|Ocular associations of metabolic syndrome.|
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|PMID: 22701846 Owner: NLM Status: PubMed-not-MEDLINE|
|Metabolic syndrome is a cluster of diseases including central obesity, dyslipidemia, hyperglycemia, and high blood pressure. People with metabolic syndrome have been shown to be at an increased risk of developing cardiovascular disease, beyond the risk associated with individual components of the syndrome. The association of diabetes and hypertension with retinopathy, cataract, and raised intraocular pressure is well known. This review highlights the association of metabolic syndrome, including all its components, with various ocular conditions such as retinopathy, central retinal artery occlusion, cataracts, and raised intraocular pressure.|
|Rupali Chopra; Ashish Chander; Jubbin J Jacob|
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|Type: Journal Article|
|Title: Indian journal of endocrinology and metabolism Volume: 16 Suppl 1 ISSN: 2230-9500 ISO Abbreviation: Indian J Endocrinol Metab Publication Date: 2012 Mar|
|Created Date: 2012-06-15 Completed Date: 2012-10-02 Revised Date: 2013-05-29|
Medline Journal Info:
|Nlm Unique ID: 101555690 Medline TA: Indian J Endocrinol Metab Country: India|
|Languages: eng Pagination: S6-S11 Citation Subset: -|
|Department of Ophthalmology, Christian Medical College, Ludhiana, India.|
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Journal ID (nlm-ta): Indian J Endocrinol Metab
Journal ID (iso-abbrev): Indian J Endocrinol Metab
Journal ID (publisher-id): IJEM
Publisher: Medknow Publications & Media Pvt Ltd, India
Copyright: © Indian Journal of Endocrinology and Metabolism
Print publication date: Month: 3 Year: 2012
Volume: 16 Issue: Suppl1
First Page: S6 Last Page: S11
PubMed Id: 22701846
Publisher Id: IJEM-16-6
|Ocular associations of metabolic syndrome|
|Jubbin J. Jacob1|
Department of Ophthalmology, Christian Medical College, Ludhiana, India
1Department of Medicine, Christian Medical College, Ludhiana, India
|Correspondence: Corresponding Author: Dr. Jubbin Jagan Jacob, Endocrine and Diabetes Unit, Department of Medicine, Christian Medical College, Ludhiana, Punjab – 141 008, India. E-mail: firstname.lastname@example.org
Almost all patients with diabetes/pre-diabetes and concomitant cardiovascular disease (CVD) risk factors of hypertension, obesity, and dyslipidemia also have insulin resistance. The clustering of these risk factors in a single patient has been termed the metabolic syndrome. The components of metabolic syndrome include abdominal obesity, diabetes, glucose intolerance, dyslipidemia, high blood pressure, and hyperuricemia. The association of diabetes and hypertension with ocular conditions such as retinopathy, cataract, and raised intraocular pressure (IOP)[5, 6] is well known. Metabolic syndrome is increasingly being recognized as a distinct identity and this review is an attempt to highlight the association between metabolic syndrome and various ocular conditions such as non-diabetic retinopathy, cataract, and primary open angle glaucoma.
According to the National Cholesterol Education Program (NCEP) guidelines, the metabolic syndrome is based on the presence of three of the following five risk factors.
- Abdominal obesity (waist circumference >40 inches in men, >35 inches in women)
- Plasma triglycerides 150 mg/dL
- Plasma high density lipoprotein (HDL) cholesterol <40 mg/dL in men and <50 mg/dL in women
- Blood pressure 130/85 mmHg
- Fasting plasma glucose 110 mg/dL.
The syndrome is increasingly being recognized as a distinct entity affecting a large proportion of US adult population. The prevalence of metabolic syndrome as defined by the NCEP guidelines has been estimated using the National Health and Nutritional Examination Survey (NHANES) database. Based on the data from NHANES collected between 1999 and 2002, the prevalence of metabolic syndrome is 34.5%. The prevalence of metabolic syndrome in our country ranges from 20 to 55%. Much higher prevalence is seen among people in urban areas and those from higher socioeconomic strata.
