Abstract
Purpose
Glaucoma incidence in patients with endogenous Cushing's syndrome (CS) has never been established. We aim to assess the risk for glaucoma among CS patients compared to controls and determine the age of disease onset.
Methods
A nationwide retrospective matched‐cohort study of patients with endogenous CS diagnosed between 2000 and 2023. Patients with CS were matched in a 1:5 ratio, with a control group individually matched for age, sex, socioeconomic status and body mass index. Main outcomes were the incidence of glaucoma and disease onset.
Results
A total of 609 patients [396 women (65%); mean age 48.1 ± 17 years] were included in the CS group and 3018 controls. Follow‐up duration was 14.6 years (IQR 9.8–20.2) for the study group. The aetiology of hypercortisolism was divided into pituitary (259, 42.6%), adrenal (206, 33.8%) and unconfirmed aetiology (144, 23.6%) patients. At baseline, 44 (7.2%) CS patients had a diagnosis of glaucoma, compared with 151 (5%) controls. The overall risk for glaucoma was 74% higher in patients with CS compared with matched controls (hazard ratio = 1.74, p = 0.002). Patients with CS who developed glaucoma were younger (mean age of 62 ± 14.7 years) than controls (mean age of 66 ± 11.3 years), (p = 0.02) [Correction added on 1 February 2025, after first online publication: The mean age has been corrected in the preceding sentence]. The overall risk for glaucoma in CS was high for both patients in remission and patients with persistent hypercortisolism (p = 0.048). Patients with active hypercortisolism experienced an earlier glaucoma onset (82.1 ± 88.0 months).
Conclusions
Endogenous CS is associated with increased risk for glaucoma regardless of remission status and develops at a younger age compared with the general population.
Keywords: Cushing's syndrome, glaucoma, onset, risk
1. INTRODUCTION
Glaucoma is a chronic, irreversible vision‐threatening disease affecting more than 80 million people worldwide (Quigley & Broman, 2006). It is the leading cause of irreversible blindness and the second cause of overall global blindness after cataracts (Tham et al., 2014).
Steroid‐induced glaucoma, categorized as secondary open‐angle glaucoma, is commonly associated with exogenous topical steroid administration rather than endogenous glucocorticoid overproduction (Phulke et al., 2017). Approximately, 30% of the general population are classified as steroid responders, experiencing elevated intraocular pressure (IOP) following corticosteroid administration (Becker, 1965).
Cushing syndrome (CS) is an endocrine disorder which results from excess cortisol production. The most common cause of CS is exogenous steroid use, followed by endogenous cortisol overproduction (Gadelha et al., 2023). In most cases (60%–70%), the corticotropin excess is produced by an adrenocorticotropic‐hormone (ACTH)‐secreting pituitary adenoma, followed by adrenal aetiologies (20%–30%) and ectopic ACTH‐producing neuroendocrine tumours (Gadelha et al., 2023; Reincke & Fleseriu, 2023).
The treatment of CS typically commences with surgical intervention to remove the source responsible for excessive cortisol production, followed by medical therapies (Fleseriu et al., 2021).
There is a known higher risk of glaucoma in patients treated with glucocorticoids; however, data concerning the risk for developing high IOP and glaucoma in patients with CS are limited to case reports and small studies (Blumenthal et al., 1999; Gupta et al., 2015; Haas & Nootens, 1974; Khaw et al., 2010; Tsushima et al., 2019; Virevialle et al., 2014).
In this retrospective matched‐cohort study, we aim to assess the risk for glaucoma in patients with CS, as compared with age, sex, socioeconomic status and body mass index (BMI)‐matched controls. Furthermore, we assess the glaucoma risk according to the CS aetiology, degree of UFC elevation and remission status.
2. MATERIALS AND METHODS
A retrospective matched‐cohort study compared patients with CS to controls without hypercortisolism. Data were sourced from Clalit Health Services (CHS), serving over 4.8 million members. Institutional ethics committee approval was obtained from Rabin Medical Center, adhering to the Declaration of Helsinki and good clinical practice (RMC‐0779‐22, 11.12.2022). As data were anonymized, written consent was deemed unnecessary.
