Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There has been recent interest in the progression of diabetic retinopathy following extracapsular cataract extraction (ECCE) especially with vitreous loss. It is well known that diabetic retinopathy progresses after intracapsular cataract extraction (ICCE) but was thought to be less common after ECCE. We present 7 patients with symmetrical non-proliferative diabetic retinopathy who underwent ECCE with intraocular lens (IOL) implantation. These patients ranged in age from 56 to 69 years; 2 were insulin-dependent diabetics (IDDM) and 5 non-IDDMs. Rubeosis iridis developed quickly between post-operative outpatient visits despite good diabetic control and a static retinal picture in the fellow eye. Visual loss following the onset of rubeosis was severe, with 3 patients needing cyclocryotherapy and eventually having no perception of light. The rapid onset of rubeosis between post-operative outpatient visits leads us to suggest much shorter periods between reviews than is current practice and the consideration of routine panretinal photocoagulation in the immediate post-operative period in diabetics with worsening retinopathy after ECCE and IOL. Possible causes of the increase in neovascularisation and rubeosis are discussed. The most important message highlighted by these case histories is that the surgery and follow-up of diabetic patients undergoing surgery should be undertaken by an ophthalmologist with an interest in diabetes. Where there is no recognised diabetic retinal specialist in a unit, then early referral to such an ophthalmologist is recommended when complications arise.
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PMID:Progression of diabetic retinopathy and rubeotic glaucoma following cataract surgery. 884 40

We investigated therapeutic effects of a rapid- and short-acting non-sulfonylurea hypoglycemic agent, calcium (2S)-2-benzyl-3-(cis-hexahydro-2-isoindolinylcarbonyl)propionate dihydrate (KAD-1229), on streptozotocin (STZ)-induced non-insulin-dependent diabetes mellitus (NIDDM) rats. The effects exerted by KAD-1229 on the post-prandial plasma glucose rise in STZ-induced mild NIDDM (mNIDDM) rats were different from those of sulfonylureas. When KAD-1229 with liquid meal (10 kcal/kg) was given to the mNIDDM rats, the plasma glucose migration was similar to that of normal healthy rats. On the contrary, glibenclamide had little or no effect on the plasma glucose rise 0.5-1 hr after oral administration, and its effect was only evident 2-5 hr after dosing. Tolbutamide showed similar hypoglycemia to that induced by glibenclamide at 2-5 hr with insufficient efficacy at 0.5 hr. Gliclazide sufficiently suppressed the level of post-prandial plasma glucose. However, its complete inhibition of post-prandial plasma glucose was associated with the extra-hypoglycemia 1-5 hr after oral administration. We also tested the efficacy of KAD-1229 in more severe STZ-induced NIDDM (sNIDDM) rats to elucidate the effects of the drug on the long-term glycemic controls and diabetic complications. When the sNIDDM rats were treated with 10 mg/kg KAD-1229 twice a day for about 17 weeks, increases in fasting plasma glucose and hemoglobin A1c were inhibited. Furthermore, treatment with KAD-1229 suppressed the development of microalbuminuria and cortical cataract. We conclude that the rapid- and short-acting insulinotropic agent KAD-1229 is able to improve the deterioration in the glycemic controls and inhibit the development of diabetic complications in STZ-induced NIDDM rats.
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PMID:A rapid- and short-acting hypoglycemic agent KAD-1229 improves post-prandial hyperglycemia and diabetic complications in streptozotocin-induced non-insulin-dependent diabetes mellitus rats. 888 29

Human and other mammalian lens proteins are composed of three major crystallins: alpha-, beta-, and gamma-crystallin. alpha-Crystallin plays a prominent role in the supramolecular assembly required to maintain lens transparency. With age, the crystallins, especially alpha-crystallin, undergo posttranslational modifications that may disrupt the supramolecular assembly, and the lens becomes susceptible to other stresses resulting in cataract formation. Because these modifications occur even at a relatively young age, it is difficult to obtain pure, unmodified crystallins for in vitro experiments. alpha-Crystallin is composed of two subunits, alphaA and alphaB. Before the application of recombinant DNA technology, these two alpha-crystallin subunits were separated from calf lens in the denatured state and reconstituted by the removal of the denaturant, but they were not refolded properly. In the present studies, we applied the recombinant DNA technology to prepare native, unmodified alphaA- and alphaB-crystallins for conformational and functional studies. The expressed proteins from Escherichia coli are in the native state and can be studied directly. First, alphaA and alphaB cDNAs were isolated from a human lens epithelial cell cDNA library. The cDNAs were cloned into a pAED4 expression vector and then expressed in E. coli strain BL21(DE3). Pure recombinant alphaA- and alphaB-crystallins were obtained after purification by gel filtration and DEAE liquid chromatography. They were subjected to conformational studies involving various spectroscopic measurements and an assessment of chaperone-like activity. alphaA- and alphaB-crystallins have not only different secondary structure, but also tertiary structure. 1-Anilino-8-naphthalene sulfonate fluorescence indicates that alphaB-crystallin is more hydrophobic than alphaA-crystallin. The chaperone-like activity, as measured by the ability to protect insulin aggregation, is about 4 times greater for alphaB- than for alphaA-crystallin. The resulting data provide a base line for further studies of human lens alpha-crystallin.
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PMID:Conformational and functional differences between recombinant human lens alphaA- and alphaB-crystallin. 904 37