Persons with metabolic syndrome are known to be at risk of developing large vessel atherosclerotic disease. Characteristics of large and small vessel disease such as inflammation and endothelial dysfunction have been reported to be associated with metabolic syndrome. The association of diabetes and hypertension with retinopathy and other microvascular changes is well known. Recent studies have shown that these retinal vascular signs are also associated with systemic markers of inflammation and endothelial dysfunction. In a population-based cross-sectional study involving 11,265 persons, retinal photographs were taken and graded for the presence of retinal microvascular signs. The data showed that persons with metabolic syndrome were significantly more likely to have retinopathy, arteriovenous nicking, focal arteriolar narrowing, smaller retinal arteriolar diameters, and larger retinal venular diameters than people without the syndrome, independent of age, gender, race, education, cigarette smoking, and alcohol consumption. With the exception of retinopathy, most associations were significant even in people without diabetes or hypertension, suggesting that factors other than hyperglycemia and high blood pressure (i.e. dyslipidemia, obesity, and inflammation) may explain the occurrence of these retinal lesions.
In another study conducted among Japanese adults, the various components of the metabolic syndrome were found to be associated with retinal microvascular signs: a larger waist circumference was associated with wider venular diameter and retinopathy lesions; a higher blood pressure level was associated with focal arteriolar narrowing, arteriovenous nicking, enhanced arteriolar wall reflex, and narrower arteriolar diameter; and a higher triglyceride level was associated with enhanced arteriolar wall reflex. Overall, persons with the metabolic syndrome were more likely to have retinopathy (odds ratio 1.64, 95% CI: 1.02–2.64) and wider venular diameter of 4.69 μm (95% CI: 1.20–8.19 μm) than persons without the metabolic syndrome in this study.
The association between metabolic syndrome and retinopathy was also studied in persons 40 years of age and older with gradable fundus photographs in the NHANES III. However, in this population-based cross-sectional study, there was no evidence of an association between the metabolic syndrome and retinopathy independent of diabetic status. Thus, prospective studies are warranted to determine the casual link between metabolic syndrome and the risk of retinopathy and other microvascular changes.
Obesity, one of the major components of metabolic syndrome, has been shown to be associated with retinopathy signs in the general and non-diabetic population. In the Hoorn Study in the Netherlands, waist–hip ratio was independently associated with a number of incident retinopathy signs including retinal hemorrhages, microaneurysms, hard exudates, and cotton wool spots in the non-diabetic general population, although the association with body mass index (BMI) failed to achieve a statistical significance. Vasoproliferative factors such as vascular endothelial growth factor (VEGF) have been proposed to have a role in the pathogenesis of diabetic retinopathy. The concentrations of serum angiogenic factors such as VEGF have been observed to be elevated in obese humans. These findings provide a potential link between obesity and retinopathy. Moreover, oxidative stress also contributes to development of diabetic retinopathy by inducing overexpression of VEGF. Obesity increases oxidative stress because of its associated hyperleptinemias.
It is one of the most sudden and dramatic events seen by the ophthalmologist. Patients usually present with a sudden painless loss of vision. The appearance of a cherry-red spot in the fundus is the main characteristic. The cherry-red spot appears because soon after the obstruction of the blood flow to the inner retina, the normally transparent retina becomes opaque and blocks the brownish-red color from the underlying choroid, which is still supplied by blood. Because the retina overlying the foveola is relatively thin, however, the normal color of the choroid is still visible in this area.
Possible risk factors for the development of central retinal artery occlusion (CRAO) [Figure 1] are arteriosclerosis, chronic atrial fibrillation, congestive heart failure, cerebrovascular accident, systemic hypertension, myocardial infarction, diabetes mellitus, primary open angle glaucoma, and rheumatic heart disease.