Using International Classification of Diseases (ICD‐10) codes, clinical diagnoses with matching dates were identified. Data were extracted from the electronic health record database via the CHS research data‐sharing platform, operated by MDClone. Collected information for potential cases included patient demographics and clinical features at CS diagnosis, along with diagnoses of various comorbidities, including glaucoma.
Diagnosis time was defined as the first occurrence of elevated UFC, CS diagnosis or pituitary/adrenal surgery. Glaucoma diagnoses for both the patients with CS and control groups were acquired through ICD‐10 coding. Patients with a diagnosis of glaucoma were identified by the appropriate ICD‐10 coding, given by the treating ophthalmologist and incorporated to the patient's medical record. Each patient with CS was matched 1:5 with controls by age, sex, socioeconomic status and BMI; notably, these controls have never had testing for hypercortisolism.
The follow‐up duration commenced from the diagnosis date for both patients with CS and their matched controls, extending until death, CHS membership cessation or the data collection cut‐off of 30 September 2023. Early biochemical remission was established as of 24‐h UFC levels normalization without requiring medical intervention for hypercortisolism or necessitating glucocorticoid replacement therapy following pituitary or adrenal surgery, occurring within 26 months from the initial diagnosis of CS. The main outcome was defined as the timing of glaucoma diagnosis following the diagnosis of CS in the study group.
In secondary analyses, the occurrence of glaucoma was compared between patients who achieved biochemical remission and those who did not as well as by aetiology of CS and degree of maximal UFC elevation.
2.1. Statistical analysis
Statistical analysis was generated using SAS Software, Version 9·4, SAS Institute Inc., Cary, NC, USA. Continuous variables were presented by mean ± standard deviation or median and interquartile range [IQR]. Categorical variables were presented by (N, %). The t‐test, the Mann–Whitney U‐test, and the Chi‐squared test were used for comparison, between cases and controls, of normally distributed, non‐normal and categorical variables, respectively. Cumulative incidence plots, for glaucoma after CS, where death without glaucoma was treated as a competing risk, were created. The Cox proportional hazard model, with death without glaucoma treated as a competing risk, was used to calculate hazard ratios (HR). The appropriateness of the proportional hazard assumption was assessed visually. Two‐sided p‐values less than 0.05 were considered statistically significant.
3. RESULTS
3.1. Study cohort and patient characteristics
Between 1 January 2000 and 30 September 2023, a cohort of 609 patients (65% women) with CS was included, with a mean age of 48.1 ± 17 years. Each patient was matched with up to five controls based on age, sex, socioeconomic status and BMI, resulting in a control group comprising 3018 patients. (Table 1).
TABLE 1.
Demographics and Clinical Characteristics of Study Patients.
| CS patients/controls | All | ||
|---|---|---|---|
| CS patients | Controls | ||
| Patients, n | 609 | 3018 | 3627 |
| Age at diagnosis, Mean ± SD | 48 ± 17.17 | 47.97 ± 17.19 | 47.99 ± 17.18 |
| Gender | |||
| Male | 213 (35%) | 1043 (35%) | 1256 (35%) |
| Female | 396 (65%) | 1975 (65%) | 2371 (65%) |
| Glaucoma | 44 (23%) | 151 (77%) | 195 (5%) |
| Socioeconomic status a | |||
| Low | 74 (13%) | 371 (13%) | 445 (13%) |
| Middle | 349 (60%) | 1719 (60%) | 2068 (60%) |
| High | 153 (27%) | 760 (27%) | 913 (27%) |
| Smoking status a | |||
| Never | 198 (60%) | 910 (63%) | 1108 (62%) |
| Current/Past smoker | 133 (40%) | 544 (37%) | 677 (38%) |
| BMI at diagnosis, Mean ± SD b | 30.9 ± 7.6 | 30 ± 6.9 | 30.2 ± 7.01 |
| Diabetes mellitus at diagnosis | 140 (23%) | 396 (13%) | 536 (15%) |
| HTN at diagnosis | 343 (56%) | 957 (32%) | 1300 (36%) |
| Dyslipidaemia at diagnosis | 258 (42%) | 874 (29%) | 1132 (31%) |
| CAD at diagnosis | 70 (11%) | 191 (6%) | 261 (7%) |
| History of stroke | 27 (4%) | 82 (3%) | 109 (3%) |
Abbreviations: BMI, body mass index; CAD, coronary artery disease; CS, Cushing's syndrome; HTN, hypertension; N, number; SD, standard deviation.
