Serum levels of vitamin D are not associated with future risk of venous thromboembolism

Brodin, Ellen; Lerstad, Gunhild; Grimnes, Guri; Brækkan, Sigrid Kufaas; Vik, Anders; Brox, Jan; Svartberg, Johan; Jorde, Rolf; Hansen, John‐Bjarne

doi:10.1160/th12-10-0728

Cited by 23 publications

(6 citation statements)

References 30 publications

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“…In addition, Khademvatani et al found a significantly higher prevalence of patients with deficient 25(OH)D in the DVT group compared to the control group [40]. However, the prospective population-based study of Brodin et al found no association between normal serum levels of 25(OH)D and decreased future risk of venous thromboembolism [42]. In addition, a large casecontrol study found that vitamin D supplementation not was associated with a decreased risk of venous thrombosis after extensive statistical adjustments, suggesting a spurious correlation in previous studies [43].…”

Section: Other Complicationsmentioning

confidence: 98%

Vitamin D status and complications, readmissions, and mortality after hip fracture

et al. 2020

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Section: Other Complicationsmentioning

confidence: 98%

Vitamin D status and complications, readmissions, and mortality after hip fracture

et al. 2020

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“…Multiple studies have provided indirect evidence for an inverse association between serum 25-hydroxyvitamin D (25(OH)D) and the predisposition to venous thromboembolism and other atherothrombotic diseases [ 34 ]. However, recent studies suggest that vitamin D deficiency does not play an important role in the pathogenesis of venous thrombosis [ 35 , 36 ]. Though, both the Tromsø and ARIC studies still maintain some doubts [ 35 , 36 ].…”

Section: Discussionmentioning

confidence: 99%

“…However, recent studies suggest that vitamin D deficiency does not play an important role in the pathogenesis of venous thrombosis [ 35 , 36 ]. Though, both the Tromsø and ARIC studies still maintain some doubts [ 35 , 36 ]. Additionally, supplementation with vitamin D seems to play a negligible effect, if any, on the risk of thrombosis [ 37 ], although some results, such as the reduced risk of idiopathic venous thromboembolisms in women randomized to calcium and vitamin D supplementation warrants further investigations [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of Regulatory Mutations in SERPINC1 Affecting Vitamin D Response Elements Associated with Antithrombin Deficiency

et al. 2016

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Antithrombin is a crucial anticoagulant serpin whose even moderate deficiency significantly increases the risk of thrombosis. Most cases with antithrombin deficiency carried genetic defects affecting exons or flanking regions of SERPINC1.We aimed to identify regulatory mutations inSERPINC1 through sequencing the promoter, intron 1 and 2 of this gene in 23 patients with antithrombin deficiency but without known genetic defects. Three cases with moderate antithrombin deficiency (63–78%) carried potential regulatory mutations. One located 200 bp before the initiation ATG and two in intron 1. These mutations disrupted two out of five potential vitamin D receptor elements (VDRE) identified in SERPINC1 with different software. One genetic defect, c.42-1060_-1057dupTTGA, was a new low prevalent polymorphism (MAF: 0.01) with functional consequences on plasma antithrombin levels. The relevance of the vitamin D pathway on the regulation of SERPINC1 was confirmed in a cell model. Incubation of HepG2 with paricalcitol, a vitamin D analog, increased dose-dependently the levels of SERPINC1transcripts and antithrombin released to the conditioned medium. This study shows further evidence of the transcriptional regulation of SERPINC1 by vitamin D and first describes the functional and pathological relevance of mutations affecting VDRE of this gene. Our study opens new perspectives in the search of new genetic defects involved in antithrombin deficiency and the risk of thrombosis as well as in the design of new antithrombotic treatments.

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“…23 Moreover, these authors also indicated that the findings of their study revealed the critical role played by 25(OH)D in the pathogenesis of deep vein thrombosis. On the other hand, the Tromsø Study examined whether high 25(OH)D levels were related to decreased risk of VTE in a prospective population-based study with 6,021 participants.The study revealed that serum vitamin D level was not related to future risk of deep vein thrombosis 24.…”

mentioning

confidence: 84%

Association between vitamin D levels and lower-extremity deep vein thrombosis: a case-control study

Korkmaz

Ersoy²,

Yüksel

et al. 2021

Sao Paulo Med. J.

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INTRODUCTIONVitamin D is a fat-soluble vitamin that is synthesized non-enzymatically in the skin and metabolized in the liver and kidneys. It arranges the immune response of the body, acts as a steroid hormone and plays a crucial role in mineral homeostasis and skeletal health. 1 Serum vitamin D levels in the range 30-60 ng/ml (75-150 nmol/l) are considered normal.Deficiency of vitamin D is associated with a variety of bone disorders (rickets, osteoporosis or osteomalacia), skin diseases and autoimmune disorders. 1,2 It also causes increased risk of cardiovascular diseases such as myocardial infarction (MI), heart failure and coronary artery disease. 2-5 Furthermore, deficiency of vitamin D has been reported in arterial diseases, including aortic aneurysm, peripheral arterial disease, arterial calcification and hypertension. [6][7][8][9] Deep vein thrombosis (DVT) is characterized by thrombus formation, usually in the lower-extremity deep venous system, which causes obstruction or occlusion of blood flow in veins. It is considered to be the third most common cardiovascular disease, after ischemic heart diseases and cerebrovascular events. 10 Although the medical and interventional treatment options for deep vein thrombosis have improved nowadays, it continues to pose a serious problem, especially in cases with inadequate treatment. It can lead to pulmonary thromboembolism, venous gangrene, chronic venous insufficiency and post-thrombotic syndrome. 11 The most well-known factors in the etiology of lower-extremity deep vein thrombosis are genetic predisposition, malignancy, history of surgical operation, immobilization, trauma, bone fractures, long journeys and oral contraceptive use. 12 Nevertheless, there may also be other factors that play a role in the etiopathogenesis of deep vein thrombosis.

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Serum levels of vitamin D are not associated with future risk of venous thromboembolism

Cited by 23 publications

References 30 publications

Vitamin D status and complications, readmissions, and mortality after hip fracture

Vitamin D status and complications, readmissions, and mortality after hip fracture

Identification of Regulatory Mutations in SERPINC1 Affecting Vitamin D Response Elements Associated with Antithrombin Deficiency

Association between vitamin D levels and lower-extremity deep vein thrombosis: a case-control study

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