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Based on the expression pattern of α and estrogen receptors in corneal cells, it has been postulated that estrogen is supplied through tears and aqueous humor at concentrations that are approximately half the concentrations found in plasma [219]. The proposed mode of action of these steroidal hormones is via the regulation of gene expression in the nucleus, leading to changes in the concentration of ECM proteins, which are critical to the maintenance of corneal integrity [220]. It is plausible that estrogen may be responsible for weakening the cornea via the stimulation of MMPs and the release of prostaglandins, causing activation of proteolytic enzymes for collagen, disruption of collagen networks, and reduction in corneal-stiffness [220]. Recently, a study reported progression of KC in 6 eyes of 3 women after receiving an in vitro fertilization treatment which increases their estrogen levels [221]. Similarly, a recent study has identified a significant elevation in salivary dehydroepiandrosterone sulfate (DHEA-S, a common precursor to other androgens) levels and a decrease in estrone (a natural estrogen) level in KC patients independent of gender [222]. Elevated DHEA-S possibly increases the expression of specific cytokines (IL-16 and stem cell factors) by blocking endogenous glucocorticoid activity and stimulating the progression of KC [222]. However, no correlation has been detected between the increased salivary DHEA-S level and increased severity of KC [222]. 2ff7e9595c
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