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Biomedical subjects

A Béchetoille

Publications and source records attributed to A Béchetoille.

At least 19 recordsLinked to original sources
PubMed2000

[Correlation between neuroretinal rim and optic disc areas in normal melanoderm and glaucoma patients].

BACKGROUND: To evaluate optic disc size and its relationship with neuroretinal rim areas. MATERIAL AND METHODS: The study was prospective; 400 hundred patients with 292 glaucomatous and 108 non glaucomatous were enrolled in this study. Optic disc size quantification was assessed by the use of Goldmann 3 mirror contact lens; diameter reading were adjusted by the magnification factor of the lens, squares of the disc and the cupping were calculated using an ellipse formula, the neuroretinal rim area was then obtained by reducing the cupping area from the whole optic disc area. RESULTS: The mean age of the sample was 36.80 years (sd: 15.68 years).The average value of the vertical disc diameter was 2.045 mm (sd: 0.254) for glaucoma patients and 1.966 mm (sd: 0.237) in the control group; p<0.001. Neuroretinal rim area was 1.886 mm(2) (sd: 0.675) in the glaucoma group; and 2.165 mm(2) (sd: 0.425) in the control one; p<0. 004. In the glaucoma group, 72.97% of large optic disc were found (vertical diameter over 1.90 mm); and 63.80% in the control one. In the control group, neuroretinal rim area was wider in the large optic discs compared to the small discs, p<0.001, Anova test. Neuroretinal rim area was thinner in the glaucoma large disc compared to the control, p<0.005, Student test. Meanwhile, there was no difference in the medium and the small discs in the glaucoma and control groups; p > 0.005, Student Newmann test. CONCLUSION: Neuroretinal rim areas are thinner in the large glaucoma discs compared to the non glaucoma large discs. In Africa, this parameter could be helpful in the diagnosis and survey of glaucoma patients.

Adolescent↗
PubMed1999

Ocular surface inflammatory changes induced by topical antiglaucoma drugs: human and animal studies.

OBJECTIVES: To investigate conjunctival and trabecular specimens from patients with glaucoma according to the duration and number of drugs received before filtration surgery, and to confirm, in a complementary experimental model, the role of preservative by comparing the effects of preserved and nonpreserved timolol. STUDY DESIGN: Experimental animal and human tissue study. PARTICIPANTS: Paired specimens of conjunctiva and trabeculum were taken from 61 patients undergoing trabeculectomy. Twenty-six patients were treated with 2 or more drugs for at least 1 year; 30 had received a beta-blocker for more than 1 year and 5 underwent primary surgery. A second study was performed in 25 rats receiving topical solutions in both eyes for 1 month. INTERVENTION: Immunohistochemistry was performed in all biopsy specimens using 12 different monoclonal antibodies. Ocular structures from rats treated for 1 month with preserved 0.5% timolol, nonpreserved 0.5% timolol, or 0.01% benzalkonium chloride were similarly investigated in an experimental study. MAIN OUTCOME MEASURES: Inflammatory cell infiltrates and fibroblasts were evaluated in biopsies, as well as in animal specimens, together with histologic changes induced by the drugs applied. RESULTS: Twenty-four of 26 conjunctivae and 21 of 24 trabecular pieces from multitreated patients were found to be abnormally infiltrated by cells expressing inflammatory or fibroblastic markers or both. Nineteen of 30 conjunctivae and 9 of 22 trabeculums in the monotherapy group and only 1 of 5 specimens from the primary surgery group were abnormal. In rats, preserved timolol and benzalkonium similarly showed infiltrates together with toxic histopathologic changes as compared to the nonpreserved timolol and control groups. CONCLUSIONS: These two combined studies confirmed histopathologic effects of antiglaucomatous drugs on the conjunctiva and showed similar effects in the trabecular meshwork. The experimental study showed that benzalkonium chloride is at least, to a large part, responsible for these toxic or immunoinflammatory effects or both on the ocular structures.

Administration, Topical↗
PubMed1999

[Cytomegalovirus retinitis and ocular complications in AIDS patients in Togo].

