Transplantation proceedings · 2020
Graft-vs-Host Disease-Induced Hyperthyroidism in a Recipient of Allogeneic Hematopoietic Stem Cell Transplantation: A Case Report.
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Huang Fen, Liao Naying, Guan Yuqing, Jin Hua, Ye Jieyu, Fan Zhiping, Xuan Li, Liu Qifa, Shi Pengcheng
Аннотация
BACKGROUND: Hyperthyroidism after hematopoietic stem cell transplantation (HSCT) is rare, and only a few cases have been reported. What is more important, the fundamental mechanisms of hyperthyroidism after HSCT remained unclear.
CASE: A 28-year-old man received an HLA haploidentical related-donor HSCT for acute myeloid leukemia and developed hyperthyroidism 31 months after HSCT. He presented with periodic paralysis as the initial symptom, his serum levels of free triiodothyronine (fT3), free thyroxine (fT4), and anti-thyroid autoantibodies increased, and thyroid-stimulating hormone level decreased. As a result, he was diagnosed with hyperthyroidism. Although systemic symptoms, signs, and laboratory findings of graft-vs-host disease (GVHD) were absent, thyroid histopathologic examination revealed thyroid follicular destruction and infiltrations of lymphocytes, which mainly consisted of CD20+ B lymphocytes and CD4+ and CD3+ T lymphocytes by immunohistochemistry. These were in accordance with the pathologic features of GVHD. The symptom of periodic paralysis resolved after treatment with prednisolone and methimazole for 1 month. The treatments lasted for 4 months, and the plasma levels of fT3, fT4, TSH, and anti-thyroid peroxidase normalized. He did not relapse after drug withdrawal with observation for 24 months to date.
CONCLUSIONS: To the best of our knowledge, the present case was the first to be confirmed with thyroid-specific GVHD-induced hyperthyroidism after allogeneic HSCT.
CASE: A 28-year-old man received an HLA haploidentical related-donor HSCT for acute myeloid leukemia and developed hyperthyroidism 31 months after HSCT. He presented with periodic paralysis as the initial symptom, his serum levels of free triiodothyronine (fT3), free thyroxine (fT4), and anti-thyroid autoantibodies increased, and thyroid-stimulating hormone level decreased. As a result, he was diagnosed with hyperthyroidism. Although systemic symptoms, signs, and laboratory findings of graft-vs-host disease (GVHD) were absent, thyroid histopathologic examination revealed thyroid follicular destruction and infiltrations of lymphocytes, which mainly consisted of CD20+ B lymphocytes and CD4+ and CD3+ T lymphocytes by immunohistochemistry. These were in accordance with the pathologic features of GVHD. The symptom of periodic paralysis resolved after treatment with prednisolone and methimazole for 1 month. The treatments lasted for 4 months, and the plasma levels of fT3, fT4, TSH, and anti-thyroid peroxidase normalized. He did not relapse after drug withdrawal with observation for 24 months to date.
CONCLUSIONS: To the best of our knowledge, the present case was the first to be confirmed with thyroid-specific GVHD-induced hyperthyroidism after allogeneic HSCT.