Our literature search reveals two case reports of CRAO wherein the patients met all the five NCEP criteria of metabolic syndrome. The pro-inflammatory markers were found to be raised in both the cases.[24, 25] Low-grade inflammation has been identified as a pivotal pathogenic factor for development of atherosclerosis and has been shown to predict myocardial infarction and stroke in patients with preexisting CVD. Increased C-reactive protein (CRP) is associated with an increase risk of CVD. CRP may also be an important marker for complications of metabolic syndrome such as CRAO. The most common risk factors for CRAO are present in metabolic syndrome. Thus, metabolic syndrome can result in CRAO causing profound visual loss. Other than these isolated case reports, our literature search did not reveal any prospective studies linking metabolic syndrome with CRAO. However, obesity has been recognized as a significant risk for retinal vein occlusion in few studies. Moreover, retinal venous and arterial occlusions are known to be associated with hypertension, diabetes mellitus, and hyperviscosity syndromes. There is evidence supporting association of obesity with diabetes, hypertension, and hypercoagulable disorders, thus providing a possible association between obesity and retinal occlusive diseases.
The relationship between age-related maculopathy (ARM) and obesity has been investigated in several studies. The Age Related Eye Disease Study (AREDS) has reported a cross-sectional association between higher BMI and more advanced ARM as documented from fundus photographs. Obesity increases systemic oxidative stress secondary to hyperleptinemia, and oxidative stress is known to play an important role in the pathogenesis of ARM.
Cataract, a leading cause of blindness and poor vision, is a major public health problem worldwide, particularly in Asia, home to half of the world's population. Diabetes and hyperglycemia have long been recognized as risk factors for cataract. Various studies conducted in the Western and Asian populations have shown an association between metabolic syndrome and cataract. In the Singapore Malay Eye Study, the prevalence of cataract increased with increasing number of metabolic syndrome components in both men and women. In this study, metabolic syndrome and two of its principal components, diabetes and high BP, were significantly associated with cataract, assessed from lens photographs in a standardized manner. Coexisting diabetes and high BP were associated with fourfold higher odds of cataract. Serum triglycerides, HDL, and BMI were not found to be associated with cataract in this study. Mechanisms linking diabetes and hyperglycemia to cataract formation include advanced glycation of lens proteins and hyperosmotic effects of sorbitol on lens fibers formed through the aldose reductase pathway. The mechanism linking hypertension and cataract is not clear. Inflammation and endothelial dysfunction could possibly play a role in the association between hypertension and cataract.
Amongst the Western studies, Tan et al. have shown that metabolic syndrome is associated with all the three types of cataract (nuclear, cortical, and posterior subcapsular) in an elderly cohort of Australians in the Blue Mountain Eye study. Paunksnis et al. have also reported an association between cataract and metabolic syndrome among middle-aged European men and women. Further, metabolic syndrome, its components, and their combination were found to be associated with an increased risk of cataract extraction in an Italian hospital population and among Swedish women aged <65 years.
Obesity, an important component of metabolic syndrome, has been proposed to be a risk factor for cataract development, though the exact mechanisms are unclear. The Physicians Health Study, a randomized trial of 22,071 healthy male American physicians aged 40-84 years, reported both overall obesity, measured as BMI, and abdominal obesity as independent risk factors for cataract. Prospective data from Framingham Eye Study also demonstrate an independent association between greater BMI and higher incidence of cortical cataract and posterior subcapsular opacities. Several pathophysiological mechanisms have been proposed to explain the association of obesity and cataract. Leptin, a cytokine expressed and secreted mainly by adipocytes, is involved in the molecular mechanisms underlying cataract formation. Individuals with obesity are likely to have hyperleptinemia and leptin resistance. Thus, hyperleptinemia associated with obesity may promote cataract formation. These studies highlight the importance of tackling metabolic syndrome and its components for the prevention of cataract.
