Endocrine Abstracts

Case history: A 38 years old Afro-Caribbean gentleman presented in June 2018 with symptoms of hyperthyroidism. He is a smoker and takes alcohol occasionally. Examination revealed fine tremors, tachycardia, moderate sized goitre with no thyroid bruit and right sided proptosis. Thyroid workup revealed suppressed TSH, raised free T4 and TRAb of 9.75 IU/L suggesting Graves’ Thyrotoxicosis. He was started on 20 mg of Carbimazole (CBZ)OD with Propanolol. After initiating carbimazole for one month, he was admitted with thrombocytopenia on July 2018. He was hemodyanamically stable with no bleeding manifestations. He was then discussed with haematology team, where suggestion was Graves’ disease or its treatment is contributing to thrombocytopenia. Carbimazole was switched to Propylthiouracil (PTU)100 mg TDS during the admission after which platelet count showed improvement. He was readmitted with thrombocytopenia in August 2018 when he was symptomatically and biochemically improving from hyperthyroidism. His propylthiouracil was stopped. He was referred to haematologist and was investigated in detail for causes of thrombocytopenia and was diagnosed with immune thrombocytopenia (ITP). He was started on steroids. He has had two further admissions with bleeding manifestations and persistent thrombocytopenia.

Investigations:

• 4/05/18: Start of CBZ, T4 >100 pmol/L, TSH<0.01 mIU/L, TRAb 9.75 IU/L, Platelet 72

• 13/07/18: First admission CBZ stopped PTU started, T4 83.7, TSH<0.01, TRAb 9.35, Platelet 9

• 25/07/18: Discharged Platelet 30

• 04/08/18: Second admission PTU Stopped and steroid started, T4 66.1, TSH<0.01, TRAb 8.34, Platelet 10

• 22/08/18: Discharge on steroid, T4 40.3, TSH<0.01, TRAb 5.49, Platelet 101

• 22/10/18: Third admission, Refractory ITP, T4 30.8, TSH 0.01, Platelet 2

• 09/11/18: Therapy for refractory ITP, Steroids, Eltrombopag, T4 17.2, TSH 0.01, Platelet 5

• 07/01/18: Rutiximab started, T4 10.6, TSH 0.11, TSH <0.4, Platelet 2

Results and treatment: He was treated with anti-thyroid drugs only for first 2 months. His anti-thyroid drugs were stopped initially with a view of contributing to thrombocytopenia. After being diagnosed with ITP, he has been repeatedly on steroids that showed improvement in his thyrotoxic state, but minimal improvement in platelets. In December 2018 admission he was started on Rituximab along with steroids for refractory ITP.

Conclusions and points for discussion: Our patient’s Graves’ disease responded to steroids, thus leading to marked reduction in T4, TRAb levels and clinical improvement, in the absence of antithyroid drugs. Because of the strong fundamental autoimmune mechanism underlying both diseases, it is known that the treatment of associated autoimmune thyroid disorder contributes to the remission of ITP, which was not in our case. I would like discuss the following:

1. Role of steroid in Graves’? Is the response transient/permanent?

2. Best long term plan in this patient Radioiodine Vs Thyroidectomy?

3. What could be done differently as opposed to our approach?