Definable causes of male osteoporosis account for only about 60% of the ost
eoporotic population. Those for whom no etiology is readily apparent are sa
id to have primary or idiopathic male osteoporosis. In these individuals, h
istomorphometric studies indicate that this is a disorder that is more typi
cally characterized by low turnover. Although antiresorptive agents such as
alendronate have been shown to increase bone mass in men, the rationale fo
r an anabolic agent that can stimulate bone formation is clear. The most at
tractive anabolic agent at this time is parathyroid hormone (PTH) administe
red in low dosage and intermittently. Such regimens in experimental animals
have been associated with marked gains in bone mass. Slovik et al. [14] sh
owed that parathyroid hormone can increase vertebral bone mass in men with
idiopathic osteoporosis. We have conducted the first controlled, randomized
, double-blind study of PTH in men with idiopathic osteoporosis. Twenty-thr
ee men, 30-68 years old (50 +/- 1.9) with Z-scores less than -2.0 were assi
gned to a placebo (n = 13) or treatment (n = 10) arm. After 18 months, thos
e who received PTH showed a 13.5 +/- 3% increase in bone mass, significantl
y greater than the placebo group whose bone density did not change. Femoral
neck bone density increased significantly by 2.9 +/- 1.5%. The distal radi
us site did not change. During an open label extension for an additional 12
months, there was no further increase in bone density in the lumbar spine
but the femoral neck continued to show gains. Markers of bone formation and
resorption increased in the PTH arm reaching a peak between 9 and 12 month
s of therapy and declining thereafter. Parathyroid hormone was well tolerat
ed. These results suggest that low-dose intermittent PTH may be an efficaci
ous therapy for men with idiopathic osteoporosis.