Endocrine Abstracts

Sweet syndrome is a febrile dermatosis characterized by painful light red patches of quite different size involving various skin zones associated with flu like symptoms, arthralgias and rarely frank arthritis. Originally considered rare, over 500 cases in the past 10 years have been described. The etiology of Sweet’s syndrome is unknown, but a type of hypersensitivity reaction leading to stimulation of a cascade of cytokines has been strongly suggested. In very few cases an association between thyroid disorders and Sweet’s syndrome has been reported.

This report describes a case of relapse of Sweet’s syndrome concomitant to changes in thyroid autoimmunity. A 50 year old women with a biopsy documented Sweet’s syndrome in 2003 was referred to our endocrine unit because of a slight overweight (BMI=28.5 kg/m²) that stressed the pain in the knees joints. Our observation occurred 2 months later a relapse of Sweet’s syndrome (February 2005) following a 2 years glucocorticoid-induced remission. In this occasion we documented anti-TPO and anti-TG positivity (previously negative) and FT4 value within the low normal range (0.76 ng/dl).

The patient described in this report offers some points of discussion: the cytokines cascade occurring in Sweet’s syndrome can stimulate HLA class II expression on immune thyroid epithelial cells, a phenomenon relevant for the amplification and progression of autoimmune thyroid diseases; furthermore, cytokines may play a cytotoxic effect on and induce apoptosis of thyroid cells. Another point of interest is represented by the cross reactivity between antigens from Yersinia Enterocolitica (highly positive in our patient) and thyroid-cell-membrane antigens.

In conclusion, many pathogenetic mechanisms proposed for Sweet’s syndrome are potentially able to affect thyroid gland, suggesting a careful evaluation of thyroid function and autoantibodies in every patient with Sweet’s syndrome.