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Propylthiouracil-Induced Vasculitis in Relapsed Graves' Disease With Recent Iodine Exposure: A Therapeutic Dilemma
Sarmad Butt1, M S Majeed1, Iftikhar Ali2
1Endocrinology and Diabetes, Ulster Hospital, Belfast, GBR.
We present a challenging case of Graves' disease complicated by propylthiouracil (PTU)-induced antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis and recent iodine contrast exposure, creating a therapeutic dilemma where standard treatment options were severely limited. A 60-year-old man was diagnosed with Graves' disease in late 2020 and treated with carbimazole for one year. When the medication was stopped, he relapsed and was switched to PTU due to side effects on restarting carbimazole. Although radioactive iodine (RAI) therapy was offered, the patient declined due to personal reasons. Nearly two years into PTU therapy, he developed worsening breathlessness, and computed tomography (CT) chest revealed a new pericardial effusion. He was treated presumptively for pericarditis, but follow-up imaging showed minimal improvement. Approximately four and a half years after the initial diagnosis, he experienced migratory joint pain, swelling, and persistently raised inflammatory markers. During his work-up, he received a significant iodine load from contrast-enhanced imaging. Autoimmune screening confirmed ANCA-associated vasculitis with anti-myeloperoxidase antibody positivity. PTU was discontinued, and corticosteroids were initiated, leading to clinical improvement. Given florid hyperthyroidism and recent iodine exposure, his case was reviewed at the Endocrine multidisciplinary meeting. Carbimazole was restarted as a bridging therapy; despite its vasculitis risk, it remained the best option until RAI, which was ineffective due to iodine saturation, could be given. Surgical thyroidectomy was unsafe due to severe thyrotoxicosis. These limitations created a narrow therapeutic window requiring careful multidisciplinary planning. This case highlights the rare but serious complication of PTU-induced vasculitis and the complexities of managing florid hyperthyroidism when drug intolerance, recent iodine exposure, and surgical risk converge, truly an endocrinologist's worst nightmare.
We present a challenging case of Graves' disease complicated by propylthiouracil (PTU)-induced antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis and recent iodine contrast exposure, creating a therapeutic dilemma where standard treatment options were severely limited. A 60-year-old man was diagnosed with Graves' disease in late 2020 and treated with carbimazole for one year. When the medication was stopped, he relapsed and was switched to PTU due to side effects on restarting carbimazole. Although radioactive iodine (RAI) therapy was offered, the patient declined due to personal reasons. Nearly two years into PTU therapy, he developed worsening breathlessness, and computed tomography (CT) chest revealed a new pericardial effusion. He was treated presumptively for pericarditis, but follow-up imaging showed minimal improvement. Approximately four and a half years after the initial diagnosis, he experienced migratory joint pain, swelling, and persistently raised inflammatory markers. During his work-up, he received a significant iodine load from contrast-enhanced imaging. Autoimmune screening confirmed ANCA-associated vasculitis with anti-myeloperoxidase antibody positivity. PTU was discontinued, and corticosteroids were initiated, leading to clinical improvement. Given florid hyperthyroidism and recent iodine exposure, his case was reviewed at the Endocrine multidisciplinary meeting. Carbimazole was restarted as a bridging therapy; despite its vasculitis risk, it remained the best option until RAI, which was ineffective due to iodine saturation, could be given. Surgical thyroidectomy was unsafe due to severe thyrotoxicosis. These limitations created a narrow therapeutic window requiring careful multidisciplinary planning. This case highlights the rare but serious complication of PTU-induced vasculitis and the complexities of managing florid hyperthyroidism when drug intolerance, recent iodine exposure, and surgical risk converge, truly an endocrinologist's worst nightmare.
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