Postmenopausal Intraocular Pressure Changes in South Indian Females

Panchami,; Pai, Sheila R; Shenoy, Jnaneshwara P; Shivakumar, J; Kole, Sharad B

doi:10.7860/jcdr/2013/5325.3145

Cited by 10 publications

(14 citation statements)

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“…Our finding that OVX decreased outflow facility is consistent with both the modest elevations in IOP (1–3 mm Hg) measured in postmenopausal women 7 , 9 – 12 and data suggesting that estrogen therapy increases outflow facility. 12 …”

Section: Discussionsupporting

confidence: 88%

“…Menopause is associated with modest IOP elevations, as IOP in postmenopausal women is 1 to 3 mm Hg higher than in age-matched premenopausal women. 7 , 8 Further, estrogen therapy in postmenopausal women causes a 0.5- to 3-mm Hg decrease in IOP. 9 – 11 Aqueous outflow facility is the major determinant of IOP, and estrogen treatment has been shown to increase outflow facility in female patients 12 ; however, it is unknown whether menopause or age at menopause affects outflow facility.…”

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confidence: 99%

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Age and Menopause Effects on Ocular Compliance and Aqueous Outflow

Feola

Sherwood

Pardue

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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Glaucoma is the second leading cause of blindness worldwide. Recent work suggests that estrogen and the timing of menopause play a role in modulating the risk of developing glaucoma. Menopause is known to cause modest changes in intraocular pressure; yet, whether this change is mediated through the outflow pathway remains unknown. Menopause also affects tissue biomechanical properties throughout the body; however, the impact of menopause on ocular biomechanical properties is not well characterized. METHODS. Here, we simultaneously assessed the impact of menopause on aqueous outflow facility and ocular compliance, as a measure of corneoscleral shell biomechanics. We used young (3-4 months old) and middle-aged (9-10 months old) Brown Norway rats. Menopause was induced by ovariectomy (OVX), and control animals underwent sham surgery, resulting in the following groups: young sham (n = 5), young OVX (n = 6), middle-aged sham (n = 5), and middle-aged OVX (n = 5). Eight weeks postoperatively, we measured outflow facility and ocular compliance. RESULTS. Menopause resulted in a 34% decrease in outflow facility and a 19% increase in ocular compliance (P = 0.011) in OVX animals compared with sham controls (P = 0.019). CONCLUSIONS. These observations reveal that menopause affects several key physiological factors known to be associated with glaucoma, suggesting that menopause may contribute to an increased risk of glaucoma in women.

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Section: Discussionsupporting

confidence: 88%

mentioning

confidence: 99%

Age and Menopause Effects on Ocular Compliance and Aqueous Outflow

Feola

Sherwood

Pardue

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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“…Research on the effects of progesterone on ocular disease in humans is sparse and often anecdotal. A variety of ocular changes have been shown to take place during times of hormonal fluctuation (Avitabile et al, 2007; Errera et al, 2013; Grant and Chung, 2013; Panchami et al, 2013; Yucel et al, 2005; Ziai et al, 1994), and gender differences are observed in rates of DR, glaucoma, AMD, dry eye, and cataracts (Wickham et al, 2000). Progesterone administered exogenously has been shown to reduce intraocular pressure, suggesting potential benefit for glaucoma (Obal, 1950; Posthumus, 1952).…”

Section: Progesteronementioning

confidence: 99%

Neuroprotective strategies for retinal disease

Pardue

Allen

2018

Progress in Retinal and Eye Research

188

160

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Diseases that affect the eye, including photoreceptor degeneration, diabetic retinopathy, and glaucoma, affect 11.8 million people in the US, resulting in vision loss and blindness. Loss of sight affects patient quality of life and puts an economic burden both on individuals and the greater healthcare system. Despite the urgent need for treatments, few effective options currently exist in the clinic. Here, we review research on promising neuroprotective strategies that promote neuronal survival with the potential to protect against vision loss and retinal cell death. Due to the large number of neuroprotective strategies, we restricted our review to approaches that we had direct experience with in the laboratory. We focus on drugs that target survival pathways, including bile acids like UDCA and TUDCA, steroid hormones like progesterone, therapies that target retinal dopamine, and neurotrophic factors. In addition, we review rehabilitative methods that increase endogenous repair mechanisms, including exercise and electrical stimulation therapies. For each approach, we provide background on the neuroprotective strategy, including history of use in other diseases; describe potential mechanisms of action; review the body of research performed in the retina thus far, both in animals and in humans; and discuss considerations when translating each treatment to the clinic and to the retina, including which therapies show the most promise for each retinal disease. Despite the high incidence of retinal diseases and the complexity of mechanisms involved, several promising neuroprotective treatments provide hope to prevent blindness. We discuss attractive candidates here with the goal of furthering retinal research in critical areas to rapidly translate neuroprotective strategies into the clinic.

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“…Postmenopausal women have a 1.5-3.5 mmHg higher IOP compared to age-matched premenopausal women (Panchami et al 2013;Qureshi 1996). However, postmenopausal women receiving hormone replacement therapy containing estrogen had a 0.5-3 mmHg lower IOP compared to postmenopausal women not receiving hormone replacement therapy (Vajaranant and Pasquale 2012;Altintas et al 2004;Vajaranant et al 2016;Affinito et al 2003).…”

Section: Menopause and Intraocular Pressurementioning

confidence: 95%

Evidence for Menopause as a Sex-Specific Risk Factor for Glaucoma

2022

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Glaucoma is a leading cause of irreversible blindness worldwide and is characterized by progressive loss of visual function and retinal ganglion cells (RGC). Current epidemiological, clinical, and basic science evidence suggest that estrogen plays a role in the aging of the optic nerve. Menopause, a major biological life event affecting all women, coincides with a decrease in circulating sex hormones, such as estrogen. While 59% of the glaucomatous population are females, sex is not considered a risk factor for developing glaucoma. In this review, we explore whether menopause is a sex-specific risk factor for glaucoma. First, we investigate how menopause is defined as a sex-specific risk factor for other pathologies, including cardiovascular disease, osteoarthritis, and bone health. Next, we discuss clinical evidence that highlights the potential role of menopause in glaucoma. We also highlight preclinical studies that demonstrate larger vision and RGC loss following surgical menopause and how estrogen is protective in models of RGC injury. Lastly, we explore how surgical menopause and estrogen signaling are related to risk factors associated with developing glaucoma (e.g., intraocular pressure, aqueous outflow resistance, and ocular biomechanics). We hypothesize that menopause potentially sets the stage to develop glaucoma and therefore is a sex-specific risk factor for this disease. Graphical Abstract

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Postmenopausal Intraocular Pressure Changes in South Indian Females

Cited by 10 publications

References 0 publications

Age and Menopause Effects on Ocular Compliance and Aqueous Outflow

Age and Menopause Effects on Ocular Compliance and Aqueous Outflow

Neuroprotective strategies for retinal disease

Evidence for Menopause as a Sex-Specific Risk Factor for Glaucoma

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