Data were not available for all patients.
Number of patients were: 363 (60%) cases, 1549 (51%) controls and 1912 (53%) total.
Follow‐up duration was 14.6 years (IQR 9.8–20.2) for the study group and 14.8 (IQR 9.9–20.2) for the matched controls.
Diabetes mellitus, hypertension, coronary artery disease, dyslipidaemia and stroke exhibited higher prevalence among CS patients compared to their matched controls (p < 0.01) (See Table 1).
The aetiology of hypercortisolism was divided into pituitary CS (pCS) in 259 (42.6%) patients and adrenal CS (aCS) in 206 (33.8%) patients. Disease aetiology could not be ascertained from the available data in 144 (23.6%) patients.
3.2. Risk factors for glaucoma in Cushing's syndrome
Overall, 78 (78/609, 12.8%) patients with CS and 250 (250/3018, 8.3%) patients without CS developed glaucoma up to the last follow‐up. When stratified by age group at the time of glaucoma diagnosis, patients with CS had the following distribution: 1.5% (nine patients) were diagnosed before the age of 40; 6.2% (38 patients) between the ages of 40 and 65; and 5% (31 patients) at the age of 65 and older. In comparison, among controls, the proportions were 0.3% (eight patients), 3.7% (113 patients) and 4.3% (129 patients) for the respective age groups.
These groups were further divided into patients with a history of glaucoma before and after the study baseline (CS diagnosis).
Reported prior history of glaucoma before CS diagnosis was noted in 34 patients with CS (5.58%), whereas among the controls, 99 patients (3.28%) had a history of glaucoma before the study baseline (p < 0.0089).
Following the diagnosis of CS, 44 (7.2%) patients with CS developed glaucoma, compared with 151 (5%) controls. (Table 1) The difference between groups was statistically significant (HR 1.74, 95% CI 1.17–2.60, p = 0.002).
The risk assessment for glaucoma, with death considered as a competing risk, revealed that by the end of the follow‐up period, CS patients had a 74% higher overall risk for glaucoma compared to their matched controls (p = 0.002), (Figure 1).
FIGURE 1.
Overall risk for glaucoma with death as a competing event. CS = Cushing's syndrome.
Patients with CS experienced glaucoma onset at a notably younger age than controls. The mean age of glaucoma onset among those with a history of glaucoma before CS diagnosis was 56.6 ± 12.9 years, in contrast to controls with a mean age of 61.6 ± 10.1 years (p = 0.005). After CS diagnosis, the age of glaucoma onset remained significantly younger in CS patients compared to their matched controls (mean age of 62 ± 14.7 years vs. 66 ± 11.3 years, respectively; p = 0.02).
We performed a subgroup analysis of patients with CS and glaucoma by the source of the excessive production of cortisol, including pituitary, adrenal and unknown‐origin CS. No difference was observed in the risk for glaucoma in patients with either pituitary, adrenal or unknown‐origin CS, compared to their matched controls. In the CD group, 15 patients (7%) were diagnosed with glaucoma, whereas in the control group, 47 patients (4%) developed glaucoma. Similarly, among patients with adrenal CS, 12 patients (7%) were diagnosed with glaucoma, compared with 45 (5%) individually‐matched controls.
A univariate analysis to examine the effect of specific variables, including diabetes mellitus, BMI, smoking history, ischemic heart disease, hypertension, dyslipidaemia, history of stroke, socio‐economic status and gender in CS patients with and without glaucoma was performed.
Severity of CS disease was evaluated by the maximal UFC levels that were ≥5 times higher in 8.1% (14/172) of patients with glaucoma, and ≤5 times higher in 8.8% (15/170). There was no correlation between maximal UFC levels and the risk for glaucoma (p = 0.19).
Of the 44 patients with CS diagnosed with glaucoma following a CS diagnosis, 13 cases (29%) had comorbid diabetes mellitus, compared to 85 of 441 (19.3%) patients without glaucoma. This suggests a trend towards an 82% higher risk of glaucoma in patients with diabetes mellitus compared to those without it (p = 0.06).
