25- hydroxyvitamin D, also known as 25-hydroxycholecalciferol, calcidiol or abbreviated 25-OH Vi t D, is the main vitamin D metabolite circulating in plasma.
The 25-hydroxy vitamin D test is the most accurate way to measure how much vitamin D is in your body.
In the kidney, 25-hydroxy vitamin D changes into an active form of the vitamin. The active form of vitamin D helps control calcium and phosphate levels in the body. Clinically speaking, things began to change in the 1970s when the blood test for vitamin D (known as the "25-OH vitamin D" test) became more accurate and widely utilized (Wolpowitz & Gilchrest, 2006; Zerwekh, 2008). This test reflected the total amount of vitamin D in the body that was coming from all sources (diet, dietary supplements, and the sun), which makes this test extremely important in the field of nutrition. Low concentrations of 25-OH vitamin D cause secondary hyperparathyroidism (high levels of parathyroid hormone or PTH). This means a person loses more calcium from his/her bones when PTH is abnormally high (PTH>65 pg/ml) and has an even greater risk for bone loss.
Newer focus is on research into the possible usefulness of vitamin D as -
Ø a screening parameter for risk estimation of osteoporosis
Ø an aid in the treatment of cancers
Ø an immune booster
Ø slowing of the aging process
Ø improving neuromuscular function
Clinical Applications and Pathophysiology
The measurement of 25-OH Vit D is becoming increasingly important in the management of patients with various disorders of calcium metabolism.
Decreased levels of 25-OH Vit D appear in patients with:
Ø nutritional rickets / osteomalacia
Ø senile / postmenopausal osteoporosis
Ø Celiac disease
Ø inflammatory bowel disease (e.g. Crohn's disease)
Ø Insufficiency of the exocrine pancreas
Ø short bowel syndrome
Ø biliary cirrhosis, liver dysfunction
Ørenal osteodystrophy
Ø nephrotic syndrome
Ø neonatal hypocalcemia
Ø hypocalcemia
Ø treatment with anticonvulsant drugs (enhanced metabolism)
Elevated levels of 25-OH Vit D appear in patients with:
Ø hypercalcemia
Ø vitamin D intoxication
Anti-Müllerian hormone (AMH) is a member of the transforming growth factor ß family of growth and differentiation factors. In the ovary, AMH has an inhibitory effect on primordial follicle recruitment as well as on the responsiveness of growing follicles to follicle-stimulating hormone (FSH). The ovary-specific expression pattern in granulosa cells of growing nonselected follicles makes AMH an ideal marker for the size of the ovarian follicle pool.
The ovarian reserve, constituted by the size of the ovarian follicle pool and the quality of the oocytes therein, declines with increasing age, resulting in the decrease of a woman's reproductive function (te Velde et al. 1998a). The size of the follicle pool is established at an early point in life. During fetal life, germ cells populate the ovary and become surrounded by somatic cells, forming the so-called primordial follicles. At birth, about 1 million oocytes are present. This number decreases during childhood, resulting in a primordial follicle pool of 300 000-500 000 follicles at menarche (Faddy et al. 1992). Throughout life, follicles leave the primordial follicle pool to enter the growing pool. The majority of these growing follicles will be lost as a result of atresia, unless they are rescued by follicle-stimulating hormone (FSH). This rescue by FSH starts after puberty when the pituitary-gonadal endocrine axis has been activated. Among the cohort of rescued follicles, only one follicle is selected to become the dominant follicle, which will ovulate under the influence of luteinizing hormone (LH) (McGee & Hsueh 2000). This process continues throughout life until the primordial follicle pool is exhausted and, as a consequence, growing follicles are no longer present in the ovary, resulting in menopause. A serum marker that reflects the number of follicles that have made the transition from the primordial pool into the growing follicle pool, and that is not controlled by gonadotropins, would benefit both patients and clinicians. In recent years, accumulated data indicate that anti-Müllerian hormone (AMH) may fulfill this role.