Hypoxia, color vision deficiencies, and blood oxygen saturation.

Chromatic thresholds were measured using the Cambridge Colour Test (CCT), the Colour Assessment and Diagnosis (CAD) test, and the Cone Specific Contrast Test (CSCT) at ground and 3780 m (12,400 ft) for subjects with normal color vision and red-green color vision defects. The CAD revealed a small (~10%) increase in the red-green thresholds for the trichromatic subjects and a similar increase in the blue-yellow thresholds for the dichromats. The other two color vision tests did not reveal any significant change in chromatic thresholds. The CAD results for the trichromats were consistent with a rotation of the discrimination ellipse counterclockwise with little change in the elliptical area. This alteration in the color discrimination ellipse can occur when retinal illumination is lowered.

Do type 2 diabetes patients without diabetic retinopathy or subjects with impaired fasting glucose have impaired colour vision? The Okubo Color Study Report.

AIMS: To investigate associations between fasting plasma glucose level and the prevalence of acquired colour vision impairment in type 2 diabetes patients without diabetic retinopathy. METHODS: Participants in this cross-sectional study of male officials aged 20-60 yr in the Japanese Self Defence Force, underwent colour vision testing, ophthalmic examination, a standardized interview and examination of venous blood samples. Ishihara plates, a Lanthony 15-hue desaturated panel and Standard Pseudoisochromatic Plates Part 2 were used to examine colour vision. The Farnsworth-Munsell 100-hue test was performed to define acquired colour vision impairment. Cardiovascular disease risk factors were determined from serum blood samples, physical records and an interview. We performed logistic regression analysis adjusted for age, diagnosed hypertension, dyslipidaemia, cataract, glaucoma, being overweight, smoking status and alcohol intake. Crude and adjusted odds ratios were calculated for three glucose levels, which included normal fasting glucose, impaired fasting glucose and diabetes. RESULTS: Out of a total of 1042 men enrolled, 872 were eligible for the study, and 31 were diagnosed with acquired colour vision impairment. As compared with the subjects with normal fasting glucose (< 5.6 mmol/l), the crude odds ratio for acquired colour vision impairment was 0.93 (95% CI 0.32-2.74) for the subjects with impaired fasting glucose (5.6-6.9 mmol/l) and 8.07 (95% CI 2.48-26.22) for the patients with type 2 diabetes. The multiple-adjusted odds ratios were 0.77 (95% CI 0.25-2.34) for the subjects with impaired fasting glucose and 5.89 (95% CI 1.55-22.40) for the patients with type 2 diabetes. CONCLUSIONS: Our findings suggest that there is a dramatically increased prevalence of acquired colour vision impairment in type 2 diabetes patients without diabetic retinopathy which might be attributable to another pathogenesis associated with diabetic retinopathy.

Serum low-density lipoprotein cholesterol level is strong risk factor for acquired color vision impairment in young to middle-aged Japanese men: the Okubo Color Study Report 2.

OBJECTIVE: To investigate associations between blood low-density lipoprotein cholesterol (LDL-C) levels and the prevalence of acquired color vision impairment (ACVI) in middle-aged Japanese men. METHODS: Participants in this cross-sectional study underwent color vision testing, ophthalmic examination, a standardized interview and examination of venous blood samples. Ishihara plates, a Lanthony 15-hue desaturated panel, and Standard pseudoisochromatic Plates part 2 were used to examine color vision ability. The Farnsworth-Munsell 100-hue test was performed to define ACVI. Smoking status and alcohol intake were recorded during the interview. We performed logistic regression analysis adjusted for age, LDL-C level, systemic hypertension, diabetes, cataract, glaucoma, overweight, smoking status, and alcohol intake. Adjusted odds ratios for four LDL-C levels were calculated. RESULTS: A total of 1042 men were enrolled, 872 participants were eligible for the study, and 31 subjects were diagnosed with ACVI. As compared to the lowest LDL-C category level (<100 mg/dl), the crude OR of ACVI was 3.85 (95% confidence interval [CI], 1.24-11.00) for the 2nd highest category (130-159 mg/dl), and 4.84 (95% CI, 1.42-16.43) for the highest level (>or=160 mg/dl). The multiple-adjusted ORs were 2.91 (95% CI, 0.87-9.70) for the 2nd highest category and 3.81 (95% CI, 1.03-14.05) for the highest level. Tests for trend were significant (P<0.05) in both analyses. CONCLUSIONS: These findings suggested that the prevalence of ACVI is higher among middle-aged Japanese men with elevated LDL-C levels. These changes might be related to deteriorated neurologic function associated with lipid metabolite abnormalities.

Associations between platelet monoamine oxidase-B activity and acquired colour vision loss in a fish-eating population.

