Autoimmune haemolytic anaemia and ulcerative colitis D. W. GORST
نویسنده
چکیده
Kriss et al. (1964) postulated that the destruction of the thyroid gland by disease (hyperthyroidism or thyroiditis) or by therapeutic agents (especially 1311) results in the release of an antigen of thyroid cell origin which then stimulates the production of the antibody, LATS. The antibody is then fixed to the tissues of the legs, the phenomenon being facilitated by a number of factors such as dependency of the lower limbs, trauma, vascular injury, cardiac failure, exposure to cold or hypothyroidism. The resulting immunological reaction then causes a local inflammatory tissue reaction which manifests as pretibial myxoedema. It is therefore interesting to note that two of our patients had elevated levels of IgG. Although the levels of LATS were not determined in these patients, the high level of IgG would support an immunological mechanism underlying the pathogenesis of pretibial myxoedema. In this context, it is significant that pretibial myxoedema has also been found in patients with Hashimoto's thyroiditis (Peard, 1961) and myxoedema with lymphocytic infiltration ofthe thyroid gland (Haydar, 1963). There may therefore be a common factor which induces inflammatory changes in the thyroid gland as well as causing exophthalmos, pretibial myxoedema and clubbing.
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