BACKGROUND: Cytomegalovirus retinitis seems to be an uncommon complication in African AIDS patients. This study was conducted in 200 patients in order to evaluate AIDS eye related complications with specific focus to cytomegalovirus retinitis. MATERIAL AND METHODS: During a period of 20 months, 200 patients (83 men and 117 women) presenting WHO AIDS case definition diagnosis were enrolled for a complete ocular examination comprising external, anterior segment and retinal fundus and fluorescein angiographic examination. RESULTS: For the whole, 200 patients underwent ocular examinations; of them 121 (60.5%) developed ocular complications. The most frequent complications were cotton wool spots (25.5%), cytomegalovirus (CMV) retinitis (21.5%), retinal hemorrhage (6%), papilloedema (3%), chorioretinal toxoplasmosis (3%), peripheral retinal vascularitis (2. 5%), herpes zoster ophthalmicus (2%). Among those with CMV retinitis, bilateral lesions were found in 30 cases, and unilateral ones in 13 cases. Poor vision was associated with the presence of CMV retinitis in 88% of cases. Death occurred in a mean range of 22 days after the "presumed" diagnosis of CMV retinitis. CONCLUSION: Cytomegalovirus retinitis represents the second ocular complication in AIDS patients in this study. Poor visual outcome was associated in 88% of cases. These results demonstrate that in some west African countries, CMV retinitis may be a common complication in AIDS patients.

AIDS-Related Opportunistic Infections↗
PubMed1997

Recurrent mutations in a single exon encoding the evolutionarily conserved olfactomedin-homology domain of TIGR in familial open-angle glaucoma.

Primary open-angle glaucoma (POAG) is a highly prevalent cause of irreversible blindness which associates cupping of the optic disc and alteration of the visual field, elevation of intraocular pressure being a major risk factor. Provided diagnosis is made at an early stage, treatments are available to prevent visual impairment. A locus, GLC1A, has been mapped on chromosome 1q23-q25 in several families affected with juvenile-onset POAG (JOAG) and also in some families affected with juvenile and middle-age onset POAG. Recently, three mutations of the TIGR (Trabecular meshwork-Induced Glucocorticoid Response) gene were shown to be responsible for the disease in several American families and in unrelated POAG patients. We now describe five new mutations in eight French families. All mutations known to date appear to concentrate in the evolutionarily conserved C-terminal domain of TIGR which bears homology to frog olfactomedin, an extracellular matrix glycoprotein of the olfactory epithelium, to rat and human neuronal olfactomedin-related proteins and to F11C3.2, a protein from Caenorhabditis elegans . Moreover, this conserved domain of TIGR is encoded by a single exon to which mutation screening could be limited. Surprisingly, the TIGR message, which is abundantly transcribed in the trabecular meshwork and also in the ciliary body and the sclera, is not expressed in the optic nerve whose degeneration is, however, the primary lesion of POAG.

Adolescent↗
PubMed1997

Genetic heterogeneity of primary open angle glaucoma and ocular hypertension: linkage to GLC1A associated with an increased risk of severe glaucomatous optic neuropathy.

The GLC1A locus for autosomal dominant juvenile and middle age onset primary open angle glaucoma (OAG) has been mapped to chromosome 1q21-q31. OAG, however, is a heterogeneous disease. We tested linkage of OAG and ocular hypertension (OHT), a major risk factor for OAG, to GLC1A in eight French families with multiple cases of juvenile and middle age onset OAG. There was strong evidence of genetic heterogeneity, four families being linked to GLC1A and two or three others being unlinked, depending on whether the complete OAG phenotype was analysed alone or jointly with OHT. Peak intraocular pressure (IOP) did not differ significantly between the two groups of families, while linkage to GLC1A conferred a highly increased risk of developing OAG and of having severe glaucomatous optic neuropathy. Testing linkage of familial OAG to GLC1A may therefore have prognostic value too.

Adult↗
PubMed1996

Age-dependent penetrance and mapping of the locus for juvenile and early-onset open-angle glaucoma on chromosome 1q (GLC1A) in a French family.