Platelet monoamine oxidase-B (MAO-B) has been considered a surrogate biochemical marker of neurotoxicity, as it may reflect changes in the monoaminergic system in the brain. Colour vision discrimination, in part a dopamine dependent process, has been used to identify early neurological effects of some environmental and industrial neurotoxicants. The objective of this cross-sectional study was to explore the relationship between platelet MAO-B activity and acquired colour discrimination capacity in fish-consumers from the St. Lawrence River region of Canada. Assessment of acquired dyschromatopsia was determined using the Lanthony D-15 desaturated panel test. Participants classified with dyschromatopsia (n=81) had significantly lower MAO-B activity when compared to those with normal colour vision (n=32) (26.5+/-9.6 versus 31.0+/-9.9 nmol/min/20 microg, P=0.030)). Similarly, Bowman's Colour Confusion Index (CCI) was inversely correlated with MAO-B activity when the vision test was performed with the worst eye only (r=-0.245, P=0.009), the best eye only (r=-0.188, P=0.048) and with both eyes together (r=-0.309, P=0.001). Associations remained significant after adjustment for age and gender when both eyes (P=0.003) and the worst eye (P=0.045) were tested. Adjustment for heavy smoking weakened the association between MAO-B and CCI in the worst eye (P=0.140), but did not alter this association for both eyes (P=0.006). Adjustment for blood-mercury concentrations did not change the association. This study suggests a relationship between reduced MAO-B activity and acquired colour vision loss and both are associated with tobacco smoking. Therefore, results show that platelet MAO-B may be used as a surrogate biochemical marker of acquired colour vision loss.

Acquired colour vision deficiency in patients receiving digoxin maintenance therapy.

BACKGROUND/AIMS: Disturbances of colour vision are a frequently reported sign of digoxin toxicity. The aim of this study was to investigate the incidence of acquired colour vision deficiency in elderly hospitalised patients receiving maintenance digoxin therapy. METHODS: 30 patients (mean age 81.3 (SD 6.1) years) receiving digoxin were tested using a battery of colour vision tests (Ishihara, AO Hardy Rand Rittler plates, City tritan test, Lanthony tritan album, and the Farnsworth D15). These were compared to an age matched control group. Serum digoxin concentrations were determined from venous blood samples. RESULTS: Slight to moderate red-green impairment was found in approximately 20-30% of patients taking digitalis, and approximately 20% showed a severe tritan deficiency. There was no correlation between colour vision impairment and serum digoxin level. CONCLUSIONS: Formal colour vision testing of elderly patients taking digitalis showed a high incidence of colour deficiency, suggesting that impairment of retinal function can occur even at therapeutic drug levels. As a result, colour vision testing in this population would have limited value for the detection of drug toxicity.

Melatonin regulation in humans with color vision deficiencies.

Light can induce an acute suppression and/or circadian phase shift of plasma melatonin levels in subjects with normal color vision. It is not known whether this photic suppression requires an integrated response from all photoreceptors or from a specialized subset of photoreceptors. To determine whether normal cone photoreceptor systems are necessary for light-induced melatonin suppression, we tested whether color vision-dificient human subjects experience light-induced melatonin suppression. In 1 study, 14 red-green color vision-deficient subjects and 7 normal controls were exposed to a 90-min, 200-lux, white light stimulus from 0200-0330 h. Melatonin suppression was observed in the controls (t = -7.04; P < 0.001), all color vision-deficient subjects (t = -4.76; P < 0.001), protanopic observers (t = -6.23; P < 0.005), and deuteranopic observers (t = -3.48; P < 0.05), with no significant difference in the magnitude of suppression between groups. In a second study, 6 red/green color vision-deficient males and 6 controls were exposed to a broad band green light stimulus (120 nm with lambda max 507 nm; mean +/- SEM, 305 +/- 10 lux) or darkness from 0030-0100 h. Hourly melatonin profiles (2000-1000 h) were not significantly different in onset, offset, or duration between the two groups. Melatonin suppression was also observed after exposure to the green light source at 0100 h (color vision deficient: t = -2.3; df = 5; P < 0.05; controls: t = -3.61; df = 5; P < 0.01) and 0115 h (color vision deficient: t = -2.74; df = 5; P < 0.05; controls: t = -3.57; df = 5; P < 0.01). These findings suggest that a normal trichromatic visual system is not necessary for light-mediated neuroendocrine regulation.

Genotype-phenotype relationships in human red/green color-vision defects: molecular and psychophysical studies.

The relationship between the molecular structure of the X-linked red and green visual pigment genes and color-vision phenotype as ascertained by anomaloscopy was studied in 64 color-defective males. The great majority of red-green defects were associated with either the deletion of the green-pigment gene or the formation of 5' red-green hybrid genes or 5' green-red hybrid genes. A rapid PCR-based method allowed detection of hybrid genes, including those undetectable by Southern blot analysis, as well as more precise localization of the fusion points in hybrid genes. Protan color-vision defects appeared always associated with 5' red-green hybrid genes. Carriers of single red-green hybrid genes with fusion in introns 1-4 were protanopes. However, carriers of hybrid genes with red-green fusions in introns 2, 3, or 4 in the presence of additional normal green genes manifested as either protanopes or protanomalous trichromats, with the majority being protanomalous. Deutan defects were associated with green-pigment gene deletions, with 5' green-red hybrid genes, or, rarely, with 5' green-red-green hybrid genes. Complete green-pigment gene deletions or green-red fusions in intron 1 were usually associated with deuteranopia, although we unexpectedly found three carriers of a single red-pigment gene without any green-pigment genes to be deuteranomalous trichromats. All but one of the other deuteranomalous subjects had green-red hybrid genes with intron 1, 2, 3, or 4 fusions, as well as several normal green-pigment genes. The one exception had a grossly normal gene array, presumably with a more subtle mutation. Amino acid differences in exon 5 largely determine whether a hybrid gene will be more redlike or more greenlike in phenotype. Various discrepancies as to severity (dichromacy or trichromacy) remain unexplained but may arise because of variability of expression, postreceptoral variation, or both. When phenotypic color-vision defects exist, the kind of defect (protan or deutan) can be predicted by molecular analysis. Red-green hybrid genes are probably always associated with protan color-vision defects, while the presence of green-red hybrid genes may not always manifest phenotypically with color-vision defects. Four subjects who were found to have 5' green-red hybrid genes in addition to normal red- and green-pigment genes had normal color vision as determined by anomaloscopy. These were discovered among a group of 129 Caucasian males who had been recruited as volunteers for a vision study.(ABSTRACT TRUNCATED AT 400 WORDS)