IOP is the only modifiable risk factor for primary open angle glaucoma. IOP is determined by the balance between aqueous humor secretion and outflow. Many cross-sectional and longitudinal epidemiological studies have reported association of elevated IOP with cardiometabolic risk factors such as type 2 diabetes mellitus, hypertension, and concurrent atherosclerotic disease, thereby suggesting a common underlying mechanism linking elevated IOP to various cardiometabolic factors.[45, 46] Chang et al. analyzed the clinical data of 1112 patients undergoing health checkup and concluded that participants with metabolic syndrome had significantly higher IOP than those without metabolic syndrome. Each additional component of metabolic syndrome was associated with a mean increase in IOP of 0.33 mm Hg. Their findings were consistent with those reported by Oh et al. in the Korean population.
The mechanism by which metabolic syndrome is associated with IOP is currently unknown. Recent research has revealed some pathophysiological links such as sympathetic stimulation, endocannabinoid overactivity, and aquaporins. Sympathetic hyperstimulation is a common feature of obesity, hypertension, and insulin resistance. Stimulation of ocular sympathetic nerve also increases IOP. Similarly, endocannabinoid overactivity contributes to the development of abdominal obesity, dyslipidemia, and hyperglycemia. In rodents, endocannabinoid receptors have been found in the trabecular meshwork where they regulate aqueous outflow and thus influence IOP. Aquaporin is a family of small membrane proteins that transport water and small molecules. They are present in various human tissues including trabecular meshwork in the eye, adipose tissue, liver, and pancreas. Aquaporins have been shown to increase aqueous fluid secretion across ciliary epithelium and regulate IOP. Unexpectedly, aquaporin knockout mice were obese and developed severe insulin resistance, pointing toward another possible link between IOP and metabolic syndrome.
Population-based data from several studies have demonstrated independent cross-sectional association between obesity and ocular hypertension. The Beaver Dam Eye Study reported a significantly positive association of IOP with several factors including BMI. Obesity exerts an effect on IOP by causing excessive intraorbital adipose tissue, increased blood viscosity, increased episcleral venous pressure, and impairment of aqueous outflow facility. Also, obesity has been shown to cause vascular endothelial dysfunction and autonomic dysfunction. This may cause abnormal ocular blood flow and perfusion instability leading to impaired vascular supply to the optic nerve head and glaucomatous changes. Data from various studies is summarized in Table 1.
The prevalence of metabolic syndrome is rapidly increasing worldwide due to the sedentary lifestyles. Its association with various ocular manifestations such as non-diabetic retinopathy, CRAO, cataract, and primary open angle glaucoma suggests that an epidemic of metabolic syndrome can have far-fetched ocular consequences as well. Amelioration of metabolic syndrome may have a therapeutic role in preventing these ocular conditions. However, most of the studies done in this regard were cross-sectional studies, and thus a causal relationship cannot be proven. Prospective, interventional studies are required to determine the causal association between metabolic syndrome, its components, and various ocular manifestations such as retinal microvascular signs, cataract, and primary open angle glaucoma.
Source of Support: Nil,
Conflict of Interest: None declared.
