Author(s)

Chris G. Velentzas

Military Hospital of Athens-Greece Toronto Western Hospital-Canada University of Athens, Greece..

Vitamin D₃ after its entrance in the organism undergoes hydroxylation on C-25 carbon atom by the action of microsomal liver enzymes giving the metabolite 25 hydroxyvitamin D₃ (25OHD₃). The function of microsomal liver enzymes is influenced in some specified states by hormones or drugs. It has approved that thyroxin is a potent stimulator of these enzymes while allopurinol suppresses their function. The aim of this issue is to examine 25OHD₃ plasma levels in thyrotoxic subjects and in those pretreated with allopurinol on the base of the afford mentioned data. In a first phase 25OHD₃ plasma levels were estimated in thyrotoxic subjects against euthytoid healthy controls. In a second phase lmg vitamin D₃ was injected intravenously (i.v.) in thyrotoxic subjects and in healthy euthyroid controls. 25OHD₃ plasma levels were measured before and in post injection period in six hours intervals for 48 hours. In a third phase a couple of subjects one thyrotoxic and one euthyroid healthy control pretreated both with allopurinol injected lmg of vitamin D₃ i.v. In all studied subjects 25OHD₃ plasma levels were measured before and in post injection period in six hours intervals for 48 hours. The pre and post injection 25OHD₃ plasma levels measured the size of activity of liver enzyme responsible for bioactivation of vitamin D₃. In the first phase was indicated that 25OHD₃ plasma levels were lower in thyrotoxic subjects comparing with that of euthyroid healthy controls (p < 0.001). In the second phase was found that the bioactivation of vitamin D₃ in thyrotoxic subjects was 2,5 to 8 times faster comparing with euthyroid healthy controls. In the third phase was shown that allopurinol decreases the activity of liver enzymes function as regard the bioactivation of vitamin D₃. The bioactivation of vitamin D₃ is accelerated in thyrotoxicosis compared with that in euthyroid state. This phenomenon produces low 25OHD₃ plasma levels in thyrotoxic subjects which initially may be normal or slightly increased depended from the vitamin D₃ status in the thyrotoxic subjects. By continuous stimulatory action of increased thyroid hormones on liver enzymes the 25OHD₃ plasma levels earlier or later decline in levels of hypo-or avitaminosis D3. The previously described biological events may explain the decreased intestinal calcium absorption of vitamin D₃ and the osteomalacic component found in a percentage of thyrotoxic bone histology. For the blocking effects of allopurinol on liver enzymes function and possibly of other pharmaceutical products in relation to vitamin D₃ bioactivation, available data are still lacking.

25-Hydroxyvitamin D; Thyroxin; Allopurinol; Microsomal Liver Enzyme’S Activity

C. G. Velentzas, "The Hydroxylation of Vitamin D on C25 in Thyrotoxicosis The Role of the Activity of Microsomal Liver Enzymes," International Journal of Clinical Medicine, Vol. 3 No. 4, 2012, pp. 295-299. doi: 10.4236/ijcm.2012.34057.