Ocular adverse effects to the therapeutic administration of digoxin.

Disturbances in colour vision are a well-reported adverse ocular effect to toxic levels of digoxin. We present a case history of a patient with both colour vision changes and transient visual field defects to therapeutic serum levels of digoxin.

Abnormal color vision and reliable self-monitoring of blood glucose.

Color vision was assessed in 103 insulin-dependent diabetic patients using the Farnsworth-Münsell 100-Hue Test. All showed color vision impairment. Thirty-four had true dyschromatopsia while 22 suffered from tritanopia or other axial defects. We evaluated how accurately diabetic patients could monitor their own blood glucose by asking them to read a series of 30 precalibrated BM Test Glycemic Strips (Chemstrip, Boehringer, Mannheim, West Germany) without a meter. Patients with axial defects performed least well regardless of 100-Hue scores. Reading accuracy of patients with no axial defects was strongly correlated to 100-Hue scores, although patients having dyschromatopsia were consistently hesitant about their readings. Our results suggest that self-monitoring of blood glucose without a meter is indicated only after color vision has been examined by the 100-Hue Test. Self-monitoring should be voided with patients suffering from axial defects or having unsatisfactory 100-Hue scores.

Whole blood cyanide levels in patients with tobacco amblyopia.

Three patients presented with painless bilateral visual failure due to tobacco amblyopia. The whole blood cyanide levels were raised above those predicted from their high tobacco consumption, approaching lethal levels reported from acute inhalation of cyanide. Each patient had an excessive alcohol intake with biochemical evidence of hepatic dysfunction, the elevated whole blood cyanide levels being attributed to the associated impairment of cyanide detoxification. In each case the improvement in visual acuities following abstinence and hydroxycobalamin therapy was accompanied by a reduction in the whole blood cyanide level to within the normal range. Serial measurements of whole blood cyanide, serum alcohol, and the detection of urinary nicotine provided valuable indices of the patient's subsequent compliance and clinical progress.

Reversible colour vision defects in obstructive jaundice.

The ocular function of 14 non-alcoholic, high icteric patients with recent occlusion of the common bile duct and 3 patients with viral hepatitis with a cholestatic pattern was studied. By means of a colour vision test panel including the Farnsworth-Munsell 100-hue test, 12 patients were initially classified as colour defective with a pattern of acquired colour vision deficiency (ACVD), predominantly of a tritan type. Visual acuity, visual field, slit lamp microscopy, intraocular pressure, ophthalmoscopy and tear secretion tests were normal, and all patients had normal levels of serum vitamin A. Retesting of 4 initially colour defective patients after disappearance of the obstructive jaundice showed a complete normalisation of the ACVD's. It is concluded, that the colour perception in patients with obstructive jaundice is related to the serum bilirubin level, and not to a deficiency of vitamin A.

The use of colour vision measurement in the diagnosis of digoxin toxicity.

Colour vision has been measured, using the Farnsworth-Munsell 100-Hue test, in control subjects and in patients taking digoxin. In 10 patients with digitalis toxicity, of whom only two described symptomatic abnormalities, colour vision was impaired compared with that of both control subjects and non-toxic patients who had been taking digoxin for more than two months. Withdrawal of digoxin from toxic patients led to improved colour vision. Colour vision scores correlated well with (a) log plasma digoxin concentrations, and (b) various measures of the pharmacodynamic effects of cardiac glycosides on cation transport in the patients' own erythrocytes. These results suggest that colour vision assessment may be of use in screening for digitalis toxicity at the bedside and in assessing the degree of digitalis intoxication in an individual patient as an aid to clinical research.

Radioligand assay in reproductive biology.

Radioligand assays have been developed for the principal reproductive steroids and peptide hormones. Specific binding reagents have included antibodies, plasma binders, and intracellular receptors. In each assay, problems of specificity, sensitivity, and nonspecific inhibitors were encountered. Many features of the endocrine physiology in childhood, during puberty, and in adulthood have been characterized. Hormonal evaluations of endocrine disorders of reproduction are characterized on the basis of their characteristic pathophysiologic alterations.