Additionally, a history of stroke was found to be more prevalent among patients with CS with glaucoma (three cases, 6.8%) compared to those without glaucoma (17 cases, 3.8%); however, the difference did not reach statistical significance. Gender did not emerge as a risk factor for glaucoma as the female‐to‐male ratio was consistent among patients with and without glaucoma.
3.3. Risk for glaucoma following remission of Cushing's syndrome
Data on early biochemical remission status following a CS diagnosis were available for 471 patients; 312 (66%) achieved early biochemical remission, while 159 (34%) had persistent hypercortisolaemia. Overall, 62 (13%) patients CS, either with or without remission, had glaucoma in this study group. To assess the risk for glaucoma following a CS diagnosis, we excluded 28 patients who developed glaucoma before the CS diagnosis. Among the remaining 34 glaucoma patients diagnosed after a CS diagnosis, 22 (7.5%) achieved early biochemical remission, while 12 (7.9%) did not. The overall risk of glaucoma in Cushing's syndrome was elevated for both individuals experiencing remission and those with persistent hypercortisolism (p = 0.048) (Figure 2). However, the difference between those who achieved remission and those who did not was not statistically significant (Table 2). Compared to their matched controls, patients with CS without early biochemical remission did not exhibit a statistically significant higher risk for glaucoma (p = 0.18). However, while the time span between CS diagnosis and glaucoma diagnosis was comparable between CS patients in remission and controls (88.6 ± 73.06 and 88.9 ± 88.4 months, respectively), CS patients not in remission experienced an earlier onset of glaucoma (82.1 ± 88.0 months).
FIGURE 2.
Risk for glaucoma in patients with and without early biochemical remission with death as a competing event.
TABLE 2.
Patients with glaucoma and Cushing's syndrome, with and without disease remission.
| CS | Glaucoma | Glaucoma prior to CS | |
|---|---|---|---|
| Total N. | 471 | 34 | 28 |
| Remission (n, %) a | 312 (66%) | 22 (65%) | 20 (71%) |
| No remission (n, %) | 159 (34%) | 12 (35%) | 8 (29%) |
Abbreviations: CS, Cushing's syndrome; N, number.
Remission is defined as a normal 24‐h UFC level without treatment for hypercortisolism, or hypocortisolism necessitating glucocorticoid replacement after pituitary or adrenal surgery, within 24 months following diagnosis of CS.
4. DISCUSSION
While data on glucocorticoid treatment and glaucoma are more established, the incidence of glaucoma in patients with CS is not known. In this nationwide retrospective matched‐cohort study, the first of its kind to assess the risk for glaucoma in patients with CS, we demonstrated that individuals with endogenous CS exhibit a heightened risk of early‐onset glaucoma. Additionally, patients with CS tended to develop glaucoma at a significantly younger age compared to matched controls from the general population. Importantly, this difference persisted even after excluding both cases and controls with a prior diagnosis of glaucoma.
The mechanism of steroid‐induced glaucoma is not well understood; decreased trabecular meshwork outflow due to increased resistance is suspected to be the main cause of IOP elevation (Kersey & Broadway, 2005).
The overall prevalence of glaucoma in the general population increases with age and ranges from 1.5% to 1.9% in ages 40 to 65 years, increasing to 2% to 7% in patients 65 and older (Friedman, 2004). In our cohort, we observed that while the incidence of glaucoma in the control group increased with age, among patients with CS, the highest incidence of glaucoma was observed among those aged between 40 and 65 years. Additionally, the incidence of glaucoma before the age of 40 was five times higher among patients with CS compared to controls, highlighting a significantly elevated risk of early‐onset glaucoma among individuals with hypercortisolism. Glaucoma prevalence in Israel is similar to worldwide reported rates (Levkovitch‐Verbin et al., 2014). The higher incidence of glaucoma observed in both the study and control groups in our study as compared to the literature may be attributed to the study's definition of glaucoma, which is based on ICD‐10 codes in patients' medical records. Furthermore, patients receiving medications potentially increasing IOP were not excluded. Thus, despite the overall higher glaucoma rates observed here, since both the study and control groups rely on the same diagnostic criteria, the increased incidence of glaucoma in patients with CS as compared to matched controls in our study is significant and warrants attention.
