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MYXEDEMA

Arch Dermatol 1981 Oct;117(10):635-8

Preradial myxedema in thyroid disease.

Wortsman J, Dietrich J, Traycoff RB, Stone S

Patients with Graves' disease were noted to have thickening of the skin on the extensor surfaces of their forearms. Skin biopsy specimens were obtained from nine consecutive patients with Graves' disease treated with sodium iodide I 131, from three patients with other thyroid disorders, and from one patient with acromegaly. Skin specimens from one patient with scleredema and one patient with scleromyxedema were used as controls for the histologic stains. Hematoxylin-eosin-stained sections of forearm skin from eight of nine patients with Graves' disease showed prominent round-cell (probably lymphocytic) infiltration around dermal capillaries and distortion of collagen fibers. In five of the patients with Graves' disease, staining with Mowry's colloidal iron disclosed dense deposits of mucin in the papillary dermis, with a distribution similar to that reported for pretibial myxedema. Mucopolysaccharide deposition in the skin on the extensor surface of the forearms may be the clinical counterpart of pretibial myxedema.

PMID: 6456700, UI: 82022454

The following study is intriguing to me because of the use of iron and gold for staining the cells of pretibial myxedema.  I may be completely wrong but I'm wondering if the fact that these cells take up iron and gold indicates that these minerals are deficient in pretibial myxedema and may be important in correcting the condition.

Thyroid 1996 Feb;6(1):41-5

Is Graves' dermopathy a generalized disorder?

Peacey SR, Flemming L, Messenger A, Weetman AP

University Department of Medicine, Clinical Sciences Centre, Northern General Hospital, Sheffield, UK.

The pathogenesis of the extrathyroidal manifestations of Graves' disease-ophthalmopathy and pretibial myxedema (Graves' dermopathy)-involves fibroblast activation and increased mucin (glycosaminoglycan) production. It is nuclear why fibroblasts are activated at these sites and evidence for site-specific and generalized fibroblast activation is conflicting. One previous report has demonstrated an increase in glycosaminoglycan deposition in the forearm skin of patients with Graves' disease but without pretibial myxedema. We have sought to confirm the existence of subclinical dermopathy in the forearm tissue from patients with untreated (UG) and treated (TG) Graves' disease and compared the histological changes with normal controls (C), treated toxic nodular goiter (MNG) and Graves' dermopathy specimens (PTM), using stains for mucin, elastin, glycosaminoglycans (GAGs), and HLA-DR molecules. Four of 4 PTM specimens stained positive for mucin, with varying sparse, fragmented, or dense elastin fibers. Four of 5 PTM specimens stained heavily for GAGs using colloidal iron and 2 of 5 stained heavily using colloidal gold. None of the patients in groups UG, TG, MNG, or the controls, showed mucin deposition or elastin changes. Mild staining with colloidal gold for GAGs was seen in 1 each of the UG, the TG, and MNG groups, and 4 of 8 controls. Heavy staining with colloidal iron for GAGs was seen in 1 TG patient and 1 control, while moderate staining was found in several TG, UG, and controls. In 2 of 4 PTM specimens the monoclonal antibody CR3/43 (against HLA-DR) stained frequent dermal fibroblast-like cells and in 2 a lymphocytic infiltrate was seen. Only 1 of 8 UG patients had multiple CR3/43 staining cells present in the dermis: 3 of 8 TG and 1 of 8 controls had a few CR3/43 stained cells. Overall we found no evidence of dermal mucin deposition in the forearms of 16 patients with Graves' disease and a similar GAG distribution to normal controls. HLA-DR expression by fibroblast-like cells in the dermis suggests activation of these cells in the dermis of the PTM specimens, but no evidence of widespread fibroblast activation was found in the forearms of patients with Graves' disease.