Отделение костной патологии  
S. Rodionova, A. Kolondaev, I. Bogdanova. Central Institute of Traumatology and Orthopaedics, Moscow, Russia.
(12-th Workshop on vitamin D (abstracts). - Maastricht. - 2003. - P. 16.)

   THE PURPOSE of this study was to estimate the dependence of BMD from biochemical markers dynamics in the treatment of senile and postmenopausal osteoporosis with alfacalcidol.
   METHODS. 75 women with senile and postmenopausal osteoporosis receiving alfacalcidol alone (43) or alfacalcidol and etidronate (32) were subjected to biochemical monitoring during one year. Calcium and phosphorus levels, alcaline phosphatase activity in blood, calcium excretion were measured on a regular basis. A change of bone mass was estimated in L2-L4 vertebra and femoral neck in one year by DEXA (Lunar DPX-L). Alfacalcidol dosage may be changed from 0,5 mcg to 1,5 mcg per a day in both groups. All patients received 0,5-1 gram of Ca per a day.
   RESULTS. In alfacalcidol group, BMD increase was significant in greater trochanter (4,5%) and L2-L4 vertebra (3,2%), not in the neck (0,6%). Correlations were found between age and BMD dynamics (Rs=0,2-0,56 in different DEXA zones), but between the change of BMD, Ca levels in blood and Ca excretion dynamics they were strongest (Rs=0,2-0,83 DEXA zones). The change of BMD in bisphosphonate+alfacalcidol group also was depended on biochemical markers. If hypocalcaemia or hypercalcaemia with high alcaline phosphatase activity developed BMD decreased in femoral neck (-1,5%) and Ward's trigonum (-0,8%), as in L2-L4 vertebra slightly increased  (2,0%). If the blood Ca level, Ca excretion and alcaline phosphatase activity were normalized significant  BMD increase was registered (from 4,0% in neck to 7,2% in vertebra).
   CONCLUSION. In the oldest osteoporotic patients Ca homeostasis disturbances were more frequent, and alfacalcidol as monotherapy or combined with bisphosphonate was more effective. Moreover, BMD decrease in one third of bisphosphonate group may be partially explained by Ca homeostasis disturbances not compensated adequately by alfacalcidol and Ca intake.
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