Autoimmune Conversion of Hashimoto's Thyroiditis to Graves' Disease With Immune Pancytopenia in a Patient With Seropositive Rheumatoid Arthritis: A Diagnostic and Therapeutic Conundrum.
- 1General Medicine, Tata Main Hospital, Jamshedpur, IND.
- 2Endocrinology, Tata Main Hospital, Jamshedpur, IND.
Abstract
Autoimmune conversion of Hashimoto's thyroiditis (HT) to Graves' disease (GD) is an uncommon phenomenon. The coexistence of GD, seropositive rheumatoid arthritis (RA), and pancytopenia presents a rare diagnostic and therapeutic challenge, particularly when antithyroid drug (ATD) therapy is contemplated in the presence of pre-existing cytopenias. A 66-year-old woman with a four-year history of hypothyroidism on levothyroxine replacement and long-standing seropositive RA presented with generalized weakness, altered bowel habits, and insomnia. Serial thyroid function tests (TFTs) had demonstrated progressive suppression of thyroid-stimulating hormone (TSH), necessitating dose reduction and eventual discontinuation of levothyroxine. Evaluation revealed thyrotoxicosis with elevated free thyroxine (FT4), free triiodothyronine (FT3), raised antithyroid peroxidase and TSH receptor antibodies, diffuse goiter with increased vascularity on Doppler ultrasonography, and diffusely increased uptake on thyroid scintigraphy, confirming Graves' disease. Concurrent investigations demonstrated pancytopenia with elevated liver enzymes and mild splenomegaly. Given the presence of seropositive rheumatoid arthritis and the exclusion of alternative causes of pancytopenia, an immune-mediated mechanism leading to bone marrow suppression was suspected. After treatment with granulocyte colony-stimulating factor, carbimazole was cautiously initiated with close hematological monitoring. The patient showed progressive clinical and hematological improvement. This case highlights the rare transition from Hashimoto's thyroiditis to Graves' disease in a patient with seropositive RA and immune-mediated pancytopenia. It underscores the importance of considering autoimmune thyroid conversion in previously hypothyroid patients with persistent TSH suppression and demonstrates that carefully monitored antithyroid therapy can be safely administered despite pre-existing pancytopenia within a multidisciplinary care framework.
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BibTeX
@article{kamath2026autoimmune,
title = {{Autoimmune Conversion of Hashimoto's Thyroiditis to Graves' Disease With Immune Pancytopenia in a Patient With Seropositive Rheumatoid Arthritis: A Diagnostic and Therapeutic Conundrum.}},
author = {Sangita D Kamath and Bijaya Jha and Vijay Kota and Prashant U Kaduskar},
journal = {Cureus},
year = {2026},
month = sep,
doi = {10.7759/cureus.116714},
url = {https://europepmc.org/article/MED/42923896},
note = {CC BY},
}
RIS
TY - JOUR
TI - Autoimmune Conversion of Hashimoto's Thyroiditis to Graves' Disease With Immune Pancytopenia in a Patient With Seropositive Rheumatoid Arthritis: A Diagnostic and Therapeutic Conundrum.
AU - Sangita D Kamath
AU - Bijaya Jha
AU - Vijay Kota
AU - Prashant U Kaduskar
PY - 2026
DA - 2026/09/22
JO - Cureus
DO - 10.7759/cureus.116714
UR - https://europepmc.org/article/MED/42923896
AB - Autoimmune conversion of Hashimoto's thyroiditis (HT) to Graves' disease (GD) is an uncommon phenomenon. The coexistence of GD, seropositive rheumatoid arthritis (RA), and pancytopenia presents a rare diagnostic and therapeutic challenge, particularly when antithyroid drug (ATD) therapy is contemplated in the presence of pre-existing cytopenias. A 66-year-old woman with a four-year history of hypothyroidism on levothyroxine replacement and long-standing seropositive RA presented with generalized weakness, altered bowel habits, and insomnia. Serial thyroid function tests (TFTs) had demonstrated progressive suppression of thyroid-stimulating hormone (TSH), necessitating dose reduction and eventual discontinuation of levothyroxine. Evaluation revealed thyrotoxicosis with elevated free thyroxine (FT4), free triiodothyronine (FT3), raised antithyroid peroxidase and TSH receptor antibodies, diffuse goiter with increased vascularity on Doppler ultrasonography, and diffusely increased uptake on thyroid scintigraphy, confirming Graves' disease. Concurrent investigations demonstrated pancytopenia with elevated liver enzymes and mild splenomegaly. Given the presence of seropositive rheumatoid arthritis and the exclusion of alternative causes of pancytopenia, an immune-mediated mechanism leading to bone marrow suppression was suspected. After treatment with granulocyte colony-stimulating factor, carbimazole was cautiously initiated with close hematological monitoring. The patient showed progressive clinical and hematological improvement. This case highlights the rare transition from Hashimoto's thyroiditis to Graves' disease in a patient with seropositive RA and immune-mediated pancytopenia. It underscores the importance of considering autoimmune thyroid conversion in previously hypothyroid patients with persistent TSH suppression and demonstrates that carefully monitored antithyroid therapy can be safely administered despite pre-existing pancytopenia within a multidisciplinary care framework.
SN - 2168-8184
ER -