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Biomedical subjects

B Becker

Publications and source records attributed to B Becker.

At least 235 records · Page 13Linked to original sources

Increased ocular and systemic responsiveness to epinephrine in primary open-angle glaucoma.

Sixteen patients with primary open-angle gaucoma (POAG) were matched as to age, sex, and race with an equal number of patients with secondary glaucoma. Although initial intraocular pressures were comparable, treatment with topical epinephrine hydrochloride, decreased intraocular pressure more than 5 mm Hg in 14 (88%) of the 16 patients with POAG but in only five (31%) of the 16 patients with secondary glaucoma (p less than .005). Eleven (69%) of the 16 patients with POAG demonstrated premature ventricular contractions during tonography as opposed to three (19%) of the 16 patients with secondary glaucoma (p less than .025). These findings suggested greater ocular as well as cardiac responsiveness to epinephrine in patients with POAG.

Age Factors↗

Increased cellular responsiveness to epinephrine in primary open-angle glaucoma.

The concentration of I-epinephrine hydrochloride necessary to inhibit lymphocyte transformation by 50% (I50 value) was determined in vitro for nine patients with primary open-angle glaucoma (POAG) and in seven controls. The lymphocytes of the patients with POAG were significantly (P less than .05) more responsive. This result is consistent with the hypothesis that patients with POAG have an increased responsiveness to agents that elevate intracellular cyclic adenosine monophosphate levels.

Adult↗

Visual field changes in ocular hypertension. A computer-based analysis.

A minicomputer system has been developed to digitize and store visual field data. In 110 cortiocosteroid-nonresponding subjects aged 10 to 75, the area of the i4e and i2e isopters and of the blind spot changed linearly as a function of age. Within this population the same visual field parameters were randomly distributed with respect to intraocular pressure. In 32 cortiocosteroid responders (increase in intraocular pressure to over 31 mm Hg after topical administration of corticosteroids) with normal visual fields, the central visual field area (i2e isopter) was reduced as a nonlinear function of IOP. Increases in IOP in excess of 8 mm Hg were required to produce significant mean reductions in central visual field area.

Adolescent↗

Corneal endothelial changes with long-term topical epinephrine therapy.

Corneal thicknesses and endothelial cell densities were studied in nine patients with ocular hypertension receiving long-term unilateral topical epinephrine hydrochloride therapy. No difference was noted in corneal thickness in the treated eyes. There was a significant (P less than .02) reduction in endothelial cell count in the treated eyes compared to their untreated fellow controls. Those patients who had the most marked intraocular pressure response to epinephrine also had the greatest endothelial cell loss.

Administration, Topical↗

Dipivefrin use in patients with intolerance to topically applied epinephrine.

Twelve patients who had previously demonstrated an intolerance to topically applied epinephrine received dipivefrin 0.1% in one eye and epinephrine 2% in the other eye. An adverse reaction occurred in only one eye (8%) receiving dipivefrin, but in ten (83%) on epinephrine. Topical dipivefrin 0.1% proved useful for lowering intraocular pressure in patients intolerant to topically applied epinephrine.

Administration, Topical↗

Thyroid function and the intraocular pressure response to topical corticosteroids.

Baseline thyroxine, thyrotropin (TSH), and triiodothyronine (T3) resin uptake levels were measured in patients classified according to their topical intraocular response to corticosteroids. Results of thyroid studies were similar in patients with primary open-angle glaucoma and noncorticosteroid responsive (NN, intraocular pressure less than 20 mmHg after six weeks of topical 0.1% dexamethasone eyedrops) subjects. Primary open-angle glaucoma was not associated with the increased prevalence of low thyroid function values. The TSH suppression induced by oral dexamethasone was similar in NN subjects and patients with primary open-angle glaucoma. Patients with primary open-angle glaucoma did not demonstrate an increased glucocorticoid sensitivity as related to thyroid function. Thus, the adenohypophysial thyrotropic cell, the major site of dexamethasone inhibition of TSH secretion, does not appear to share the enhanced corticosteroid sensitivity of the eye, the hypothalamus, and the lymphocyte in patients with primary open-angle glaucoma.

