title: High incidence of adrenal suppression in children with Kawasaki disease treated with intravenous immunoglobulin plus prednisolone.
abstract: Combination treatment with intravenous immunoglobulin (IVIG) plus prednisolone, newly designed for children with severe Kawasaki disease (KD), reduces coronary artery abnormalities significantly. As prednisolone is administered for approximately 20 days in this regimen, we examined whether adrenal function of the treated patients is suppressed. A prospective study was performed at one medical institution in 21 children with KD (age range 0.3-10.4 years, median 3.1 years) who were treated with the regimen between February and June, 2012. We assessed cortisol and ACTH values before the initiation and after the cessation of prednisolone administration as well as peak cortisol and ACTH values at corticotropin-releasing hormone (CRH) stimulation tests, which were repeated 0, 2, and 6 months after the treatment. Morning cortisol and ACTH values after the cessation of prednisolone treatment were suppressed. Peak cortisol values at the first CRH stimulation test ranged from 5.1 to 25.4 μg/dL and were less than 20 μg/dL in 17 of 21 patients, but were restored to more than 14.6 μg/dL in all patients by 6 months after the prednisolone treatment. A significant positive correlation was observed between cortisol values at 09:00 h after the prednisolone treatment and peak cortisol values at the following CRH stimulation test (r = 0.727, p < 0.001). We conclude that adrenal suppression can occur in a high proportion of children with KD treated with IVIG plus prednisolone, despite rather short duration and relatively small amounts of administered glucocorticoids.
authors.affiliation: Division of Endocrinology and Metabolism, Tokyo Metropolitan Children's Medical Center, Fuchu 183-8561, Japan.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Goto
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Miyagawa
authors.forename: Kaori
authors.initials: K
authors.lastname: Kikunaga
authors.forename: Masaru
authors.initials: M
authors.lastname: Miura
authors.forename: Yukihiro
authors.initials: Y
authors.lastname: Hasegawa
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D000309:Adrenal Insufficiency / Q000139:chemically induced* / Q000453:epidemiology / Q000517:prevention & control; D000324:Adrenocorticotropic Hormone / Q000037:antagonists & inhibitors / Q000097:blood / Q000378:metabolism; D000893:Anti-Inflammatory Agents / Q000009:adverse effects* / Q000627:therapeutic use; D002648:Child; D002675:Child, Preschool; D003131:Combined Modality Therapy / Q000009:adverse effects; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D006854:Hydrocortisone / Q000009:adverse effects / Q000037:antagonists & inhibitors / Q000097:blood / Q000378:metabolism / Q000627:therapeutic use; D016756:Immunoglobulins, Intravenous / Q000009:adverse effects* / Q000627:therapeutic use; D015994:Incidence; D007223:Infant; D007564:Japan / Q000453:epidemiology; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D011239:Prednisolone / Q000009:adverse effects* / Q000627:therapeutic use; D011446:Prospective Studies; D012306:Risk
chemical_list: D000893:Anti-Inflammatory Agents; D005938:Glucocorticoids; D016756:Immunoglobulins, Intravenous; D000324:Adrenocorticotropic Hormone; D011239:Prednisolone; D006854:Hydrocortisone