Kits
1,25-(OH)2-Vitamin D3/D2 ImmuTube®, LC-MS/MS Extraction Kit
Kits
Description
Vitamin D is either produced in the skin (under the influence of UV light) or taken up
from nourishment. The storage type of vitamin D, namely 25-hydroxy vitamin D, is
formed in the liver. The hormone 1,25-dihydroxy vitamin D (D hormone) is formed
in a second hydroxylation step in the kidney. The responsible enzyme, the kidney
1α-hydroxylase, is subjected to a rigid control through hormones (especially parathyroid
hormone) and its activity is influenced by the serum concentrations of calcium
and phosphate.
The serum concentration of 1,25-dihydroxy vitamin D normally re-adjusts itself to
the demands of metabolism. Deviations from the normal range of 1,25-dihydroxy
vitamin D must therefore always be interpreted in the context of the remaining parameters
of the calcium metabolism. The serum concentration of 1,25-dihydroxy vitamin
D decreases only in seldom cases of vitamin D deficiency. For the diagnosis
of vitamin D deficiency the precursor metabolite, 25-hydroxyvitamin D, should be
measured.
The reason for a non-physiological deficiency of 1,25-dihydroxy vitamin D can be
found in metabolic disturbances, caused either by genetic defects of the enzyme
1α-hydroxylase (rare) or kidney malfunctions (more common). Even a slightly impaired
kidney function can lead to a decrease of the 1,25-dihydroxy vitamin D concentration.
Since 1,25-dihydroxy vitamin D has important functions in calcium metabolism
as well as supplementing secretion of parathyroid hormone from the parathyroid
glands, increasing kidney malfunctioning leads to development of renal osteopathy,
which is characterized by osteomalacia and osteitis fibrosa.
Treatment of renal osteopathy consists of the administration of 1,25-dihydroxy vitamin
D (calcitriol) or the prohormone 1α-hydroxy vitamin D. In renal tubules malfunctions
decreased or relatively low levels of 1,25-dihydroxy vitamin D (e.g. diabetes
insipidus, Fanconi syndrome) are found. A non-physiological over-production
of 1,25-dihydroxy vitamin D arises in granulomatosis (e.g. sarcoidosis), where extrarenal
synthesis of 1,25-dihydroxy vitamin D occurs. This can lead to hypercalcaemia.
Also in idiopathic hypercalciuria a relatively high level of 1,25-dihydroxy vitamin D is
found. Increased concentrations of 1,25-dihydroxy vitamin D can be seen in case of non-functional vitamin D receptors (rare), during calcium deficient nutrition, as well
as a result from overproduction of parathyroid hormone (primary hyperthyroidism).
Supplemental vitamin D is available in two distinct forms: ergocalciferol (vitamin D2)
and cholecalciferol (vitamin D3
). Pharmacopoeias have officially regarded these two
forms as equivalent and interchangeable, based on studies of rickets prevention in
infants. The determination of 1,25-dihydroxy vitamin D3
/D2
as a measure of 1,25-dihydroxy
vitamin D status provides an objective, quantitative measure of the biological
response to vitamin D administration.
from nourishment. The storage type of vitamin D, namely 25-hydroxy vitamin D, is
formed in the liver. The hormone 1,25-dihydroxy vitamin D (D hormone) is formed
in a second hydroxylation step in the kidney. The responsible enzyme, the kidney
1α-hydroxylase, is subjected to a rigid control through hormones (especially parathyroid
hormone) and its activity is influenced by the serum concentrations of calcium
and phosphate.
The serum concentration of 1,25-dihydroxy vitamin D normally re-adjusts itself to
the demands of metabolism. Deviations from the normal range of 1,25-dihydroxy
vitamin D must therefore always be interpreted in the context of the remaining parameters
of the calcium metabolism. The serum concentration of 1,25-dihydroxy vitamin
D decreases only in seldom cases of vitamin D deficiency. For the diagnosis
of vitamin D deficiency the precursor metabolite, 25-hydroxyvitamin D, should be
measured.
The reason for a non-physiological deficiency of 1,25-dihydroxy vitamin D can be
found in metabolic disturbances, caused either by genetic defects of the enzyme
1α-hydroxylase (rare) or kidney malfunctions (more common). Even a slightly impaired
kidney function can lead to a decrease of the 1,25-dihydroxy vitamin D concentration.
Since 1,25-dihydroxy vitamin D has important functions in calcium metabolism
as well as supplementing secretion of parathyroid hormone from the parathyroid
glands, increasing kidney malfunctioning leads to development of renal osteopathy,
which is characterized by osteomalacia and osteitis fibrosa.
Treatment of renal osteopathy consists of the administration of 1,25-dihydroxy vitamin
D (calcitriol) or the prohormone 1α-hydroxy vitamin D. In renal tubules malfunctions
decreased or relatively low levels of 1,25-dihydroxy vitamin D (e.g. diabetes
insipidus, Fanconi syndrome) are found. A non-physiological over-production
of 1,25-dihydroxy vitamin D arises in granulomatosis (e.g. sarcoidosis), where extrarenal
synthesis of 1,25-dihydroxy vitamin D occurs. This can lead to hypercalcaemia.
Also in idiopathic hypercalciuria a relatively high level of 1,25-dihydroxy vitamin D is
found. Increased concentrations of 1,25-dihydroxy vitamin D can be seen in case of non-functional vitamin D receptors (rare), during calcium deficient nutrition, as well
as a result from overproduction of parathyroid hormone (primary hyperthyroidism).
Supplemental vitamin D is available in two distinct forms: ergocalciferol (vitamin D2)
and cholecalciferol (vitamin D3
). Pharmacopoeias have officially regarded these two
forms as equivalent and interchangeable, based on studies of rickets prevention in
infants. The determination of 1,25-dihydroxy vitamin D3
/D2
as a measure of 1,25-dihydroxy
vitamin D status provides an objective, quantitative measure of the biological
response to vitamin D administration.