This case report concerns a 14-year-old female patient, whose insulin-dependent diabetes mellitus was displayed by one infrequent complication, the cataract. This is an unusual manifestation in a 14-year-old patient; indeed, there are many findings in experimental animals demonstrating the development of this complication by maintaining blood glucose levels above 12 mM. After surgical therapy, complete vision was recovered, but we think that an earlier diagnosis and therapy of metabolic derangement of diabetes may have avoided this complication.
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PMID:The diabetic cataract: an unusual presentation in a young subject: case report. 920 5

Mouse lens cultures were employed to study the progression of cataracts initiated by injection of buthionine sulfoximine, an inhibitor of glutathione (GSH) biosynthesis. Culture of lenses removed from untreated mice on postnatal day 7, for 48 hr in the presence of 4 mm BSO, resulted in only limited cataractous changes. To enable substantial progression of cataracts in vitro, it was therefore necessary to pretreat the mice with BSO prior to lens culture. A single injection of BSO (4 nmol mg-1 lens), administered on day 7, resulted in >90% depletion of lens GSH within 3 days, but no visible cataractous changes. The clear lenses were incubated for 29+/-1 hr at 37 degrees C in Medium HL-1, supplemented with EGF, insulin and Ca2+, in the presence or absence of BSO, and were scored for cataract development by previously described criteria. In the absence of BSO, only 4 of 10 lenses developed large opacities. However, in the presence of 4 mm BSO, 40 out of 45 experimental lenses developed opacities affecting at least 50% of the lens visual field and were scored as stages 1C-4, depending upon the extent and density of the cataracts. In addition, three lenses had opacities involving 20-50% of the field (stage 1B). By contrast, less than 10% of lenses from untreated mice incubated in the absence of BSO developed opacities. The cataracts developed in 4 mm BSO were accompanied by reduction of lens glutathione levels to <0.010 nmol mg-1 lens. They were almost completely prevented by 1 mm ascorbate, 2 mm GSH, 2 mm GSH monoethyl ester and 2 mm cysteamine. GSH and GSH ester maintained lens glutathione content between 0.1 and 0.2 nmol mg-1 in the presence of BSO, whereas ascorbate did not prevent near-total GSH depletion. The prevention of cataracts by thiols and ascorbate was confirmed by lens Na/K ratios not significantly different from those in control lenses. The above combination of GSH depletion in vivo by a single injection of BSO, followed 3 days later with lens culture in the presence of BSO, may yield a useful system to elucidate and control the biochemical mechanisms involved in oxidative cataract induction by this GSH-depleting agent.
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PMID:Progression of mouse buthionine sulfoximine cataracts in vitro is inhibited by thiols or ascorbate. 929 71

FK506 (tacrolimus), a potent immunosuppressant, is used for inhibiting allograft rejection in the organ transplantation field. In a preclinical toxicity study in rats, FK506 induced various toxicities, including renal and pancreatic injuries. One of these toxic findings was cataract, and we have found that cataract appeared in rats dosed orally with FK506 for 13 weeks and more. Therefore, to better elucidate the onset mechanism of FK506-induced cataract, we measured biochemical parameters, such as sorbitol, Na,K-ATPase and glutathione in the lens of rats. Rats were dosed with FK506 in oral daily doses of 0.2, 1 or 5 mg/kg for 13 weeks, the lowest dose of which approximated the expected clinical dosage. Cataract developed in the 5-mg/kg/day group, with an incidence of 25%, whereas no cataract formation was observed in the 0.2- or 1-mg/kg/day groups. Five mg/kg/day led an increase of sorbitol and a decrease of reduced type glutathione, but did not affect Na,K-ATPase activity of the lens. FK506 is known to have diabetogenicity mediated through pancreatic injury, which appears as vacuolation of islet cell in rats. Five mg/kg/day of FK506 induced an elevation of blood glucose associated with glucose intolerance, and decrease of both basal insulin level and insulin content in the pancreas, and the changes were in parallel with the cataract development in the present study. On the other hand, diabetic parameters did not change in the 0.2- or 1-mg/kg/day groups. These observation suggest that diabetes developed in the rats dosed with 5 mg/kg/day of FK506. Coadministration of a novel aldose reductase inhibitor, Zenarestat, at an oral dose of 50 mg/kg/day resulted in a reduction of incidence of the FK506-induced cataract and a decrease of sorbitol levels in the lens when compared to that in the lens of rats dosed with 5 mg/kg/day of FK506. These results suggest that FK506-induced cataract in rats is due to an accumulation of sorbitol in the lens, secondary to the diabetogenic effect of FK506. FK506 treatment at the doses of 0.2 and 1 mg/kg/day neither affected parameters indicative of diabetes nor induced cataract in rats, suggesting that the cataract would not develop with FK506 if diabetic parameters were kept under control.
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PMID:Cataract development induced by repeated oral dosing with FK506 (tacrolimus) in adult rats. 935 35

