Importance of vitamin D-calcidiol and calcitriol in endometriosis

Abstract

Background: Vitamin D has multiple extraskeletal functions. Among them are some important roles in reproductive system and many aspects are still under evaluation. It is not surprising because vitamin D seems to be involved in almost every physiological process that takes place in the reproductive system. Active form of vitamin D –calcitriol – 1,25OH2D3 plays a significant role in anti-proliferative and immunosuppressive processes in the body. Evaluation of endometriosis in some studies showed changed vitamin D metabolism in tissue and advanced parallel activation and degradation of calcitriol in cells of endometriosis.
Aim of the study: We aimed to observe literature to review current knowledge about the connection of endometriosis and vitamin D – calcidiol and calcitriol. Our main interest is to summarize latest studies, based on them make some conclusions and suggest directions for future studies. Key interest is to find out how affects vitamin D endometriosis and vice versa in both clinical and experimental studies.
Materials and Methods: Electronic databases such: Pubmed, Medline, Cochrane Library, Web of Science, Science Direct, Springer were searched. 75 articles were reviewed. 29 articles that had statistically significant results were included in our review.
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Results: Clinical studies from the last few years are more about the associative connection of low 25OHD3 and endometriosis. Researchers are concentrated more on calcidiol-25OHD3 and do not pay much attention to calcitriol-1,25OHD3. Mainly they see low calcidiol as a risk factor for endometriosis and few think that low 25OHD3 may be the consequence of active conversion of 25OHD3 to 1,25OHD3. Association between low calcidiol -25OHD3 and endometriosis is studied the most. Most of the studies have found that patients with endometriosis have lower levels of 25OHD3. Only two studies measured both calcitriol and calcidiol in blood of women with endometriosis and result are controversial. Evidence is low and insufficient to discuss about the reasons and consequences of changed metabolism.
Conclusions: According to reviewed research we do not have enough data to insist that vitamin D metabolism is different in endometriosis. But it seems to be so. It is important to understand which is risk factor for another- low 25OHD3 raises risk of endometriosis or vice versa? If high activation of 25OHD3 to 1,25OHD3 and following high degradation of 1,25OHD3 occurs during endometriosis in endometrial tissue, what is the consequence of it in blood and are this consequences important enough to notice? May it affect calcium homeostasis? It should be mentioned that experimental treatment of endometriosis with calcitriol analogs shows promising effects. If management of endometriosis with help of calcitriol analogs will be available in the future, it will be important to have some basic knowledge about calcitriol and calcidiol levels in blood. Outcome of this different vitamin D metabolism in endometrial tissue may be high, low or normal calcitriol levels in blood. But substrate for conversion – 25OHD3 calcidiol should be
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theoretically low, because of high demand. Persistent hypercalcitriolemia may lead to hypercalcemia and cause harm to multiple organ systems. Thus normalization of vitamin D metabolites should receive proper attention and be corrected as well.