Hormones and dry eye disease

Abstract

The endocrine system influences all tissues and cells in the human body. The ocular surface is constantly exposed to circulating hormones and expresses their specific receptors. Dry eye disease (DED) is a disorder with multifactorial etiology, and endocrine anomalies are one of the inciting factors. The endocrine anomalies that cause DED include physiological conditions such as menopause, menstrual cycle variations, pathologies such as polycystic ovarian syndrome, androgen resistance, iatrogenic conditions such as contraceptive use, and antiandrogen treatment. This review highlights the status of these hormones in DED along with the mechanism of action of different hormones on the ocular surface structures and the clinical implications of these effects. The influence of androgens, estrogens, and progesterone on the ocular surface tissues, and the implications of androgen-deficient states in DED are also discussed. The physiological and pathological effects of menopause and sex hormone replacement therapy are discussed. The effects of insulin and insulin resistance on the ocular surface and DED, and the growing potential of topical insulin therapeutics for DED are mentioned. Thyroid-associated ophthalmopathy, its impact on the ocular surface, and the tissue effects of thyroid hormone in the context of DED are reviewed. Finally, the potential role of hormonal therapeutics in the management of DED has also been discussed. The compelling evidence suggests that it would be clinically beneficial to consider the possibility of hormonal imbalances and their impact while treating patients with DED.

CD4+T cells drive corneal nerve damage but not epitheliopathy in an acute aqueous-deficient dry eye model

“…Finally, female sex is the most influential risk factor for DED in patients (88,89), and our findings also shed light on this association: female mice develop worse DED in terms of corneal epithelial and neural impairment in part due to greater pathogenic activity of CD4 + T cells in this sex (Supplementary Figures 1 and 2). However, the difference in disease severity between sexes cannot be solely attributed to these cells because female mice adoptively transferred with CD4 + T cells from female DED mice do not develop worse corneal neuropathy than their male counterparts (Supplementary Figure 6A), indicating that sex influences other pathogenic factors that are triggered by desiccation in the ocular surface.…”

The Association between Ovarian Cancer and the Incidence of Newly Developed Dry Eye Disease: A Nationwide Population-Based Study

“…As a consequence, elevated oxidative stress could be the reason for the increasing DED incidence in the ovarian cancer population. In addition to oxidative stress, serum sex hormones level like estrogen are crucial for the onset of DED during in vitro fertilization [41], and both the elevation of estrogen and progesterone are associated with the development of DED, despite a few papers demonstrating contrary results [42]. Since ovarian cancer featured with increased estrogen and progesterone [11], this may be another mechanism for DED development in individuals with ovarian cancer.…”

Morphometric and volumetric analysis of lacrimal glands in patients with thyroid eye disease

“…According to previous investigations, estrogens’ role in anatomy of lacrimal glands is very debatable. While some researchers claim minimal invasiveness of estrogen in morphology of lacrimal glands others state adverse influence on the lacrimal gland, such as inducing glandular regression, acinar cell disruption, and necrosis 30 , 31 . Characteristic ophthalmic signs of TED that sometimes precede laboratory analysis include exophthalmos, eyelid retraction, eyelid oedema, restrictive extraocular myopathy, and optic neuropathy associated with thyroid dysfunction.…”