Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year-old woman has been suffering from recurrent corneal edema without ocular hypertension since her early childhood. When the cornea is clear, visual acuity-with correction for high myopia-is 5/10 to 5/15 and Nieden I; when the cornea is swollen, it decrease to 5/50 and 1/10, respectively, and Nieden VII. Furthermore, there is an atypical pigment degeneration of the retina combined with deafness, a progressive ptosis since her 10th year of life, and a progressive dystrophy of the outer eye muscles, having developed in the past few years. In addition, the mentally normal developed patient presents a proportional dwarfism (no dysostosis) and a diabetes mellitus. This combination of symptoms is compared with the well known Bardet-Biedl syndrome and the De Grouchy syndrome and is found to constitute a new syndrome.
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PMID:[Recurrent corneal edema without ocular hypertension, pigment degeneration combined with deafness, progressive dystrophy of the outer eye-muscles in a patient with proportional dwarfism and diabetes mellitus (author's transl)]. 30 14

Ocular involvement in Yersinia enterocolitica infection presenting as a Parinaud's oculoglandular syndrome occurred in a 77-year-old woman with diabetes. Yersinia enterocolitica was recovered from cultures of the conjunctiva, cornea, fistula tract, and blood. The patient responded to parenteral and topical administration of gentamicin and a corneal transplant. While hospitalized, she developed peritonsillar inflammation and enlarged, tender lymph nodes in the preauricular, submaxillary, and submandibular areas. The combination of the unilateral granulomatous conjunctivitis and enlarged regional lymph nodes was consistent with the diagnosis of Parinaud's oculoglandular syndrome. Yersinia enterocolitica may be another cause of Parinaud's oculoglandular syndrome.
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PMID:Ocular involvement in Yersinia enterocolitica infection presenting as Parinaud's oculoglandular syndrome. 83 62

A 45-year-old woman with juvenile-onset diabetes had persistent corneal edema after a pars plana vitrectomy and lensectomy procedure. Phase contrast and electron microscopic observation of the patient's cornea revealed extreme attenuation of the endothelial cell layer and abnormal collagenous and basement membrane material interposed between Descemet's membrane and the endothelium. Endothelial fibrous proliferations in this case were consistent with the development of ultrastructurally identical fibrous proliferations in many other situations involving dysfunction of the corneal endothelium.
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PMID:Corneal endothelial degeneration and fibrous proliferation after plana vitrectomy. 126 29

High L-ascorbic acid (AA) levels in aqueous humor and intraocular tissues including lens and cornea are thought to protect against the harmful effects of the photochemical and ambient oxidation reactions involving oxygen and its radicals. Our pulse-chase studies follow a bolus of radiolabeled test molecules including [14C]L-ascorbic acid and [3H]L-glucose (L-glu) introduced into the blood at time t = 0, and determine the time-dependent concentrations of these labeled molecules as they move into aqueous humor, corneal endothelium and stroma tissues. Calculated entry and exit rate constants provide a representative measure of the functional state of passive and carrier mediated transport mechanisms in situ in normal and diabetic animals. Diabetic rats were categorized in terms of length of time exposed to a uniform, monitored streptozotocin (stz) diabetes as: short term (10-20 days); mid-term (40-60 days); and long term (100+ days). In the rat, we observed little change in entry rate of L-glu (a passive marker) into aqueous humor [control Ki = 0.0216 +/- 0.0021 (n = 14)/mid-term stz-diabetes Ki = 0.0202 +/- 0.0027 (n = 10)] and a modest decrease in the entry rate of AA into aqueous humor [control KAi = 0.0231 +/- 0.0022 (n = 14)/mid-term stz-diabetes KAi = 0.0201 +/- 0.0034 (n = 10)]. At corneal endothelium, we noted a significant decrease in the active movement of AA [control KE = 0.614 +/- 0.053 (n = 14)/mid-term stz-diabetes KE = 0.220 +/- 0.026 (n = 9)] while the passive L-glu entry rate remained essentially unchanged.+
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PMID:Decreased ascorbic acid entry into cornea of streptozotocin-diabetic rats and guinea-pigs. 142 66

The cornea was thought to be not for a long time saved from the havoc of the diabetes. Last time a series of authors talk about a diabetic keratopathy. For the beginning the cornea endothelium was involved (changes of density and form of the cells) and last time the cornea epithelium was involved, some authors making a correlation between the diabetic neuropathy and keratopathy that consider a special entity, the diabetic keratopathy. We kept under the observation a group of diabetic patients who were hospitalized at our clinic of ambulatory examined for various complications of diabetes, in order to discover if it exist a relationship between the two affection, neuropathy and keratopathy. The number of the diabetic neuropathies is more less (13.3%) than that of the diabetic retinopathies or nephropathies. The keratopathies were observed for 6.6% (much inferior to other statistics). Half of the cases of keratopathies have presented either symptom of neuropathies or any other neurological charge; though for the first time it could be done the relationship between the two affections, the examination of the patients often pleads for coincidences; it's why we wonder if it really exist a diabetic keratopathy or a keratopathy at the diabetic patient.
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PMID:[Does diabetic keratitis exist?]. 152 43

