The dry eye syndrome (DED) is a pathological condition of a multifactorial nature, thus related to several causative factors, including both physiological and environmental conditions. Of the many factors that can contribute to DED, increased tear osmolarity and inflammation of the ocular surface and endocrine abnormalities are certainly important contributors. In fact, like any other organ in our body, the ocular surface is affected by many hormones circulating and is under the constant control of these mediators. In particular, several hormones, including sex steroids, thyroid hormones, vitamin D, prolactin, growth hormone, play a key role in sustaining ocular surface morphology and function.
On the occasion of the National Dry Eye Prevention and Diagnosis Campaign in May, we find out more about the role of hormones in the onset and progression of dry eye syndrome.
Biological sex as a variable in ocular physiology and DED
Gender diversity is a critical variable that influences every single biological function in the living world, and the ocular surface is no exception. In the case of dry eye syndrome, in fact, it has been shown by many studies that the incidence is higher in women than in men. Not only that, women often report more prominent symptoms. Furthermore, in Sjögren, an autoimmune disease of which DED is one of the most prominent symptoms, androgen deficiency has been identified as an aetiological factor.
Other female conditions associated with DED include polycystic ovary syndrome (PCOS), one of the most common endocrine disorders in women of reproductive age. Studies have shown that women with PCOS have more severe symptoms of DED than healthy women. Altered sex steroids and insulin resistance are said to cause eye surface disorders in these patients.
The role of hormones in DED
- AndrogensAndrogens exert a trophic effect on the growth and functioning of the Meibomian glands, which are responsible for secreting the lipid layer of the tear film. Androgens, in fact, stimulate genes involved in the production, transport and secretion of lipids by these glands. Thus, androgen deficiency has detrimental effects on the morphology and function of the Meibomian gland. In particular, testosterone regulates the expression of several genes in the lacrimal glands, including those involved in cell growth and metabolism, cell communication and transport, and signalling at the molecular level. This important influence of androgen hormones contributes to many of the sex differences in tear gland function.
- Oestrogen and progesteroneoestrogen and progesterone receptors are present in various structures of the ocular surface, including the cornea, conjunctiva, Meibomian glands and lacrimal glands. However, the nature of the influence of oestrogens on these structures is more controversial than that of androgens. Some studies suggest that oestrogens play only a minimal role in the anatomy and physiology of the lacrimal glands, while other studies have shown that oestrogens have a negative influence, e.g. by inducing glandular regression, acinar cell rupture and necrosis. In contrast, there are studies that support a beneficial effect of oestrogen on the lacrimal glands and the reduction of lacrimal gland function in postmenopausal, oestrogen-deficient women seems to support this theory.
- Thyroid hormonesThere are several thyroid-associated ophthalmopathies that have a strong impact on the ocular surface and the onset of DED. With regard to autoimmune thyroid diseases, one of the mechanisms by which these disorders contribute to the onset of DED is reduced tear secretion and increased inflammation due to autoimmune damage. However, it has been shown that decreased thyroid hormone stimulation of the lacrimal glands could also be a possible etiopathogenetic factor in these patients.
- Vitamin Dis considered a pro-hormone and several studies report that vitamin D levels are reduced on the ocular surface of patients with DED. Indeed, under physiological conditions, vitamin D improves the epithelial barrier function of the ocular surface, reduces inflammation, improves tear osmolarity and relieves hyperosmotic stress.
- Insulininsulin is known to improve tear gland secretion and function and has a synergistic action with androgens. Indeed, patients with diabetes mellitus have a higher prevalence of DED and serum glycated haemoglobin (HbA1c) levels have been shown to be significantly associated with tear film stability and dry eye disease symptoms.
- Glucocorticoids, prolactin, growth hormoneglucocorticoids are modulators of inflammation and may therefore be involved in ocular surface homeostasis. Prolactin also has pro-inflammatory effects and it has been observed that in patients with Sjögren serum prolactin levels are significantly higher. Growth hormone (GH), on the other hand, appears to have a positive influence on the physiology of ocular surface structures such as the Meibomian glands.
In conclusion, all conditions that can cause hormonal alterations - both physiological ones, such as menopause, and pathological ones, such as polycystic ovary syndrome or thyroid diseases - can contribute to the development of DED and, in these cases, a collaboration between the ophthalmologist and the endocrinologist can be very helpful for an optimal management of this condition.
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