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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case-control study was planned as a part of the Casteldaccia Eye Study in order to investigate about risk factors of ocular hypertension and glaucoma. Cases were 44 subjects with glaucoma or intraocular pressure of 24 mm Hg or more. Controls were 220 subjects with intraocular pressure of 20 mm Hg or less and no signs of glaucoma. A number of environmental, behavioral, systemic and ocular variables were studied. Among the others we investigated the following: sunlight exposure, smoking, alcohol intake, pregnancies, systemic hypertension, diabetes, use of corticosteroids, refractive status, anterior chamber depth, lens nuclear sclerosis, iris color and texture. After univariate analysis the use of ocular corticosteroids and antibiotics, myopia, shallow anterior chamber and myopic macular degeneration were associated with ocular hypertension or glaucoma. However, the logistic regression showed that only the use of ocular corticosteroids (odds ratio = 7.79) and the myopia (odds ratio = 5.56) were independently associated.
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PMID:Risk factors of ocular hypertension and glaucoma. The Casteldaccia Eye Study. 792 48

A pilot study was carried out to determine the prevalence of ophthalmic disease in the Indian community of Southall and to ascertain the best methods applicable for a larger formal study. Three sites were chosen for the study, a Sikh gurdwara, a mosque and a Hindu temple. The subjects were volunteers aged 30 years and over who had visited the appropriate place of worship at least twice in the previous month. A total of 184 subjects were examined. The prevalence of blindness was 2.7% by the World Health Organization (WHO) criteria, while 9.8% had uniocular blindness. The prevalence of glaucoma and ocular hypertension was 2.7% and 7%, respectively. Of the 184 subjects examined, 58% had cataract and 3.8% had age-related maculopathy. The prevalence of visually disabling trachomatous eye disease was 9.7%. The prevalence of diabetes mellitus was 17.9%, and that of hypertension 22.8%. This small study suggests that people with origins from the Indian subcontinent have a higher prevalence of ophthalmic disease than the Caucasian population.
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PMID:A pilot study into the prevalence of ophthalmic disease in the Indian population of Southall. 819 34

Glucocorticoid-induced ocular hypertension has been demonstrated in both animals and humans. It is possible that glucocorticoid-induced changes in trabecular meshwork (TM) cells are responsible for this hypertension. In order to elaborate further the effect of glucocorticoids on the trabecular meshwork, the ultrastructural consequences of dexamethasone (DEX) treatment were examined in three different human TM cell lines. Confluent TM cells were treated with 0.1 microM of DEX for 14 days, and then processed for light, epifluorescent microscopy or transmission electron microscopy (TEM). The effect of DEX treatment on TM cell and nuclear size was quantified using computer assisted morphometrics. Morphometric analysis showed a significant increase in both TM cell and nuclear size after 14 days of DEX treatment. Epifluorescent microscopy of rhodamine-phalloidin stained, control TM cells showed the normal arrangement of stress fibers. In contrast, DEX-treated TM cells showed unusual geodesic dome-like cross-linked actin networks. Control TM cells had the normal complement and arrangement of organelles as well as electron dense inclusions and large vacuoles. DEX-treated TM cells showed stacked arrangements of smooth and rough endoplasmic reticulum, proliferation of the Golgi apparatus, pleomorphic nuclei and increased amounts of extracellular matrix material. The DEX-induced alterations observed in the present study may be an indication of the processes that are occurring in the in vivo disease process.
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PMID:Dexamethasone induced ultrastructural changes in cultured human trabecular meshwork cells. 826 90

To investigate pattern electroretinogram changes in treated ocular hypertension, we evaluated pattern electroretinogram recordings of 48 hypertensive eyes following an 8-month timolol maleate therapy. During treatment, 27 of 48 eyes had normalized intraocular pressures (15-18 mm Hg), while 21 retained elevated values (21-25 mm Hg). Twenty-eight eyes with untreated hypertension (22-25 mm Hg) lasting at least 8 months, as well as 32 untreated, normotensive eyes served as controls. When compared to untreated normotensive controls, timolol-treated eyes with either elevated or normalized intraocular pressures showed reductions in the mean electroretinographic amplitudes. However, these amplitude reductions were substantially greater in treated eyes with elevated pressures as compared to those with normalized ones. Untreated hypertensive controls showed pattern electroretinogram reductions, with respect to normal values, that were comparable to those of treated hypertensive eyes, but larger than those of treated normotensive ones. These results indicate that, in treated ocular hypertension, pattern electroretinogram losses tend to be associated with moderately increased intraocular pressures in the range of 21-25 mm Hg. Electroretinographic abnormalities may be, at least in part, prevented only by lowering intraocular pressure into a normal range.
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PMID:Pattern electroretinogram in treated ocular hypertension: a cross-sectional study after timolol maleate therapy. 853 95

