While GAG is normally found throughout the body, in GD there are excessive amounts. The excess production of GAG is caused by the same stimulating TSH receptor antibodies that cause hyperthyroidism. However, rather than affecting receptors in thyroid cells, these antibodies activate early fibroblast cells to produce GAG.
Most patients who develop PTM also have Graves’ ophthalmopathy and a more severe form of GD. Approximately 5% of patients with clinically evident Graves' ophthalmopathy (GO) have PTM, and 12% to 15% of patients with severe GO also have PTM.
I’m an exception, having PTM with mild GO and mild hyperthyroidism. I developed PTM shortly after having radioiodine ablation (RAI) treatment. RAI is known to induce the development of PTM. The connection here is that RAI causes an increase in blood levels of stimulating TSH receptor antibodies since these antibodies are released from dying thyroid cells.
PTM occurs in both a pitting and non-pitting form, although the non-pitting form is more common. Pitting is a condition in which an indentation or pit is formed when the swollen skin is pressed with a finger. The skin in PTM is typically leathery and swollen or edematous (fluid filled. The skin is characterized by prominent hair follicle openings and brownish waxy plaques may be present on the skin surface. Itching of the affected area is common, although the area is not usually painful.
Treatment of PTM is primarily medical, consisting of oral and topical corticosteroids designed to reduce the inflammatory process. Several GD patients with PTM have reported seeing improvement when the skin surface is exposed to sunlight. In rare instances plaques or nodules associated with PTM may form pseudotumorous masses, which must be surgically removed. While these are not true tumors, they may interfere with the nerves and blood vessels in this area.
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