Spontaneous recovery of bone mass after cure of endogenous hypercortisolism

Abstract

Patients with Cushing's syndrome (CS) develop osteopenia-osteoporosis. The present study evaluates the recovery of bone mass within 2 years after remission of hypercortisolism and in long term follow up, an issue rarely addressed. Twenty patients (6M, 14F, 3 post-menopausal, 15-64 years old), 15 with Cushing's disease, 2 with ectopic ACTH syndrome, 3 with ACTH-independent CS were studied. BMD, T and Z scores at lumbar spine and proximal femur were assessed by dual-energy X-ray absorptiometry before and 7-33 months after treatment of hypercortisolism. Five patients were treated with bisphosphonates. Four patients had hypogonadism and 4 GH-deficiency. At baseline all patients showed osteopenia/osteoporosis and the spine appeared more damaged than the femur; femur BMD was positively related with body mass index (BMI). No correlations were observed between spine and femur bone parameters and duration of disease or severity of hypercortisolism. Bone parameters did not differ in patients with or without GH or other pituitary deficiencies. After cure of hypercortisolism a significant improvement in spine BMD, Z and T scores and in femur Z and T scores was observed with normalization in 3 patients; there was no significant difference in percent improvement between femur and spine. The increase in bone parameters at spine and femur was independent from values at baseline. The percent increase in spine T and Z scores was positively related with time elapsed since cure. Bisphosphonates did not influence the recovery of bone mineralization. In long term follow up, after a median period of 7 years a further improvement in bone density was observed in 100% of patients at spine and in 9/11 at femur, although 8/11 patients still had femoral and/or vertebral T score in the range of osteopenia/osteoporosis. Spontaneous improvement of osteoporosis after cure of hypercortisolism occurs both at spine and femur, is independent from basal conditions and not affected by bisphosphonates. The improvement at spine depends on time since cure.

MECHANISMS IN ENDOCRINOLOGY: Endogenous subclinical hypercortisolism and bone: a clinical review

“…However, it must be considered that in the past years, the daily dose of steroid replacement was definitely higher than that currently used (112), and, therefore, these data have probably been biased by an overtreatment of postsurgical hypoadrenalism. In addition, the usefulness of bisphosphonates after recovery from endogenous hypercortisolism is questioned (113). Therefore, after recovery from SH, a bone-active drug should be initiated only in the presence of BMD decrease and/or if a fragility fracture occurs during follow-up (Fig.…”

Pituitary Diseases and Bone

“…6,33 Bone health does not always completely recover after correction of endogenous hypercortisolism. 34 In fact, some patients may experience an increase in bone formation soon after resolution of glucocorticoid excess with secondary improvement of BMD and a decrease in fracture risk, 35 whereas in other patients the risk of fracture continue to remain high over the long term after the cure of disease, 36 needing personalized treatment with bone-active drugs. 37 Hypopituitarism Low bone turnover and decreased BMD is reported in patients with GH deficiency (GHD) (see Box 1), either isolated or combined with other pituitary hormone deficiencies.…”

Clinical Perspective: What Do Addison and Cushing Tell Us About Glucocorticoid Action?

“…Although it is prudent to treat with either an anabolic or anti-resorptive in a patient with active endogenous hypercortisolism to prevent active bone loss, the case for anti-resorptive after a surgical cure is less clear. This is due to the fact that there is spontaneous recovery of bone mass following cure [ 16 ], which theoretically could be blunted by an anti-resorptive.…”