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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As the endothelial cells of the human cornea cannot perform mitosis, any metabolic alteration that destroys the cells should result into a decrease in cell density. This study was designed to demonstrate this phenomenon in diabetics as we know that diabetes alters endothelial cells, capillaries at least. On the assumption that capillary endothelium has the same mesodermal origin and almost the same metabolic function as the corneal endothelium, we tried to verify whether the corneal endothelium from diabetic subjects differs from non diabetic controls. As corneal endothelium can be studied in vivo by specular microscopy, it was interesting to verify whether this method could provide evidence of the conditions of the endothelial cells in the diabetic subject. Our study in specular microscopy involved 101 cases. We found slightly inferior values of the corneal endothelial cells density in diabetic subjects compared to the control subjects but no correlation between the values of endothelial cell density and the various parameters in diabetic patients: age, duration of diabetes, corneal thickness. This is correlated to other studies in which the morphology of endothelial cells differed between diabetic and non-diabetic subjects. We concluded that diabetes alters but does not significantly destroy the corneal endothelial cell. This result must be taken into account in corneal surgery as the diabetic cornea is a high risk cornea.
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PMID:[The corneal endothelium of diabetic patients. A study using specular microscopy]. 344 21

Diabetes mellitus, which affects millions of people all over the world, produces significant ocular morbidity. Corneal complications such as tear film dysfunction, elevated glucose in tears, different forms of epitheliopathy, neurotrophic ulcers, corneal edema, wrinkles in Descemet's membrane and decrease in corneal sensitivity have been reported. While a few reports described altered epithelial morphology as the possible basis for epithelial disease, all other clinical phenomena have been unexplained thus far. In this first-ever multifaceted approach to study the pathogenesis of diabetic keratopathy, striking abnormalities were observed in corneal nerves, corneal epithelium and corneal endothelium of diabetics. We have clearly demonstrated the existence of neuropathy in diabetic cornea, both in an animal model and in the humans, -- the first demonstration of such an abnormality. Our in vivo specular microscopic observations on epithelium confirmed in vitro observations in our study as well as of others while the analysis of endothelium provided the basis for the problems noticed in the diabetic cornea following intraocular surgical procedures. Our observations should help the clinician in the understanding of diabetic keratopathy and in developing better prophylactic and therapeutic strategy against some recalcitrant forms of corneal disease in this group of individuals.
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PMID:Dr. P. Siva Reddy Oration. Diabetic keratopathy. 350 67

There are few previous estimates of the size of the human lens epithelium. In this study the lens epithelium is measured by specular reflex photography with a macro camera. The results are corrected for cornea magnification. One hundred subjects were studied ranging in age from 11 to 75 and including 20 diabetics and 18 subjects with cataract. The results show a range of epithelial cell diameters from 8-21 microns with 97% of the measurements lying in the 9-17 microns range. Pleomorphism is marked. The mean cell size was 12.7 microns. Large differences exist in mean cell size between individuals, but no correlation was found with age, diabetes or cataract.
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PMID:An estimate of the human lens epithelial cell size in vivo. 365 80

Corneal sensitivity was tested in 145 cases of clear corneal transplants using Cochet-Bonnet aesthesiometer. The central area of corneal transplants was found to be either completely anesthetic or markedly hypesthetic even 32 years following corneal transplantation, as exemplified in a patient who had surgery for keratoconus. Age, preoperative diagnosis, contact lens wear, diabetes, or length of postoperative period had no correlation with sensitivity in corneal grafts. In cases with a preoperative diagnosis of failed graft, even the peripheral recipient cornea was found to be relatively hypesthetic. The observations from this study that the central area of corneal graft never recovers normal sensitivity may have significant implications on the epithelial cell integrity of corneal grafts.
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PMID:Recovery of corneal sensitivity in grafts following penetrating keratoplasty. 390 90

Acetylcholine (ACh), choline acetyltransferases and cholinesterases occur in cornea, iris-ciliary body complex and retina of several vertebrates. In cornea, ACh may serve as a sensory transmitter as well as a local hormone, the function of which is not delineated. The function of ACh as the parasympathetic neurotransmitter at the iris and ciliary body is well established. The muscarinic receptors on the iris smooth muscle are similar to the muscarinic receptors (M2 type in two way classification) at other smooth muscles towards their interaction with agonists and antagonists. Binding studies using radiolabeled antagonists and their displacement by agonists indicate that muscarinic receptors in membranes of iris-ciliary body complex are heterogeneous indicating more than one subtype of muscarinic receptors. A subtype other than M2 receptors may occur at the presynaptic sites of parasympathetic nerves, which have yet to be investigated using specific agonists and antagonists. Cholinergic markers, choline acetyltransferase and acetylcholinesterase, differ quantitatively and qualitatively in retinas of different species. However, amacrine cells are cholinergic in all vertebrate species. Although they make up 1% of retinal neurons, they influence the activity of a majority of ganglion cells. Cholinergic effects in ganglia are mediated through nicotinic and muscarinic receptors. Both of these types of cholinergic receptors are heterogeneous. They have yet to be investigated for their subtypes using specific agonists and antagonists. Although the role of cholinergic retinal neurons in the processing of visual information is not known, their input to ganglion cells generally increases the rate of spontaneous activity or the number of action potentials in light-evoked responses. Thus, the cholinergic input seems to modify the overall neuronal input to the ganglion cells from the receptive fields. Endothelial cells of blood vessels contain muscarinic receptors, which are activated by ACh to cause relaxation. Although retinal blood vessels provide recognizable characteristic signs in diabetes mellitus and hypertensive disease, no information is available on the muscarinic receptors of these vessels.
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PMID:Cholinergic systems and multiple cholinergic receptors in ocular tissues. 391 49

