Abstract
BackgroundInhibition of hypoxia-inducible factor prolyl hydroxylase (HIF-PH) is a novel choice for the treatment of renal anemia, and an oral HIF-PH inhibitor roxadustat was approved for renal anemia. Roxadustat has high affinity to thyroid hormone receptor beta, which may affect thyroid hormone homeostasis.Case presentationWe present here a patient undergoing hemodialysis with primary hypothyroidism receiving levothyroxine replacement, who showed decreased free thyroxine (FT4) and thyroid stimulating hormone (TSH) after starting roxadustat. Pituitary stimulation test revealed selective suppression of TSH secretion. Recovery of TSH and FT4 levels after stopping roxadustat suggested the suppression of TSH was reversible.ConclusionsPhysicians should pay special attention to thyroid hormone abnormalities in treatment with roxadustat.
Highlights
Inhibition of hypoxia-inducible factor prolyl hydroxylase (HIF-PH) is a novel choice for the treatment of renal anemia, and an oral Hypoxia-inducible factor (HIF)-PH inhibitor roxadustat was approved for renal anemia
Thyroid hormone is tightly controlled by the feedback regulation in the hypothalamus-pituitary-thyroid axis, and Thyroid hormone receptor (THR) play essential roles in the actions of thyroid hormone
thyroid hormone receptor β (THRβ) plays an important role in hypothalamus and pituitary gland
Summary
Inhibition of hypoxia-inducible factor prolyl hydroxylase (HIF-PH) is a novel choice for the treatment of renal anemia, and an oral HIF-PH inhibitor roxadustat was approved for renal anemia. We describe a hemodialysis patient who showed suppression of thyroid stimulating hormone (TSH, or thyrotropin) and decreased free thyroxine (FT4) levels following roxadustat treatment for renal anemia.
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