In addition, patients with CS experienced the onset of glaucoma at a notably younger age compared to controls, with CS patients exhibiting glaucoma onset 4 years earlier than controls. When examining the ages of patients before their CS diagnosis, those diagnosed with glaucoma were statistically significantly younger than controls, with mean ages of 56 and 61 years, respectively. This observation, coupled with the well‐documented diagnostic delay of CS (Rubinstein et al., 2020), suggests that the hypercortisolism before the formal diagnosis of CS did put them at a heightened risk of developing glaucoma at a younger age.
Notably, we did not find any correlation between maximum elevation of UFC and the risk of developing glaucoma. We postulate that extended hypercortisolism exposure could exert a more significant influence than the maximum UFC levels measured in the urine, which has known significant variability also.
The association between diabetes mellitus and glaucoma remains inconclusive due to conflicting findings in cohort and epidemiological studies (de Voogd et al., 2006; Hennis et al., 2003). However, a comprehensive meta‐analysis published in 2014 suggested that individuals with diabetes mellitus face an elevated risk of developing glaucoma (Zhou et al., 2014). In our study, we observed that patients with CS and diabetes mellitus were more likely to develop glaucoma compared to those without diabetes mellitus. Another significant risk factor for developing high IOP and consequently glaucoma is chronic corticosteroids use, specifically topical steroids. When the IOP remains high for a prolonged duration, damage to the optic nerve (steroid‐induced secondary glaucoma) may occur (Kersey & Broadway, 2005).
Though it seems intuitive that endogenous CS could match the exogenous CS numbers, there are no large population studies examining the association between CS and glaucoma. Several studies suggested a role for endogenous cortisol in the development of ocular hypertension and glaucoma, noting increased plasma and aqueous humour cortisol levels in glaucoma patients (Patel et al., 2023). However, only a few small cohort clinical studies have been performed on endogenous hypercortisolism in patients with CS causing increased IOP and glaucoma (Jonas et al., 1990; Ma et al., 2022), while another study showed no correlation between endogenous hypercortisolism and increased IOP (Mishra et al., 2017). There are several published case reports on endogenous hypercortisolism as a cause for secondary glaucoma; Virevialle et al. reported a case of a young female with painless loss of vision who had severe open‐angle glaucoma with uncontrolled high IOP, requiring glaucoma surgery, which later was found to be secondary to CS related to an adrenal adenoma (Virevialle et al., 2014). Another case report published by Blumenthal et al. described a 33‐year‐old man with increased IOP represented as a manifestation of hypercortisolism caused by ectopic CS. Importantly, after surgical removal of the tumour, the high IOP resolved (Blumenthal et al., 1999). CD has also led to ocular hypertension and glaucoma in two cases, with IOP returning to normal levels in all four eyes after transsphenoidal tumour resection (Gupta et al., 2015). Noteworthy, in some of the reports, ocular hypertension and glaucoma were the presenting manifestations for CS diagnosis (Jonas et al., 1990; Ma et al., 2022; Mishra et al., 2017).
The overall risk for glaucoma was high for both patients with early biochemical remission and patients with no remission, which can be due to the limited number of patients in each group. However, patients with persistent hypercortisolaemia were diagnosed with glaucoma approximately 6 months earlier compared to both patients with CS in remission and controls. This observation could be attributed to the prolonged hypercortisolaemia in patients with CS without remission, leading to elevated IOP and subsequent development of glaucoma.
This study has several strengths, including a sufficiently large sample size for the primary analysis, long‐term follow‐up, and strict criteria for diagnosing CS, along with consideration of disease aetiology and remission status. The control group was carefully matched to minimize the influence of factors like age, sex, socioeconomic status and BMI on cancer risk. Additionally, the database encompasses the entire population, eliminating the risk of selection bias. Given the increased mortality associated with CS, we accounted for death as a competing risk in all analyses. Lastly, we performed necessary sensitivity analyses to ensure the robustness of our results.