The GLC1A locus for autosomal dominant primary open-angle glaucoma (POAG) with juvenile onset (before 20 years) has been mapped to chromosome 1q21-q31. Recently, a French-Canadian family was described in which both juvenile-onset and middle-age or early-onset POAG were observed and linked to GLC1A. We now describe a second POAG family with variable age of onset (range 11-51, median 36 years of age). Linkage to GLC1A was established with a maximum lod score of 6.21 at the D1S452 locus. A recombination event in a severely glaucomatous patient restricted the distal boundary of the GLC1A interval proximal to the AFM154xc9 marker. This study strengthens the idea that early-onset POAG may also be determined by the GLC1A genetic region.

Adolescent↗
PubMed1996

Vascular risk factors in glaucoma.

The role of the villain in high-pressure glaucoma is played by ocular hypertension. Alterations of lamina cribosa, other mechanical alterations, and a possible loss of optic nerve head capillaries are all accountable, and from a therapeutic standpoint most clinicians readily perceive that lowering ocular pressure is the single most important management goal and are satisfied with such results. Yet, when confronted with normal intraocular pressure, other perturbing factors or at least other accomplices must be studied; in this case, an ischemic origin becomes the primary suspect, potentially engendering therapeutic consequences of a different nature.

Animals↗
PubMed1995

[Acute angle-closure glaucoma].

Acute angle-closure glaucoma is an ocular disorder essentially linked to specific anatomical formations, particularly hereditary, in which, as of a critical age and influenced by random triggering factors, unilateral or bilateral blockage of the pupil occurs. This leads to closing of the iridocorneal angle followed by severe ocular hypertonia and, if emergency treatment is not begun, to severe complications of the eye and the vision. Treatment is first by osmotic agents (acetazolamide), beta-blocking collyria and myotic agents, followed obligatorily by surgical or laser iridectomy of the affected eye, then of the other eye as a preventive measure.

Acute Disease↗
PubMed1995

[Arterial hypotension in glaucoma of normal or moderately high pressure].

BACKGROUND: Arterial hypotension, by decreasing blood flow in the optic nerve head, may be a risk factor for glaucomatous damage. The purpose of this study was to compare blood pressure in different types of glaucoma patients, using ambulatory recording. METHODS: An ambulatory blood pressure recording was performed in 55 glaucoma patients over a 24-hour period. Two groups of patients could have been differentiated according to pretreatment intra-ocular pressure level: a group of 38 patients (GPNM) with normal or moderately elevated intra-ocular pressure, and a group of 17 patients (GPH) with high intra-ocular pressure. RESULTS: A statistically significant different lower blood pressure was found in group GPNM for: diastolic mean blood pressure (76.4 versus 81.4 mmmHg p = 0.05), diastolic nocturnal (71.8 versus 78.1 mmHg p = 0.025), and for some hourly intervals: from 2:00 to 3:00 (p = 0.008), 8:00 to 9:00 (p = 0.01) and 15:00 to 18:00 (p = 0.03). The mean lowest readings were lower (p < 0.05) in group GPNM (95.8/54.4 versus 102/59.9 mmHg). The percentage of low readings (9.9% versus 5.1% p = 0.01) and systolic drops (0.226 versus 0.192 p = 0.018) were also higher in this group. CONCLUSION: Hypoperfusion of optic nerve head may be a significant factor in glaucomatous damage by compromising blood supply. It is important to identify arterial hypotension when examining of normal or moderately elevated pressure glaucoma patients, and ambulatory monitoring of blood pressure is currently the best test. These episodes should be taken into consideration, especially when initiating systemic antihypertensive therapy, in order to maintain, as well as possible, perfusion of the optic nerve head.

Blood Pressure Monitoring, Ambulatory↗
PubMed1995

[Toxicity of 5-FU].

Explore the source record for details and available documents.

Administration, Topical↗
PubMed1994

Diurnal and nocturnal blood pressure drops in patients with focal ischemic glaucoma.

