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Increased public awareness of vitamin D–related health benefits might increase the risk of VDT due to self-administration of vitamin D in doses higher then recommended for age and body weight or even higher than the established upper limit intake values. Those processes include elevated activity of 1α-hydroxylase or inhibited activity of 24-hydroxylase, both leading to increased concentration of 1,25(OH)D increased number of vitamin D receptors and saturation of the capacity of vitamin D binding protein. Researchers have proposed many processes to explain VDT. That phenomenon, called hypersensitivity to vitamin D, reflects dysregulated vitamin D metabolism. Laboratory testing during routine clinical examinations may reveal asymptomatic hypercalcemia caused by the intake of vitamin D even in doses recommended for the general population and considered safe. Endogenous VDT may also develop from an excessive production of 25(OH)D and 1,25(OH) 2D in congenital disorders, such as Williams–Beuren syndrome. Endogenous VDT may develop from excessive production of an active vitamin D metabolite – 1,25(OH) 2D in granulomatous disorders and in some lymphomas or from the reduced degradation of that metabolite in idiopathic infantile hypercalcemia. Serum 25-hydroxyvitamin D concentrations higher than 150 ng/ml (375 nmol/l) are the hallmark of VDT due to vitamin D overdosing. Exogenous VDT is usually caused by the inadvertent or improper intake of extremely high doses of pharmacological preparations of vitamin D and is associated with hypercalcemia. Many forms of exogenous (iatrogenic) and endogenous VDT exist. Although VDT is rare, the health effects can be serious if it is not promptly identified. VDT and its clinical manifestation, severe hypercalcemia, are related to excessive long-term intake of vitamin D, malfunctions of the vitamin D metabolic pathway, or the existence of coincident disease that produces the active vitamin D metabolite locally.