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PubMed1985

Metabolism of fluorescein after intravenous administration.

The measurement of plasma unbound (free) fluorescein is important in the study of blood-ocular barrier kinetics. The authors became concerned about the quantitative significance of the presumed glucuronide metabolite of fluorescein to the measurement of plasma fluorescence in diabetic and normal subjects. Fluorescein was given intravenously (14 mg/kg) to seven normal subjects and eight diabetic subjects. Plasma samples taken during 60 min were subjected to microfiltration, from which aliquots of ultrafiltrate were incubated with beta-glucuronidase. Samples were subjected to high-performance liquid chromatography, and fluorescence activity was measured in the eluent. All subjects showed an additional fluorescence peak to that of fluorescein in plasma and ultrafiltrate 5 min after fluorescein administration and increased thereafter. This additional peak was abolished by incubation of ultrafiltrate with beta-glucuronidase and resulted in a marked increase in fluorescence due to the liberation of fluorescein from its presumed glucuronide. There were no pharmacokinetic differences between normal and diabetic subjects in plasma-free fluorescein and fluorescein glucuronide pharmacokinetics or in their respective binding to plasma proteins. The glucuronide had only 4.5% of the fluorescence of fluorescein, but because more of the glucuronide was unbound (32%) compared with fluorescein (10%) and its concentration increased while that of fluorescein decreased, it constituted an increasing proportion of the fluorescence in the ultrafiltrate. At 60 min, 80% of the fluorescein was present as glucuronide and contributed 20% of the total fluorescence in the ultrafiltrate. Fluorescein-glucuronide is a potential source of variability in studies on blood-ocular barrier kinetics.

Adult↗

PubMed1998

The effect of acetazolamide on passive and active transport of fluorescein across the blood-retina barrier in retinitis pigmentosa complicated by macular oedema.

BACKGROUND: The carbonic anhydrase inhibitor acetazolamide (AZM) reduces macular oedema in some patients with retinitis pigmentosa. To better understand the oedema-reducing effect of AZM, the effect of AZM on passive permeability and active transport of fluorescein across the blood-retina barrier was studied in patients with retinitis pigmentosa and varying degrees of macular oedema. METHOD: The selection of patients was based on an introductory examination including vitreous fluorometry for qualitative assessment of the vitreous. Macular oedema was graded by fluorescein angiographic leakage. The effect of AZM on the transport properties of the blood-retina barrier was determined by differential spectrofluorometry, in a randomised, double-masked, cross-over study, comprising 2 weeks' treatment with AZM (500 mg/day) and 2 weeks' treatment with placebo. The penetration ratio, defined as the ratio between vitreous concentration 3 mm in front of the retina and the plasma integral, was determined for fluorescein and its metabolite fluorescein glucuronide at 30-60 min and at 120 min after fluorescein injection. Passive permeability and unidirectional permeability in the direction vitreous to blood, due to outward active transport of fluorescein, were determined in those cases where the curves for vitreous concentration of fluorescein could be fitted to a mathematical model. Visual acuity was tested by use of ETDRS standard logarithmic charts. RESULTS: Twenty-two patients volunteered to participate in the study. Signs of significant vitreous detachment/liquefaction caused the exclusion of ten patients after the introductory examination. Nine patients with approximately intact vitreous and varying degrees of oedema completed the cross-over study. AZM treatment was related to a decrease in the penetration ratio of 21% for fluorescein (P=0.01) and of 22% for fluorescein glucuronide (P=0.004). Passive permeability and unidirectional permeability were determined in seven patients. AZM caused a decrease of 27% in the passive permeability of fluorescein (from 1.1 x 10(1) nm/s, P=0.031), and a 95% increase in unidirectional permeability of fluorescein (from 1.2 x 10(2) nm/s, P=0.047). AZM led to a reduction in the grade of macular oedema as determined by fluorescein angiography in three out of seven patients. Only small improvements (< or =5 letters) in visual acuity were noted. CONCLUSION: The present study indicates that the oedema-reducing effect of AZM is due to decreased leakage and stimulated active transport across the blood-retina barrier.

Acetazolamide↗

PubMed1990

[Fundus video fluorescein angiography with low steady light].