|1.||Bonora E,Kiechl S,Willeit J,Oberhollenzer F,Egger G,Targher G,et al. Prevalence of insulin resistance in metabolic disorders: The Bruneck StudyDiabetesYear: 199847164399753305|
|2.||Meigs JB. Invited commentary: Insulin resistance syndrome? Syndrome X? Multiple metabolic syndrome? A syndrome at all? Factor analysis reveals patterns in the fabric of correlated metabolic risk factorsAm J EpidemiolYear: 20001529081111092432|
|3.||Wong TY,Klein R,Klein BE,Tielsch JM,Hubbard LD,Nieto FJ. Retinal microvascular abnormalities and their relations with hypertension, cardiovascular disease and mortalitySurv OphthalmolYear: 200146598011525792|
|4.||Tan JS,Wang JJ,Mitchell P. Influence of diabetes and cardiovascular disease on the long term incidence of cataract: The Blue Mountains eye studyOphthalmic EpidemiolYear: 2008153172718850468|
|5.||Mitchell P,Smith W,Chey T,Healy PR. Open angle glaucoma and diabetes: The Blue Mountain eye study, AustraliaOphthalmologyYear: 1997104712189111268|
|6.||Dielemans I,Vingerling JR,Algra D,Hofman A,Grobbee DE,de Jong PT. Primary open angle glaucoma, intraocular pressure, and systemic blood pressure in the general elderly populationOphthalmologyYear: 199510254607831042|
|7.||National Cholesterol Education Program (NCEP) Expert panel on the Detection, Evaluation and Treatment of high blood cholesterol in adults (Adult Treatment Panel III). Third report of the National Cholesterol Education Program (NCEP) Expert panel on the Detection, Evaluation and Treatment of high blood cholesterol in adults (Adult Treatment Panel III). Final reportCirculationYear: 2002106314342112485966|
|8.||Ford ES,Giles WH,Dietz WH. Prevalence of the metabolic syndrome among US adults: Findings from the third National Health and Nutrition Examination SurveyJAMAYear: 2002287356911790215|
|9.||Ford ES. Prevalence of the metabolic syndrome defined by the International Diabetes Federation among adults in the USDiabetes CareYear: 2005282745916249550|
|10.||Misra A,Khurana L. Obesity and the metabolic syndrome in developing countriesJ Clin Endocrinol MetabYear: 20089311 Suppl 1S93018987276|
|11.||Golden SH,Folsom AR,Coresh J,Sharrett AR,Szklo M,Brancati F. Risk factor groupings related to insulin resistance and their synergistic effects on subclinical atherosclerosis: The Atherosclerosis Risk in Communities StudyDiabetesYear: 20025130697612351449|
|12.||Duncan BB,Schmidt MI,Pankow JS,Boerwinkle E. Low grade systemic inflammation and the development of type 2 diabetes: The Atherosclerosis Risk in Communities StudyDiabetesYear: 200352179980512829649|
|13.||Klein R,Sharrett AR,Klein BE,Chambless LE,Cooper LS,Hubbard LD,et al. Are retinal arteiolar abnormalities related to atherosclerosis.The Atherosclerosis Risk in Communities Study?Arterioscler Thromb Vasc BiolYear: 20002016445010845884|
|14.||Wong TY,Duncan BB,Golden SH,Klein R,Couper DJ,Klein BE,et al. Associations between the metabolic syndrome and retinal microvascular signs: Atherosclerosis Risk in Communities StudyInvest Ophthalmol Vis SciYear: 20044529495415326106|
|15.||Kawasaki R,Tielsch JM,Wang JJ,Wong TY,Mitchell P,Tano Y,et al. The metabolic syndrome and retinal microvascular signs in a Japanese population: The Funagata StudyBr J OphthalmolYear: 200892161617965107|
|16.||Keenan JD,Fan AZ,Klein R. Retinopathy in non diabetic persons with the metabolic syndrome: Findings from the Third National Health and Nutrition Examination SurveyAm J OphthalmolYear: 20091479344419243735|
|17.||Cheung N,Wong TY. Obesity and eye diseasesSurv OphthalmolYear: 2007521809517355856|
