Severely hunched over with a broken leg to boot, 78-year-old
Lillian S sits waiting in her doctor's office. Lillian
has osteoporosis and is taking alendronate and a calcium
supplement, but no vitamin D. To remedy this, her doctor
advises her to hobble out and get a bottle of vitamin
D as soon as possible. But it may be wise to reconsider
this decision. The results of a new study suggest that
prescription vitamin D analogues may be superior to traditional
over-the-counter vitamin D supplements for preventive
treatment of osteoporosis.
It's been established that the
sunshine vitamin can counteract all major mechanisms
of osteoporotic fractures, yet most studies have been
unable to provide conclusive results as to which form
works best. The majority of studies to date have been
too small (350 or fewer subjects) to answer this question
and few have actually compared different forms of vitamin
D head-to-head. Fortunately, a meta-analysis published
online February 7, 2005 in Calcified Tissue International
compares the effects of vitamin D and hydroxylated vitamin
D analogues (alfacalcidol and calcitriol) on bone mineral
density and osteoporotic fractures.
THE
ANALOGue ADVANTAGE
The analysis demonstrates "superiority of the D analogues
alfacalcidol and calcitriol in preventing bone loss
and spinal fractures in primary osteoporosis, including
postmenopausal women," said lead study author Dr Florent
Richy and his colleagues from the University of Liege,
Belgium. Fourteen native vitamin D, nine alfacalcidol
and 10 calcitriol trials met the inclusion criteria,
along with two studies directly comparing native vitamin
D and alfacalcidol in glucocorticoid-induced osteoporosis
(GIOP). The effects in GIOP were less clear, but direct
comparison suggested a similar benefit.
What about treating osteoporosis
caused by a vitamin D deficiency? In a 2004 review of
vitamin D and its analogues published in the journal
Rheumatology International, authors Drs Johann
Ringe and Erich Schacht noted that both primary and
secondary vitamin D deficiency may contribute to osteoporosis
in the elderly. The treatment differences between the
two were reviewed.
Primary deficiency of vitamin D,
caused by low dietary vitamin D, intestinal malabsorption
or reduced exposure to sunlight, can be corrected with
native vitamin D supplements. Vitamin D is converted
to calcitriol, its most metabolically active form, through
the addition of two hydroxyl groups — the first
by the liver, the second by the kidney. These supplements
are safe, cheap and readily available without prescription.
Feedback inhibition of calcitriol production prevents
hypercalcemia.
Reduced renal activation, which
may occur in the elderly, can cause secondary vitamin
D deficiency. Native vitamin D cannot correct this type
of deficiency but vitamin D analogues are effective
— though neither will correct tissue resistance.
Alfacalcidol requires activation
by the liver, which can occur even
with serious liver disease. Calcitriol needs no activation
but may induce hypercalcemia when taken due to its unregulated
concentrations. Hypercalcemia is less likely with alfacalcidol
as conversion to calcitriol is relatively slow, producing
lower peak concentrations.
Vitamin D analogues appear to outshine
native vitamin D supplements for preventive treatment
of osteoporosis. The vitamin D analogues don't accumulate
in tissue and can be used in all age groups and types
of osteoporosis. One drawback, however, is that they're
more expensive and require a prescription. So, vitamin
D analogues may just be the sunshine vitamin of choice
for Lillian — if she can afford it.
Calcif Tissue Int published
online Feb 7, 2005
|