The limitations of this study include the potential for missing data, which, due to its retrospective design, may have affected our ability to identify patients with CS and glaucoma, as well as to determine disease aetiology or remission status in some cases. Additionally, ascertainment bias cannot be excluded, as patients with CS may have been diagnosed with glaucoma more frequently due to more regular ophthalmologic examinations. Surveillance bias, where patients with more frequent healthcare visits or monitoring are more likely to be diagnosed with additional conditions due to being examined more often than others, could also result in an overestimation of the association between CS and glaucoma.
In this large nationwide retrospective matched‐cohort study, we have shown for the first time that endogenous CS, whether caused by a pituitary or adrenal adenoma, is associated with an increased risk for glaucoma and a clinical manifestation at an earlier age versus general population, regardless of remission status or degree of UFC elevation. A delay in diagnosing both CS and glaucoma can result in significant ocular and systemic morbidities. Guidelines should also incorporate recommendations for periodic monitoring for intraocular pressure and/or glaucoma development to be routinely performed for patients with CS, especially if they also have concomitant comorbidities. Further research using larger multinational databases is warranted to validate our findings and uncover additional insights.
FUNDING INFORMATION
This research did not receive any specific grant from funding agencies in the public, commercial or not‐for‐profit sectors.
CONFLICT OF INTEREST STATEMENT
Y.S., A.Z., Y.R., S.K., I.S. and T.S. do not have any financial or personal relationships with other people or organizations to disclose. A.A. has received occasional scientific fee for scientific consulting and advisory boards from Medison, C.T.S. pharma and Neopharm. M.F. has received research support from Oregon Health & Science University as a principal investigator from Recordati, Sparrow and Xeris and has performed occasional scientific consultancy for Recordati, Sparrow and Xeris.
Sharon, Y. , Shochat, T. , Rudman, Y. , Kushnir, S. , Zahavi, A. , Shimon, I. et al. (2025) Higher risk and earlier onset glaucoma in Cushing's syndrome. Acta Ophthalmologica, 103, e176–e182. Available from: 10.1111/aos.16787
REFERENCES
- Becker, B. (1965) Intraocular Pressure Response to Topical Corticosteroids. Investigative Ophthalmology & Visual Science, 4, 198–205. [PubMed] [Google Scholar]
- Blumenthal, E.Z. , Muszkat, M. , Pe'Er, J. & Ticho, U. (1999) Corticosteroid‐induced glaucoma attributable to an adrenocorticotropin‐ secreting malignant carcinoid tumor of the thymus. American Journal of Ophthalmology, 128, 100–101. [DOI] [PubMed] [Google Scholar]
- de Voogd, S. , Ikram, M.K. , Wolfs, R.C.W. , Jansonius, N.M. , Witteman, J.C.M. , Hofman, A. et al. (2006) Is diabetes mellitus a risk factor for open‐angle glaucoma? The Rotterdam study. Ophthalmology, 113, 1827–1831. [DOI] [PubMed] [Google Scholar]
- Fleseriu, M. , Auchus, R. , Bancos, I. , Ben‐Shlomo, A. , Bertherat, J. , Biermasz, N.R. et al. (2021) Consensus on diagnosis and management of Cushing's disease: a guideline update. The Lancet Diabetes and Endocrinology, 9, 847–875. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Friedman, D.S. (2004) Prevalence of open‐angle glaucoma among adults in the United States. Archives of Ophthalmology, 122, 532–538. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Gadelha, M. , Gatto, F. , Wildemberg, L.E. & Fleseriu, M. (2023) Cushing's syndrome. Lancet, 402, 2237–2252. [DOI] [PubMed] [Google Scholar]
- Gupta, S. , Sihota, R. , Gupta, V. , Dada, T. , Gogia, V. & Sharma, A. (2015) Functional pituitary tumors masquerading as primary glaucoma and effect of hypophysectomy on intraocular tension. Journal of Glaucoma, 24, e7–e13. [DOI] [PubMed] [Google Scholar]