This case-control study evaluated risk factors for open-angle glaucoma (OAG) and high intraocular pressure (IOP), including systemic hypertension and its treatment, other systemic factors, familial, and demographic variables. The three study groups were based on masked ophthalmologic gradings of visual fields and fundus photographs, as well as tonometry. The OAG group (n = 122) had OAG field defects, IOP > 21 mmHG, and cup-disc ratios > or = 0.5 and/or evidence of glaucoma disc damage. The ocular hypertensives (n = 108) had no field defects, IOP > 21 mmHg and normal discs. The controls (n = 190) had no field defects, IOP < 21 mmHg and normal discs. The data collection protocol included a standardized interview and measurements. Medical history was confirmed by contacting the primary care physicians (89% response from physicians). Study groups were compared by polychotomous logistic regression analyses. Men were more likely to have OAG and less likely to have ocular hypertension. Systemic hypertension was more frequent in ocular hypertensives (Odds Ratio = 2.36); high diastolic pressure was associated with OAG and ocular hypertension (OR = 2.13 and 2.21, respectively). Treatment for systemic hypertension was unrelated to OAG risk. Low perfusion pressures (blood pressure-IOP differences) were strongly associated with OAG and ocular hypertension, a finding that could be due to the high IOP in these groups. A family history of glaucoma was more frequent in OAG (OR = 3.08) and ocular hypertension (OR = 2.38) than in controls. Alcohol consumption was related to ocular hypertension (OR = 2.32). No other associations were significant. The results confirm an association of blood pressure with intraocular pressure. Since the OAG and ocular hypertensive groups had similar blood pressure results, an independent effect of blood pressure on OAG was not substantiated.
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PMID:Open-angle glaucoma and ocular hypertension: the Long Island Glaucoma Case-control Study. 884 Oct 60

Intravenous fenoldopam, a selective dopamine-1 receptor agonist, was compared with placebo in this randomized, double-blind, two-period crossover study to evaluate its effects on intraocular pressure, aqueous dynamics, and macular blood flow in patients with elevated intraocular pressure or primary open-angle glaucoma. Doses of fenoldopam were titrated up to a maximum of 0.5 microgram/kg/min. Intraocular pressure, measured by pneumotonometry, was the primary outcome variable. Other outcomes included macular blood flow assessed by blue field examination, visual field examined by automated perimetry, aqueous outflow facility measured by tonography, and aqueous humor production determined by fluorophotometry. During infusions of fenoldopam, intraocular pressure increased from a mean baseline level of 29.2 mmHg to a mean maximum level of 35.7 mmHg. During the placebo infusions, pressure increased from a mean baseline of 28.4 mmHg to a mean of 29.0 mmHg at the time point that corresponded to the mean maximum intraocular pressure on the day intravenous fenoldopam was administered, to yield a mean difference in pressure between study days of 6.7 mmHg (P < 0.05). There were no apparent changes in macular blood flow, visual fields, or production or outflow of aqueous humor associated with fenoldopam infusion. The increase in intraocular pressure seen in this population of patients with ocular hypertension during infusions of fenoldopam is consistent with fenoldopam-associated increases in intraocular pressure reported in previous studies of healthy volunteers and of patients with accelerated systemic hypertension. These results further suggest that dopamine-1 receptors play a role in the regulation of intraocular pressure.
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PMID:Effect of intravenous fenoldopam on intraocular pressure in ocular hypertension. 911 57

