No satisfactory treatment is available for metabolic bone disease asso
ciated with primary biliary cirrhosis. On the basis of the similaritie
s to postmenopausal osteoporosis, the rationale exists for calcitonin
to be tested in clinical studies in patients with primary biliary cirr
hosis-associated osteoporosis. We evaluated the effect of calcitonin o
n bone metabolism and mineral density in 25 women with primary biliary
cirrhosis and severe osteopenia. After 6 mo of observation, patients
received a synthetic calcitonin or a control treatment consisting of l
ess than one hundredth of the recommended dose of porcine calcitonin.
The two treatments were administered in sequence to each patient for t
wo 6-mo periods, with a 3-mo washout between them, according to a cros
sover design. After the observation period, oral calcium supplementati
on was started. Bone mineral density was measured by dual-photon absor
ptiometry of the lumbar spine at study entry and at the beginning and
the end of each treatment period. During the observation period bone m
ineral density fell by 3.5% whereas during the following 6 mo it incre
ased in both the patients who received calcitonin (4.3%) and those who
received the control treatment (4.9%). Conversely, after the crossove
r, bone mineral density decreased during both calcitonin (-2.7%) and c
ontrol treatment (-2.9%). A significant difference was observed betwee
n the two periods but not between the two treatments or between the tw
o sequences of treatment administration. In conclusion, our findings i
ndicate that parenterally administered calcitonin for 6 mo is ineffect
ive in halting bone loss in patients with primary biliary cirrhosis-as
sociated metabolic bone disease, whereas calcium supplementation may h
ave a transient beneficial effect.