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Nivolumab-induced hypophysitis causing secondary adrenal insufficiency after transient ACTH elevation
Title: | Nivolumab-induced hypophysitis causing secondary adrenal insufficiency after transient ACTH elevation |
Authors: | Sekizaki, Tomonori Browse this author | Kameda, Hiraku Browse this author →KAKEN DB | Oba, Chiho Browse this author | Yong Cho, Kyu Browse this author | Nakamura, Akinobu Browse this author →KAKEN DB | Miyoshi, Hideaki Browse this author →KAKEN DB | Osawa, Takahiro Browse this author →KAKEN DB | Shinohara, Nobuo Browse this author →KAKEN DB | Atsumi, Tatsuya Browse this author →KAKEN DB |
Keywords: | Nivolumab | Immune checkpoint inhibitor | Hypophysitis | ACTH | Secondary adrenal insufficiency |
Issue Date: | 2019 |
Publisher: | The Japan Endocrine Society |
Journal Title: | Endocrine Journal |
Volume: | 66 |
Issue: | 10 |
Start Page: | 937 |
End Page: | 941 |
Publisher DOI: | 10.1507/endocrj.EJ19-0076 |
Abstract: | A 62-year-old man was referred to our department for elevation of plasma ACTH and cortisol levels during nivolumab administration for renal cell carcinoma. Although his ACTH and cortisol levels had been maintained within their reference ranges, they were elevated to 232.7 pg/mL and 21.9 μg/dL, respectively, after eight courses of nivolumab without any subjective symptoms or Cushing’s sign. He was hospitalized for endocrinological investigation. ACTH and cortisol returned to their normal ranges (29.18 pg/mL and 11.4 μg/dL, respectively) in the early morning on day 1, but fell down sharply to 3.7 pg/mL and 1.6 μg/dL, respectively, in the early morning on day 2 without subjective symptoms or vital sign changes. Brain magnetic resonance imaging showed no abnormality in his pituitary gland. ACTH response to CRH was apparently normal, but cortisol did not respond to increased ACTH. A rapid ACTH stimulation test showed slightly reduced response of cortisol to exogenous ACTH (1-24). These findings and his clinical course suggested secondary adrenal insufficiency arising from nivolumab-induced hypophysitis. In previous reports, most cases of immune checkpoint inhibitor (ICI)-induced hypophysitis were diagnosed based on adrenal insufficiency symptoms or hyponatremia with low ACTH and cortisol. The ACTH elevation observed in the present case may reflect destruction of the pituitary gland, suggesting that this finding may be important for early detection of ICI-induced hypophysitis. Our case underlines the necessity of close monitoring for subsequent onset of adrenal insufficiency when ACTH elevation is observed during ICI administration |
Type: | article |
URI: | http://hdl.handle.net/2115/78818 |
Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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