Q016

Human chorionic gonadotrophin induced gestational thyrotoxicosis: 2 case reports and a discussion.

R W Carroll, N Mahadevan, S R Mehta

 

Case 1

SM, a 29 year old female had multiple admissions during the first trimester of her 3^rd pregnancy as a result of severe vomiting.  Hyperemesis gravidarum was confirmed clinically at week 8 and at this stage biochemical hyperthyroidism was also noted.  She was clinically euthyroid and TSH receptor antibodies were not detected.  Peak free T4 levels were 34.56 pmol/L.  Supportive management was administered consisting of anti-emetics and rehydration.  Thyroid function tests normalized with the TSH falling to 0.439 mIU/L (0.27-4.2) and free T4 to 16.21 pmol/L (12-22) in parallel with a fall in B-HCG levels..

 

Case 2

YPN, a 28 year old female presented with biochemical hyperthyroidism at 10 weeks gestation.  She had had three admissions as a result of hyperemesis gravidarum and had received supportive treatment with fluids and anti-emetics. Peak free T4 levels were 53.06 pmol/L at 10 weeks gestation.  TSH receptor antibodies were not detected.  Her symptoms improved as the pregnancy progressed and Free T4 and Free T3 returned to normal by week 20, (free T4 13.76 pmol/L (12-22) and Free T3  4.3 pmol/L (4-6.8), as B-HCG levels decreased, but TSH remained suppressed at <0.01 mIU/L (0.27-4.2).

 

Discussion

In both cases a diagnosis of HCG induced gestational thyrotoxicosis with associated hyperemesis gravidarum was made.  The management involved supportive care and monitoring of improvement in biochemical thyroid function.  We discuss the mechanism of HCG induced gestational thyrotoxicosis and the management of this common scenario.  The role of thionamide therapy is reviewed.  TSH receptor antibodies should be measured so as to exclude Graves’ disease, the management of which differs from that of HCG induced gestational thyrotoxicosis. The assessment of the pregnant female with clinical or biochemical hyperthyroidism is discussed.