To decrease both the intensity of the exciting light and the amount of sodium fluorescein, we attached a compact image intensifier incorporating a microchannel plate with a fundus photoscope and tried to record video-fluorescein angiography with low steady light. We preliminarily examined the relationships of exciting and emitted light intensity with various concentrations of sodium fluorescein. The strongest fluorescence was obtained with a concentration of 0.01 mg/ml solution of sodium fluorescein. When the compact image intensifier was attached to the equipment, the exciting light intensity could be decreased to 1/300 with an exciting filter of lambda max of 486 nm. When sodium fluorescein of 0.01 mg/ml solution was injected directly into the heart of Rana catesbeiana, complete video-fluorescein angiography with sufficient brightness and resolution was possible. With the same machine, we recorded video-fluorescein angiography in a normal human subject with injection of 5 ml of 10% sodium fluorescein. The ordinary observing light of the machine was strong enough for video-recording. This exciting light intensity caused no trouble and elicited no complaint from the examinee. These results showed that the use of a compact image intensifier incorporated microchannel plate with a fundus photoscope made it possible to record video-fluorescein angiography and to decrease exciting light intensity and the amount of fluorescein dye. This means that light damage to photoreceptors by exciting light and problems induced by allergic reaction with fluorescein dye might be decreased. These aspects might be very important to obtain information about both retinal circulation and disruption of the blood-retinal barrier and also to perform safe fluorescein angiography examination.

Animals↗

PubMedDate not supplied

Fluorescein angiography and adverse drug reactions revisited: the Lions Eye experience.

BACKGROUND: The last major survey of adverse reactions to intravenous fluorescein angiography was performed more than 20 years ago. There have been two recent fatalities involving intravenous fluorescein in Australia. It is important to review the current incidence of adverse reactions and latest literature on the pathogenesis, prophylaxis and alternatives to intravenous fluorescein angiography. METHODS: A retrospective review of all adverse reactions to intravenous sodium fluorescein in patients undergoing fluorescein angiography between June 1998 and June 2004 was undertaken. The total number of fluorescein angiograms performed and the number of patients with adverse reactions were identified from the photographic department database and the fluorescein adverse reaction register at the Lions Eye Institute. RESULTS: A total of 11 898 fluorescein angiograms were performed during the study period. There were 132 adverse reactions recorded. The commonest adverse reactions were nausea and vomiting. There were no serious adverse reactions or deaths recorded. There was a statistically significant difference in the incidence of adverse reactions between sodium fluorescein used from two manufacturers. CONCLUSIONS: Fluorescein angiography is a relative safe procedure and comparable to other intravenous radiocontrast media angiography or investigation. The present results are consistent with previous studies. Prophylactic treatment, fluorescein desensitization or oral fluorescein angiography should be considered in high-risk patients. Safe guards should be in place to manage potential serious adverse reactions. Other imaging techniques, like optical coherence tomography, should be considered as an alternative in selected cases.

Adverse Drug Reaction Reporting Systems↗

PubMed2001

Transport of fluorescein in MDCKII-MRP1 transfected cells and mrp1-knockout mice.

The multidrug resistant-associated protein 1 (MRP1) is a membrane-bound transport protein that is involved in the efflux of organic anions and has been implicated in multidrug resistance in cancer. MRP1 has also been reported to be ubiquitously expressed in normal tissues, including the brain. The presence of functional organic anion transporters in the blood-brain and blood-CSF barriers that influence the distribution of various compounds to the brain has long been known. The purpose of this study was to examine the role of MRP1 in the brain distribution of a model organic anion, fluorescein. The substrate specificity of MRP1 for fluorescein was initially determined by examining the accumulation of fluorescein in MDCKII MRP1-transfected cells. The distribution of fluorescein in the brain was then examined in wild-type and mrp1 gene knockout mice. The results show that in MDCKII MRP1-transfected cells, the accumulation of fluorescein was significantly lower (about 40% lower) than that in wild-type MDCKII cells. MRP1 inhibitors such as probenecid, MK-571, and LY402913 enhanced fluorescein accumulation in MDCKII MRP1-transfected cells to a greater extent than in wild-type MDCKII cells. In an in vivo study, after intravenous injection of fluorescein, the fluorescein brain-to-plasma concentration ratio in mrp1 knockout mice was not significantly different than that in wild-type mice. However, when probenecid was co-administered with fluorescein in wild-type mice, the fluorescein brain-to-plasma ratio was significantly increased (1.5-fold). These findings suggest that fluorescein is a substrate for MRP1. Furthermore, the in vivo study also suggests that MRP1 has a limited role in the transport and distribution of fluorescein in the brain. Therefore, other organic anion transport proteins, including the various isoforms of the MRP family, may be responsible for the accumulation and transport of organic anions in the brain.