BACKGROUND: The purpose of this study was to assess the role of arterial hypotension in the pathogenesis of certain types of glaucoma. METHODS: We compared diurnal and nocturnal fluctuations in blood pressure by using an ambulatory recording over a 24-h period in two different groups of patients: one of 16 patients with focal ischemic glaucoma (FIG) and another of 16 patients with primary open angle glaucoma (POAG). RESULTS: In patients with FIG, compared to those with POAG, we found: lower diastolic blood pressure (BP; 75.7 vs 82.5 mmHg, P < 0.05), systolic BP (121.7 vs 131.2 mmHg, P < 0.05) and mean BP (90.5 vs 101.5 mmHg, P < 0.05) over 24 h; lower diurnal diastolic BP (78.1 vs 85.5 mmHg, P < 0.05), and systolic BP (124.6 vs 134.2 mmHg, P < 0.05); greater nocturnal systolic BP variability (8.2% vs 6.2%, P < 0.05); and a greater percentage of diurnal low readings (14.53% vs 2.8%, P < 0.05), compared with the literature limits (101/61 mmHg). However, the number of nocturnal low readings was not different for either group. CONCLUSION: It is important to detect arterial hypotension - one of the components of the vascular factor - during examination of a patient with normal-pressure glaucoma. This is one element in preserving the best possible perfusion of the optic nerve.

Adult↗
PubMed1994

[Linkage between juvenile glaucoma and chromosome 1q in 2 French families].

Primary open-angle glaucoma is a major cause of irreversible blindness in Western countries for which there is presently no curative treatment. Linkage of hereditary juvenile glaucoma with chromosome 1q21-q23 was recently described in 2 American families. Here we have studied two large French pedigrees with a similar form of familial autosomal dominant juvenile-onset glaucoma. Linkage of glaucoma with chromosome 1 was confirmed in these 2 families. Maximal lod-score of 7.60 was reached at the D1S212 marker for a recombination fraction of 4.4%. The typing of this marker should facilitate the screening of glaucoma families and the identification of individuals at risk for the disease. It will also provide a reference to evaluate the genetic heterogeneity of glaucoma.

Adolescent↗
PubMed1992

Sezolamide: additivity to timolol twice daily.

Sezolamide, a potent topical carbonic anhydrase inhibitor previously known as MK-417, was studied to determine its ocular hypotensive activity in patients with elevated intraocular pressure while on continuing therapy with topical timolol. This was a three-centre, double-masked, randomised, placebo-controlled, parallel study in 36 patients with bilateral primary open angle glaucoma or ocular hypertension on therapy receiving 0.5% timolol twice daily, with a morning intraocular pressure greater than or equal to 22 mmHg in both eyes 2-4 hours following an 8 a.m. dose of timolol. Sezolamide 1.8% or placebo twice daily was added to treatment with timolol on the evening of day 1 and continued for 2 weeks. Twelve-hour diurnal curves were performed before the study on day 1 (timolol alone) and on day 15. Intraocular pressure measurements were also taken on days 2 and 8 at 8 a.m. and 9 a.m. Patients who received timolol and sezolamide showed additional intraocular pressure reductions from day 1 (timolol alone) of 8.0 to 15.5%, which were significant at all times. At hours 1, 2, 4 and 8 the reductions in intraocular pressure observed in the group receiving sezolamide and timolol were significantly greater than those in the group receiving timolol and placebo.

Aged↗
PubMed1991

[Additive effect of timolol and the local carbonic anhydrase inhibitor MK-417 (sezolamide)].

MK-417 (sezolamide) is a topically active carbonic anhydrase inhibitor. The effect of additional treatment with sezolamide 1.8% twice daily to patient already receiving timolol 0.5% twice daily was investigated. For this purpose, 12-h diurnal curves were used in a double-masked, randomized, placebo-controlled, parallel study in 36 patients with bilateral primary open angle glaucoma or ocular hypertension who during beta blocker therapy had intraocular pressures (IOP) greater than or equal to 22 mmHg. For 15 days patients received sezolamide or placebo 10 min after 0.5% timolol given at 8 a.m. and 8 p.m. On treatment day 15, this addition of sezolamide twice daily induced a further mean decrease in IOP of approximately 4 mm Hg (about 15%) at 1, 2 and 4 h and of approximately 2-3 mm Hg at 0, 6, 8, 10 and 12 h after drug administration, thus demonstrating a partial additive effect of sezolamide and timolol. Thus, sezolamide may be a useful addition to the treatment of glaucoma in patients not adequately controlled by beta blocker therapy.

Aged↗