Administration, Oral↗

Low-dose methazolamide and intraocular pressure.

Sixteen patients with increased intraocular pressure (over 20 mm Hg) received 25 and 50 mg of oral methazolamide, twice daily, during consecutive weeks and then 500 mg (Sequels) of acetazolamide. The two methazolamide regimens produced significant decreases in intraocular pressure. Acetazolamide treatment resulted in a greater decrease in intraocular pressure but more systemic acidosis and side effects.

Acetazolamide↗

The effect of hyperthermia on aqueous humor dynamics in rabbits.

Hyperthermia increased intraocular pressure (Po) by approximately 5 mm Hg in rabbit eyes. This increase was not associated with changes in plasma osmolarity, blood lactate, or pH. Episcleral venous pressure (Pv) decreased from a baseline of 11 +/- 1 mm Hg(mean +/- SEM) to 8 +/- 1 mm Hg after one hour of hyperthermia. Outflow facility (c) as measured by tonography remained unchanged. Aqueous humor flow [c(Po - Pv)] as estimated by tonography increased by about 126%. The elevation of intraocular pressure was not prevented by aspirin pretreatment nor altered by unilateral optic nerve transection.

Animals↗

The pigment dispersion syndrome.

The pigment dispersion syndrome was noted in 10% of white and black subjects with and without glaucoma. This suggested pigment dispersion was not a high risk factor in the development of glaucoma. The HLA-B7 antigen was less prevalent and HLA-B13 and Bw17 antigens were significantly more prevalent in individuals with the pigment dispersion syndrome than in subjects without the syndrome. Either HLA-B13 or Bw17 antigen was found in 23 (77%) of 30 patients with the pigment dispersion syndrome and in only 13 (6%) of the 203 subjects without pigment dispersion. Pigmentary glaucoma was characterized by a significantly higher prevalence of combinations of HLA-B12 and B13 or HLA-B12 and Bw17 antigens as compared to the pigment dispersion syndrome without glaucoma, primary open-angle glaucoma, or the general population. This suggested that pigmentary glaucoma differed genetically from primary open-angle glaucoma and was a separate entity.

Glaucoma↗

Anterior segment ischemia after cyclocryotherapy.

The syndrome of anterior segment ischemia occurred in three patients as a complication of cyclocryotherapy for hemorrhagic glaucoma. Cryotherapy was applied with a retinal probe (2.5 mm in diameter) for 12 one-minute applications (-60 degrees or -80 degrees C) over the entire 360-degree circumference at the globe. The pathogenesis for this complication may be related, and unique, to chronic ocular ischemia associated with rubeosis iridis.

Adult↗

The association of HLA-B7 and HLA-B12 antigens with cup/disk ratio, family history of glaucoma, and intraocular pressure.

The presence of either HLA-B7 or HLA-B12 antigens was associated with a higher prevalence of cup/disk ratios greater than 0.3 in the GG responders (intraocular pressure greater than 31 mm Hg after six weeks of topical dexamethasone 0.1%, four times daily) and in the combined NN-NG (intraocular pressure less than or equal to 31 mm Hg) groups. The presence of either antigen was associated with a higher prevalence of a family history of glaucoma in the GG group. N association was noted between the antigens and age, sex, race, or mean intraocular pressure in either of the groups studied.

Dexamethasone↗

Prognostic value of HLA-A 3, BW 35, B 7, and B 12 in ocular hypertension.

The prevalences of HLA-A 3, BW 35, B 7 and B 12 in 80 Caucasian patients with ocular hypertension were intermediate between values found in ocular normotensives and in patients with primary open-angle glaucoma. The presence of HLA-B 7 or B 12 had significant predictive value for the development of glaucomatous damage to the optic nerve in patients with ocular hypertension. The HLA-A 3 antigen by itself, or in combination with B 7 and B 12 did not improve the prognostic value of the B 7 and B 12 antigens. Only one of the 20 white ocular hypertensives in this series with HLA BW 35 antigen developed glaucomatous visual field loss.