ATP-Binding Cassette Transporters↗

PubMed1997

Excretion of fluorescein in the urine of women with interstitial cystitis.

PURPOSE: Altered bladder permeability may have a role in the pathogenesis of interstitial cystitis. Fluorescein, a fluorescent dye of molecular weight 325, has been used to assess membrane permeability. Orally ingested fluorescein normally is rapidly conjugated to glucuronate by the liver and excreted in the urine. MATERIALS AND METHODS: To test its use as a marker of bladder permeability, we administered fluorescein orally to 6 patients with interstitial cystitis who satisfied National Institutes of Health, National Institute for Diabetes and Digestive and Kidney Diseases criteria and to 6 normal female control subjects. After emptying the bladder and collection of a baseline blood sample, fasted subjects ingested 20 mg. fluorescein and blood samples were collected 1, 2, 3, 4 and 24 hours later. Urine was collected during each of the first 4 hours, and then from 4 to 10, 10 to 16 and 16 to 24 hours. Urine volume was measured, and all plasma and urine samples were analyzed for fluorescein. RESULTS: Plasma fluorescein concentrations (ng./ml.) were significantly (p < 0.05) higher in interstitial cystitis patients than in control subjects at 1 and 2 hours after fluorescein ingestion. Urine fluorescein excretion (mg.) was significantly (p < 0.05) lower in interstitial cystitis patients than in control subjects at 4 to 10 hours after fluorescein ingestion, and for the entire 24 hours. CONCLUSIONS: The increased fluorescein concentration in the plasma and decreased excretion in the urine of interstitial cystitis patients suggest that fluorescein may be a useful marker of altered membrane permeability.

Adult↗

PubMed1981

Intracellular binding of fluorescein in lymphocytes.

The fluorescence characteristics of intracellular fluorescein, formed by the hydrolysis of fluorescein diacetate in peripheral human lymphocytes, were studied by fluorometry on cell suspensions and compared to those of albumin bound and free fluorescein in solution. The absorption and fluorescence spectra of both intracellular fluorescein and fluorescein in aqueous solutions of albumin and glycerol were red shifted by 2-10 nm as compared to the spectra of fluorescein in phosphate buffered saline. The fluorescence polarization (P) of both intracellular fluorescein and a mixture of albumin-bound and free fluorescein showed a decrease towards low emission wavelengths and an increase toward high excitation wavelengths. The results were found to be consistent with a simple model assuming that part of the intracellular fluorescein is dissolved in the aqueous phase of the cytoplasm, giving P less than 0.1, while the rest is bound to macromolecules, giving P = 0.33. The fraction of bound intracellular fluorescein was estimated to be about 70%. Fluorescein was found to bind with high affinity and more rigidly (P = 0.43) to albumin than to intracellular macromolecules in general.

Blood Proteins↗

PubMed1989

Characterization by flow cytometry of fluorescein-methotrexate transport in Chinese hamster ovary cells.

We have studied by flow cytometry the transport of fluorescein-methotrexate in Chinese hamster ovary cells. Fluorescein-methotrexate appears to enter cells via a mechanism different from the carrier-mediated system for methotrexate. This conclusion is supported by the following observations: 1) Fluorescein-methotrexate is transported equally well into normal and mutant cells defective in the inward methotrexate uptake. 2) Folic acid and its reduced states, which competitively inhibit methotrexate uptake, do not alter fluorescein-methotrexate transport. 3) Fluorescein-methotrexate accumulation exhibits a low temperature coefficient (Q10 = 1.6) compared with the influx of methotrexate (Q10 = 6-8). 4) Initial rates of fluorescein-methotrexate uptake are concentration dependent but are not saturable. 5) Fluorescein-methotrexate uptake is very slow and reaches steady state after 8 h, whereas at an equimolar concentration methotrexate reaches saturation after 20 min. 6) Initial influx rates of fluorescein-methotrexate are not affected by the presence of methotrexate. 7) Sulfhydryl-reactive mercurials, which block methotrexate transport, do not reduce fluorescein-methotrexate influx, but rather stimulate it. Thus, based on the nonsaturability of fluorescein-methotrexate inward transport, its low temperature coefficient, and lack of inhibition with structural analogs, we conclude that fluorescein-methotrexate is accumulated in hamster cells by a passive diffusion process.

