Thyroid dysfunction and thrombosis potential

Dr Ramzi Ajjan, University of Leeds


Summary of the work

Overactivity of the thyroid gland, a common condition, is associated with an increased risk of blood clot formation resulting in blood vessel obstruction. The blood clot is composed of a mesh of fibres (known as fibrin fibres) with blood cells embedded in this network. Previous work has shown that a dense clot (many fibres and small pores) is associated with premature and more severe heart disease, which is probably related to difficulties in dissolving clot having a dense structure.

The aim of the current work is to investigate blood clot structure in individuals with an overactive thyroid and study the effects of normalising thyroid function on the fibrin clot.

Since the work started, we have established a number of collaborations and the study has been extended significantly (detailed below), with the extra funding needed covered from other sources.

Progress of the study

We have recruited 24 patients as planned but some did not attend the follow up and therefore we have a total of 21 patients who completed the study. Analysis of the data shows that hyperthyroidism is associated with a denser clot structure without affecting fibrinolysis (clot breakdown) time. Results from our work have been submitted to the annual American Endocrine Society meeting to be held in San Diego California in June 2010.

In vitro work to study the effects of carbimazole is still ongoing and should complete by the 20th of March.

We have recently established a collaboration with a group in Amsterdam (SC Cannegieten and B van Zaane) to study the effects of mild hyperthyroidism, induced by thyroxine treatment of healthy volunteers, on clot structure and lysis. Samples have been delivered and analysis will be completed by the end of March 2010.

We also have a long standing collaboration with a group in Newcastle (SH Pearce and J Weaver) and sample analysis of hyperthyroid and hypothyroid patients as well as healthy controls has been completed.

Finally, in order to fully understand the effects of thyroid dysfunction on thrombosis potential, we will also analyse samples from individuals with hypothyroidism (in collaboration with S Atkin-Hull). Analysis of these samples is scheduled to be completed by the end of March.

Taken together, this will be the first and most comprehensive study analysing blood clot structure in individuals with thyroid dysfunction. As detailed above, the study has been expanded significantly and additional funding has been covered using other resources.