(22.03) Coexisting Immune Thrombocytopenic Purpura and Grave's Disease: A Therapeutic Challenge

It is known that a patient with a diagnosed autoimmune disorder has a predisposition for developing other autoimmune disorders. However, it is unknown when and which disorder can be developed. Some associations of autoimmune disorders are well documented, but others are barely studied due to their rarity of presentation. Overlapping of Immune Thrombocytopenic Purpura (ITP) and Grave’s Disease has been described in case reports, but the appropriate treatment approach is unclear. Antithyroid drugs usually recommended for Grave’s disease such as methimazole and PTU are known to have agranulocytosis as an adverse effect. Radioiodine therapy may also be considered but it has been associated with an increased thyroid autoimmune response which could potentially also affect platelet autoantibodies.  Surgery is an alternative but may not be preferred if thrombocytopenia is severe. Therefore, no clear treatment strategy has proved preferred in these cases.

Case(s) Description :

A 42 year old woman with past medical history of ITP for 8 years not responsive to corticosteroid therapy was referred due to thyrotoxicosis symptoms. Patient presented with palpitations, heat intolerance, and irritability. Physical exam was remarkable for tachycardia, elevated systolic blood pressure and enlarged goiter, without ophthalmopathy. Thyroid function tests (TFTS) showed TSH: 0.007uIU/mL(0.45-5.33uIU/mL), FT4: >5.00ng/dL(0.71-1.85uIU/mL), TT3: 7.55ng/mL(0.8-2.0ng/mL) and platelet levels at 56k. Thyroid ultrasound showed enlarged and heterogenous gland with left isoechoic nodule 2.1x1.8x1.7cm. Patient was started on methimazole 10mg PO every 8 hours and atenolol 25mg PO daily. Follow up CBC revealed platelet levels above 40k with no bleeding which had remained stable when compared with previous platelet levels for the past year. Patient used methimazole and beta blocker therapy temporarily with improvement of thyrotoxic symptoms before stopping them for thyroid scan preparation. She then developed severe thrombocytopenia of 20k with epistaxis along with thyrotoxicosis symptoms for which she was administered IVIG and Beta blocker therapy inpatient. Thyroid uptake scan showed diffusely increased radiotracer at 79% consistent with Grave’s Disease. On follow up evaluation outpatient, TFTS showed suppressed TSH, elevated FT4 and TSI along with elevated liver enzymes >4 times upper limit of normal for which methimazole was discontinued and patient was referred to radioiodine ablation therapy.

Discussion :

Several mechanisms have been postulated for immune mediated thrombocytopenia as well as for thrombocytopenia in Grave’s Disease which may be overlapping. Upon review of literature, in case studies, hyperthyroidism correction has led to improvement of platelet levels especially in patients with steroid resistant ITP. In other case reports, thrombocytopenia has worsened after use of methimazole or PTU. In this scenario, the choice of therapy is challenging, and no definitive recommendations are available. In this case we raise awareness of the association of immune thrombocytopenic purpura and Grave’s disease and need for more studies in treatment approach.