PubMed Health⌕ Search

Biomedical subjects

B Becker

Publications and source records attributed to B Becker.

At least 253 records · Page 14Linked to original sources
PubMed1977

Glucocorticoid responsiveness associated with HLA-B12.

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.

Aged↗
PubMed1977

HLA antigens and primary open-angle glaucoma in black Americans.

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.

Black People↗
PubMed1977

The ocular hypotensive effect of epinephrine in high and low corticosteroid responders.

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.

Administration, Topical↗
PubMed1977

Acidosis, alkalosis, and aqueous humor dynamics in rabbits.

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.

Acidosis↗
PubMed1976

HLA antigens and corticosteroid response.

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.

Glaucoma↗
PubMed1976

Topical corticosteroid therapy and pituitary-adrenal function.

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.

Administration, Topical↗
PubMed1976

Prognostic factors in glaucomatous visual field loss.

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.

Female↗
PubMed1976

Response to topical epinephrine. A practical prognostic test in patients with ocular hypertension.

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.

Administration, Topical↗
PubMed1976

Long-term epinephrine therapy of ocular hypertension.

Nineteen patients with symmetrical ocular hypertension and symmetrical cupping of the optic nerves were made asymmetric with respect to intraocular pressure for one to five years by unilateral topical treatment with epinephrine hydrochloride. Development of glaucomatous visual field defects was observed in 32% of the untreated eyes and in none of the treated eyes (P less than .05). Progressive cupping of the optic nerve was noted in 53% of the untreated eyes and in 11% of the treated eyes (P less than .025). Evidence of glaucomatous damage was observed more frequently in subjects maintained on this regimen for longer periods and in subjects with initial horizontal cup/disc ratios greater than 0.4 (P less than .05). None of the eyes, either treated or untreated, with mean intraocular pressures less than 24 mm Hg developed glaucomatous damage during the period of this study.

Administration, Topical↗
PubMed1976

The prognostic value of HLA-B12 and HLA-B7 antigens in patients with increased intraocular pressure.

The presence of the histocompatibility antigens HLA-B12 or HLA-B7 in 76 patients with increased intraocular pressure and a GG response to topical corticosteroids (intraocular pressure over 31 mm Hg after six weeks of topical 0.1% dexamethasone eyedrops, four times daily) correlated with the development of glaucomatous visual field loss. In close agreement with prevalences in patients with primary open-angle glaucoma, 14 (88%) of the 16 patients with increased intraocular pressure and a GG response who developed glaucomatous visual field loss had either HLA-B12 or B7 antigens. Fourteen (41%) of 34 patients with increased intraocular pressure and a GG response who had B12 or B7 antigens developed glaucomatous visual field loss but only two (5%) of 42 similar patients without either antigen had visual field loss. Other factors such as the initial intraocular pressure, the horizontal cup/disk ratio, and family history of glaucoma proved less valuable as prognostic indicators in this series.

Adrenal Cortex Hormones↗
PubMed1976

Increased intraocular pressure after third ventricle injections of prostaglandin E1 and arachidonic acid.

Prostaglandin E1 administered into the third ventricle of rabbits produced increased intraocular pressure and body temperature. Similar responses were observed after third ventricle instillation of arachidonic acid, a precursor of prostaglandin E2. Increase of body temperature occurred with lower doses of prostaglandin E1 and arachidonic acid while the intraocular pressure response required larger amounts of these drugs. Pretreatment with aspirin rectal suppositories had no effect on the third ventricle responses induced by prostaglandin E1. Aspirin pretreatment before third ventricle instillation of arachidonic acid blocked the increases of intraocular pressure and temperature.

Animals↗
PubMed1976

Relative afferent pupillary defect in glaucoma.

Seven patients with asymmetrical open-angle glaucoma had relative afferent pupillary defects. This defect may have occurred during any stage of glaucoma, but the presence of this sign may be indicative of the earliest onset of optic nerve damage in patients with ocular hypertension. Although the presence of an afferent pupillary defect should suggest the consideration of a neurologic lesion, glaucomatous damage may be the sole explanation for this phenomenon.

Adult↗
PubMed1976

The effects of dipivalyl epinephrine on the eye.

We treated one eye each of ten patients with ocular hypertension with dipivalyl epinephrine (DPE), a congener of epinephrine. Pupil size and intraocular pressure were measured before and at intervals up to 240 minutes after instillation of a single drop of DPE in concentrations from 0.005 to 0.5%. Concentrations of 0.025% DPE and greater significantly reduced IOP, and mydriasis was induced by concentrations of 0.1% DPE or greater. Comcentrations of 0.1% DPE, instilled twice daily for one month, significantly reduced intraocular pressure during diurnal testing on days 2 and 31. No toxic side effects were noted. The DPE produced dose-related increases of cyclic adenosine monophosphate in the aqueous humor of rabbits.

Animals↗
PubMed1976

Positive FTA-ABS tests in subjects with corticosteroid-induced uveitis.

Of 17 subjects who developed severe anterior nongranulomatous uveitis during or immediatelyy after testing with topical corticosteroid preparations, 14 (82%) had a positive fluorescent-treponemal-antibody absorption (FTA-ABS) test. No association was found between corticosteroid-induced uveitis and any specific HL-A locus.

Adrenal Cortex Hormones↗
PubMed1976

Plasma cortisol suppression test used to predict the development of primary open-angle glaucoma.

Forty patients classified as high responders (GG) to dexamethasone testing (intraocular pressure greater than 31 mm Hg) without visual field loss were subjected to plasma cortisol suppression testing. After a five-year follow-up adequate data were available on 35 patients. Eighteen responded to 1.0 mg of dexamethasone-diphenylhydantoin suppression testing in a similar fashion to patients with primary open-angle glaucoma while 17 responded in a similar fashion to subjects classified as low (NN, intraocular pressure less than 20 mm Hg) and intermediate (NG, intraocular pressure 20 to 31 mm Hg) responders to dexamethasone testing. Eight of the 35 patients developed glaucomatous visual field loss during the follow-up period. These eight patients were not more sensitive to suppression of plasma cortisol than the 27 patients maintaining normal visual fields. Thus, plasma cortisol suppression testing failed to predict the development of primary open-angle glaucoma in GG responders.

Dexamethasone↗
PubMed1976

Valve implants in filtering surgery.

A valve implant for glaucoma incorporated upper and lower intraocular pressure limits for outflow. The device consisted of an open Supramid tube sealed to a Silastic tube with a slit valve. The valve implants had opening pressures of 11 to 16 mm Hg and closing pressures 1 to 3 mm Hg lower. A surgical technique was developed in monkey eyes and applied later in modified form to three patients with glaucoma. In four of seven monkey eyes the implants remained in place and were patent for over one year. Follow-up studies were carried out for over six months in the three patients. In two patients the valve implants were functioning with controlled intraocular pressures. In one patient the implant migrated posteriorly. This was replaced by using a new valve and a buried fixation suture and has since functioned without problem. The valve implants were well tolerated and offered possibilities for predictable intraocular pressures after glaucoma surgery.

Adolescent↗