Endocrine Abstracts

PTH has been reported to enhance steroid secretion in vitro from human adrenocortical cells and some reports indicate an increased cortisol secretion in patients with PHPT that normalizes after surgery. Thus, the possible stimulatory effect of PTH on cortisol secretion could contribute to the impairment of bone status in primary hyperparathyroidism (PHPT). The aim of this study was to evaluate the relationship between parameters of adrenal function, bone metabolism and density as well as biochemical indices of PHPT in a group of consecutive patients at the time of the diagnosis, referred to us from 1993 through 2004. In 191 patients (age, mean±S.D., 60.1±13.2 yrs; F/M 145/46, BMI: 25.8±4.8 kg/m², symptomatic/asymptomatic: 91/100, PTH: 235.6±200.1 pg/ml, total Ca_s:11.2±0.09 mg/dl, Ca_s⁺⁺:1.5±0.01 mMol/l) morning and midnight ACTH and cortisol levels, urinary free cortisol (UFC), osteocalcin (OC), total and bone ALP, urinary cross-links (XL), DXA at lumbar spine, total femur and forearm were evaluated. Univariate analysis with Spearman rank correlation test was performed. Mean levels of morning and midnight ACTH and cortisol as well as of UFC were in the normal range. Bone markers were all increased; osteoporosis (T score <−2.5 DS) was diagnosed in 67.6% of PHPT patients, mostly at lumbar spine and forearm level. PTH negatively correlated with morning ACTH levels (P<0.02) while it did not correlate either with morning or midnight cortisol levels or UFC. Negative correlations (P<0.05) were found: a) between morning cortisol and femoral BMD, b) between midnight cortisol and radial as well as femoral BMD. The morning/midnight cortisol ratio showed positive correlation with radial T and Z scores, while negatively correlated with total Ca_s. In conclusions, our findings indicate some relationship between ACTH and cortisol secretion and PTH/calcium levels in PHPT. They also show a clear association between cortisol levels and bone impairment, particularly at cortical bone. All together these findings suggest a potential role of cortisol secretion in the pathogenesis of bone impairment in PHPT.