The corneal endothelium was photographed through a wide-field specular microscope in 38 eyes, in 20 successive diabetic outpatients receiving laser therapy because of underlying proliferative or background retinopathy. Areas of 100 individual endothelial cells from each central cornea were analysed using a digitizer. No statistically significant correlations were observed between mean cell areas or standard deviations of mean and total amount of previous laser energy received. Laser therapy or the type of diabetes did not seem to cause statistically significant changes in the endothelial cell areas examined.
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PMID:Corneal endothelium after photocoagulation in diabetic patients. 404 Nov 14

Tissues of the eye affected by diabetes are the lens, cornea, and retina. The lens becomes cataractous through osmotic swelling of its cortical fibers. Sorbitol, formed in the presence of aldose reductase, accumulates in the lens during hyperglycemia. Dulcitol similarly accumulates in the presence of galactosemia. Cataractogenesis in both cases can be prevented by inhibitors of aldose reductase. The efficacy of synthetic inhibitors differs in various tissues and species, but they react with aldose reductase at a common structural site. The most promising inhibitor is sorbinil . Diabetic retinopathy is similarly related to sorbitol accumulation and may be prevented or reversed by inhibition of aldose reductase. Healing of corneal wounds in diabetes is facilitated by enzyme inhibition. Retinal vasculopathy of diabetes is due to selective loss of the intramural pericytes that normally form structural elements in the retinal capillary walls. The vulnerability of these cells is due to their aldose reductase content. Whether inhibition of aldose reductase will prevent retinopathy is being tested in a randomized trial conducted by the National Eye Institute.
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PMID:NIH conference. Aldose reductase and complications of diabetes. 620 54

The morphologic status of corneal innervation was studied in rats with streptozocin-induced diabetes. Animals were killed at 1, 4, 16, and 36 weeks. Corneal innervation was studied by light and electron microscopy using nonspecific cholinesterase reaction, gold chloride impregnation, and plastic-embedded sections. Increased irregularity in the periodicity of nerve fiber beading was observed in diabetic corneas with gold impregnation. Ultrastructural evidence of irregularities in the basal lamina of Schwann cells was demonstrated in 16- and 36-week-old diabetic animals, along with occasional axonal degeneration. These alterations constitute a constellation of early pathologic manifestations in the innervation of diabetic cornea. To our knowledge, this study represents the first demonstration of neural changes in diabetic corneas as well as nerve fiber changes in an avascular tissue in diabetes.
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PMID:Corneal nerve alterations in diabetes mellitus. 623 81

The presence of the enzyme aldose reductase is increasingly being linked to diabetic complications. The distribution of this enzyme in human cornea, lens, retina, and optic nerve has been studied using specific antibodies against purified human placental aldose reductase raised in both rabbit and goat. The antisera from both animals gave equal, specific reactions. In frozen sections of ocular tissues, significant aldose reductase localization was reproducibly demonstrated in the endothelium and epithelium of the cornea and in the basal cell layers of the conjunctiva. In the lens, staining was observed in the epithelium and superficial lens fibers. In retinal sections, the presence of aldose reductase was demonstrated in the Mueller's cells, especially near the inner limiting membrane. It was also found in some ganglion and cone cells. In the optic nerve, positive staining was observed in the axon. All other cells of the tissues examined revealed only weak, nonspecific staining.
Diabetes 1984 Jun
PMID:Localization of aldose reductase in the human eye. 642 40

Forty-six corneas from 25 patients who had had type II (adult-onset) diabetes for more than ten years were examined by specular microscopy with quantitative morphometric analyses of individual endothelial cells. Thirty-four corneas from 21 age-matched nondiabetic subjects were examined for comparison. We also examined 31 corneas from 17 patients with type I (juvenile-onset) diabetes and compared them to 41 corneas from 23 age-matched normal volunteers. The corneal endothelium in type II diabetes showed no difference in cell density but demonstrated a significantly higher coefficient of variation, a decrease in the percentage of hexagonal cells, and a low figure coefficient compared to an age-matched nondiabetic population. Type I diabetes produced similar cell changes, but these changes occurred in the earlier decades. Moreover, we detected a significantly higher rate of cell loss in type I diabetes, resulting in a significant decrease in cell density in the fourth and fifth decades. These results clearly indicate that the diabetic endothelium is morphologically abnormal. The observed anatomic changes result in a less stable and more vulnerable cell layer, possibly explaining some of the persistent clinical changes in the diabetic cornea after surgical trauma.
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PMID:Corneal endothelial changes in type I and type II diabetes mellitus. 648 11


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