Department of Medical Endocrinology, Copenhagen University Hospital, Rigshospitalet, Copenhagen.
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen.
Rheumatology (Oxford). 2020 Oct 1;59(10):2764-2773. doi: 10.1093/rheumatology/keaa011.
Glucocorticoid treatment is fundamental in polymyalgia rheumatica (PMR) and giant cell arteritis (GCA), but carries a risk of glucocorticoid-induced adrenal insufficiency. Adrenal insufficiency can cause reluctance to stop glucocorticoid treatment after disease remission as symptoms can resemble PMR/GCA flare. We aimed to determine the prevalence of adrenal insufficiency in prednisolone-treated patients with PMR/GCA.
We included 47 patients with PMR (n = 37), GCA (n = 1) or both (n = 9), treated with prednisolone for ≥5.4 months, current dose 2.5-10 mg/day. Adrenal function was evaluated using a corticotropin (Synacthen®) stimulation test following 48 h prednisolone pause. Two years' clinical follow-up data are provided.
Seven patients (15%) had adrenal insufficiency, 4 (11%) of the 37 patients with PMR alone, and 3 (30%) of the 10 patients with GCA. Corticotropin-stimulated P-cortisol was significantly associated with current prednisolone dose, mean daily dose the last 3 and 6 months before testing, and basal P-cortisol, but not with total dose or treatment duration. Adrenal insufficiency occurred with all current prednisolone doses (2.5-10 mg/day). Five (71%) of the glucocorticoid-insufficient patients could discontinue prednisolone treatment; two of them recovered glucocorticoid function, whereas three still needed hydrocortisone replacement 2 years later. Two patients experienced in total four acute hospital admissions with symptoms of adrenal crises.
Glucocorticoid-induced adrenal insufficiency occurred in 15% of patients with PMR/GCA. Mean prednisolone dose the last 3 months and basal P-cortisol were the best and simplest predictors of adrenal function. Most of the glucocorticoid-insufficient patients could discontinue prednisolone with appropriate treatment for adrenal insufficiency.
糖皮质激素治疗是巨细胞动脉炎（GCA）和多发性肌炎（PMR）的基础，但存在糖皮质激素诱导的肾上腺功能不全的风险。肾上腺功能不全可能导致疾病缓解后不愿停止糖皮质激素治疗，因为症状可能类似于 PMR/GCA 发作。我们旨在确定接受泼尼松龙治疗的 PMR/GCA 患者中肾上腺功能不全的患病率。
我们纳入了 47 名接受泼尼松龙治疗≥5.4 个月的 PMR（n=37）、GCA（n=1）或两者（n=9）的患者，当前剂量为 2.5-10mg/天。在停用泼尼松龙 48 小时后，使用促皮质素（Synacthen®）刺激试验评估肾上腺功能。提供了两年的临床随访数据。
7 名患者（15%）存在肾上腺功能不全，37 名单独患有 PMR 的患者中有 4 名（11%），10 名患有 GCA 的患者中有 3 名（30%）。促皮质素刺激后的 P 皮质醇与当前泼尼松龙剂量、测试前 3 个月和 6 个月的平均每日剂量以及基础 P 皮质醇显著相关，但与总剂量或治疗持续时间无关。所有当前的泼尼松龙剂量（2.5-10mg/天）都出现了肾上腺功能不全。5 名（71%）糖皮质激素不足的患者能够停止泼尼松龙治疗；其中 2 名恢复了糖皮质激素功能，而 3 名在 2 年后仍需要氢化可的松替代治疗。2 名患者总共经历了 4 次因肾上腺危象症状而急性住院。
PMR/GCA 患者中，糖皮质激素诱导的肾上腺功能不全发生率为 15%。最近 3 个月的平均泼尼松龙剂量和基础 P 皮质醇是预测肾上腺功能的最佳和最简单的指标。大多数糖皮质激素不足的患者可以在适当治疗肾上腺功能不全后停止使用泼尼松龙。
