A2 Refereed review article in a scientific journal
Significance of vitamin D responsiveness on the etiology of vitamin D-related diseases
Authors: Järvelin, Ulla M.; Järvelin, Juho M.
Publisher: Elsevier
Publication year: 2024
Journal: Steroids
Journal name in source: Steroids
Article number: 109437
Volume: 207
ISSN: 0039-128X
eISSN: 1878-5867
DOI: https://doi.org/10.1016/j.steroids.2024.109437(external)
Web address : https://doi.org/10.1016/j.steroids.2024.109437(external)
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/393518820(external)
Abstract
Vitamin D resistance (VDRES) explains the necessity for higher doses of Vitamin D (VD) than those recommended for treatment success. VD receptor (VDR) signaling blockade, such as that caused by infections and poisons, is one basis for VDRES etiology. Mutations within genes affecting the VD system cause susceptibility to developing low VD responsiveness and autoimmunity. In contrast, VD hypersensitivity (VDHY) occurs if there is extra VD in the body; for example, as a result of an overdose of a VD supplement. Excess 1,25(OH)2D3 is produced in lymphomas and granulomatous diseases. The placenta produces excess 1,25(OH)2D3. Gene mutations regulating the production or degradation of 1,25(OH)2D3 enhance the effects of 1,25(OH)2D3. Increased 1,25(OH)2D3 levels stimulate calcium absorption in the gut, leading to hypercalcemia. Hypercalcemia can result in the calcification of the kidneys, circulatory system, or placenta, leading to kidney failure, cardiovascular disease, and pregnancy complications. The primary treatment involves avoiding exposure to the sun and VD supplements. The prevalence rates of VDRES and VDHY remain unclear. One estimate was that 25%, 51%, and 24% of the patients had strong, medium, and poor responses, respectively. Heavy-dose VD therapy may be a promising method for the treatment of autoimmune diseases; however, assessing its potential side effects is essential. To avoid VD-mediated hypercalcemia, responsiveness must be considered when treating pregnancies or cardiovascular diseases associated with VD. Furthermore, how VD is associated with the related disorders remains unclear. Investigating responsiveness to VD may provide more accurate results.
Vitamin D resistance (VDRES) explains the necessity for higher doses of Vitamin D (VD) than those recommended for treatment success. VD receptor (VDR) signaling blockade, such as that caused by infections and poisons, is one basis for VDRES etiology. Mutations within genes affecting the VD system cause susceptibility to developing low VD responsiveness and autoimmunity. In contrast, VD hypersensitivity (VDHY) occurs if there is extra VD in the body; for example, as a result of an overdose of a VD supplement. Excess 1,25(OH)2D3 is produced in lymphomas and granulomatous diseases. The placenta produces excess 1,25(OH)2D3. Gene mutations regulating the production or degradation of 1,25(OH)2D3 enhance the effects of 1,25(OH)2D3. Increased 1,25(OH)2D3 levels stimulate calcium absorption in the gut, leading to hypercalcemia. Hypercalcemia can result in the calcification of the kidneys, circulatory system, or placenta, leading to kidney failure, cardiovascular disease, and pregnancy complications. The primary treatment involves avoiding exposure to the sun and VD supplements. The prevalence rates of VDRES and VDHY remain unclear. One estimate was that 25%, 51%, and 24% of the patients had strong, medium, and poor responses, respectively. Heavy-dose VD therapy may be a promising method for the treatment of autoimmune diseases; however, assessing its potential side effects is essential. To avoid VD-mediated hypercalcemia, responsiveness must be considered when treating pregnancies or cardiovascular diseases associated with VD. Furthermore, how VD is associated with the related disorders remains unclear. Investigating responsiveness to VD may provide more accurate results.
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