Animals↗

PubMed1985

Fluorescein distribution in retinas of normal and diabetic rats.

Quantitative fluorescence microscopy was used to study fluorescein distribution across the blood-retinal barrier in control and streptozotocin diabetic rats at 2 min, 1 and 2 hr after dye injection (12.5 and 125 mg kg-1 i.v.). Fluorescence intensities of choriocapillaris and retina were compared with plasma fluorescein levels. Diabetic rats had only one-half the total plasma fluorescein concentration of controls by 1 hr after injection, but the proportion of free fluorescein was greater in diabetic animals than in controls, providing the total plasma dye levels did not exceed the binding capacity of plasma proteins. Diabetic rats also had more unbound fluorescein glucuronide in plasma. With fluorescence microscopy no focal fluorescein leakage from retinal capillaries or pigment epithelium was seen in any diabetic or control eye. However, the dye was detected in retinas of diabetic and control animals at all intervals except 2 hr after injection of the lower dose when its fluorescence was too low to measure. Initial fluorescein entry occurred from the choroid by diffusion through pigment epithelial cells creating a steep intensity gradient decreasing from outer to inner retinal layers. With time this gradient flattened and then completely reversed, suggesting removal of dye from outer retinal layers and concomitant equilibration of inner layers with a pool of fluorescein in vitreous humor. Although the pattern of transretinal fluorescence distribution was similar in all rats, in specific instances, retinal fluorescence intensity differed significantly between control and diabetic animals. Fluorescence intensity was higher in diabetic than in control rats at 2 min after the 12.5 mg kg-1 dose and lower at 1 hr after the 125 mg kg-1 dose (P less than 0.05). These differences were directly related to transient differences in plasma free fluorescein concentrations, and in both cases, retinal fluorescence in diabetic rats returned to control values in conjunction with return to control levels of their plasma free fluorescein concentrations. The amount of dye detected in diabetic retinas was not in excess of normal levels at any interval after injection when related to concurrent plasma free fluorescein concentrations. These data do not indicate blood-retinal barrier dysfunction in the diabetic rat, but interpretation of the results is limited by the experimental conditions. With the high dose there was probably initial saturation of active transport mechanisms for dye removal, and with the low dose, dye distribution could not be followed to 2 hr when evidence of abnormal accumulation in retina may be more apparent.

Animals↗

PubMed1997

Fluorescein as a marker for subretinal transplantation of human fetal neural retina.

PURPOSE: To investigate the effect of fluorescein on human fetal neural retina and adult rat retina; and to use fluorescein to map the area of subretinal transplantation. METHODS: In vitro: Human fetal neural retina (8 to 14 weeks gestational age) was incubated in 0.03% fluorescein in Dulbecco's Modified Eagles Medium (DMEM) or DMEM alone for 30 min. Viability was determined using the trypan blue exclusion test, and results were compared. Effects of the fluorescein on cell morphology were assessed by observation of primary cultures for 1 week. In vivo: Human fetal neural retina was mechanically dissociated in 0.03% fluorescein in DMEM and transplanted to the subretinal space of immunosuppressed rats. To control for the effect of fluorescein on the grafted tissue, transplants were also performed in DMEM only. After transplantation, indirect ophthalmoscopy and true color fundus photography were performed to document the area covered by the transplant. One month after transplantation, the appearance of grafts exposed to fluorescein was compared to those that were not, at the light microscopic level. RESULTS: In vitro: Exposure of human fetal neural retina to fluorescein had no effect on viability. Similarly, in tissue culture, the fluorescein-exposed cells exhibited the same phenotype as the controls. In vivo: Immediately after transplantation the graft site was clearly outlined within the subretinal area and fluoresced intensely. There were no traces of the dye 2 h after transplantation. Cells that were transplanted with fluorescein survived transplantation, and one month after transplantation could be seen forming subretinal grafts. No differences were noted between these and control grafts. CONCLUSIONS: Fluorescein is an effective dye for immediate and transient localization of trans-scleral transplants to the subretinal space. It allows mapping of the area covered by the injection without interfering with the viability and differentiation of the transplanted cells. It allows unequivocal photo- and video-documentation in both the albino and pigmented fundi. It is already FDA approved for many other extra- and intraocular studies and now has directly been shown to be non-toxic to both human fetal neural retina and adult rodent retina.

Animals↗

PubMed1981

Goldmann applanation tonometry without fluorescein.

