Biomedical subjects
Publications and source records attributed to B Becker.
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.
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.
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.
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).
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.
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.
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.
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.
Primary open-angle galucoma (POAG) patients are more responsive to glucocorticoids, and have increased prevalences of the histocompatibility antigens HLA-B7 and HLA-B12. We report herein a comparison of in vitro cellular responsiveness to glucocorticoids and HLA classification for 25 POAG patients, and 25 individuals who respond to topical dexamethasone with intraocular pressure is greater than 31 mm. HG. (GG responders). Within both the POAG and GG groups, significantly greater responsiveness to prednisolone occurs in patients with HLA-B12 antigen. No such association occurs for patients with HLA-B7.
Black patients with primary open-angle glaucoma, when compared to nonglaucomatous individuals, demonstrate significantly increased prevalences of the HLA antigens B7 and B12 and significantly decreased frequencies of A1 and A11. White patients with primary open-angle glaucoma have in common with blacks the increases in B7 and B12 and the decrease in A11, but present no deficit of A1. In addition, white patients with primary open-angle glaucoma demonstrate a significant increase of A3 and a decrease of Bw35, both of which are not found in blacks.
Nonglaucomatous individuals were classified by their intraocular pressure response to 6 weeks of topical dexamethasone, 0.1%, four times daily. Twenty GG responders (over 31 mm. Hg after dexamethasone) and 20 NN responders (below 20 mm. Hg after dexamethasone) of similar age, sex, race, initial intraocular pressure, and facility of outflow were selected. After 24 hr. of treatment (two doses) with 1% epinephrine HCl, the GG subjects demonstrated a mean (+/-sigma) corrected decrease in intraocular pressure of 4.2 mm. Hg (+/- 2.5) as opposed to 1.8 mm. Hg (+/- 2.1) in the NN subjects (p less than 0.005). The relationship between increased responsiveness to corticosteroids, to epinephrine, and to theophylline suggested cyclic nucleotides as a possible common pathway.
Systemic acidosis induced by intravenous administration of hydrochloric acid lowered intraocular pressure in unanesthetized rabbits. Aqueous humor flow was reduced by approximately 50%, as measured by the iodide method and as calculated from tonographic data. Outflow facility, episcleral venous pressure, plasma osmolality, blood pressure, pulse, and body temperature were not altered by systemic acidosis. Systemic alkalosis induced by intravenously administered sodium bicarbonate was associated with an increased intraocular pressure. Aqueous humor flow following systemic alkalosis was increased by approximately 100%, as measured by the iodide method and as calculated from tonographic data. Alkalosis was not associated with alterations in outflow facility, episcleral venous pressure, plasma osmality, blood pressure, pulse, or rectal temperature.
Compared with normal individuals, patients with primary open-angle glaucoma have increased prevalences of HLA-B12 and B7 antigens and are more responsive to glucocorticoids. Lymphocytes from both ocular normotensive and glaucomatous individuals with the HLA-B12 antigen require significantly (P less than .02) lower concentrations of prednisolone to inhibit phytohemagglutinin-induced transformation.
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Systemic absorption has been reported after the use of corticosteroid eye drops. Prolonged use could result in adrenocortical insufficiency and an associated adrenal crisis under stressful situations. For that reason, we studied the hypothalamic-pituitary-adrenal axis of patients receiving corticosteroid eye drope. Fifteen patients were given 0.1% dexamethasone sodium phosphate eye drops, one drop (approximately 1/30 ml) to each eye four times a day for six weeks. This dosage resulted in partial adrenal suppression, manifested by reduced levels of plasma cortisol. However, in each case, the hypothalamic-pituitary-adrenal axis, as evaluated with the use of the oral metyrapone tartrate test, was intact.
A retrospective review was conducted of 31 patients with bilateral elevations of intraocular pressure and unilateral glaucomatous visual field loss. Nine (29%) of the fellow eyes developed visual field loss during a three- to seven-year follow-up period. Of the 13 fellow eyes that had an initial intraocular pressure greater than 26 mm Hg, eight (62%) developed visual field loss, as opposed to one (6%) of the 18 eyes that had lower intraocular pressures. Of the 11 fellow eyes whose intraocular pressures exceeded 24 mm Hg, either treated or untreated, on more than 50% of the measurements, seven (64%) lost visual field, whereas in the 20 eyes whose intraocular pressures were lower, only two )10%) lost visual field.
Eighty patients with ocular hypertension (intraocular pressure greater than 20 mm Hg) and GG-response to topical corticosteroids (over 31 mm Hg after six weeks of topical dexamethasome 0.1% four times a day) were tested for ocular hypotensive response to topical epinephrine. Of 80 patients observed for five to ten years, 20 (25%) developed gluacomatous visual field defects, and 34 (43%) were "responders" to topical epinephrine (IOP reduction of greater than 5 mm Hg). Of 20 patients who developed glaucomatous visual field defects, 17 (85%) had responded to topical epinephrine, but only 28% of those who did not have visual field defects showed this type of epinephrine response. Of 34 epinephrine responders, 17 (50%) developed glaucomatous visual field defects as compared to three of 46 (6.5%) nonresponders. The initial applanation IOP level proved less valuable as a prognostic indicator.