A 40-year-old man presented to the outpatient department with complaints of multiple, nontender, raised nodular lesions on his shins bilaterally for the past year (Figure 1). The lesions had an insidious onset and were progressively increasing in size. He was evaluated at an outside clinic. Biopsy was performed multiple times, and possibility of spindle cell lipoma and myxoid liposarcoma was kept. The patient was referred to our institute for further management. However, on eliciting a detailed history, he had easy fatigability and cold intolerance. General physical examination revealed dry and coarse skin. The thyroid gland was not palpable. Deep tendon reflexes were delayed, suggestive of hypothyroidism. Laboratory investigations revealed suppressed FT4 (0.7 ng/mL), and elevated thyroid-stimulating hormone levels (104 mU/L), thus confirming the diagnosis of primary hypothyroidism. Thyroid peroxidase antibodies were raised (860 U/mL). Review of histopathology slides revealed marked dermal mucin, consistent with pretibial myxedema. The patient was started on levothyroxine therapy and steroid occlusive dressings for primary hypothyroidism and pretibial myxedema, respectively.
Thyroid dermopathy is classically seen in patients who have Graves disease with ophthalmopathy. Rarely, it can develop in patients with chronic autoimmune thyroiditis with or without hypothyroidism.1 In a study using pretibial ultrasound in patients with autoimmune thyroid disease, pretibial myxedema was found in 17.1% in Hashimoto thyroiditis, and 6.5% in idiopathic hypothyroidism.2 Typically, there is diffuse, nonpitting edema with “orange-peel” appearance. Due to its dependent position and increased exposure to mechanical stress, the pretibial region is the site most commonly involved. Other forms of lesions are plaque, nodular, and elephantiasic form. Nodular lesions are seen in <10% of patients with thyroid dermopathy.3 Increased production of glycosaminoglycan by fibroblast in dermal tissue due to stimulation by thyroid-stimulating hormone (TSH) receptor antibodies leads to expansion of connective tissue and obstruction of lymphatic microcirculation, resulting in nonpitting edema. All the patients with thyroid dermopathy have high levels of TSH receptor antibodies. Because TSH receptor antibodies are elevated in approximately 15% of patients with autoimmune hypothyroidism, this could possibly explain the occurrence of dermopathy in these patients. Histologically, there is excessive accumulation of glycosaminoglycans in reticular dermis, along with fragmentation and fraying of collagen fibers. Diagnosis is obvious in the presence of pretibial lesions and ophthalmopathy. However, skin biopsy is necessary in lesions at an atypical location or in the absence of ophthalmopathy. Treatment includes local corticosteroid, compressive therapy, systemic immunomodulation, and surgical excision in refractory cases.4 In the index case, the patient underwent multiple biopsies despite the presence of typical lesions in the pretibial region. Thus, presence of pretibial skin lesions in the presence of thyroid dysfunction confirms the diagnosis of thyroid dermopathy, and skin biopsy could be avoided in these patients.
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-Mandeep Singla, MD, DM, Abhinav Gupta, MD
-This article originally appeared in the March issue of The American Journal of Medicine.