Recently, there have been several suggestions that Goldmann applanation tonometry can be performed without fluorescein. In order to determine the clinical efficacy of performing Goldmann applanation tonometry without fluorescein, 100 consecutive patients had applanation tonometry performed without fluorescein (Ophthetic only) and with fluorescein (Fluress), according to a predetermined randomization schedule. It was found that the average difference between readings with fluorescein and without fluorescein was 7.01 mm Hg. Tonometry readings without fluorescein were lower than readings with fluorescein. In addition, regression analysis indicated that the differences between the readings with and without fluorescein increased as intraocular pressure increased. By not utilizing fluorescein in Goldmann applanation tonometry, the clinician will record lower readings. In addition, greater errors in measurement occur with increasing intraocular pressures. Because eyes with higher intraocular pressures are at a greater risk to develop glaucomatous optic atrophy and loss of visual field, the merits of Goldmann applanation tonometry without fluorescein are speculative.

Fluoresceins↗

PubMed1996

Vitreous laser absorption following fluorescein angiography in diabetic patients.

BACKGROUND: Sodium fluorescein staining of the vitreous following fluorescein angiography may interact with laser photocoagulation. METHODS: We evaluated the laser absorption by fluorescein in the vitreous when photocoagulation is performed following fluorescein angiography in 15 eyes of nine diabetic patients. Axial fluorescein concentration in the vitreous was measured by a scanning vitreal fluorophotometer. The amount of light absorbed by the fluorescein within the vitreous was calculated according to the Lambert-Beer law. RESULTS: The mean fluorescein concentration ranged from 2.93 ng cm-3 to 105.16 ng cm-3 at 1 h after injection of fluorescein and from 8.03 to 188.56 ng cm-3 after 4 h. Maximum laser absorption at 488 nm ranged from 6.79% (after 1 h) to 14.53% (after 4 h); at 514.5 nm it ranged from 0.96% to 2.14%; at 532 nm it ranged from 0.03% to 0.07%. At lambda > 550 nm, laser absorption was found to be negligible. CONCLUSIONS: In order to optimize the effect of photocoagulation, especially during long photocoagulation sessions, argon blue laser (488 nm) should be avoided following fluorescein angiography. Argon green laser (514.5 nm) should be used within 1 h after fluorescein injection. Frequency-doubled Nd:YAG laser (532 nm), krypton laser (647 nm) or semiconductor diode laser (810 nm) may be used at any time.

Absorption↗

PubMed1988

Transport of fluorescein in the rabbit eye after treatment with sodium iodate.

The outward active transport and the inward permeability of the blood-retinal barrier were studied in the rabbit eye after i.v. administration of sodium iodate. The active transport was evaluated from the half-time of disappearance of the vitreous fluorescein following intravitreal administration, and the inward permeability was evaluated from the vitreous concentration of fluorescein monoglucuronide after i.v. administration. The half-time of the vitreous fluorescein was 3.5 +/- 0.3 (mean +/- S.D.) hr, and 3.9 +/- 0.2 hr before and within 6 hr after iodate administration, respectively. After 24 hr, the half-time was 11.7 +/- 1.7 hr, similar to that of fluorescein monoglucuronide, 12.0 +/- 2.7 hr. The vitreous and the anterior chamber concentration of fluorescein monoglucuronide was measured at 1 hr after the i.v. dye injection. The vitreous concentration in the rabbits given iodate 3 hr before the dye injection was significantly greater than in the normal eyes, while the anterior chamber concentration was not different. Since fluorescein is rapidly metabolized to fluorescein monoglucuronide, differences in parameters determined using systemic fluorescein under two treatments or in disease states may be the result of alteration of the dynamics of fluorescein, fluorescein monoglucuronide, or both.

Animals↗

PubMed1994

Fluorescein transport across the human blood-retina barrier in the direction vitreous to blood. Quantitative assessment in vivo.

