Mitsuru Ichii1, Katsuhito Mori2, Daichi Miyaoka3, Mika Sonoda1, Yoshihiro Tsujimoto1, Shinya Nakatani3, Tetsuo Shoji4, Masanori Emoto5,3. 1. Division of Internal Medicine, Inoue Hospital, Suita, Japan. 2. Department of Nephrology, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, 545-8585, Osaka, Japan. ktmori@med.osaka-cu.ac.jp. 3. Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan. 4. Department of Vascular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan. 5. Department of Nephrology, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, 545-8585, Osaka, Japan.
Abstract
BACKGROUND: 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. Roxadustat has high affinity to thyroid hormone receptor beta, which may affect thyroid hormone homeostasis. CASE PRESENTATION: We 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. CONCLUSIONS: Physicians should pay special attention to thyroid hormone abnormalities in treatment with roxadustat.
BACKGROUND: 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. Roxadustat has high affinity to thyroid hormone receptor beta, which may affect thyroid hormone homeostasis. CASE PRESENTATION: We 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. CONCLUSIONS: Physicians should pay special attention to thyroid hormone abnormalities in treatment with roxadustat.
Authors: Olympia Koulouri; Carla Moran; David Halsall; Krishna Chatterjee; Mark Gurnell Journal: Best Pract Res Clin Endocrinol Metab Date: 2013-10-17 Impact factor: 4.690