2013
DOI: 10.1016/j.contraception.2012.12.008
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Endothelial function in women using levonorgestrel-releasing intrauterine system (LNG-IUS)

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Cited by 15 publications
(8 citation statements)
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“…The use of long-acting reversible contraceptives (LARC), such as levonorgestrel intrauterine devices (IUD) or contraceptive implants, yields a state of extended exogenous hormone exposure. There is limited data regarding the impact of IUDs on markers of vascular or endothelial function, but studies that have been conducted suggest no changes in IUD users compared to non-users (Selim and Hussein, 2013;Zueff et al, 2017). To our knowledge, there are no studies that directly assess vascular or endothelial function and contraceptive implant use.…”
Section: Pharmacological Conditionsmentioning
confidence: 99%
“…The use of long-acting reversible contraceptives (LARC), such as levonorgestrel intrauterine devices (IUD) or contraceptive implants, yields a state of extended exogenous hormone exposure. There is limited data regarding the impact of IUDs on markers of vascular or endothelial function, but studies that have been conducted suggest no changes in IUD users compared to non-users (Selim and Hussein, 2013;Zueff et al, 2017). To our knowledge, there are no studies that directly assess vascular or endothelial function and contraceptive implant use.…”
Section: Pharmacological Conditionsmentioning
confidence: 99%
“…Levonorgestrel is a progestin or a synthetic form of the naturally occurring female sex hormone, progesterone [ 8 ]. Although the exact mechanism remains elusive, the mechanisms by which levonorgestrel may cause vasoconstriction are suggested as follows: (1) Endothelin-1 decreases during the menstrual cycle when estrogen is elevated [ 9 ]. Endothelin-1 is an endothelial-derived vasoconstricting substance [ 10 ].…”
Section: Discussionmentioning
confidence: 99%
“…Endothelin-1 is an endothelial-derived vasoconstricting substance [ 10 ]. Levonorgestrel reduces estrogen secretion, which increases the production of endothelin-1 and can cause vasoconstriction [ 9 , 10 ]. (2) Maintenance of nitric oxide (NO) bioavailability through the activation of endothelial NO synthesis is essential for maintaining vascular homeostasis [ 9 , 11 ].…”
Section: Discussionmentioning
confidence: 99%
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“…Analysing the physiopathological aspects of morphological alterations in the endometrium after LNG-IUS insertion, recent studies show that exposure to the levonorgestrel concentrations released by this kind of device would result in increased expression of tissue factor (TF), interleukin-8 (IL-8), interleukin-13 (IL-13) and interleukin-15 (IL-15), cyclooxygenase-2 and matrix metalloproteinases (MMPs). These markers could facilitate leukocyte infiltration, especially of natural killer cells specific for uterine endometrium, and epithelial degradation, with posterior formation of foci of necrosis and calcification 4,6,[7][8][9][10][11][12] . There would also be increased expression of vascular endothelial growth factor (VEGF), which would act as to increase vascular permeability, promoting aberrant angiogenesis and resulting in haemorrhages, microthromboses and ulceration of the epithelium 4,7,10,12 .…”
Section: Discussionmentioning
confidence: 99%