. 3. Omohundro C, Dijkstra JW, Camisa C, et al. Early onset pretibial myxedema in the absence of ophthalmopathy: A morphologic evolution. Cutis 1996;58:211–4. 4. Wu SL, Chang TC, Chang TJ, et al. Cloning and sequencing of complete thyrotropin receptor transcripts in pretibial fibroblast culture cells. J Endocrinol Invest 1996;19:365–70. 5. Cheung HS, Nicoloff JT, Kamiel MB, et al. Stimulation of fibroblast biosynthetic activity by serum of patients with pretibial myxedema. J Invest Dermatol 1978;71:12–7. 6. Peacey SR, Flemming L, Messenger A, et al. Is Graves’ dermopathy a generalized disorder? Thyroid 1996;6:41–5. 7. Wortsman J, Dietrich J, Traycoff RB, et al. Preradial myxedema in thyroid disease. Arch Dermatol 1981;117:635–8. 8. Somach SC, Helm TN, Lawlor KB, et al. Pretibial mucin. Histologic patterns and clinical correlation. Arch Dermatol 1993;129:1152–6. 9. Kriss JP. Pathogenesis and treatment of pretibial myxedema. Endocrinol Metab Clin North Am 1987;16:409–15. 10. Chang CC, Chang TC, Kao SC, et al. Pentoxifylline inhibits the proliferation and glycosaminoglycan synthesis of cultured fibroblasts derived from patients with Graves’ ophthalmopathy and pretibial myxedema. Acta Endocrinol 1993;129:322–7. 11. Antonelli A, Navarranne A, Palla R, et al. Pretibial myxedema and high-dose intravenous immunoglobulin treatment. Thyroid 1994;4:399–408. 12. Chang TC, Kao SC, Huang KM. Octreotide and Graves’ ophthalmopathy and pretibial myxedema. BMJ 1992;304:158.