The biologically active form of vitamin D is 1,25-dihydroxyvitamin D (1,25(OH)2D). Measurement ofserum levels of 1,25(OH)2D need to be considered upon uncertainty of deficiency or excess of this kind of the vitamin.

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Reference rangesfor 1,25(OH)2D might be reported together either pg/mL or pmol/L. The molecular load of 1,25(OH)2D is about 416.7, yielding the adhering to conversion factors: 1 pmol/L = 0.42 pg/mL; whereas 1 pg/mL = 2.4 pmol/L.


Plasma 1,25-dihydroxyvitamin D (1,25(OH)2 D) is tightly controlled by plasma parathyroid hormone (PTH), serum calcium, serum phosphate, and also fibroblast-like development factor 23 (FGF-23).

Decreased 1,25-dihydroxyvitamin D levels

Decreased levels of 1,25(OH)2 D can an outcome from chronic kidney disease, various heritable disorders, tumor-induced osteomalacia, the usage of HIV protease inhibitors, or serious vitamin D deficiency.

Chronic kidney disease: short 1,25(OH)2 D levels have actually been shown to current even in beforehand stages that kidney failure. The diminish of 1,25(OH)2 D level is more prominent as soon as kidney fail progresses. In a study by Levin et al (2007), 13% that patients with an approximated glomerular filtration rate (eGFR) greater than 80 mL/min and much more than 60% that patients with an eGFR of less than 30 mL/min had actually low serum levels of 1,25(OH)2 D. <2> Impaired production of the enzyme 1α-hydroxylase in kidney failure was believed to be the key mechanism. However, phosphate retention and FGF-23 additionally contribute to the diminished synthesis of 1,25(OH)2 D. <3>

Heritable disorders connected with short 1,25(OH)2 D levels encompass vitamin D–dependent rickets form 1 (inactivating mutation in the 1-hydroxylase gene), <4> autosomal-dominant hypophosphatemic rickets (mutation that the gene coding for FGF-23, which stays clear of its breakdown), <5> and also X-linked hypophosphatemic rickets (mutations the elevate level of FGF-23). <6>

In tumor-induced osteomalacia, tumor-secreted FGF-23 inhibits enzyme 1α-hydroxylase and subsequently results in lessened 1,25(OH)2 D synthesis. <7>

HIV protease inhibitors have actually been report to markedly suppress the tasks of 25- and 1α-hydroxylase and also thus influence 1,25(OH)2 D synthesis. <8> In a cohort study including 671 patients, progression to bone demineralization was observed in 28% of the patients end a average of 2.5 years. Patients who were concurrently using protease inhibitors to be at better risk because that worsening bone demineralization than those that were not making use of protease inhibitors (OR 1.64; 95% CI, 1.35-2.04; P <9>

Severe vitamin D deficiency: 25(OH)D is the key substrate the 1,25(OH)2 D. Vitamin D deficiency can impact the manufacturing of 1,25(OH)2 D owing to the absence of substrate. A positive correlation between serum level of 25(OH)D and 1,25(OH)2 D to be observed throughout seasonal changes. Treatment through 25(OH)D deserve to normalize 1,25(OH)2 D concentrations in patients through vitamin D deficiency. <10>

Increased 1,25-dihydroxyvitamin D levels

Increased 1,25(OH)2 D level can result from extrarenal 1α-hydroxylation or hereditary vitamin D–resistant rickets.

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In granulomatous disease such as lymphoproliferative disorders, sarcoidosis, tuberculosis, and also inflammatory bowel disease, 1α-hydroxylase enzyme activity was found in macrophages together the extrarenal resource of 1,25(OH)2 D. Once 1α-hydroxylase is activated, the converts 25(OH)D come 1,25(OH)2 D, just as what occurs under physiologic conditions in the kidneys. <11> However, unequal the kidney, the 1α-hydroxylase in the macrophages in granulomatous diseases is not managed by the normal physiologic regulators. Moreover, not all conditions or every patients with boosted macrophage task manifest rises in 1α-hydroxylase activity. In vitro researches of monocytes/macrophages show that gamma interferon is crucial regulator the 1α-hydroxylase however only when other crucial signaling pathways are also activated (eg, JAK-STAT and MAP-Kinase). <12>

Hereditary vitamin D-resistant rickets is a an extremely rare autosomal recessive disorder in i m sorry mutations the vitamin D receptor (VDR) coding genes reason failure or abnormal binding of vitamin D to VDRs. <13, 14> patients usually present with hypocalcemia, early-onset rickets, alopecia, and also other ectodermal anomalies.