Cortical venous drainage has been described as one of the major risk factors for dural arteriovenous fistula, which may induce venous hypertension leading to venous ischemia or intracerebral hemorrhage. However, it is rather rare to observe cortical venous drainage manifesting in this way in the cavernous sinus region. We report a case of a 55-year-old gentleman with a right cavernous dural arteriovenous fistula, presenting with conjunctival chemosis, exophthalmus and ocular hypertension on the affected side. Magnetic resonance imaging showed a small intracerebral hemorrhage in the right frontal lobe. Cerebral angiography revealed a dural arteriovenous fistula in the right cavernous sinus draining into the right olfactory vein via the uncal vein, as well as into the superior and inferior ophthalmic veins. This unusual cortical venous reflux was thought to be consistent with the intracerebral hemorrhage found on the magnetic resonance imaging. The patient underwent transvenous embolization for the dural arteriovenous fistula using an inferior petrosal catheterization into the uncal vein was difficult, and the cortical venous reflux through the vein seemed to be slight. However, extravasation of the contrast material occurred in the right frontal lobe after obliteration of the ophthalmic veins during the procedure. The cause of the extravasation was suspected to be the same olfactory vein that had been involved in the previous intracerebral hemorrhage. The obliteration of the dural fistula was continued rapidly, and the fistula disappeared after the embolization. Neurologically, the patient had no noticeable troubles, except for a mild headache. The pretreatment symptoms were alleviated within several days, and the patient was discharged in a week. We emphasize the following points from this rare case in order to facilitate a safer procedure during transvenous embolization for cavernous dural arteriovenous fistula. It is important to obliterate the cortical venous drainage as early as possible, even if the reflux is small or the catheterization is difficult. Repeated, careful sinography is useful for the evaluation of the drainage pattern at certain stages during the transvenous embolization procedure.
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PMID:[A case of cavernous dural arteriovenous fistula resulting in intracerebral extravasation during transvenous embolization]. 926 67

The effects of single or multiple topical doses of the relatively selective A1 adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N6-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20-250 micrograms) or CHA (20-500 micrograms) produced ocular hypertension (maximum rise = 4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall = 2.1 or 3.6 mmHg) from 2-6 hr. The relatively selective adenosine A2 antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 micrograms) inhibited the early hypertension, without influencing the hypotension. Neither 100 micrograms R-PIA nor 500 micrograms CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 micrograms R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A2 receptors, while the subsequent hypotension appears to be mediated by adenosine A1 receptors and results primarily from increased outflow facility.
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PMID:Effects of adenosine agonists on intraocular pressure and aqueous humor dynamics in cynomolgus monkeys. 930 79

The aim of the study was to determine whether certain factors are related to an increased risk of developing open-angle glaucoma. A total of 345 untreated glaucoma suspects with intraocular pressure (IOP) > or = 21 mmHg, cup to disc ratio 0.4 or less and no visual field defects, were followed up for 6 to 8 years (mean 7.3). During the follow-up 71 patients developed established glaucoma and were compared to the remaining 274 patients. The following factors were analysed: age, family history of glaucoma, IOP, Humphrey 30-2 visual fields, optic disc appearance, myopia, exfoliation, arterial hypertension and diabetes. Analysis yielded statistically significant results regarding a number of these factors in the patients who subsequently developed open-angle glaucoma. A significant association with the subsequent development of field loss in ocular hypertension (OHT) included: heredity (p < 0.001), age > or = 60 years (p = 0.013), axial myopia (0.001 < p < 0.01) and arterial hypertension (p = 0.05). About 20% of patients with ocular hypertension developed glaucoma over a period of seven years. Risk factors such as heredity, age, myopia and arterial hypertension, among others, must be considered in the follow-up of glaucoma suspects.
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PMID:Risk factors in ocular hypertension. 945 59

Corticosteroids (glucocorticoids), used frequently as potent anti-inflammatory agents, increase the risk of glaucoma by raising the intraocular pressure (IOP) when administered exogenously (topically, periocularly or systemically) and in certain conditions of increased endogenous production (e.g. Cushing's syndrome). Approximately 18 to 36% of the general population are corticosteroid responders. This response is increased to 46 to 92% in patients with primary open-angle glaucoma (POAG). Patients over 40 years of age and with certain systemic diseases (e.g. diabetes mellitus, high myopia) as well as relatives of patients with POAG are more vulnerable to corticosteroid-induced glaucoma. The association of corticosteroid-induced ocular hypertension in other conditions which are considered as risk factors for glaucoma (racial origins, hypertension, migraine, vasospasm) is likely but not fully established. The proposed mechanism of corticosteroid-induced glaucoma includes morphological and functional changes in the trabecular meshwork system and is similar to the pathogenesis of POAG. Trabecular cells exposed to corticosteroids in vitro show endoreplication of nuclei, an increase in cell size and excessive production of an approximately 56kD glycoprotein, identified as myocilin and transcribed by the GLC1A gene. Induction of ocular hypertension after corticosteroid administration depends on the specific drug, the dose, the frequency of administration and the corticosteroid responsiveness of the patient. The risk of corticosteroid-induced glaucoma can be minimised with judicious use of corticosteroids, as well as education of patients and medical practitioners. New treatment modalities include modified steroids and nonsteroidal anti-inflammatory agents that will have less effect on the elevation of IOP.
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PMID:Corticosteroids and glaucoma risk. 1064 55


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