|18.||Van Leiden HA,Dekker JM,Moll AC. Risk factors for incident retinopathy in a diabetic and non diabetic population; the Hoorn studyArch OphthalmolYear: 20031212455112583792|
|19.||Aiello LP,Avery RL,Arrigg PG. Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disordersN Engl J MedYear: 1994331148077526212|
|20.||Miyazawa S,Takahasi K,Bujo H. Elevated serum vascular endothelial growth factor is associated with visceral fat accumulation in human obese subjectsDiabetologiaYear: 2003461483814534780|
|21.||Caldwell RB,Bartoli M,Behzadian MA. Vascular endothelial growth factor and diabetic retinopathy: Role of oxidative stressCurr Drug TargetsYear: 200565112416026270|
|22.||Bouloumine A,Marummo T,Lafontan M. Leptin induces oxidative stress in human endothelial cellsFASEB JYear: 1999131231810385613|
|23.||Mangat HS. Retinal artery OcclusionSurv OphthalmolYear: 199540145568533103|
|24.||Kosanovic-Jakovic N,Petrovic L,Risimic D,Milenkovic S,Danica M. Metabolic syndrome and central retinal artery occlusionVojnosanit PreglYear: 200562935816375224|
|25.||Cekic SP,Petkovic T,Stankovic-Babic GL,Mrsic JM. Central retinal artery occlusion in a patient with Metabolic Syndrome XJ Ophthalmol Vis ResYear: 201055760|
|26.||Alexander RW. Inflammation and coronary artery diseaseN Engl J MedYear: 199433146898035844|
|27.||Haverkate F,Thompson SG,Pyke SD,Gallimore JR,Pepys MB. Production of C-reactive protein and risk of coronary events in stable and unstable angina.European concerted Action on Thrombosis and Disabilities Angina Pectoris Study GroupLancetYear: 199734946269040576|
|28.||Backhouse O,Parapia L,Mahomed l. Familial thrombophilia and retinal vein occlusionEyeYear: 20001413710755093|
|29.||Lahey JM,Kearney JJ,Tune M. Hypercoagulable states and central retinal vein occlusionCurr Opin Pulm MedYear: 200393859212904708|
|30.||Abramson N,Abramson S. Hypercoagulable: Clinical assessment and treatmentSouth Med JYear: 20019410132011702813|
|31.||Risk factors associated with age related macular degeneration. A case control study in the age related eye disease study: Age Related Eye Disease Study Report Number 3OphthalmologyYear: 200010722243211097601|
|32.||Congdon NG,Friedman DS,Lietman T. Important causes of visual impairment in the world todayJAMAYear: 200329020576014559961|
|33.||Sabanayagam C,Wang JJ,Mitchell P,Tan AG,Tai ES,Aung T,et al. Metabolic syndrome components and age related Cataract: The Singapore Malay Eye StudyInvest Ophthalmol Vis SciYear: 201152239740421228391|
|34.||Stitt AW. Advanced glycation: An important pathological event in diabetic and age related ocular diseaseBr J OphthalmolYear: 2001857465311371498|
|35.||Klein BE,Klein R,Lee KE,Knudtson MD,Tsai MY. Markers of inflammation, vascular endothelial dysfunction and age related cataractAm J OphthalmolYear: 20061411162216386984|
|36.||Paunksnis A,Bojarskiene F,Cimbalas A,Cerniauskeine LR,Luksiene DI,Tamosiunas A. Relationship between cataract and metabolic syndrome and its componentsEur J OphthalmolYear: 2007176051417671938|
|37.||Galeone C,Petracci E,Pelucchi C,Zucchetto A,Lai VC,Tavani A. Metabolic syndrome, its components and risk of age related cataract extraction: A case control study in ItalyAnn EpidemiolYear: 201020380420382339|
|38.||Lindblad BE,Hakansson N,Philipson B,Wolk A. Metabolic syndrome components in relation to risk of cataract extraction: A prospective cohort study of womenOphthalmologyYear: 200811516879218538408|
|39.||Glynn RJ,Christen WG,Manson JE,Bernheimer J,Hennekens CH. Body mass index. An independent predictor of cataractArch OphthalmolYear: 1995113113177661746|
