than cyclo-oxygenase-2 inhibitors do (category I A).39 In deciding on the prescription of cyclooxygenase-2 inhibitors and conventional NSAIDs, cardiovascular risk factors should also be taken into account.40–45 8. All patients on glucocorticoid therapy for longer than 1 month, who will undergo surgery, need perioperative management with adequate glucocorticoid replacement to overcome potential adrenal insufficiency. N Level of evidence: IV N Strength of recommendation (95% CI): 91 (84–99) Adrenal insufficiency due to surgical stress has already been described in the 1950s.46 As patients with RA and PMR are considered to have relative adrenal insufficiency due to their disease,47 they might be more prone to adrenal insufficiency at surgery. The incidence and duration of GC-induced adrenal insufficiency depend, apart from possible individual differences in sensitivity for GC, on the type and dosage of GC48 49 and the duration of therapy. GC-treatment of less than 3 weeks or alternate-day therapy does not exclude the risk of suppression of the hypothalamic–pituitary–adrenal axis,50 51 but the risk is still dose-dependent.52 GC-replacement is recommended in case of surgery for patients at risk of adrenal insufficiency (category IV). For moderate physical stress-inducing procedures, a single dose of 100 mg of hydrocortisone intravenously has been proposed, and for major surgery, 100 mg of hydrocortisone intravenously before anaesthesia and every 8 h 4 times thereafter.53 The dose can be gradually tapered by half per day afterwards. However, several other schemes of GC-replacement exist. 9. Glucocorticoids during pregnancy have no additional risk for mother and child. N Level of evidence: – Mother: IV – Child: I–III N Strength of recommendation (95% CI): 87 (78 to 96) Safety of GC-usage during pregnancy refers to both the mother and the unborn child. First, for the pregnant mother, the spectrum of AEs associated with the use of GCs is believed not to differ between a pregnant patient and a non-pregnant patient (category IV evidence), but since pregnant or lactating women are more at risk for pregnancy-associated Aes, which are also seen as AE of GC-therapy (eg, osteoporosis,54 diabetes,55 hypertension56), this risk of these AEs could be especially increased by GC-therapy for these women, but no data are available. Second, regarding the safety of GCs for the fetus and neonate, dexamethasone can be used to treat fetal conditions such as immature lungs, because it is not metabolised well by the placenta, and so higher dosages are available to the fetus. Prednisone, prednisolone and methylprednisolone are less available to the fetus (10% of the maternal dose), and so these substances are preferred for the treatment of maternal disorders.57 GCs prior to and during pregnancy do not seem to have a negative impact on the development of the fetus. GCs in high doses have caused low birth weights in humans and cleft palate in experimental animal models,58 59 but there is no evidence that in humans prednisone or methylprednisolone are teratogenic (Food and Drug Administration risk category B,60), category III evidence.61 The incidence of infection was not increased in neonates who had been exposed to GCs in utero (category IB).62 GCs are excreted minimally into breast milk,63 64 and breastfeeding by women on low-dose GC-therapy is generally considered to be safe.65 Exposure of an infant can be further minimised if breastfeeding is avoided during the first 4 h after GC-intake, because there is an equilibrium between the concentration of prednisolone in mother milk and serum.64 10. Children receiving glucocorticoids should be checked regularly for linear growth