Purpose: To estimate the impact and the frequency of development thyroid disorders (TD) after heart transplantation (HT).
Methods: From 2010 to 2016 we performed 80 HT (mean age 46,0±14,0 yrs). Before HT 33% (n=26) of patients had TD: autoimmune thyroiditis - 42,3% (n=11), amiodarone-induced thyrotoxicosis type 1 (Graves' disease) - 3,8% (n=1), amiodarone-induced thyrotoxicosis (AIT) type 2 – 38,5% (n=10), diffuse nodular goiter - 11,5% (n=3) and thyroid adenoma - 3,8% (n=1). Before HT the level of thyroid stimulating hormone (TSH) in all recipients was normal or matched to subclinical hypothyroidism (SCH) (2,209±1,251 mMe/l vs. 7,115±4,533 mMe/l, p<0,05). Before HT 1 patient underwent hemithyroidectomy due to thyroid adenoma. All recipients were treated with triple-drug therapy (steroids, calcineurin inhibitors, mycophenolate mofetil) and induction (basiliximab – 76% (n=61), thymoglobulin – 24% (n=19)). Every 6 months the level of TSH was controlled or more frequent in case of pretransplantation thyroid history. If TSH was not in normal values, other thyroid hormones were measured and ultrasound investigation performed.
Results: After HT TD developed in 7,4% (n=4) patients without previous thyroiditis history: 1 - hypothyroidism, 3 - post-transplanted thyrotoxicosis (PTT). During 1st yr after HT PTT was diagnosed in 6,3% (n=5) recipients who were successfully treated by thiamazole or/and prednisone (TSH - 0,008 [0,003;0,163] mMe/l vs. 3,327 [1,539;3,836] mMe/l). Moreover, 2 of them had TD history: 1- autoimmune thyroiditis, 1 – AIT type 2. In long-term follow-up there was no evidence of PTT. During 1st yr hypothyroidism was found in 10% (n=8) patients and then were treated with levothyroxine therapy (TSH – 8,006 [5,681;23,640] mMe/l vs. 1,963 [1,882;2,482] mMe/l). After HT in 10 from 17 recipients (58,8%) with hypothyroidism and in 3 from 9 (33,3%) – with euthyroidism the level of TSH increased. In 2 months after HT significant hypothyroidism manifested in 1 recipient: TSH increased (59,922 mMe/l), free thyroxine (T4) decreased (5,2 pmol/l). In 5 yrs after HT AIT type 2 was diagnosed in 3 other patients. In long-term follow-up induction did not impact on the level of TSH. We found correlation between time spent on mechanical ventilatory support (MVS) and PTT (r=0,8; p<0,05). Development of TD did not relate to endomyocardial biopsies results but donor-specific HLA sensibilisation was positive (PRA>30%). After HT imbalance of thyroid status was found in 15 from 26 recipients (57,7%) with TD history and in 4 from 54 (7,4%) – without it. The absolute risk of TD deterioration or development was 36,6% in TD group vs. 6,9% - the onset of TD (p<0,001).
Conclusion: Thyroid status deteriorated in majority of heart transplanted patients. After HT level of TSH needs to be under control in all recipients, especially in those with thyroid disease history. Anti-thyroid medications are successfull.