|40.||Hiller R,Podgor MJ,Sperduto RD,Nowroozi L,Wilson PW,Calton T,et al. A longitudinal study of boby mass index and lens opacities.The Framingham StudiesOphthalmologyYear: 19981051244509663229|
|41.||Gomez-Ambrosi J,Salvador J,Fruhbeck G. Is hyperleptinemia involved in the development of age related lens opacities?Am J Clin NutrYear: 200479888915113732|
|42.||Narin F,Atabek ME,Karakukcu M,Narin N,Kurtoglu S,Gumus H,et al. The association of plasma homocysteine levels with serum leptin and apolipoprotein B levels in childhood obesityAnn Saudi MedYear: 2005252091416119521|
|43.||Lazaro C,Garcia-Feijoo J,Castillo A,Perea J,Martinez-Casa JM,Garcia-Sanchez J. Impact of intraocular pressure after filteration surgery on visual field progression in primary open angle glaucomaEur J OphthalmolYear: 2007173576217534816|
|44.||Civan MM,Macknight AD. The ins and outs of aqueous humour secretionExp Eye ResYear: 2004786253115106942|
|45.||Lee JS,Lee SH,Oum BS,Chung JS,Cho BM,Hong JW. Relationship between intraocular pressure and systemic health parameters in a Korean populationClin Experiment OphthalmolYear: 2002302374112121360|
|46.||Memarzadeh F,Ying-Lai M,Azen SP,Varma R. Associations with intraocular pressure in Latinos: The Los Angeles Latino Eye StudyAm J OphthalmolYear: 2008146697618486096|
|47.||Chang YC,Lin JW,Wang LC,Chen HM,Hwang JJ,Chuang LM. Associations of intraocular pressure with the metabolic syndrome and novel cardiometabolic risk factorsEyeYear: 20102410374319816514|
|48.||Oh SW,Lee S,Park C,Kim DJ. Elevated intraocular pressure is associated with insulin resistance and metabolic syndromeDiabetes Metab Res RevYear: 2005214344015651065|
|49.||Mancia G,Bousquet P,Elgozi JL,Esler M,Grassi G,Julius S,et al. The sympathetic nervous system and the metabolic syndromeJ HypertensYear: 2007259092017414649|
|50.||Belmonte C,Bartels SP,Liu JH,Neufeld AH. Effects of stimulation of the ocular sympathetic nerves on IOP and aqueous humor flowInvest Ophthalmol Vis SciYear: 1987281649542820890|
|51.||Jarvinen T,Pate DW,Laine K. Cannabinoids in the treatment of glaucomaPharmacol TherYear: 2002952032012182967|
|52.||Verkman AS. Role of aquaporin water channels in eye functionExp Eye ResYear: 2003761374312565800|
|53.||MacDougald OA,Burant CF. Obesity and metabolic perturbations after loss of aquaporin 7, the adipose glycerol transporterProct Natl Acad Sci U S AYear: 20051021075960|
|54.||Klein BE,Klein R,Linton KL. Intraocular pressure in an American community.The Beaver Dam Eye StudyInvest Ophthalmol Vis SciYear: 199233222481607232|
|55.||Shiose Y,Kawase Y. A new approach to stratified normal intraocular pressure in a general populationAm J OphthalmolYear: 1986101714213717257|
|56.||Glowinska B,Urban M,Hryniewicz A,Peczynska J,Florys B,Hwish M. Endothelin–I plasma concentration in children and adolescents with atherogenic risk factorsKardiol PolYear: 2004613293815841114|
|57.||Broadway DC,Drance SM. Glaucoma and vasospasmBr J OphthalmolYear: 199882862709828767|
|58.||Teuscher AU,Meienberg O. Ischaemic oculomotor nerve palsy.Clinical features and vascular risk factors in 23 patientsJ NeurolYear: 198523214494031956|
|59.||Raina J,Foster JA. Obesity as a cause of mechanical entropionAm J OphthalmolYear: 199612212358659588|
|60.||Purvin VA,Kawasaki A,Yee RD. Papilledema and obstructive sleep apnea syndromeArch OphthalmolYear: 200011816263011115256|
|61.||McNab AA. The eye and sleepClin Exp OphthalmolYear: 20053311725|
[Figure ID: F1]
Central retinal artery occlusion
Keywords: Cataract, central retinal artery occlusion, intraocular pressure, metabolic syndrome, retinopathy.
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