Eye Diseases↗

HLA in primary open-angle glaucoma.

Histocompatibility antigen typing was carried out in 50 Caucasian patients with primary open-angle glaucoma (POAG) and 50 Caucasian ocular-normotensive subjects. HLA-A 3 was present in 46%, B7 in 52%, B12 in 50%, and either B7 or B12 in 88% of p,tients with POAG. These prevalences in POAG patients were significantly greater than in ocular-normotensive subjects (p less than 0.01, p less than 0.0005, p less than 0.001, and p less than less than 0.0005, respectively). The prevalences of A 3-B 7, A 3-B 12 and either combination were also significantly greater in POAG patients than in the ocular normotensives (p less than 0.005, p less than 0.005, and p less than 0.0005, respectively). HLA-BW 35 was noted to be in deficit in Caucasian POAG patients (8%) as compared to Caucasian ocular normotensives (32%; p less than 0.01).

Glaucoma↗

Histocompatibility antigens and diabetic retinopathy.

Of 160 patients with onset of diabetes at or after 30 years of age, the 84 with no evidence prevalences of HLA-A1 and B8 when compared with the 76 with retinal complications or with the 282 healthy blood donors. In addition, in 90 patients with onset of diabetes before age 30 years, we could confirm the reported significant increase of HLA-B8 and decrease of B7, but no differences were noted between those juvenile-onset diabetics with and those without retinopathy.

Adult↗

Topical corticosteroid response and retinopathy in juvenile-onset diabetes mellitus.

In a prospective study, 64 patients with insulin-dependent juvenile-onset diabetes mellitus were followed for eight to 12 years to determine if those with higher spontaneous intraocular pressures (IOPs) would be protected from the development of retinopathy. The patients were also classified initially as high (GG), intermediate (NG), or low (NN), responders on the basis of their IOP response to corticosteroid eyedrops. High responders were found to be considerably in excess (25 per cent) of the proportion found in the general population (6 per cent). Retinopathy developed significantly less often and was less severe in the high (GG) corticosteroid responders. Although the GG diabetics had significantly higher mean baseline IOPs than the less responsive NN and NG groups in each corticosteroid response category, the mean IOP of the group with retinopathy was not significantly different from that without retinopathy. This suggested that factors associated with the GG response other than increased IOP might be important in the relative resistance to diabetic retinopathy.

Administration, Topical↗

The ocular anti-inflammatory action of imidazole.

Imidazole administered intraperitoneally to albino rabbits at a dose of 250 mg. per kilogram inhibited the rise of aqueous humor protein concentration by approximately 50 per cent 30 minutes after paracentesis. Systemic imidazole administered daily to albino rabbits injected with intravitreal Shigella endotoxin decreased the conjunctival and iris hyperemia and reduced the anterior chamber cell and flare and the haziness of the optical media. Systemically administered imidazole had no effect on the aqueous humor concentrations of c-AMP or c-GMP in the rabbit. In vitro studies of rabbit ciliary body-iris phosphodiesterase activity indicated no effect of imidazole at a concentration of 10(-3) molar.

Adenosine Monophosphate↗

Increased intraocular pressure following topical azide or nitroprusside.

In rabbits the topical administration of sodium azide (NaNs) or sodium nitroprusside (SNP) increased intraocular pressure in a dose-response manner. These agents, which activate guanylate cyclase, elevated cyclic GMP in the aqueous humor. Systemic blood pressure and pulse were not altered. Tonographic outflow facility was unchanged, suggesting an increase in aqueous humor flow as the mechanism for the elevation of intraocular pressure. Posterior chamber aqueous humor ascorbate concentration was decreased in the eye receiving the NaN3 or SNP. Systemic pretreatment with phenoxybenzamine, an alpha-adrenergic blocking agent, prevented the elevation of intraocular pressure observed following NaN3 and SNP. Pretreatment with systemic indomethacin, propranolol, or acetazolamide or the topical application of atropine or epinephrine failed to alter the elevation of intraocular pressure by either NaN3 or SNP.

Administration, Topical↗