Endocrine Abstracts (2010) 22 P841

Effects of rhTSH administration on 24 h arterial pressure in subjects undergoing evaluation for differentiated thyroid cancer

Gianna Rentziou1, Eustathios Manios3, Emily Mantzou2, Katerina Saltiki1,2, Fotios Michas3, Nikos Zakopoulos3 & Maria Alevizaki1,2

1Endocrine Unit, Department of Medical Therapeutics, Alexandra Hospital, Athens University School of Medicine, Athens, Greece; 2Endocrine Unit, Evgenidion Hospital, Athens University School of Medicine, Athens, Greece; 3Hypertension Unit, Department of Medical Therapeutics, Alexandra Hospital, Athens University School of Medicine, Athens, Greece.

Background: TSH levels within the normal range have been associated with increased blood pressure (BP). TSH itself might be involved, especially as extrathyroidal actions of TSH exist.

We investigated whether elevated TSH levels after acute rhTSH administration may result in alterations in BP in euthyroid individuals.

Methods: Twenty-six euthyroid female subjects thyroidectomised and on T4 suppressive dose, were evaluated by the rhTSH (Thyrogen) test to assess cure of the disease. A 24 h ambulatory blood pressure monitoring (24 h ABPM) was performed on days 2–3 (D2–3) of the test, immediately after the second intramuscular rhTSH injection (0.9 mg/day on D1&2), when TSH levels are highest. TSH levels were measured on D1, D3, D5. Twelve subjects underwent one further 24 h BPM 1–3 weeks before the Thyrogen test (control). Patients took stable T4 dose throughout the study.

Results: All subjects were euthyroid. TSH levels were D1: 0.059±0.039 mU/l, D3: 125.13±33.40 mU/l, D5: 14.21±5.58 mU/l (P<0.001). There were no significant associations between TSH levels on D3 and any BP measurements either systolic (SBP), or diastolic(DBP) on day and night time measurements. There was a significant positive correlation of TSH on D5 with SBP and DBP (r values=0.396, 0.461, P<0.05).

In the group with control measurements mean SBP was significantly higher at the time when the rhTSH was administered compared to control (paired sample T test), (SBP control=111.1±12.0 mmHg, after rhTSH=115.0±9.7 mmHg, P=0.024). Similar differences were found when day-time and night-time SBP measurements were assessed. Both groups did not differ significantly regarding DBP (control=68.6±6.3 mmHg, after rhTSH=69.8±6.5 mmHg, P=0.135).

Conclusions: This study provides indirect evidence that TSH per se, when acutely elevated, may increase diastolic and systolic arterial pressure. Although night measurements were also elevated, one cannot exclude the possibility that the stress related to ‘medical test performance’ may have contributed to this increase in BP.

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