In vivo measurement of metabolic changes in diabetic cornea and lens were performed using redox fluorometry in nonobese diabetic (NOD) mice. Autofluorescence from reduced pyridine nucleotides (PN) and oxidized flavoproteins (Fp) were measured, and the PN/Fp ratio was used as a tissue metabolism indicator. The PN/Fp ratios were significantly higher in the diabetic corneal endothelium. Morphometric analysis of the corneal endothelium using specular microscopy revealed no significant differences between the two groups. These results indicate that redox fluorometry is able to detect early metabolic changes in the corneal endothelium and lens epithelium, which are induced by diabetes mellitus. Activation of the polyol pathway may be responsible for the change. Corneal epithelia may be less susceptible to diabetic changes than the corneal endothelium and lens epithelium.
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PMID:[Noninvasive metabolic analysis of the diabetic cornea and lens: in vivo measurement]. 155 9

The scope of ocular fluorometry is to monitor exogenous and endogenous fluorophores in ocular tissues, in relation with ophthalmic and systemic diseases using the unique optical prospectives of the eye. The elderly population and the incidence of blindness are increasing rapidly due to more cases of diabetes, glaucoma, cataract and age-related macular degeneration. Monitoring changes in specific fluorophores in the eye may help identify the high risk groups in these diseases. New developments in instrumentation include differential fluorometry and introduction of confocal optics. Differential fluorometry has already achieved significant progress for the study of the autofluorescence of the lens and cornea and measurements in the aqueous. Improved spatial resolution obtained with improved optics opens interesting possibilities like measurement of corneal endothelial permeability and retinal vascular permeability. The results already obtained will be presented with particular incidence on measurements of lens fluorescence (normals--336.2 +/- 56.3; diabetes--659.9 +/- 123.9; age group--40-50 y) and corneal endothelial permeability (normals--3.14 +/- 60.10(-1) cm-1).
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PMID:[Future developments in ocular fluorophotometry instrumentation]. 157 Jul 48

A method is described for the separate quantitation of fluorescein and fluorescein glucuronide in the vitreous by differential spectrofluorometry. An ocular fluorometer was equipped with monochromatic laser excitation at two rapidly interchangeable wavelengths. The data analysis accounts for absorption of light in the cornea, lens, and extrinsic ocular fluorophores. Examination of seven patients with insulin-dependent diabetes and different degrees of diabetic retinopathy demonstrated that both fluorescein and fluorescein glucuronide enter the eye through the blood-retina barrier. The mean ratio between the permeabilities of fluorescein glucuronide and fluorescein was 0.9 (range, 0.3-1.9). Thus, differences in the molecular size and lipid solubility of the two substances appear to be of little or no importance for their inward penetration of the barrier. No association was found between the relative permeability and the degree of retinopathy.
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PMID:Differential spectrofluorometry in the human vitreous: blood-retina barrier permeability to fluorescein and fluorescein glucuronide. 191 23

Disorders of lipid metabolism, either hyperlipidemia or hypolipidemia, are associated with the formation of corneal opacities. Corneal arcus, the most commonly encountered peripheral corneal opacity, is frequently associated with abnormal serum lipid levels, but may occur without any predisposing factors. Reports also have linked corneal arcus with alcoholism, diabetes mellitus and atherosclerotic heart disease. Unilateral arcus is a rare entity that is associated with carotid artery disease or ocular hypotony. Diffuse corneal opacities associated with hypolipidemic disorders such as LCAT deficiency, fish eye disease and Tangier disease, may be the initial manifestation of these disorders and puts the ophthalmologist in a position to make an early diagnosis. Corneal arcus, along with a central corneal opacity, is seen in Schnyder's crystalline stromal distrophy. The association of the disorder with a dyslipidemia remains controversial. A review of lipid metabolism, corneal arcus and several disorders of lipid metabolism that affect the cornea are presented.
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PMID:The cornea and disorders of lipid metabolism. 192 41

We report six eyes in six patients in which corneal decompensation developed 18 or more months after argon laser iridectomy (ALI). In addition to the level of laser energy used, other risk factors included performing ALI during an attack, diabetes, and a cornea damaged by glaucomatous attack. The interval between the ALI and corneal decompensation ranged from 18 months to 3 1/2 years.
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PMID:Corneal decompensation after argon laser iridectomy--a delayed complication. 196 12


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