We describe a Thai family with three children, two of whom presented with Wolfram syndrome, which is a rare syndrome characterised by diabetes insipidus, diabetes mellitus, optic atrophy, deafness and urinary tract dilatation. A girl and her younger brother had insulin-dependent diabetes mellitus at 11 years old with early onset of renal impairment, proteinuria and hypertension. Urinary tract dilatation was demonstrated in both patients. Kidney biopsies were compatible with diabetic nephropathy. Both children also had bilateral sensorineural hearing loss. Optic atrophy with severe loss of vision was detected in the girl and bilateral cataract in her brother. Both patients were HLA DR2 positive. At 16 years old, her creatinine clearance was 16 ml/min/1.73 m2. Her brother's creatinine clearance was 25 ml/min/1.73 m2 at 13 years old. We conclude that renal function should be evaluated in patients with Wolfram syndrome and the cause of renal failure in these patients may be rapid and severe diabetic nephropathy.
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PMID:Renal failure in two patients with Wolfram syndrome. 946 37

A prospective study of the effect of cataract extraction with intraocular lens implantation on the course of diabetic retinopathy (DR) in 44 patients (59 eyes) was carried out. It showed that in the 1-3 years following surgery, there was progression of DR (including development of newly formed retinopathy) in 35% of the patients (28.8% of eyes). Progression was more marked in patients with pre-operative bilateral DR compared to those without bilateral DR (77% and 16% respectively). Insulin dependence did not play a role in progression. Final visual acuity was better in patients without pre-operative DR, as well as in eyes without progressive retinopathy.
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PMID:[Progression of diabetic retinopathy after cataract extraction]. 951 69

Postural stability in 55 non-insulin dependent diabetics was compared with 53 non-diabetic controls matched for age and gender. The study was conducted in a primary care clinic, using a computerised postural sway system. Changes in the centre of pressure while the subjects stood on a force platform were recorded, and sway parameters computed using customised software. Clinical data were obtained by interview, physical examination, and from case records. Results of the study showed that non-insulin dependent diabetics were more unstable than the non-diabetic controls for four out of the six parameters studied (namely L, length of sway path; Vel, average speed of centre of pressure along its path; Ao, area included within the path of the centre of pressure; and Ae, 95% confidence elliptical area), after adjusting for height, weight, adequate sleep and alcohol intake the night before, and history of bone or thyroid disorders. Amongst diabetic subjects, significant factors associated with postural stability were age, weight, presence of peripheral neuropathy or cataract, metformin, use, and HbAlc levels > 9%. Further studies are indicated to look into factors affecting postural stability (other than diabetic neuropathy) in greater depth.
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PMID:Postural stability in non-insulin dependent diabetics. 952 70

Investigations on the specific idiotypes of autoantibodies are supposed to help with the understanding of the control mechanisms participating in the pathogenesis of autoimmune diseases. This study describes three monoclonal antibodies (Mabs) that recognize distinct idiotypic determinants on anti-insulin autoantibodies. The preabsorption by IAA-positive sera of insulin inhibits their subsequent binding to the anti-Id, thus suggesting that the Mabs recognize epitopes located at or near the binding site of insulin autoantibodies (IAA). These idiotypes are detected in sera from patients with insulin-dependent diabetes mellitus (IDDM), which are IAA-negative, also. It is possible that the expression of the idiotypes recognized might generally be associated with induction of autoantibodies, since they were found in sera from patients with rheumatoid arthritis (RA), autoimmune thyroid disease (AITD), and cataract (K). It can be assumed that the corresponding idiotypes of these Mabs, or similar structures (sequential or conformational), are expressed on autoantibodies with various antigen-binding specificities. These data suggest that some autoimmune diseases are preceded by the secretion of autoantibodies which express a common or similar pathological idiotype.
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PMID:Cross-reacting idiotypes on anti-insulin autoantibodies in autoimmune diseases, identified by monoclonal antibodies. 961 27


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