Vol 62, No 5 (2011)
Original paper
Published online: 2011-11-08

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Fibrinogen and D-dimers levels in patients with hyperthyroidism before and after radioiodine therapy

Anna Brona, Anna Bohdanowicz-Pawlak, Diana Jędrzejuk, Andrzej Milewicz
Endokrynol Pol 2011;62(5):409-415.

Abstract

Background: Various abnormalities of haemostasis have been described in patients with hyperthyroidism. The results of different studies point to the underlying thyroid disease, especially severity of hyperthyroidism and autoimmune processes, as important factors contributing to coagulation-fibrinolytic balance. The objective of this study was to investigate the association between hyperthyroidism (concerning severity of thyroid dysfunction and anti-thyroid perioxidase antibodies level) and plasma fibrinogen and D-dimers levels before and after radioiodine therapy.
Material and methods: The study included 35 non-smoking, postmenopausal women, aged 51–69, with subclinical or overt hyperthyroidism treated with radioiodine. Analysis comprised serum TSH (thyroid stimulating hormone), fT4 (free thyroxine), fT3 (free triiodothyronine), TPO antibodies (anti-thyroid perioxidase) levels, and plasma D-dimers and fibrinogen levels before and 12-16 weeks and 24–28 weeks after radioiodine therapy.
Results: Elevated fibrinogen (3.82 g/L ± 0.75, reference range 2–4.5 g/L) and D-dimers (674.26 ng/mL ± 652.71, reference range 70–490 ng/mL) levels were observed in subjects with hyperthyroidism. They decreased after radioiodine therapy. A negative correlation between plasma fibrinogen and D-dimers levels and anti-thyroid perioxidase antibodies level was found. TSH, fT4 and fT3 correlated with D-dimers level in overt hyperthyroidism.
Conclusions: Hyperthyroidism is associated with a tendency toward hypercoagulation and hyperfibrinolysis. The changes observed in plasma fibrinogen and D-dimers levels are reversible. Fibrinogen level decreases within reference range and D-dimers level decreases almost to the upper reference range. They depend on severity and autoimmunity of the underlying thyroid disease and may be modified by restoring euthyroidism. (Pol J Endocrinol 2011; 62 (5): 409–415)

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