Bone loss in hyperthyroid patients and in former hyperthyroid patients controlled on medical therapy: influence of...

The effect of hyperthyroidism on osteoporosis risk and its reversal after control of hyperthyroidism remains somewhat controversial. We assessed the values of bone mineral density in hyperthyroid patients and in former hyperthyroid patients euthyroid on medical therapy, as well as the influence of aetiology and menopause upon bone mass.

The values of bone mineral density in hyperthyroid patients (active) and former hyperthyroid patients euthyroid on medical therapy (controlled), were compared, together with data from our control group and from the Spanish reference population. We also compared the values of bone mineral density in patients with Graves' disease with those in patients with toxic nodular goitre and assessed the influence of the menopause.

We studied 127 consecutive hyperthyroid patients (age 41 +/- 16 years; 110 females, 17 males; 102 Graves' disease and 25 toxic nodular goitre); 78 were active (group A) and 49 controlled on medical therapy (carbimazole, mean time of euthyroidism 7.5 +/- 9.1 months; group B). We also studied 43 healthy subjects (age 40 +/- 14 years; 41 females, two males; group C).

Bone mineral density was assessed by dual X-ray absorptiometry at lumbar spine (L2-L4), femoral neck and Ward's triangle. Data were expressed as g/cm2 and as a Z score (SD vs Spanish reference population adjusted by age and sex). Blood was obtained to measure the levels of free T4, TSH and TSH receptor antibody.

Patients with active hyperthyroidism showed a generalized reduction in axial bone mineral density in comparison with both the control group and the reference population, whereas former hyperthyroid patients showed partial recovery of bone mass in lumbar spine and Ward's triangle. Mean Z scores at lumbar spine, femoral neck and Ward's triangle were: -0.92, -0.79 and -0.89 in group A; -0.74, -0.23 and -0.44 in group B and 0.18, 0.09 and 0.36 in group C, respectively. No differences were found between bone mineral density values from patients with Graves' disease and those with toxic nodular goitre, nor between pre and postmenopausal hyperthyroid women once adjusted by age and sex.

Our data suggest that hyperthyroid patients show a generalized reduction of bone mass in the axial skeleton and that only partial recovery is present in former hyperthyroid patients after a mean of 7.5 months of biochemical euthyroidism. This recovery is insufficient to normalize the bone density in lumbar spine and Ward's triangle, although femoral bone mass was not different from that of the control group. The extent and degree of hyperthyroid bone disease surpass the effects of the menopause on the bone mass. The aetiology of hyperthyroidism does not seem to play any role in the severity of hyperthyroid bone disease.