Inward and outward movement of flourescein across the human blood-retina barrier was studied in five healthy volunteers, using a differential spectrofluorometry method that eliminates the contribution of fluorescein glucuronide to the total fluorescence in the vitreous and in plasma. The inward permeability across the blood-retina barrier, which is presumed to be passive, and the diffusion coefficient in the vitreous for fluorescein was calculated from data obtained 1 h after intravenous injection of fluorescein. The rate of elimination of fluorescein from the vitreous across the blood-retina barrier was estimated from data obtained 7 to 12 h after injection of fluorescein. The calculations were based upon the free plasma fluorescein decay curve and the preretinal fluorescein gradient in the vitreous. The mean inward permeability of fluorescein was 1.39 x 10(-7) cm/sec (range: 0.70-2.06 x 10(-7) cm/sec), whereas the mean outward permeability was 1.51 x 10(-5) cm/sec (range: 1.14-1.73 x 10(-5) cm/sec). We have thus found that the movement of fluorescein across the blood-retina barrier is highly asymmetric, the outward transport being more than 100 times faster than the passive inward leakage. This could indicate the presence of an active pumping mechanism in the blood-retina barrier, responsible for fluorescein transport in the direction from the vitreous to the blood.

Biological Transport, Active↗

PubMed1991

Measurement of the tear meniscus height using 0.25% fluorescein sodium.

Measuring the tear meniscus height (TMH) is easy after fluorescein installation, but the TMH after fluorescein instillation is higher than the TMH before fluorescein instillation. Therefore, we measured the time that the TMH after fluorescein instillation became the same with the TMH, we studied the difference in the TMH between normal eyes and dry eyes. The TMH 0.19 +/- 0.05 mm in the normal eyes and 0.10 +/- 0.04 mm in the dry eyes, and there was a significant difference between the 2 groups. The time that the TMH after fluorescein instillation became the same with the TMH before fluorescein instillation was 2.19 +/- 0.81 min. in the normal eyes and 2.29 +/- 0.73 min. in the dry eyes. Within 4 min. after fluorescein instillation, the TMH became the same with the TMH before fluorescein instillation in all cases and the height persisted until 7 min. after fluorescein instillation. Therefore, measuring the TMH will be easy if it is measured at 4-7 min. after fluorescein instillation.

Dry Eye Syndromes↗

PubMed1976

Interaction of a fluorescent reagent, fluorescein mercuric acetate, with nucleic acids.

Fluorescein mercuric acetate (fluorescein Hg Ac), which is a fluorescent thiol reagent, was shown to bind to various nucleic acids by measuring the changes in its absorption and fluorescence properties. Up to a critical concentration of free fluorescein Hg Ac (1-10(-7) M for calf thymus DNA, with 42% GC, and 2-10(-7) M for Micrococcus lysodeikticus DNA, with 72% GC) this reagent appears to bind selectively to single-stranded sections in DNA. Above this critical concentration, cooperative binding to double helical DNA occurs, and denatured DNA is obtained after removal of bound fluorescein Hg Ac by dialysis against 1 M KCl. These facts indicate that fluorescein Hg Ac causes the denaturation of double helical DNA prior to binding as has been shown in the case of methylmercuric hydroxide. The binding of fluorescein Hg Ac to DNA is much stronger than that of methylmercuric hydroxide. The number of total binding sites for fluorescein Hg Ac is close to the number of base pairs for both calf thymus DNA and M. lysodeikticus DNA. Furthermore, it was shown that fluorescein Hg Ac binds to thymidine, deoxyguanosine, poly(U) and poly(G). Since fluorescence quenching of fluorescein Hg Ac accompanies its complex formation with DNA and the affinity is markedly high as indicated by the association constant of 6.8-10(7) M(-1) for single-stranded calf thymus DNA, fluorescein Hg Ac can be used for the structural studies of small amounts of nucleic acids.

Binding Sites↗

PubMed2000

A standardized visual scale for evaluation of tear fluorescein clearance.

