TY - ABST
T1 - Adrenal insufficiency during prednisolone treatment in patients with polymyalgia rheumatica or giant cell arteritis - prevalence and clinical approach
AU - Willemoes, Borresen Stina
AU - Laursen, Toke
AU - Jensen, Bente
AU - Hilsted, Linda
AU - Marie, Bartels Else
AU - Feldt-rasmussen, Ulla
AU - Locht, Henning
PY - 2018
Y1 - 2018
N2 - Introduction: Prednisolone is standard treatment of polymyalgia rheumatica (PMR) and giant cell arteritis (GCA), but many patients are reluctant to discontinue prednisolone treatment even after remission of the inflammatory conditions. Prednisolone-induced adrenal insufficiency can give manifest or latent symptoms, causing failure to taper and withdraw prednisolone. We therefore aimed to find the prevalence of adrenal insufficiency in prednisolone-treated patients with PMR/GCA.
Methods: A cross-sectional study of PMR/GCA patients treated with prednisolone for >6 months, currently 2.5–10 mg/day. Forty-seven patients (34 women) were included consecutively from the Rheumatology Outpatient Clinic. Adrenal function was evaluated by a fasting 250 μg Synacthen test in the morning following being prednisolone-free for 48-hours and oestrogen treatment free for 6-weeks. P-cortisol concentrations were measured by Roche Elecsys® Cortisol II assay. Adrenal insufficiency was defined as P-cortisol <420 nmol/l 30 minutes after Synacthen injection (local assay specific cut-off). All patients with adrenal insufficiency were subsequently followed in a close rheumatologic-endocrine collaboration. Prednisolone tapering was based on PMR/GCA remission, Synacthen tests were performed regularly and the need for hydrocortisone stress doses/daily supplementations was adjusted accordingly.
Results: The 47 patients (mean age 73 years (SD 7.3)) were treated with prednisolone for median 23 months (range 5.4–139 months), with a mean current prednisolone dose of 5.3 mg/day (SD 2.0). Seven patients (15%, CI95%: 7.4–28%) had adrenal insufficiency. Current prednisolone dose correlated negatively with 30 min P-cortisol (-32 nmol/l/mg prednisolone, CI95%: -9.5–-55 nmol/l/mg, P=0.0066, r=−0.39), but adrenal insufficiency occurred across the entire prednisolone dose range (2.5–10 mg/day). There was no correlation between duration of treatment and 30 min P-cortisol (P=0.24, r=−0.17). ACTH levels were low within reference range (mean 4.6 pmol/l (SD 2.9)). Insufficient patients were informed of the condition and administration of necessary hydrocortisone stress doses. Subsequently, 5 patients were able to discontinue prednisolone treatment, 2 of whom recovered adrenal function, whereas 3 still need daily hydrocortisone replacement. Two patients were unable to stop prednisolone treatment due to PMR/GCA disease activity, and have occasionally needed excess steroid doses to overcome stress/adrenal crises.
Conclusion: Iatrogenic adrenal insufficiency occurred in 15% of low-dose prednisolone treated patients with PMR/GCA. In most patients prednisolone could be discontinued due to recovery of adrenal function or by switching to oral hydrocortisone. This illustrates the importance of a close collaboration between rheumatology and endocrinology.
AB - Introduction: Prednisolone is standard treatment of polymyalgia rheumatica (PMR) and giant cell arteritis (GCA), but many patients are reluctant to discontinue prednisolone treatment even after remission of the inflammatory conditions. Prednisolone-induced adrenal insufficiency can give manifest or latent symptoms, causing failure to taper and withdraw prednisolone. We therefore aimed to find the prevalence of adrenal insufficiency in prednisolone-treated patients with PMR/GCA.
Methods: A cross-sectional study of PMR/GCA patients treated with prednisolone for >6 months, currently 2.5–10 mg/day. Forty-seven patients (34 women) were included consecutively from the Rheumatology Outpatient Clinic. Adrenal function was evaluated by a fasting 250 μg Synacthen test in the morning following being prednisolone-free for 48-hours and oestrogen treatment free for 6-weeks. P-cortisol concentrations were measured by Roche Elecsys® Cortisol II assay. Adrenal insufficiency was defined as P-cortisol <420 nmol/l 30 minutes after Synacthen injection (local assay specific cut-off). All patients with adrenal insufficiency were subsequently followed in a close rheumatologic-endocrine collaboration. Prednisolone tapering was based on PMR/GCA remission, Synacthen tests were performed regularly and the need for hydrocortisone stress doses/daily supplementations was adjusted accordingly.
Results: The 47 patients (mean age 73 years (SD 7.3)) were treated with prednisolone for median 23 months (range 5.4–139 months), with a mean current prednisolone dose of 5.3 mg/day (SD 2.0). Seven patients (15%, CI95%: 7.4–28%) had adrenal insufficiency. Current prednisolone dose correlated negatively with 30 min P-cortisol (-32 nmol/l/mg prednisolone, CI95%: -9.5–-55 nmol/l/mg, P=0.0066, r=−0.39), but adrenal insufficiency occurred across the entire prednisolone dose range (2.5–10 mg/day). There was no correlation between duration of treatment and 30 min P-cortisol (P=0.24, r=−0.17). ACTH levels were low within reference range (mean 4.6 pmol/l (SD 2.9)). Insufficient patients were informed of the condition and administration of necessary hydrocortisone stress doses. Subsequently, 5 patients were able to discontinue prednisolone treatment, 2 of whom recovered adrenal function, whereas 3 still need daily hydrocortisone replacement. Two patients were unable to stop prednisolone treatment due to PMR/GCA disease activity, and have occasionally needed excess steroid doses to overcome stress/adrenal crises.
Conclusion: Iatrogenic adrenal insufficiency occurred in 15% of low-dose prednisolone treated patients with PMR/GCA. In most patients prednisolone could be discontinued due to recovery of adrenal function or by switching to oral hydrocortisone. This illustrates the importance of a close collaboration between rheumatology and endocrinology.
U2 - 10.1530/endoabs.56.P19
DO - 10.1530/endoabs.56.P19
M3 - Conference abstract in journal
SN - 1470-3947
VL - 56
JO - Endocrine Abstracts
JF - Endocrine Abstracts
M1 - P19
ER -