- Haas, J.S. & Nootens, R.H. (1974) Glaucoma secondary to benign adrenal adenoma. American Journal of Ophthalmology, 78, 497–500. [DOI] [PubMed] [Google Scholar]
- Hennis, A. , Wu, S.Y. , Nemesure, B. & Leske, M.C. (2003) Hypertension, diabetes, and longitudinal changes in intraocular pressure. Ophthalmology, 110, 908–914. [DOI] [PubMed] [Google Scholar]
- Jonas, J.B. , Huschle, O. , Koniszewski, G. , Buchfelder, M. & Fahlbusch, R. (1990) Intraocular pressure in patients with Cushing's disease. Graefe's Archive for Clinical and Experimental Ophthalmology, 228, 407–409. [DOI] [PubMed] [Google Scholar]
- Kersey, J.P. & Broadway, D.C. (2005) Corticosteroid‐induced glaucoma: a review of the literature. Eye, 20, 407–416. [DOI] [PubMed] [Google Scholar]
- Khaw, K.W. , Jalaludin, M.Y. , Suhaimi, H. , Harun, F. & Subrayan, V. (2010) Endogenous cushing syndrome from an ectopic adrenocorticotropic hormone production as a rare cause of ocular hypertension. Journal of AAPOS, 14, 356–357. [DOI] [PubMed] [Google Scholar]
- Levkovitch‐Verbin, H. , Goldshtein, I. , Chodick, G. , Zigman, N. & Shalev, V. (2014) The Maccabi glaucoma study: prevalence and incidence of glaucoma in a large Israeli health maintenance organization. American Journal of Ophthalmology, 158, 402–408.e1. [DOI] [PubMed] [Google Scholar]
- Ma, Y. , Chen, Z. , Ma, Z. , Ye, H. , Zhang, Z. , Wang, Y. et al. (2022) Increased risk of ocular hypertension in patients with Cushing's disease. Journal of Glaucoma, 31, 941–946. [DOI] [PubMed] [Google Scholar]
- Mishra, P. , Singh, A. , Kanaujia, V. , Agarwal, R. , Mishra, P. , Guleria, A. et al. (2017) Intraocular pressure and its correlation with midnight plasma cortisol level in Cushing's disease and other endogenous Cushing's syndrome. Indian Journal of Ophthalmology, 65, 826–829. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Patel, P.D. , Kodati, B. & Clark, A.F. (2023) Role of glucocorticoids and glucocorticoid receptors in glaucoma pathogenesis. Cells, 12, 2452. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Phulke, S. , Kaushik, S. , Kaur, S. & Pandav, S.S. (2017) Steroid‐induced glaucoma: an avoidable irreversible blindness. Journal of Current Glaucoma Practice, 11, 67–72. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Quigley, H. & Broman, A.T. (2006) The number of people with glaucoma worldwide in 2010 and 2020. The British Journal of Ophthalmology, 90, 262–267. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Reincke, M. & Fleseriu, M. (2023) Cushing syndrome: a review. JAMA, 330, 170–181. [DOI] [PubMed] [Google Scholar]
- Rubinstein, G. , Osswald, A. , Hoster, E. , Losa, M. , Elenkova, A. , Zacharieva, S. et al. (2020) Time to diagnosis in Cushing's syndrome: a meta‐analysis based on 5367 patients. Journal of Clinical Endocrinology and Metabolism, 105, e12–e22. [DOI] [PubMed] [Google Scholar]
- Tham, Y.C. , Li, X. , Wong, T.Y. , Quigley, H.A. , Aung, T. & Cheng, C.Y. (2014) Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta‐analysis. Ophthalmology, 121, 2081–2090. [DOI] [PubMed] [Google Scholar]
- Tsushima, Y. , Munshi, L.B. , Taneja, C. & Kim, S. (2019) Cushing disease masquerading as glaucoma. ACE Clinical Case Reports, 5, e290–e293. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Virevialle, C. , Brasnu, E. , Fior, R. & Baudouin, C. (2014) Open‐angle glaucoma secondary to Cushing syndrome related to an adrenal adenoma: case report. Journal Français d'Ophtalmologie, 37, e169. [DOI] [PubMed] [Google Scholar]
- Zhou, M. , Wang, W. , Huang, W. & Zhang, X. (2014) Diabetes mellitus as a risk factor for open‐angle glaucoma: a systematic review and meta‐analysis. PLoS One, 9, e102972. [DOI] [PMC free article] [PubMed] [Google Scholar]