OBJECTIVE: To evaluate the correlation and the agreement between a validated fluorometric technique (fluorescein clearance test) and a newly developed, clinically practical standardized visual scale to evaluate tear fluorescein clearance. Also, the ability of this new method to distinguish healthy persons from patients reporting ocular irritation associated with meibomian gland disease (MGD), aqueous tear deficiency (ATD), or both was tested. DESIGN: Case-controlled study. PARTICIPANTS: Healthy persons (n = 32), patients with MGD associated with rosacea (n = 30), patients with noninflammatory atrophic MGD (n = 24), and patients with ATD (n = 39) were evaluated. There was a similar age and gender distribution in each group. METHODS: Each subject completed a symptom questionnaire and had the following tests performed: fluorescein clearance test (FCT), standardized visual scale test (SVST), corneal fluorescein staining, Schirmer 1 test, corneal and conjunctiva sensitivity, and eyelid margin and meibomian gland examination. MAIN OUTCOME MEASURES: The FCT was performed with a CytoFluor II fluorophotometer by measuring the fluorescein concentration in minimally stimulated tear samples collected from the inferior tear meniscus 15 minutes after instillation of 5 microl of 2% sodium fluorescein. The SVST score, ranging from 0 to 6, was obtained by comparing the colors of the standardized visual scale with the color of the lateral inferior tear meniscus immediately before tear collection for the FCT. Severity of ocular irritation was assessed with a symptom questionnaire. Schirmer 1 test (without anesthesia), biomicroscopic meibomian gland evaluation, and corneal fluorescein staining were performed. Corneal and conjunctival sensitivity scores were assessed with the Cochet-Bonnet aesthesiometer. The correlation and the agreement between FCT, FCT corrected for Schirmer test (corrected FCT), SVST, and SVST corrected for Schirmer test (corrected SVST) in separating healthy persons from patients with ATD, MGD, or both were studied. Furthermore, the correlations of FCT, corrected FCT, SVST and corrected SVST, corneal fluorescein staining score, corneal and conjunctiva sensitivity, meibomian gland and eyelid evaluation, and questionnaire score were studied. RESULTS: The FCT, the corrected FCT, the SVST, and the corrected SVST all showed strong correlation with irritation symptoms, corneal fluorescein staining, Schirmer 1 test score, cornea and conjunctiva sensitivity, and meibomian gland and eyelid pathologic characteristics. The FCT, the corrected FCT, the SVST, and the corrected SVST had a sensitivity in diagnosing MGD, respectively, of 67%, 72%, 69%, and 76%, and of 95%, 97%, 97%, and 97% in diagnosing ATD. The specificity was, respectively, 97%, 96%, 97%, and 94%. CONCLUSIONS: The new standardized visual scale test was equivalent to fluorometric assessment of tear clearance in its correlation with irritation symptoms, ocular surface and eyelid disease, and ocular surface sensitivity. Its ability to separate healthy persons from patients with MGD and ATD was improved by applying a correction factor based on Schirmer test score. The new standardized visual scale test is an accurate and practical method for clinical assessment of fluorescein tear clearance.

Case-Control Studies↗

PubMed1976

Fluorescein angiography of degenerative lesions of the peripheral fundus and rhegmatogenous retinal detachment.

Since the number of cases for each of the conditions in our study was small, only preliminary conclusions can be made; in order to establish the fluorescein pattern of each of these peripheral retinal lesions, additional studies will be required. The following summarizes our preliminary observations. 1. Areas of retinal white-with-pressure or without and peripheral retinal cystoid degeneration did not reveal remarkable fluorescein angiographic findings. One exception was in an area of pigment epithelial disturbance characterized by atrophy and proliferation, which showed a "window and masking" effect of choroidal fluorescence. 2. Fluorescein angiography of areas of the fundus with lattice retinal degeneration showed little or no findings in early or mild cases. In severe or advanced cases, the affected retina revealed poor or absent perfusion caused by vascular occlusion. The retinal and choroidal circulation was devoid of fluorescein leakage. Advanced lesions displayed choroidal hypofluorescence in areas of pigment proliferation and hyperfluorescence in areas of pigment atrophy. 3. In advanced cases, occlusive vascular changes over areas of acquired retinoschisis were observed. There was intraretinal leakage of the dye from deep capillaries and pooling of the dye in cystic cavities near the margin of the retinoschisis. 4. There was no perfusion of the choroid and retina in the area of the hole and in the retina surrounding it. This finding suggests choroidal and retinal ischemia in the pathogenesis of a retinal hole. 5. Fluorescein angiography of retinal tears revealed fluorescein leakage along the edge of the tear and absent perfusion of the retinal flap. The retinal and choroidal circulation-around the tear was otherwise unremarkable. The choroidal fluorescein underlying the retinal flap was not visible, perhaps because it was masked by the retinal flap. 6. Our fluorescein angiographic findings in cases of rhegmatogenous retinal detachment confirmed those of others [7, 8, 10]. Transit of fluorescein through the retinal circulation was sluggish. The retinal capillaries were dilated. 7. In cases of rhegmatogenous retinal detachment which had become reattached surgically, areas treated with diathermy or cryoapplications showed absent or diminished choroidal and retinal perfusion. Leakage of the fluorescein from capillaries in the optic disc and retina in the posterior pole was sometimes persistent several months postoperatively.

Fluorescein Angiography↗